Questions and videos are attached
Watch the video (
https://screencast-o-matic.com/watch/creXn0VcTJe
)
For each case, try to identify the diagnosis. Support your answer by summarizing the key information from the video [symptoms, observations, or other information]. If you are unsure between more than one disorder, include what you would need to know to confirm [tests or questions you could ask].
[it could be any disorder from all chapters covered so far] book is attached and look at chapters 5-7
I am expecting at least 3 observations/points of support and at least 1 potential diagnosis for each disorder.
Second
edition
Robin S. Rosenberg
Stephen M. Kosslyn
AbnormAl Psychology
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Robin S. Rosenberg
University of California at San Francisco
Stephen M. Kosslyn
Minerva Schools at the Keck Graduate Institute
ABNORMAL PSYCHOLOGY
A Macmillan Higher Education Company
WORTH PUBLISHERS
SECOND
EDITION
Senior Vice President, Editorial and Production: Catherine Woods
Publisher: Kevin Feyen
Associate Publisher: Jessica Bayne
Executive Marketing Manager: Katherine Nurre
Developmental Editor: Thomas Finn
Director of Print and Digital Development: Tracey Kuehn
Associate Managing Editor: Lisa Kinne
Media Editor: Anthony Casciano
Editorial Assistant: Catherine Michaelsen
Photo Editor: Robin Fadool
Photo Researchers: Roman Barnes and Donna Ranieri
Project Editor: Christine Cervoni, TSI Graphics, Inc.
Art Director: Barbara Reingold
Cover Designers: Barbara Reingold and Lyndall Culbertson
Interior Designers: Charles Yuen and Lyndall Culbertson
Production Manager: Barbara Anne Seixas
Composition and Line Art: TSI Graphics, Inc.
Anatomical and Studio Art: Matthew Holt, Keith Kasnot, and Chris Notarile
Printing and Binding: Quad/Graphics
Cover Art: coloroftime/E+/Getty Images
Library of Congress Control Number: 2013955446
ISBN-13: 978-1-4292-4216-5
ISBN-10: 1-4292-4216-7
© 2014, 2011 by Worth Publishers
All rights reserved
Printed in the United States of America
First printing
Worth Publishers
41 Madison Avenue
New York, NY 10010
www.worthpublishers.com
To our families
FM-CT
iv
Robin S. Rosenberg is a clinical psychologist in private practice in both Menlo
Park and San Francisco, California. She is board certified in clinical psychology by the
American Board of Professional Psychology, and has been certified in clinical hypnosis.
Dr. Rosenberg is a fellow of the American Academy
of Clinical Psychology, member of the Academy for
Eating Disorders, President of the Santa Clara County
Psychological Association, member of the California
Psychological Association Ethics Committee, and
assistant clinical professor at the University of California
at San Francisco. She has taught psychology classes at
Lesley University and Harvard University.
Dr. Rosenberg received her B.A. in psychology
from New York University, and her M.A. and Ph.D. in
clinical psychology from the University of Maryland, College Park. She completed her
clinical internship at Massachusetts Mental Health Center, had a postdoctoral fellowship
at Harvard Community Health Plan, and was a staff member at Newton-Wellesley
Hospital’s Outpatient Services. Dr. Rosenberg specializes in treating people with anxiety
disorders, eating disorders, depression, and sexual dysfunctions.
In addition, Dr. Rosenberg writes about fictional popular culture figures and
the psychological phenomena their stories reveal. She is author of Superhero Origins:
What Makes Superheroes Tick and Why We Care and What’s the Matter with Batman? An
Unauthorized Clinical Look Under the Mask of the Caped Crusader, as well as college-level
psychology textbooks. She is the editor of The Psychology of the Girl With the Dragon
Tattoo; The Psychology of Superheroes; Our Superheroes, Ourselves; and What Is a Superhero?
Dr. Rosenberg is also a blogger at Psychology Today and the Huffington Post.
Stephen M. Kosslyn is the Founding Dean of the Minerva Schools at KGI (Keck
Graduate Institute). Previously, he served as Director of the Center for Advanced
Study in the Behavioral Sciences and as Professor of Psychology at Stanford University.
Kosslyn also is the former chair of the Department of
Psychology, Dean of Social Science, and John Lindsley
Professor of Psychology at Harvard University. He
received a B.A. from UCLA and a Ph.D. from Stanford
University, both in psychology.
Kosslyn’s research has focused primarily on the
nature of visual cognition, visual communication, and
individual differences; he has authored or coauthored
14 books and over 300 papers on these topics. Kosslyn
has received the following accolades: the American
Psychological Association’s Boyd R. McCandless Young
Scientist Award, the National Academy of Sciences Initiatives in Research Award, the
Cattell Award, a Guggenheim Fellowship, and the J-L. Signoret Prize (France). He has
honorary Doctorates from the University of Caen, the University of Paris Descartes, and
University of Bern. Kosslyn has been elected to Academia Rodinensis pro Remediatione
(Switzerland), the Society of Experimental Psychologists, and the American Academy
of Arts and Sciences.
ABOUT THE AUTHORS
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Preface xvii
CHAPTER 1 The History of Abnormal Psychology 3
CHAPTER 2 Understanding Psychological Disorders:
The Neuropsychosocial Approach 29
CHAPTER 3 Clinical Diagnosis and Assessment 59
CHAPTER 4 Research Methods 87
CHAPTER 5 Mood Disorders and Suicide 115
CHAPTER 6 Anxiety Disorders 155
CHAPTER 7 Obsessive-Compulsive-Related and
Trauma-Related Disorders 195
CHAPTER 8 Dissociative and Somatic Symptom Disorders 223
CHAPTER 9 Substance Use Disorders 257
CHAPTER 10 Eating Disorders 297
CHAPTER 11 Gender and Sexual Disorders 327
CHAPTER 12 Schizophrenia and Other Psychotic Disorders 365
CHAPTER 13 Personality Disorders 401
CHAPTER 14 Neurodevelopmental and
Disruptive Behavior Disorders 443
CHAPTER 15 Neurocognitive Disorders 477
CHAPTER 16 Ethical and Legal Issues 503
Glossary G-1
References R-1
Permissions and Attributions P-1
Name Index N-1
Subject Index S-1
LIST OF CHAPTERS
FM-TOC-i2-T-a
FM-CT
vi
CONTENTS
CHAPTER 2
Understanding Psychological Disorders:
The Neuropsychosocial Approach …………….. 29
Neurological Factors in Psychological Disorders 30
Brain Structure and Brain Function 30
A Quick Tour of the Nervous System 30
Neurons 32
Chemical Signals 34
Hormones and the Endocrine System 36
The Genetics of Psychopathology 36
Behavioral Genetics 37
Feedback Loops in Understanding Genes
and the Environment 39
The Environment Affects the Genes 39
The Genes Affect the Environment 40
Psychological Factors in Psychological Disorders 41
Behavior and Learning 41
Classical Conditioning 41
Operant Conditioning 42
Feedback Loops in Understanding Classical
Conditioning and Operant Conditioning 44
Observational Learning 45
Mental Processes and Mental Contents 45
Mental Processes 45
Mental Contents 46
Emotion 47
Emotions and Behavior 47
Emotions, Mental Processes, and Mental Contents 48
Emotional Regulation and Psychological Disorders 48
Neurological Bases of Emotion 48
Temperament 49
Social Factors in Psychological Disorders 50
Family Matters 50
Family Interaction Style and Relapse 51
Child Maltreatment 51
Parental Psychological Disorders 52
Community Support 52
Social Stressors 52
Socioeconomic Status 53
Discrimination, Bullying, and War 54
Culture 54
A Neuropsychosocial Last Word on the Beales 56
Preface xvii
CHAPTER 1
The History of Abnormal Psychology …………. 3
The Three Criteria for Determining
Psychological Disorders 4
Distress 4
Impairment in Daily Life 5
Risk of Harm 6
Context and Culture 7
Views of Psychological Disorders
Before Science 10
Ancient Views of Psychopathology 10
Supernatural Forces 11
Imbalance of Substances Within the Body 11
Forces of Evil in the Middle Ages and the
Renaissance 12
Rationality and Reason in the 18th and
19th Centuries 12
Asylums 13
Pinel and Mental Treatment 13
Moral Treatment 13
The Transition to Scientific Accounts of
Psychological Disorders 14
Freud and the Importance of Unconscious Forces 14
Psychoanalytic Theory 15
Psychosexual Stages 16
Mental Illness, According to Freud 16
Defense Mechanisms 16
Psychoanalytic Theory Beyond Freud 17
Evaluating the Contributions of Freud and His Followers 17
The Humanist Response 18
Scientific Accounts of Psychological Disorders 19
Behaviorism 19
The Cognitive Contribution 20
Social Forces 21
Biological Explanations 22
The Modern Synthesis of Explanations of
Psychopathology 23
The Diathesis-Stress Model 23
The Biopsychosocial and Neuropsychosocial Approaches 23
Contents v ii
Types of Scientific Research 90
Conducting Research with Experiments 90
Quasi-Experimental Design 93
Correlational Research 93
Case Studies 96
Meta-Analysis 97
Ethical Guidelines for Research 98
Research Challenges in Understanding
Abnormality 100
Challenges in Researching Neurological Factors 100
Challenges in Researching Psychological Factors 101
Biases in Mental Processes That Affect Assessment 101
Research Challenges with Clinical Interviews 101
Research Challenges with Questionnaires 101
Challenges in Researching Social Factors 102
Investigator-Influenced Biases 103
Cultural Differences in Evaluating Symptoms 103
Researching Treatment 104
Researching Treatments That Target Neurological
Factors 104
Drug Effect or Placebo Effect? 105
Dropouts 105
Researching Treatments That Target Psychological
Factors 105
Common Factors and Specific Factors 106
Is Therapy Better Than No Treatment? 107
Is One Type of Therapy Generally More Effective
Than Another? 108
The Therapy Dose–Response Relationship 109
Researching Treatments That Target Social Factors 110
Gender and Ethnicity of Patient and Therapist 111
Culturally Sanctioned Placebo Effects 111
Ethical Research on Experimental Treatments 112
CHAPTER 5
Mood Disorders and Suicide …………………….. 115
Depressive Disorders 116
Major Depressive Episode 116
Affect: The Mood Symptoms of Depression 116
Behavioral and Physical Symptoms of Depression 116
Cognitive Symptoms of Depression 117
CHAPTER 3
Clinical Diagnosis and Assessment ……………. 59
Diagnosing Psychological Disorders 61
Why Diagnose? 62
A Cautionary Note About Diagnosis 63
Reliability and Validity in Classification Systems 64
The Diagnostic and Statistical Manual of Mental
Disorders 65
The Evolution of DSM 65
The Evolution of DSM-5 66
The People Who Diagnose Psychological Disorders 70
Clinical Psychologists and Counseling Psychologists 70
Psychiatrists, Psychiatric Nurses, and General
Practitioners 71
Mental Health Professionals with Master’s Degrees 71
Assessing Psychological Disorders 72
Assessing Neurological and Other Biological Factors 72
Assessing Abnormal Brain Structures with X-Rays,
CT Scans, and MRIs 73
Assessing Brain Function with PET Scans and fMRI 73
Neuropsychological Assessment 74
Assessing Psychological Factors 75
Clinical Interview 75
Tests of Psychological Functioning 78
Assessing Social Factors 81
Family Functioning 81
Community 82
Culture 82
Assessment as an Interactive Process 83
Diagnosing and Assessing Rose Mary
and Rex Walls? 84
CHAPTER 4
Research Methods ……………………………………… 87
Using the Scientific Method to Understand
Abnormality 88
The Scientific Method 88
Collect Initial Observations 88
Identify a Question 88
Develop and Test a Hypothesis 89
Develop a Theory 89
Test the Theory 89
v iii Contents
CHAPTER 6
Anxiety Disorders …………………………………….. 155
Common Features of Anxiety Disorders 155
What Is Anxiety? 156
The Fight-or-Flight Response Gone Awry 156
Comorbidity of Anxiety Disorders 157
Generalized Anxiety Disorder 158
What Is Generalized Anxiety Disorder? 158
Understanding Generalized Anxiety Disorder 159
Neurological Factors 160
Psychological Factors: Hypervigilance and the Illusion
of Control 160
Social Factors: Stressors 161
Feedback Loops in Understanding Generalized
Anxiety Disorder 161
Treating Generalized Anxiety Disorder 161
Targeting Neurological Factors: Medication 161
Targeting Psychological Factors 162
Targeting Social Factors 163
Feedback Loops in Treating Generalized Anxiety Disorder 164
Panic Disorder and Agoraphobia 165
The Panic Attack—A Key Ingredient of Panic Disorder 165
What Is Panic Disorder? 166
What Is Agoraphobia? 167
Understanding Panic Disorder and Agoraphobia 168
Neurological Factors 169
Psychological Factors 170
Social Factors: Stressors, a Sign of the Times,
and “Safe People” 170
Feedback Loops in Understanding Panic Disorder
and Agoraphobia 171
Treating Panic Disorder and Agoraphobia 171
Targeting Neurological Factors: Medication 171
Targeting Psychological Factors 172
Targeting Social Factors: Group and Couples Therapy 174
Feedback Loops in Treating Panic Disorder and
Agoraphobia 174
Social Anxiety Disorder (Social Phobia) 175
What Is Social Anxiety Disorder? 176
Understanding Social Anxiety Disorder 177
Neurological Factors 177
Psychological Factors 178
Social Factors 179
Major Depressive Disorder 118
Depression in Children and Adolescents 120
Persistent Depressive Disorder 120
Current Controversy: Disruptive Mood
Dysregulation Disorder: Overlabeling of Tantrums? 121
Understanding Depressive Disorders 122
Neurological Factors 122
Psychological Factors 124
Social Factors 126
Feedback Loops in Understanding Depressive Disorders 128
Treating Depressive Disorders 130
Targeting Neurological Factors 130
Targeting Psychological Factors 132
Targeting Social Factors 133
Feedback Loops in Treating Depressive Disorders 135
Bipolar Disorders 136
Mood Episodes for Bipolar Disorders 136
Manic Episode 136
Hypomanic Episode 138
The Two Types of Bipolar Disorder 139
Cyclothymic Disorder 140
Understanding Bipolar Disorders 141
Neurological Factors 141
Psychological Factors: Thoughts and Attributions 142
Social Factors: Social and Environmental Stressors 143
Feedback Loops in Understanding Bipolar Disorders 143
Treating Bipolar Disorders 143
Targeting Neurological Factors: Medication 144
Targeting Psychological Factors: Thoughts, Moods,
and Relapse Prevention 144
Targeting Social Factors: Interacting with Others 145
Feedback Loops in Treating Bipolar Disorder 145
Suicide 146
Suicidal Thoughts and Suicide Risks 146
Thinking About, Planning, and Attempting Suicide 146
Risk and Protective Factors for Suicide 148
Understanding Suicide 149
Neurological Factors 149
Psychological Factors: Hopelessness and Impulsivity 150
Social Factors: Alienation and Cultural Stress 150
Feedback Loops in Understanding Suicide 150
Preventing Suicide 151
Crisis Intervention 151
Long-Term Prevention 151
Contents ix
Treating Obsessive-Compulsive Disorder 205
Targeting Neurological Factors: Medication 205
Targeting Psychological Factors 205
Targeting Social Factors: Family Therapy 206
Feedback Loops in Treating
Obsessive-Compulsive Disorder 206
Trauma-Related Disorders 207
What Are the Trauma-Related Disorders? 208
What Is Posttraumatic Stress Disorder? 209
What Is Acute Stress Disorder? 211
Understanding Trauma-Related Disorders: PTSD 213
Neurological Factors 213
Psychological Factors: History of Trauma, Comorbidity,
and Conditioning 214
Social Factors: Socioeconomic Factors, Social Support,
and Culture 215
Feedback Loops in Understanding Posttraumatic
Stress Disorder 215
Treating Posttraumatic Stress Disorder 216
Targeting Neurological Factors: Medication 217
Targeting Psychological Factors 217
Current Controversy: Eye Movement
Desensitization and Reprocessing (EMDR)
Treatment for Posttraumatic Stress Disorder 217
Targeting Social Factors: Safety, Support, and Family
Education 218
Feedback Loops in Treating Posttraumatic Stress
Disorder 218
Follow-up on Howard Hughes 220
CHAPTER 8
Dissociative and Somatic Symptom
Disorders ………………………………………………….. 223
Dissociative Disorders 224
Dissociative Disorders: An Overview 224
Normal Versus Abnormal Dissociation 225
Types of Dissociative Disorders 226
Dissociative Amnesia 226
What Is Dissociative Amnesia? 226
Understanding Dissociative Amnesia 228
Depersonalization-Derealization Disorder 229
What Is Depersonalization-Derealization Disorder? 229
Understanding Depersonalization-Derealization Disorder 231
Feedback Loops in Understanding Social Anxiety
Disorder 179
Treating Social Anxiety Disorder 180
Targeting Neurological Factors: Medication 180
Targeting Psychological Factors: Exposure and
Cognitive Restructuring 180
Targeting Social Factors: Group Interactions 181
Feedback Loops in Treating Social Anxiety Disorder 181
Specific Phobia 182
What Is Specific Phobia? 182
Specifics About Specific Phobia 183
Understanding Specific Phobia 184
Neurological Factors 184
Psychological Factors 185
Social Factors: Modeling and Culture 185
Feedback Loops in Understanding Specific Phobia 186
Treating Specific Phobia 186
Targeting Neurological Factors: Medication 186
Targeting Psychological Factors 186
Targeting Social Factors: A Limited Role for
Observational Learning 187
Feedback Loops in Treating Specific Phobia 187
Separation Anxiety Disorder 188
What Is Separation Anxiety Disorder? 188
Current Controversy: Separation Anxiety Disorder:
Anxiety Disorder or Developmental Difference? 190
Understanding and Treating Separation Anxiety
Disorder 191
Follow-up on Earl Campbell 191
CHAPTER 7
Obsessive-Compulsive-Related and
Trauma-Related Disorders ……………………….. 195
Obsessive-Compulsive Disorder and
Related Disorders 196
What Is Obsessive-Compulsive Disorder? 196
What Is Body Dysmorphic Disorder? 199
Understanding Obsessive-Compulsive Disorder 202
Neurological Factors 202
Psychological Factors 203
Social Factors 204
Feedback Loops in Understanding
Obsessive-Compulsive Disorder 205
x Contents
Polysubstance Abuse 262
Prevalence and Costs 262
Culture and Context 263
Stimulants 263
What Are Stimulants? 263
Cocaine and Crack 264
Amphetamines 264
Methamphetamine 265
Ritalin 265
MDMA (Ecstasy) 265
“Bath Salts” 266
Understanding Stimulants 266
Brain Systems and Neural Communication: Dopamine
and Abuse 267
Psychological Factors: From Learning to Coping 268
Social Factors 269
Depressants 271
What Are Depressants? 271
Alcohol 272
Sedative-Hypnotic Drugs 274
Understanding Depressants 275
Neurological Factors 275
Psychological Factors 276
Social Factors 277
Other Abused Substances 278
What Are Other Abused Substances? 278
Opioids: Narcotic Analgesics 278
Hallucinogens 279
Dissociative Anesthetics 280
Understanding Other Abused Substances 281
Neurological Factors 281
Psychological Factors 282
Social Factors 282
Feedback Loops in Understanding Substance Use
Disorders 282
Treating Substance Use Disorders 284
Goals of Treatment 284
Current Controversy: Once an Alcoholic, Always
an Alcoholic? 285
Targeting Neurological Factors 285
Detoxification 285
Medications 286
Dissociative Identity Disorder 232
What Is Dissociative Identity Disorder? 232
Criticisms of the DSM-5 Criteria 234
Understanding Dissociative Identity Disorder 234
Treating Dissociative Disorders 238
Targeting Neurological Factors: Medication 238
Targeting Psychological and Social Factors: Coping and
Integration 238
Feedback Loops in Treating Dissociative Disorders 239
Somatic Symptom Disorders 240
Somatic Symptom Disorders: An Overview 240
Somatic Symptom Disorder 241
What Is Somatic Symptom Disorder? 241
Understanding Somatic Symptom Disorder 242
Conversion Disorder 244
What Is Conversion Disorder? 245
Criticisms of the DSM-5 Criteria 247
Understanding Conversion Disorder 247
Illness Anxiety Disorder 248
Current Controversy: Omission of Hypochondriasis
from DSM-5: Appropriate or Overreaction? 249
What Is Illness Anxiety Disorder? 249
Illness Anxiety Disorder, Anxiety Disorders, and OCD:
Shared Features 250
Understanding Illness Anxiety Disorder 250
Treating Somatic Symptom Disorders 251
Targeting Neurological Factors 251
Targeting Psychological Factors: Cognitive-Behavior
Therapy 252
Targeting Social Factors: Support and Family Education 252
Feedback Loops in Treating Somatic Symptom
Disorders 253
Follow-up on Anna O. 254
CHAPTER 9
Substance Use Disorders …………………………. 257
Substance Use: When Use Becomes a Disorder 257
Substance Use Versus Intoxication 258
Substance Use Disorders 258
Substance Use Disorder as a Category or on a
Continuum? 260
Use Becomes a Problem 261
Comorbidity 262
Contents x i
Dieting, Restrained Eating, and Disinhibited Eating 313
Other Psychological Disorders as Risk Factors 313
Social Factors: The Body in Context 313
The Role of Family and Peers 314
The Role of Culture 314
Eating Disorders Across Cultures 315
The Power of the Media 315
Objectification Theory: Explaining the Gender Difference 316
Feedback Loops in Understanding Eating Disorders 317
Treating Eating Disorders 318
Targeting Neurological and Biological Factors:
Nourishing the Body 319
A Focus on Nutrition 319
Medical Hospitalization 319
Medication 319
Targeting Psychological Factors:
Cognitive-Behavior Therapy 320
CBT for Anorexia 320
CBT for Bulimia 320
Efficacy of CBT for Treating Eating Disorders 321
Targeting Social Factors 321
Interpersonal Therapy 321
Family Therapy 321
Psychiatric Hospitalization 322
Prevention Programs 323
Feedback Loops in Treating Eating Disorders 323
Follow-up on Marya Hornbacher 324
CHAPTER 1 1
Gender and Sexual Disorders …………………… 327
Gender Dysphoria 328
What Is Gender Dysphoria? 328
Understanding Gender Dysphoria 331
Neurological Factors 332
Psychological Factors: A Correlation with Play Activities? 332
Social Factors: Responses From Others 332
Treating Gender Dysphoria 333
Targeting Neurological and Other Biological Factors:
Altered Appearance 333
Targeting Psychological Factors: Understanding the
Choices 334
Targeting Social Factors: Family Support 334
Targeting Psychological Factors 287
Motivation 288
Cognitive-Behavior Therapy 289
Twelve-Step Facilitation (TSF) 290
Targeting Social Factors 291
Residential Treatment 291
Group-Based Treatment 291
Family Therapy 292
Feedback Loops in Treating Substance Use
Disorders 292
CHAPTER 1 0
Eating Disorders ……………………………………….. 297
Anorexia Nervosa 298
What Is Anorexia Nervosa? 298
Anorexia Nervosa According to DSM-5 298
Two Types of Anorexia Nervosa: Restricting and Binge
Eating/Purging 300
Medical, Psychological, and Social Effects of
Anorexia Nervosa 300
Medical Effects of Anorexia 301
Psychological and Social Effects of Starvation 301
Bulimia Nervosa 302
What Is Bulimia Nervosa? 302
Medical Effects of Bulimia Nervosa 304
Is Bulimia Distinct From Anorexia? 305
Binge Eating Disorder and “Other” Eating
Disorders 305
What Is Binge Eating Disorder? 305
Current Controversy: Is Binge Eating Disorder
Diagnosis a Good Idea? 307
Disordered Eating: “Other” Eating Disorders 307
Understanding Eating Disorders 308
Neurological Factors: Setting the Stage 309
Brain Systems 309
Neural Communication: Serotonin 310
Genetics 310
Psychological Factors: Thoughts of and Feelings
About Food 310
Thinking About Weight, Appearance, and Food 311
Operant Conditioning: Reinforcing Disordered Eating 311
Personality Traits as Risk Factors 312
x ii Contents
CHAPTER 1 2
Schizophrenia and Other Psychotic
Disorders ………………………………………………….. 365
What Are Schizophrenia and Other
Psychotic Disorders? 366
The Symptoms of Schizophrenia 366
Positive Symptoms 366
Negative Symptoms 369
Cognitive Deficits: The Specifics 369
Deficits in Attention 369
Deficits in Working Memory 369
Deficits in Executive Functioning 370
Cognitive Deficits Endure Over Time 370
Limitations of DSM-5 Criteria 370
Deficit/Nondeficit Subtypes 371
Distinguishing Between Schizophrenia and Other
Disorders 371
Psychotic Symptoms in Schizophrenia,
Mood Disorders, and Substance-Related Disorders 371
Other Psychotic Disorders 372
Current Controversy: Attenuated Psychosis
Syndrome: The Diagnosis That Wasn’t 375
Schizophrenia Facts in Detail 376
Prevalence 376
Comorbidity 376
Course 377
Gender Differences 377
Culture 377
Prognosis 379
Understanding Schizophrenia 380
Neurological Factors in Schizophrenia 380
Brain Systems 380
Neural Communication 383
Genetics 384
Psychological Factors in Schizophrenia 385
Mental Processes and Cognitive Difficulties:
Attention, Memory, and Executive Functions 385
Beliefs and Attributions 386
Emotional Expression 387
Social Factors in Schizophrenia 387
Understanding the Social World 388
Stressful Environments 388
Paraphilic Disorders 335
What Are Paraphilic Disorders? 335
Paraphilic Disorders Involving Nonconsenting People 336
Sexual Sadism Disorder and Sexual Masochism
Disorder: Pain and Humiliation 340
Paraphilic Disorders Involving Nonhuman Objects 341
Assessing Paraphilic Disorders 343
Criticisms of the DSM-5 Paraphilic Disorders 343
Understanding Paraphilic Disorders 343
Neurological Factors 344
Psychological Factors: Conditioned Arousal 344
Social Factors: More Erotica? 344
Treating Paraphilic Disorders 345
Targeting Neurological and Other Biological Factors:
Medication 345
Current Controversy: Sex Offenders: Is Surgical
Castration an Ethical Solution? 345
Targeting Psychological Factors: Cognitive-Behavior
Therapy 346
Targeting Social Factors 346
Sexual Dysfunctions 346
An Overview of Sexual Functioning and Sexual
Dysfunctions 346
The Normal Sexual Response Cycle 347
Sexual Dysfunctions According to DSM-5 348
Sexual Desire Disorders and Sexual Arousal Disorders 349
Orgasmic Disorders 350
Sexual Pain Disorder: Genito-Pelvic Pain/Penetration
Disorder 352
Criticisms of the Sexual Dysfunctions in DSM-5 354
Understanding Sexual Dysfunctions 354
Neurological and Other Biological Factors 354
Psychological Factors in Sexual Dysfunctions 355
Social Factors 356
Feedback Loops in Understanding Sexual
Dysfunctions 356
Treating Sexual Dysfunctions 358
Targeting Neurological and Other Biological Factors:
Medications 358
Targeting Psychological Factors: Shifting Thoughts,
Learning Behaviors 359
Targeting Social Factors: Couples Therapy 360
Feedback Loops in Treating Sexual Dysfunctions 360
Contents x iii
Odd/Eccentric Personality Disorders 410
Paranoid Personality Disorder 411
Schizoid Personality Disorder 413
Schizotypal Personality Disorder 414
What Is Schizotypal Personality Disorder? 414
Understanding Schizotypal Personality Disorder 415
Treating Odd/Eccentric Personality Disorders 417
Dramatic/Erratic Personality Disorders 417
Antisocial Personality Disorder 418
Understanding Antisocial Personality Disorder and
Psychopathy 419
Treating Antisocial Personality Disorder and Psychopathy 421
Current Controversy: Should Psychopaths Receive
Treatment? 422
Borderline Personality Disorder 422
Understanding Borderline Personality Disorder 424
Treating Borderline Personality Disorder:
New Treatments 427
Histrionic Personality Disorder 429
What Is Histrionic Personality Disorder? 430
Distinguishing Between Histrionic Personality
Disorder and Other Disorders 431
Treating Histrionic Personality Disorder 431
Narcissistic Personality Disorder 431
What Is Narcissistic Personality Disorder? 431
Treating Narcissistic Personality Disorder 432
Fearful/Anxious Personality Disorders 433
Avoidant Personality Disorder 433
What Is Avoidant Personality Disorder? 433
Distinguishing Between Avoidant Personality
Disorder and Other Disorders 434
Dependent Personality Disorder 435
Obsessive-Compulsive Personality Disorder 436
What Is Obsessive-Compulsive Personality Disorder? 436
Distinguishing Between Obsessive-Compulsive
Personality Disorder and OCD 438
Understanding Fearful/Anxious Personality Disorders 438
Treating Fearful/Anxious Personality Disorders 438
Follow-up on Rachel Reiland 440
Immigration 389
Economic Factors 390
Cultural Factors: Recovery in Different Countries 390
Feedback Loops in Understanding Schizophrenia 391
Treating Schizophrenia 392
Targeting Neurological Factors in Treating
Schizophrenia 393
Medication 393
Brain Stimulation: ECT 394
Targeting Psychological Factors in Treating
Schizophrenia 394
Cognitive-Behavior Therapy 394
Treating Comorbid Substance Abuse: Motivational
Enhancement 395
Targeting Social Factors in Treating Schizophrenia 395
Family Education and Therapy 395
Group Therapy: Social Skills Training 395
Inpatient Treatment 396
Minimizing Hospitalizations: Community-Based
Interventions 396
Feedback Loops in Treating Schizophrenia 397
CHAPTER 1 3
Personality Disorders ………………………………. 401
Diagnosing Personality Disorders 402
What Are Personality Disorders? 403
Assessing Personality Disorders 404
DSM-5 Personality Clusters 405
Criticisms of the DSM-5 Category of Personality
Disorders 405
Understanding Personality Disorders in General 406
Neurological Factors in Personality Disorders:
Genes and Temperament 407
Psychological Factors in Personality Disorders:
Temperament and the Consequences of Behavior 408
Social Factors in Personality Disorders: Insecurely
Attached 408
Feedback Loops in Understanding Personality
Disorders 408
Treating Personality Disorders: General Issues 409
Targeting Neurological Factors in Personality Disorders 409
Targeting Psychological Factors in Personality Disorders 409
Targeting Social Factors in Personality Disorders 410
x iv Contents
What Is Oppositional Defiant Disorder? 463
What Is Attention-Deficit/Hyperactivity Disorder? 464
Understanding Disorders of Disruptive Behavior
and Attention 468
Neurological Factors 468
Psychological Factors: Recognizing Facial Expressions,
Low Self-Esteem 469
Social Factors: Blame and Credit 469
Feedback Loops in Understanding Attention-Deficit/
Hyperactivity Disorder 470
Treating Disorders of Disruptive Behavior and
Attention: Focus on ADHD 470
Targeting Neurological Factors: Medication 470
Targeting Psychological Factors: Treating Disruptive
Behavior 472
Targeting Social Factors: Reinforcement in Relationships 473
Feedback Loops in Treating Attention-Deficit/
Hyperactivity Disorder 473
CHAPTER 15
Neurocognitive Disorders ………………………… 477
Normal Versus Abnormal Aging and
Cognitive Functioning 478
Cognitive Functioning in Normal Aging 479
Intelligence 479
Memory 480
Processing Speed, Attention, and Working Memory 480
Psychological Disorders and Cognition 481
Depression 481
Anxiety Disorders 482
Schizophrenia 482
Medical Factors That Can Affect Cognition 482
Diseases and Illnesses 482
Stroke 483
Head Injury 484
Substance-Induced Changes in Cognition 484
Delirium 484
What Is Delirium? 484
Understanding Delirium: A Side Effect? 487
Delirium Caused by Substance Use 487
Delirium Caused by a General Medical Condition 487
Treating Delirium: Rectify the Cause 487
CHAPTER 1 4
Neurodevelopmental and Disruptive
Behavior Disorders …………………………………… 443
Intellectual Disability (Intellectual
Developmental Disorder) 444
What Is Intellectual Disability? 444
Current Controversy: Changing Mental Retardation
to Intellectual Disability: Will Such a Switch Be
Beneficial? 446
Understanding Intellectual Disability 447
Neurological Factors: Teratogens and Genes 447
Psychological Factors: Problem Behaviors 448
Social Factors: Understimulation 448
Treating Intellectual Disability 448
Targeting Neurological Factors: Prevention 448
Targeting Psychological and Social Factors:
Communication 449
Targeting Social Factors: Accommodation in the
Classroom—It’s the Law 449
Autism Spectrum Disorder 449
What Is Autism Spectrum Disorder? 450
Understanding Autism Spectrum Disorder 453
Neurological Factors 453
Psychological Factors: Cognitive Deficits 453
Social Factors: Communication Problems 454
Treating Autism Spectrum Disorder 454
Targeting Neurological Factors 454
Targeting Psychological Factors: Applied Behavior Analysis 454
Targeting Social Factors: Communication 455
Specific Learning Disorder: Problems with
the Three Rs 455
What Is Specific Learning Disorder? 455
Understanding Specific Learning Disorder 457
Neurological Factors 457
Psychological Factors 458
Social Factors 458
Treating Dyslexia 458
Disorders of Disruptive Behavior and
Attention 459
What Is Conduct Disorder? 460
Adolescent-Onset Type 462
Childhood-Onset Type 462
Contents x v
The Insanity Defense: Current Issues 511
Assessing Insanity for the Insanity Defense 512
States’ Rights: Doing Away with the Insanity Defense 513
Current Controversy: Criminal Behavior:
Does Abnormal Neural Functioning Make It
More Excusable? 513
With the Insanity Defense, Do People Really
“Get Away with Murder”? 514
After Committing the Crime: Competent to
Stand Trial? 514
Dangerousness: Legal Consequences 515
Evaluating Dangerousness 516
Actual Dangerousness 516
Confidentiality and the Dangerous Patient: Duty to
Warn and Duty to Protect 516
Maintaining Safety: Confining the Dangerously
Mentally Ill Patient 518
Criminal Commitment 518
Civil Commitment 518
Sexual Predator Laws 521
Legal Issues Related to Treatment 521
Right to Treatment 522
Right to Refuse Treatment 522
Competence to Refuse Treatment 522
Mental Health and Drug Courts 523
The Wheels of Justice: Follow-up on
Andrew Goldstein 524
Glossary G-1
References R-1
Permissions and Attributions P-1
Name Index N-1
Subject Index S-1
Dementia (and Mild Versus Major
Neurocognitive Disorders) 488
What Is Dementia? 488
Mild and Major Neurocognitive Disorders 489
Current Controversy: Miid and
Major Neurocognitive Disorders 490
Dementia and Alzheimer’s Disease 490
Understanding Dementia 492
Alzheimer’s Disease 492
Vascular Dementia 494
Dementia Due to Other Medical Conditions 495
Treating Dementia 497
Targeting Neurological Factors 498
Targeting Psychological Factors 498
Targeting Social Factors 499
Diagnosing Mrs. B.’s Problems 499
CHAPTER 1 6
Ethical and Legal Issues ……………………………. 503
Ethical Issues 504
An Ethical Principle: The Role of Confidentiality 504
Ambiguities Regarding Confidentiality 505
Limits of Confidentiality: HIPAA in Action 505
Legal Restrictions on Confidentiality 506
Privileged Communication 506
Informed Consent to Participate in Research on
Mental Illness: Can Patients Truly Be Informed? 507
Criminal Actions and Insanity 507
While Committing the Crime: Sane or Insane? 508
From the M’Naghten Test to the Durham Test 508
The American Legal Institute Test 509
Insanity Defense Reform Acts 509
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FM-CT PREFACE
xvii
T his is an exciting time to study psychopathology. Research on the entire range of psychological disorders has blossomed during the last several decades, producing dramatic new insights about psychological disorders and their treatments. However,
the research results are outpacing the popular media’s ability to explain them. We’ve
noticed that when study results are explained in a news report or an online magazine
article, “causes” of mental illness are often reduced to a single factor, such as genes, brain
chemistry, irrational thoughts, or social rejection. But that is not an accurate picture.
Research increasingly reveals that psychopathology arises from a confluence of three
types of factors: neurological (brain and body, including genes), psychological (thoughts,
feelings, and behaviors), and social (relationships, communities, and culture). Moreover,
these three sorts of factors do not exist in isolation, but rather mutually influence each
other. It’s often tempting to seek a single cause of psychopathology, but this effort is
fundamentally misguided.
We are a clinical psychologist (Rosenberg) and a cognitive neuroscientist (Kosslyn)
who have been writing collaboratively for many years. Our observations about the
state of the field of psychopathology—and the problems with how it is sometimes
portrayed—led us to envision an abnormal psychology textbook that is guided by a
central idea, which we call the neuropsychosocial approach. This approach allows us to
conceptualize the ways in which neurological, psychological, and social factors interact
to give rise to mental disorders. These interactions take the form of feedback loops in
which each type of factor affects every other type. Take depression, for instance, which
we discuss in Chapter 5: Someone who attributes the cause of a negative event to his
or her own personal characteristics or behavior (such attributions are a psychological
factor) is more likely to become depressed. But this tendency to attribute the cause of
negative events to oneself is influenced by social experiences, such as being criticized
or abused. In turn, such social factors can alter brain functioning (particularly if one has
certain genes), and abnormalities in brain functioning affect one’s thoughts and social
interactions, and so on—round and round.
The neuropsychosocial approach grew out of the venerable biopsychosocial
approach—but instead of focusing broadly on biology, we take advantage of the
bountiful harvest of findings about the brain that have filled the scientific journals over
the past two decades. Specifically, the name change signals a focus on the brain itself; we
derive much insight from the findings of neuroimaging studies, which reveal how brain
systems function normally and how they have gone awry with mental disorders, and we
also learn an enormous amount from findings regarding neurotransmitters and genetics.
Although mental disorders cannot be fully understood without reference to the
brain, neurological factors alone cannot explain these disorders; rather, mental disorders
develop through the complex interaction of neurological factors with psychological and
social factors. Without question, psychopathology cannot be reduced to “brain disease,”
akin to a problem someone might have with his or her liver or lungs. Instead, we show
that the effects of neurological factors can only be understood in the context of the
other two types of factors addressed within the neuropsychosocial approach. (In fact, an
understanding of a psychological disorder cannot be reduced to any single type of factor,
whether genetics, irrational thoughts, or family interaction patterns.) Thus, we present
cutting-edge neuroscience research results and put them in context, explaining how
they illuminate issues in psychopathology.
Our emphasis on feedback loops among neurological, psychological, and social
factors led us to reconceptualize and incorporate the classic diathesis-stress model
(which posits a precondition that makes a person vulnerable and an environmental
trigger—the diathesis and stress, respectively). In the classic view, the diathesis was almost
always treated as a biological state, and the stress was viewed as a result of environmental
x v iii Preface
events. In contrast, after describing the conventional diathesis-stress model in Chapter 1,
we explain how the neuropsychosocial approach provides a new way to think about the
relationship between diathesis and stress. Specifically, we show how one can view any
of the three sorts of factors as a potential source of either a diathesis or a stressor. For
example, living in a dangerous neighborhood, which is a social factor, creates a diathesis for
which psychological events can serve as the stressor, triggering an episode of depression.
Alternatively, being born with a very sensitive amygdala (a brain structure involved in
fear and other strong emotions) may act as a diathesis for which social events—such as
observing someone else being mugged—can serve as a stressor that triggers an anxiety
disorder.
Thus, the neuropsychosocial approach is not simply a change in terminology (“bio”
to “neuro”), but rather a change in basic orientation: We do not view any one sort of
factor as “privileged” over the others, but regard the interactions among the factors—the
feedback loops—as paramount. In our view, this approach incorporates what was best
about the biopsychosocial approach and the diathesis-stress model.
Our new approach should lead students who use this textbook to think critically
about theories and research on etiology, diagnosis and treatment of mental disorders.
We want students to come away from the course with the knowledge and skills to
understand why no single type of findings alone can explain psychopathology, and to
have compassion for people suffering from psychological disorders. One of our goals is to
put a “human face” on mental illness, which we do by using case studies to illustrate and
make concrete each disorder. These goals are especially important because this course
will be the last psychology course many students take—and this might be the last book
about psychology they read.
The new approach we have adopted led naturally to a set of unique features, as we
outline next.
Unique Coverage
By integrating cutting-edge neuroscience research and more traditional psychosocial
research on psychopathology and its treatment, this textbook provides students with a
sense of the field as a coherent whole, in which different research methods illuminate
different aspects of abnormal psychology. Our integrated neuropsychosocial approach
allows students to learn not only how neurological factors affect mental processes (such
as executive functions) and mental contents (such as distorted beliefs), but also how
neurological factors affect emotions, behavior, social interactions, and responses to
environmental events—and vice versa.
The 16 chapters included in this book span the traditional topics covered in
an abnormal psychology course. The neuropsychosocial theme is reflected in both
the overall organization of the text and the organization of its individual chapters.
We present the material in a decidedly contemporary context that infuses both the
foundational chapters (Chapters 1–4) as well as the chapters that address specific
disorders (Chapters 5–15).
In Chapter 2, we provide an overview of explanations of abnormality and discuss
neurological, psychological, and social factors. Our coverage is not limited merely
to categorizing causes as examples of a given type of factor; rather, we explain how
a given type of factor influences and creates feedback loops with other factors.
Consider depression again: The loss of a relationship (social factor) can affect thoughts
and feelings (psychological factors), which—given a certain genetic predisposition
(neurological factor)—can trigger depression. Using the neuropsychosocial approach,
we show how disparate fields of psychology and psychiatry (such as neuroscience and
Preface x ix
clinical practice) are providing a unified and overarching understanding of abnormal
psychology.
Our chapter on diagnosis and assessment (Chapter 3) uses the neuropsychosocial
framework to organize methods of assessing abnormality. We discuss how abnormality
may be assessed through measures that address the different types of factors: neurological
(e.g., neuroimaging data or certain types of blood tests), psychological (e.g., clinical
interviews or questionnaires), and social (e.g., family interviews or a history of legal
problems).
The research methods chapter (Chapter 4) also provides unique
coverage. We explain the general scientific method, but we do so
within the neuropsychosocial framework. Specifically, we consider
methods used to study neurological factors (e.g., neuroimaging),
psychological factors (e.g., self-reports of thoughts and moods),
and social factors (e.g., observational studies of dyads or groups
or of cultural values and expectations). We show how the various
measures themselves reflect the interactions among the different
types of factors. For instance, when researchers ask participants to
report family dynamics, they are relying on psychological factors—
participants’ memories and impressions—to provide measures of
social factors. Similarly, when researchers use the number of items
checked on a stressful-life events scale to infer the actual stress
experienced by a person, social factors provide a proxy measure
of the psychological and neurological consequences of stress. We
also discuss research on treatment from the neuropsychosocial
framework.
The clinical chapters (Chapters 5–15), which address specific disorders, also
rely on the neuropsychosocial approach to organize the discussions of both etiology
and treatment of the disorders. Moreover, when we discuss a particular disorder, we
address the three basic questions of psychopathology: What exactly constitutes this
psychological disorder? What neuropsychosocial factors are associated with it? How
is it treated?
Pedagogy
All abnormal psychology textbooks cover a lot of ground: Students must learn many
novel concepts, facts, and theories. We want to make that task easier, to help students
come to a deeper understanding of what they learn and to consolidate that material
effectively. The textbook uses a number of pedagogical tools to achieve this goal.
Feedback Loops Within the Neuropsychosocial Approach
This textbook highlights and reinforces the theme of feedback loops among neurological,
psychological, and social factors in several ways:
• In each clinical chapter, we include a section on “Feedback Loops in Understanding,”
which specifically explores how disorders result from interactions among the
neuropsychosocial factors. We also include a section on “Feedback Loops in Treating,”
which specifically explores how successful treatment results from interactions among
the neuropsychosocial factors.
• We include neuropsychosocial “Feedback Loop” diagrams as part of these sections.
For example, in Chapter 7 we provide a Feedback Loop diagram for understanding
posttraumatic stress disorder and another for treating posttraumatic stress disorder.
During times of political unrest, violence, or
terrorism, rates of trauma-related disorders
are likely to increase.
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These diagrams illustrate the feedback loops among the neurological, psychological,
and social factors. Additional feedback loop diagrams can be found on the book’s
website at: www.worthpublishers.com/launchpad/rkabpsych2e.
• The Feedback Loops in Understanding diagrams serve several purposes: (1) they
provide a visual summary of the most important neuropsychosocial factors that
contribute to various disorders; (2) they illustrate the interactive nature of the factors;
(3) because their overall structure is the same for each disorder, students can compare
and contrast the specifics of the feedback loops across disorders.
Brain Systems
Mental Processes and
Mental Contents
Family
Hippocampus
Genetics
Inherited tendency to seek
out situations that may have
a higher likelihood of trauma
Dissociation during
trauma
Beliefs that one is unable
to control stressors and
that the world is a
dangerous place
Behavior
Conditioned emotional
response to stimuli
associated with trauma
Negative reinforcement
of avoidance
Affect
Anxiety
Fear
Stressful Life Events
Socioeconomic stress
Lack of social support
Specific characteristics
of the traumatic event
No known major
contribution
Gender/Culture
Cultural influences on
symptom expression
NeuroPsychoSocial
NeuroPsychoSocial NeuroPsychoSocial
Neural Communication
Norepinephrine
Serotonin
FI G U RE 7.2 • Feedback Loops in Understanding PTSD
Treatments Targeting
Neurological Factors
Medication: SSRIs
Changes neural
activity
Decreases isolation
and shame
Increases social
support
Improves
relationships
Treatments Targeting
Social Factors
Group therapy
Couples or family
therapy
Changes thoughts,
feelings, and
behaviors
Treatments Targeting
Psychological Factors
CBT: Breathing,
relaxation, exposure,
cognitive restructuring,
psychoeducation
EMDR
FI G U RE 7.3 • Feedback Loops in Treating PTSD
Preface x x i
• Like the Feedback Loops in Understanding diagrams, the Feedback Loops in Treating
diagrams serve several purposes: (1) they provide a visual summary of the treatments for
various disorders; (2) they illustrate the interactive nature of successful treatment (the
fact that a treatment may directly target one type of factor, but changes in that factor in
turn affect other factors); (3) because their overall structure is the same for each disorder,
students can compare and contrast the specifics of the feedback loops across disorders.
Clinical Material
Abnormal psychology is a fascinating topic, but we want students to go beyond
fascination; we want them to understand the human toll of psychological disorders—
what it’s like to suffer from and cope with such disorders. To do this, we’ve incorporated
several pedagogical elements. The textbook includes three types of clinical material:
chapter stories—each chapter has a story woven through, traditional third-person cases
(From the Outside), and first-person accounts (From the Inside).
Chapter Stories: Illustration and Integration
Each chapter opens with a story about a person (or, in some cases, several people) who
has symptoms of psychological distress or dysfunction. Observations about the person
or people are then woven throughout the chapter. These chapter stories illustrate the
common threads that run throughout the chapter (and thereby integrate the material),
serve as retrieval cues for later recall of the material, and show students how the theories
and research presented in each chapter apply to real people in the real world; the stories
x x ii Preface
humanize the clinical descriptions and discussions of research presented
in the chapters.
The chapter stories present people as clinicians and researchers often
find them—with sets of symptoms in context. It is up to the clinician or
researcher to make sense of the symptoms, determining which of them may
meet the criteria for a particular disorder, which may indicate an atypical
presentation, and which may arise from a comorbid disorder. Thus, we
ask the student to see situations from the point of view of clinicians and
researchers, who must sift through the available information to develop
hypotheses about possible diagnoses and then obtain more information to
confirm or disconfirm these hypotheses.
In the first two chapters, the opening story is about a mother and
daughter—Big Edie and Little Edie Beale—who were the subject of a
famous documentary in the 1970s and whose lives have been portrayed
more recently in the play and HBO film Grey Gardens. In these initial
chapters, we offer a description of the Beales’ lives and examples of their
very eccentric behavior to address two questions central to psychopathology:
How is abnormality defined? Why do psychological disorders arise?
The stories in subsequent chapters focus on different examples
of symptoms of psychological disorders, drawn from the lives of other
people. For example, in Chapter 6 we discuss football star Earl Campbell
(who suffered from symptoms of anxiety); in Chapter 7 we discuss the
reclusive billionaire Howard Hughes (who suffered from symptoms of
obsessive-compulsive disorder and who experienced multiple traumatic
events); and in Chapter 12 we discuss the Genain quadruplets—all four
of whom were diagnosed with schizophrenia.
We return often to these stories throughout each chapter in an effort
to illustrate the complexity of mental disorders and to show the human
side of mental illness, how it can affect people throughout a lifetime,
rather than merely a moment in time.
From the Outside
The feature called From the Outside provides third-person accounts (typically case
presentations by mental health clinicians) of disorders or particular symptoms of
disorders. These accounts provide an additional opportunity for memory consolidation
of the material (because they mention symptoms the person experienced), an additional
set of retrieval cues, and a further sense of how symptoms and disorders affect real
people; these cases also serve to expose students to professional case material. The From
the Outside feature covers an array of disorders, such as cyclothymic disorder, panic
disorder, transvestic disorder, and separation anxiety disorder. Often several From the
Outside cases are included in a chapter.
From the Inside
In every chapter in which we address a disorder in depth, we present at least one first-
person account of what it is like to live with that disorder or particular symptoms of it.
In addition to providing high-interest personal narratives, these From the Inside cases help
students to consolidate memory of the material, provide additional retrieval cues, and are
another way to link the descriptions of disorders and research findings to real people’s
experiences. The From the Inside cases illuminate what it is like to live with disorders
such as agoraphobia, obsessive-compulsive disorder, illness anxiety disorder, alcohol use
disorder, gender dysphoria, and schizophrenia, among others.
Using this book’s definition of a psychological
disorder, did either of the Beales have a
disorder? Big Edie exhibited distress that
was inappropriate to her situation; both
women appeared to have an impaired ability
to function. The risk of harm to the women,
however, is less clear-cut.
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Learning About Disorders:
Consolidated Tables to
Consolidate Learning
In the clinical chapters, we provide two types of tables to help students organize and
consolidate information related to diagnosis: DSM-5 diagnostic criteria tables, and Facts
at a Glance tables.
DSM-5 Diagnostic Criteria Tables
The American Psychiatric Association’s manual of psychiatric disorders—the Diagnostic
and Statistical Manual of Mental Disorders, 5th edition (DSM-5)—provides tables of the
diagnostic criteria for each of the listed disorders. For each disorder that we discuss at
length, we present the DSM-5 diagnostic criteria table; we also explain and discuss the
criteria—and criticisms of them—in the body of the chapters themselves.
Facts at a Glance Tables for Disorders
Another important innovation is our summary tables for each disorder, which provide
key facts about prevalence, comorbidity, onset, course, and gender and cultural factors.
These tables are clearly titled with the name of the disorder, which is followed by the
term “Facts at a Glance” (for instance, Obsessive-Compulsive Disorder Facts at a Glance).
These tables give students the opportunity to access this relevant information in one
place and to compare and contrast the facts for different disorders.
New Features
This edition has two new features: Current Controversy boxes and Getting the Picture
critical thinking photo sets.
Current Controversies
New to this edition, each clinical chapter includes a brief discussion about a current
controversy related to a disorder—its diagnosis or its treatment. Examples include
whether the new diagnoses in DSM-5 of mild and major neurocognitive disorders
are net positive or negative changes from DSM-IV, and whether eye movement
desensitization and reprocessing (EMDR) provides additional benefit beyond that
of other treatments for posttraumatic stress disorder. These discussions help students
understand the iterative and sometimes controversial nature of classifying “problems”
and symptoms as disorders, and whether and when treatments might be appropriate.
Many of these discussions were contributed by instructors who teach Abnormal
Psychology—including: Ken Abrams, Carleton College; Randy Arnau, University of
Southern Mississippi; Glenn Callaghan, San Jose State University; Richard Conti, Kean
University; Patrice Dow-Nelson, New Jersey City University; James Foley, College
of Wooster; Rick Fry, Youngstown State University; Farrah Hughes, Francis Marion
University; Meghana Karnik-Henry, Green Mountain College; Kevin Meehan, Long
Island University; Jan Mendoza, Golden West College; Meera Rastogi, University of
Cincinnati, Clermont College; Harold Rosenberg, Bowling Green State University;
Anthony Smith, Baybath College; and Janet Todaro, Salem State University.
Getting the Picture
Also new to this edition are brief visual features that help to consolidate learning, which
we call Getting the Picture: We offer two photos and ask students to decide which one
x x iv Preface
best illustrates a clinical phenomenon described in the chapter. Each chapter contains
several of these features.
Summarizing and Consolidating
We include two more key features to help students learn the material: end-of-section
application exercises and end-of-chapter summaries (called Summing Up).
Thinking Like a Clinician: End-of-Section Application
Exercises
At the end of each major section in the clinical chapters, we provide Thinking Like a Clinician
questions. These questions ask students to apply what they have learned to other people and
situations. These questions allow students to test their knowledge of the chapter’s material;
they may be assigned as homework or used to foster small-group or class discussion.
End-of-Chapter Review: Summing Up
The end-of-chapter review is designed to help students further consolidate the material
in memory:
• Section Summaries: These summaries allow students to review what they have
learned in the broader context of the entire chapter’s material.
• Key Terms: At the end of each chapter we list the key terms used in that chapter—
the terms that are presented in boldface in the text and are defined in the marginal
glossaries—with the pages where the definitions can be found.
Imagine that you know that both of these women are afraid of getting fat and believe themselves to
be overweight. If you had to guess based on their appearance, which of these models would you think
didn’t meet all the criteria for anorexia nervosa and instead had a partial case? The woman on the
right is more likely to have a partial case because, based on these photos, she does not appear to be
significantly underweight.
GETTING THE PICTURE
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• At the very end of Summing Up, students are directed to the online study aids and
resources pertinent to the chapter.
Integrated Gender and Cultural Coverage
We have included extensive culture and gender coverage, and integrated it throughout
the entire textbook. You’ll find a complete list of this coverage on the book’s catalog
page. Some of our coverage of culture and gender include:
• Facts at a Glance tables provide relevant cultural and gender data for each specific disorder
• Cultural differences in evaluating symptoms of disorders in psychological research, 63, 66
• Cultural differences in assessing social factors in psychological assessment, 75, 103–104
• Gender and cultural consideration in depressive disorders, 127
• Suicide—cultural factors, 150
• Cultural influence of substance abuse, 263
• Alcoholism rate variations by gender and culture, 271–273, 411
• Gender and culture differences in schizophrenia, 377
• Oppositional defiant disorder—cultural considerations for diagnosis, 468
• Gender differences in different types of dementia (Table 15.9), 501
Media and Supplements
The second edition of our book features a wide array of multimedia tools designed to
meet the needs of both students and teachers. For more information about any of the
items below, visit Worth Publishers’ online catalog at www.worthpublishers.com.
LAUNCHPAD WITH LEARNINGCURVE QUIZZING A comprehensive Web resource for
teaching and learning psychology, LaunchPad combines rich media resources and an
easy-to-use platform. For students, it is the ultimate online study guide with videos,
e-Book, and the LearningCurve adaptive quizzing system. For instructors, LaunchPad
is a full course space where class documents can be posted, quizzes are easily assigned
and graded, and students’ progress can be assessed and recorded. The LaunchPad for
our second edition can be previewed at: www.worthpublishers.com/launchpad/
rkabpsych2e. You’ll find the following in our LaunchPad:
The LearningCurve quizzing system was designed based on the latest findings from
learning and memory research. It combines adaptive question selection, immediate and
valuable feedback, and a game-like interface to engage students in a learning experience
that is unique to them. Each LearningCurve quiz is fully integrated with other resources
in LaunchPad through the Personalized Study Plan, so students will be able to review
with Worth’s extensive library of videos and activities. State-of-the-art question analysis
reports allow instructors to track the progress of individual students as well as the class
as a whole. The many questions in LearningCurve have been prepared by a talented
team of instructors including Kanoa Meriwether from the University of Hawaii, West
Oahu, Danielle Gunraj from the State University of New York at Binghamton, and
Anna Aulette Root from the University of Capetown.
• Diagnostic Quizzing developed by Diana Joy of Denver Community College and
Judith Levine from Farmingdale State College includes more than 400 questions for
every chapter that help students identify their areas of strength and weakness.
• An interactive e-Book allows students to highlight, bookmark, and make their own
notes, just as they would with a printed textbook. Digital enhancements include full-
text search and in-text glossary definitions.
x x v i Preface
• Student Video Activities include more than 60 engaging and gradeable video
activities, including archival footage, explorations of current research, case studies, and
documentaries.
• The Scientific American Newsfeed delivers weekly articles, podcasts, and news briefs
on the very latest developments in psychology from the first name in popular science
journalism.
COURSESMART E-BOOK The CourseSmart e-Book offers the complete text in an easy-
to-use, flexible format. Students can choose to view the CourseSmart e-Book online
or download it to a personal computer or a portable media player, such as a smart
phone or iPad. The CourseSmart e-Book for Abnormal Psychology, Second Edition, can
be previewed and purchased at www.coursesmart.com.
Also Available for Instructors
The Abnormal Psychology video collection on Flash Drive and DVD. This comprehensive
collection of more than 130 videos includes a balanced set of cases, experiments, and
current research clips. Instructors can play clips to introduce key topics, to illustrate
and reinforce specific core concepts, or to stimulate small-group or full-classroom
discussions. Clips may also be used to challenge students’ critical thinking skills—either
in class or via independent, out-of-class assignments.
INSTRUCTOR’S RESOURCE MANUAL, by Kanoa Meriwether, University of Hawaii, West
Oahu and Meera Rastogi, University of Cincinnati: The manual offers chapter-by-
chapter support for instructors using the text, as well as tips for explaining to students
Preface x x v ii
the neuropsychosocial approach to abnormal psychology. For each chapter, the manual
offers a brief outline of learning objectives and a list of key terms. In addition, it includes
a chapter guide, including an extended chapter outline, point-of-use references to art in
the text, and listings of class discussions/activities, assignments, and extra-credit projects
for each section.
TEST BANK, by James Rodgers from Hawkeye Community College, Joy Crawford,
University of Washington, and Judith Levine, Farmingdale State College: The test
bank offers over 1700 questions, including multiple-choice, true/false, fill-in, and essay
questions. The Diploma-based CD version makes it easy for instructors to add, edit, and
change the order of questions.
PRESENTATION SLIDES are available in three formats that can be used as they are or can
be customized. One set includes all the textbook’s illustrations and tables. The second
set consists of lecture slides that focus on key themes and terms in the book and include
text illustrations and tables. A third set of PowerPoint slides provides an easy way to
integrate the supplementary video clips into classroom lectures. In addition, we have
lecture outline slides correlated to each chapter of the book created by Pauline Davey
Zeece from University of Nebraska-Lincoln.
Acknowledgments
We want to thank the following people, who generously gave of their time to review
one or more—in some cases all—of the chapters in this book. Their feedback has
helped make this a better book.
REVIEWERS OF THE FIRST EDITION
Eileen Achorn, University of Texas at San Antonio
Tsippa Ackerman, Queens College
Paula Alderette, University of Hartford
Richard Alexander, Muskegon Community College
Leatrice Allen, Prairie State College
Liana Apostolova, University of California, Los Angeles
Hal Arkowitz, University of Arizona
Randolph Arnau, University of Southern Mississippi
Tim Atchison, West Texas A&M University
Linda Bacheller, Barry University
Yvonne Barry, John Tyler Community College
David J. Baxter, University of Ottawa
Bethann Bierer, Metropolitan State College of Denver
Dawn Bishop Mclin, Jackson State University
Nancy Blum, California State University, Northridge
Robert Boland, Brown University
Kathryn Bottonari, University at Buffalo/SUNY
Joan Brandt Jensen, Central Piedmont Community College
Franklin Brown, Eastern Connecticut State University
Eric Bruns, Campbellsville University
Gregory Buchanan, Beloit College
Jeffrey Buchanan, Minnesota State University–Mankato
NiCole Buchanan, Michigan State University
Danielle Burchett, Kent State University
x x v iii Preface
Glenn M. Callaghan, San Jose State University
Christine Calmes, University at Buffalo/SUNY
Rebecca Cameron, California State University, Sacramento
Alastair Cardno, University of Leeds
Kan Chandras, Fort Valley State University
Jennifer Cina, University of St. Thomas
Carolyn Cohen, Northern Essex Community College
Sharon Cool, University of Sioux Falls
Craig Cowden, Northern Virginia Community College
Judy Cusumano, Jefferson College of Health Sciences
Daneen Deptula, Fitchburg State College
Dallas Dolan, The Community College of Baltimore County
Mitchell Earleywine, University at Albany/SUNY
Christopher I. Eckhardt, Purdue University
Diane Edmond, Harrisburg Area Community College
James Eisenberg, Lake Erie College
Frederick Ernst, University of Texas–Pan American
John P. Garofalo, Washington State University–Vancouver
Franklin Foote, University of Miami
Sandra Jean Foster, Clark Atlantic University
Richard Fry, Youngstown State
Murray Fullman, Nassau Community College
Irit Gat, Antelope Valley College
Marjorie Getz, Bradley University
Andrea Goldstein, South University
Steven Gomez, Harper College
Carol Globiana, Fitchburg State University
Cathy Hall, East Carolina University
Debbie Hanke, Roanoke Chowan Community College
Sheryl Hartman, Miami Dade College
Wanda Haynie, Greenville Technical College
Brian Higley, University of North Florida
Debra Hollister, Valencia Community College
Kris Homan, Grove City College
Farrah Hughes, Francis Marion University
Kristin M. Jacquin, Mississippi State University
Annette Jankiewicz, Iowa Western Community College
Paul Jenkins, National University
Cynthia Kalodner, Towson University
Richard Kandus, Mt. San Jacinto College
Jason Kaufman, Inver Hills Community College
Jonathan Keigher, Brooklyn College
Mark Kirschner, Quinnipiac University
Cynthia Kreutzer, Georgia Perimeter College, Clarkston
Thomas Kwapil, University of North Carolina at Greensboro
Preface x x ix
Kristin Larson, Monmouth College
Dean Lauterbach, Eastern Michigan University
Robert Lichtman, John Jay College of Criminal Justice
Michael Loftin, Belmont University
Jacquelyn Loupis, Rowan-Cabarrus Community College
Donald Lucas, Northwest Vista College
Mikhail Lyubansky, University of Illinois, Urbana-Champaign
Eric J. Mash, University of Calgary
Janet Matthews, Loyola University
Dena Matzenbacher, McNeese State University
Timothy May, Eastern Kentucky University
Paul Mazeroff, McDaniel University
Dorothy Mercer, Eastern Kentucky University
Paulina Multhaupt, Macomb Community College
Mark Nafziger, Utah State University
Craig Neumann, University of North Texas
Christina Newhill, University of Pittsburgh
Bonnie Nichols, Arkansas NorthEastern College
Rani Nijjar, Chabot College
Janine Ogden, Marist College
Randall Osborne, Texas State University–San Marcos
Patricia Owen, St. Mary’s University
Crystal Park, University of Connecticut
Karen Pfost, Illinois State University
Daniel Philip, University of North Florida
Skip Pollack, Mesa Community College
William Price, North Country Community College
Linda Raasch, Normandale Community College
Christopher Ralston, Grinnell College
Lillian Range, Our Lady of Holy Cross College
Judith Rauenzahn, Kutztown University
Jacqueline Reihman, State University of New York at Oswego
Sean Reilley, Morehead State University
David Richard, Rollins College
Harvey Richman, Columbus State University
J.D. Rodgers, Hawkeye Community College
David Romano, Barry University
Sandra Rouce, Texas Southern University
David Rowland, Valparaiso University
Lawrence Rubin, St. Thomas University
Stephen Rudin, Nova Southeastern University
Michael Rutter, Canisius College
Thomas Schoeneman, Lewis and Clark College
Stefan E. Schulenberg, University of Mississippi
Christopher Scribner, Lindenwood University
x x x Preface
Russell Searight, Lake Superior State University
Daniel Segal, University of Colorado at Colorado Springs
Frances Sessa, Pennsylvania State University, Abington
Fredric Shaffer, Truman State University
Eric Shiraev, George Mason University
Susan J. Simonian, College of Charleston
Melissa Snarski, University of Alabama
Jason Spiegelman, Community College of Beaver County
Michael Spiegler, Providence College
Barry Stennett, Gainesville State College
Carla Strassle, York College of Pennsylvania
Nicole Taylor, Drake University
Paige Telan, Florida International University
Carolyn Turner, Texas Lutheran University
MaryEllen Vandenberg, Potomac State College of West Virginia
Elaine Walker, Emory University
David Watson, MacEwan University
Karen Wolford, State University of New York at Oswego
Shirley Yen, Brown University
Valerie Zurawski, St. John’s University
Barry Zwibelman, University of Miami
REVIEWERS OF THE SECOND EDITION
Mildred Cordero, Texas State University
Brenda East, Durham Technical Community College
Jared F. Edwards, Southwestern Oklahoma State University
Rick Fry, Youngstown State University
Kelly Hagan, Bluegrass Community & Technical College
Jay Kosegarten, Southern New Hampshire University
Katherine Lau, University of New Orleans
Linda Lelii, St. Josephs University
Tammy L. Mahan, College of the Canyons
David McAllister, Salem State University
Kanoa Meriwether, University of Hawaii, West Oahu
Bryan Neighbors, Southwestern University
Katherine Noll, University of Illinois-Chicago
G. Michael Poteat, East Carolina University
Kimberly Renk, University of Central Florida
JD Rodgers, Hawkeye Community College
Eric Rogers, College of Lake County
Ty S. Schepis, Southwest Texas State University
Gwendolyn Scott-Jones, Delaware State University
Jason Shankle, Community College of Denver
Jeff Sinkele, Anderson University
Marc Wolpoff, Riverside Community College
Preface x x x i
Many thanks also go to our Advisory Board for the helpful insights and suggestions:
Randy Arnau, University of Southern Mississippi
Carolyn Cohen, Northern Essex Community College
Christopher Dyszelski, Madison Area Technical College
Brenda East, Durham Technical Community College
Rick Fry, Youngstown State University
Jeff Henriques, University of Wisconsin
Katherine Noll, University of Illinois at Chicago
Marilee Ogren, Boston College
Linda Raasch, Normandale Community College
Judith Rauenzahn, Kutztown University
Susan Simonian, College of Charleston
For double checking our DSM-5 information, we want to give a loud shout out of thanks to:
Rosemary McCullough, New England Counseling Associates
Jim Foley, College of Wooster
Although our names are on the title page, this book has been a group effort. Special
thanks to a handful of people who did armfuls of work in the early stages of bringing
the book to life in the first edition: Nancy Snidman, Children’s Hospital Boston, for help
with the chapter on developmental disorders; Shelley Greenfield, McLean Hospital, for
advice about the etiology and treatment of substance abuse; Adam Kissel, for help in
preparing the first draft of some of the manuscript; Lisa McLellan, senior development
editor, for conceiving the idea of “Facts at a Glance” tables; Susan Clancy for help in
gathering relevant literature; and Lori Gara-Matthews and Anne Perry for sharing a
typical workday of a pediatrician and a school psychologist, respectively.
To the people at Worth Publishers who have helped us bring this book from
conception through gestation and birth, many thanks for your wise counsel, creativity,
and patience. Specifically, for the second edition, thanks to: Jessica Bayne, our acquisitions
editor and rock; Thomas Finn, our development editor who went over and over and over
each chapter with good humor, patience, and a needed “outside” eye; Jim Strandberg,
our pre-development editor, whose advice, support, and amazing attention to detail
were sorely appreciated; Christine Cervoni and her crew at TSI Graphics for getting the
manuscript ready to become a book; Babs Reingold (again), art director, for her out-of-
the-box visual thinking. We’d also like to thank Roman Barnes and Robin Fadool for their
help with photo research; Eileen Lang and Catherine Michaelsen for helping prepare the
manuscript for turnover; Anthony Casciano for helping to wrangle our supplements and
media packages; and Kate Nurre for marketing our book. And a special note of thanks to
Carlise Stembridge for organizing and helping us with our advisory board.
On the personal side, we’d like to thank our children—Neil, David, and Justin—for
their unflagging love and support during this project and for their patience with our foibles
and passions. We also want to thank: our mothers—Bunny and Rhoda—for allowing us
to know what it means to grow up with supportive and loving parents; Steven Rosenberg,
for numerous chapter story suggestions; Merrill Mead-Fox, Melissa Robbins, Jeanne
Serafin, Amy Mayer, Kim Rawlins, and Susan Pollak, for sharing their clinical and personal
wisdom over the last three decades; Michael Friedman and Steven Hyman, for answering
our esoteric pharmacology questions; and Jennifer Shephard and Bill Thompson, who
helped track down facts and findings related to the neurological side of the project.
Robin S. Rosenberg
Stephen M. Kosslyn
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ABNORMAL PSYCHOLOGY
3
CHAPTER 1
The History of
Abnormal Psychology
ig Edie” (Edith Bouvier Beale, 1894–1977) and her
daughter, “Little Edie” (Edith Beale, 1917–2002 ),
lived together as adults for 29 years. Their home was
a 28-room mansion, called Grey Gardens, in the chic town of East
Hampton, New York. But the Beales were not rich society women,
entertaining in grand style. They had few visitors, other than people
who delivered food to them daily, and they lived in impoverished
circumstances. For the most part, they inhabited only two of the
second-floor rooms and an upstairs porch of a house that was fall-
ing apart. These intelligent women were not simply poor recluses,
though. They were unconventional, eccentric women who flaunted
the rules of their time and social class.
Let’s consider Big Edie first. In her later years, Big Edie had dif-
ficulty walking, and her bedroom was the hub of the Beale women’s
lives and full of squalor. It contained a small refrigerator, a hot plate
on which food was heated or cooked, and up to 52 cats. The room
had two twin beds, one for Little Edie, the other for Big Edie. Big
Edie made her bed into an unusual nest of blankets (no sheets). Cats
constantly walked across the bed or rested on it; because the women
didn’t provide the cats with a litter box, the bed was one of the spots
the cats left their droppings. Big Edie’s mattress was so soiled that the
grime and the cat droppings were indistinguishable.
Big Edie hadn’t left the house in decades (except for one occa-
sion; Sheehy, 1972) and would let Little Edie out of her sight for only
a few minutes before yelling for her to return to the bedroom. When
Big Edie fell off a chair and broke her leg at the age of 80, she refused
to leave the house to see a doctor, and refused to allow a doctor to
come to the house to examine her leg. As a result, she developed
bedsores that became infected and she died at Grey Gardens 7 months
later (Wright, 2007).
The Three Criteria for Determining
Psychological Disorders
Distress
Impairment in Daily Life
Risk of Harm
Context and Culture
Views of Psychological
Disorders Before Science
Ancient Views of Psychopathology
Forces of Evil in the Middle Ages and
the Renaissance
Rationality and Reason in the 18th and
19th Centuries
The Transition to Scientific Accounts
of Psychological Disorders
Freud and the Importance of Unconscious Forces
The Humanist Response
Scientific Accounts of
Psychological Disorders
Behaviorism
The Cognitive Contribution
Social Forces
Biological Explanations
The Modern Synthesis of Explanations
of Psychopathology
Wildcard Images/Glasshouse. Photo for illustrative purposes only; any individual depicted is a model.
Little Edie was also unusual, most obviously in her style of dress. Little Edie always
covered her head, usually with a sweater that she kept in place with a piece of jewelry. She
professed not to like women in skirts, but invariably wore skirts herself, typically wearing
them upside down so that the waistband was around her knees or calves and the skirt hem
bunched around her waist. She advocated wearing stockings over pants, and she suggested
that women “take off the skirt, and use it as a cape” (Maysles & Maysles, 1976).
Although both of these women were odd, could their behavior be
chalked up to eccentricity or did one or both of them have a psychological disorder?
It depends on how psychological disorder is defined.
The sort of psychologist who would evaluate Big Edie and Little Edie would
specialize in abnormal psychology (or psychopathology), the subfield of psychol-
og y that addresses the causes and progression of psychological disorders (also
referred to as psychiatric disorders, mental disorders, or mental illness). How would
a mental health clinician—a mental health professional who evaluates or treats
people with psychological disorders—determine whether Big Edie or Little Edie
(or both of them) had a psychological disorder? The clinician would need to
evaluate whether the women’s behavior and experience met three general criteria
for psychological disorders.
The Three Criteria for Determining
Psychological Disorders
Big Edie and Little Edie came to public attention in 1971, when their unusual
living situation was described in the national press. Health Department inspectors
had raided their house and found the structure to be in violation of virtually every
regulation. “In the dining room, they found a 5-foot mountain of empty cans;
in the upstairs bedrooms, they saw human waste. The stor y became a national
scandal. Health Department officials said they would evict the women unless the
house was cleaned” (Martin, 2002). The Beales were able to remain in their house
after Big Edie’s niece ( Jacqueline Kennedy Onassis, the former first lady) paid to
have the dwelling brought up to the Health Department’s standards.
To determine whether Big Edie or Little Edie had a psychological disorder,
we must first define psychological disorder: a pattern of thoughts, feelings, or
behaviors that causes significant personal distress, significant impairment in daily life,
and/or significant risk of harm, any of which is unusual for the context and culture
in which it arises (American Psychiatric Association, 2013). Notice the word signifi-
cant in the definition, which indicates that the diagnosis of psychological disorder is
applied only when the symptoms have a substantial effect on a person’s life. As we
shall see shortly, all three elements (distress, impairment, and risk of harm) do not
need to be present; if two (or even one) of the elements are present to a severe
enough degree, then the person’s condition may merit the diagnosis of a psycho-
logical disorder (see Figure 1.1). Let’s consider these three elements in more detail.
Distress
Distress can be defined as anguish or suffering, and all of us experience distress at
different times in our lives. However, when a person with a psychological disorder
experiences distress, it is often out of proportion to a situation. The state of being
Determination
of psychological
disorder
Pattern of
thoughts,
feelings,
or behaviors
Risk of harmImpairmentDistressDistress
FI G U RE 1.1 • Determining a
Psychological Disorder: Three
Criteria The severity of a person’s distress,
impairment in daily life, and/or risk of harm
determine whether he or she is said to have
a psychological disorder. All three elements
don’t need to be present at a significant
level: When one or two elements are present
to a significant degree, this may indicate a
psychological disorder, provided that the
person’s behavior and experience are not
normal for the context and culture in which
they arise.
Abnormal psychology
The subfield of psychology that addresses
the causes and progression of psychological
disorders; also referred to as psychopathology.
Psychological disorder
A pattern of thoughts, feelings, or behaviors
that causes significant personal distress,
significant impairment in daily life, and/
or significant risk of harm, any of which is
unusual for the context and culture in which
it arises.
4 C H A P T E R 1
distressed, in and of itself, does not indicate a psychological
disorder—it is the degree of distress or the circumstances in
which the distress arises that mark abnormality. Some people
with psychological disorders exhibit their distress: They may
cry in front of others, share their anxieties, or vent their an-
ger on those around them. But other people with psychological
disorders contain their distress, leaving family and friends un-
aware of their emotional suffering. For example, a person may
worry excessively but not talk about the worries, or a depressed
person may cry only when alone, putting on a mask to con-
vince others that everything is all right.
Severe distress, by itself, doesn’t necessarily indicate a
psychological disorder. The opposite is also true: The absence
of distress doesn’t necessarily indicate the absence of a psycho-
logical disorder. A person can have a psychological disorder without experiencing
distress, although it is uncommon. For instance, someone who chronically abuses
stimulant medication, such as amphetamines, may not feel distress about misusing
the drug, but that person nonetheless has a psychological disorder (specifically, a
type of substance use disorder).
Did either Big Edie or Little Edie exhibit distress? People who knew them describe
the Beale women as free spirits, making the best of life. Like many other people, they
were distressed about their financial circumstances; but they in fact had real financial
difficulties, so these worries were not unfounded. Little Edie did show significant
distress in other ways, though. She was angry and resentful about having to be a full-
time caretaker for her mother, and the documentary film Grey Gardens (as well as the
HBO film and Broadway play of the same name) clearly portrays this: When Big Edie
yells for Little Edie to return to her side, Little Edie says in front of the camera, “I’ve
been a subterranean prisoner here for 20 years” (Maysles & Maysles, 1976).
Although Little Edie appears to have been significantly distressed, her distress
was reasonable given the situation. Being the full-time caretaker to an eccentric and
demanding mother for decades would undoubtedly distress most people. Because her
distress made sense in its context, it is not an element of a psychological disorder. Big
Edie, in contrast, appears to have become significantly distressed when she was alone
for more than a few minutes, and this response is unusual for the context. We can
consider Big Edie’s distress as meeting this criterion for a psychological disorder.
Impairment in Daily Life
Impairment is a significant reduction of a person’s ability to function in some important
area of life. A person with a psychological disorder may be impaired in functioning at
school, at work, in taking adequate care of himself or herself, or in relationships. For
example, a woman’s drinking problem may interfere with her ability to do her job or
to attend to her bills; a middle-aged, married man’s continually worrying about his
increasing baldness—spending hours and hours each day “fixing” his hair—might
impair his ability to get to work on time.
Where do mental health clinicians draw the line between normal functioning
and impaired functioning? It is the degree of impairment that indicates a psychological
disorder. When feeling “down” or nervous, we are all likely to function less well—
for example, we may feel irritable or have difficulty concentrating. With a psycho-
logical disorder, though, the degree of impairment is atypical for the context—the
person is impaired to a greater degree than most people in a similar situation. For in-
stance, after a relationship breakup, most people go through a difficult week or two,
but they still go to school or to work. They may not accomplish much, but they soon
Big Edie and Little Edie Beale were clearly
unconventional and eccentric. But did either
of them have a psychological disorder?
Psychological disorders involve significant
distress, impairment in daily life, and/or risk
of harm.
A
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The History of Abnormal Psychology 5
begin to bounce back. Some people, however, are more impaired after a breakup—
they may not make it out of the house or even out of bed; they may not bounce back
after a few weeks. These people are significantly impaired.
One type of impairment directly reflects a particular pattern of mental events: A
psychosis is an impaired ability to perceive reality to the extent that normal func-
tioning is difficult or not possible. The two forms of psychotic symptoms are hal-
lucinations and delusions. Hallucinations are sensations that are so vivid that the
perceived objects or events seem real, although they are not. Hallucinations can oc-
cur in any of the five senses, but the most common type is auditory hallucinations, in
particular, hearing voices. However, a hallucination—in and of itself—does not in-
dicate psychosis or a psychological disorder. Rather, this form of psychotic symptom
must arise in a context that renders it unusual and impairs functioning.
The other psychotic symptom is delusions—persistent false beliefs that are held
despite evidence that the beliefs are incorrect or exaggerate reality. The content of
delusions can vary across psychological disorders. Common themes include a person’s
belief that:
• other people or organizations—the FBI, aliens, the neighbor across the street—are
after the person (paranoid or persecutory delusions);
• his or her intimate partner is dating or interested in another person (delusional jealousy);
• he or she is more powerful, knowledgeable, or influential than is true in reality and/
or that he or she is a different person, such as the president or Jesus (grandiose delusions);
• his or her body—or a part of it—is defective or functioning abnormally (somatic delusion).
Were the Beale women impaired? The fact that they lived in such squalor implies
an inability to function normally in daily life. They knew about hygienic standards
but didn’t live up to them. Whether the Beales were impaired is complicated by the
fact that they viewed themselves as bohemians, set their own standards, and did not
want to conform to mainstream values (Sheehy, personal communication, December
29, 2006). However, their withdrawal from the world can be seen as clear evidence
that they were impaired. Perhaps they couldn’t function in the world and so retreated
to Grey Gardens.
The women also appear to have been somewhat paranoid: In the heat of
summer, they left the windows nailed shut (even on the second floor) for fear of
possible intruders. The women’s social functioning was impaired to the extent that
their paranoid beliefs led to strange behaviors that isolated them. In addition, their
beliefs led them to behave in ways that made the house so uncomfortable— extreme
temperatures and fleas—that relatives wouldn’t visit. And Big Edie’s distress at being
alone for even a few minutes indicates that her ability to function independently was
impaired. It seems, then, that a case could be made that both of them—Big Edie
more so than Little Edie—were impaired and not functioning normally.
Risk of Harm
Some people take more risks than others. They may drive too fast or drink too much.
They may diet too strenuously, exercise to an extreme, gamble away too much money,
or have unprotected sex with multiple partners. For such behavior to indicate a psy-
chological disorder, it must be outside the normal range. The criterion of danger,
then, refers to symptoms of a psychological disorder that lead to life or property being
put at risk, either accidentally or intentionally. For example, a person with a psycho-
logical disorder may be in danger when:
• depression and hopelessness lead him or her to attempt suicide;
• hallucinations interfere with normal safety precautions, such as checking for cars
before crossing the street;
We don’t know why this woman is so upset,
but being persistently upset at work might
qualify as an impairment—a significant
reduction in a person’s ability to function in
some important area of life, such as work.
Researchers have attempted to measure
the effects of impairment associated with
psychological disorders on the ability to
function at work: For every 100 workers, an
average of 37 work days per month are lost
because of reduced productivity or absences
due to psychological disorders (Kessler &
Frank, 1997).
©
A
le
x
M
a
lo
n
ey
/z
ef
a
/C
o
rb
is
Psychosis
An impaired ability to perceive reality to the
extent that normal functioning is difficult
or not possible. The two types of psychotic
symptoms are hallucinations and delusions.
Hallucinations
Sensations that are so vivid that the perceived
objects or events seem real, although they are
not. Hallucinations can occur in any of the five
senses.
Delusions
Persistent false beliefs that are held despite
evidence that the beliefs are incorrect or
exaggerate reality.
6 C H A P T E R 1
• a distorted body image and other psychological disturbances lead the person to
refuse to eat enough food to maintain a healthy weight, which in turn leads to
malnutrition and medical problems.
Psychological disorders can also lead people to put other people’s lives at risk.
Examples of this type of danger include:
• auditory hallucinations that command the person to harm another person;
• suicide attempts that put the lives of other people at risk, such as driving a car into
oncoming traffic;
• paranoia so extreme that a parent kills his or her children in order to “save” them
from a greater evil.
The house in which Little Edie and Big Edie lived had clearly become dan-
gerous. Wild animals—raccoons and rats—roamed the house, and the ceiling was
falling down. But having too little money to make home repairs doesn’t mean
that someone has a psychological disorder. Some might argue that perhaps the
Beale women simply weren’t aware of the danger. The women
were, however, aware of some dangers: When their heat stopped
working, they called a heating company to repair it, and ditto
for the electricit y. They had a handyman come in regularly to
repair fallen ceilings and walls, and to fill holes that rats might
use to enter (Wright, 2007). It’s hard to say, however, whether
they realized the extent to which their house itself had become
dangerous.
On at least one occasion in her early 30s, Little Edie appears to
have been a danger to herself. Her cousin John told someone about
“a summer afternoon when he watched Little Edie climb a catalpa
tree outside Grey Gardens. She took out a lighter. He begged her
not to do it. She set her hair ablaze” (Sheehy, 2006). From then on,
her head was at least partially bald, explaining her ever-present head
covering.
Aside from Little Edie’s single episode with the lighter, it’s not
clear how much the Beale women’s behavior led to a significant risk
of harm. Big Edie recognized most imminent dangers and took
steps to ensure her and her daughter’s safety. The women were not
overtly suicidal nor did they harm others. The only aspect of their
lives that suggests a significant risk of harm was the poor hygienic
standards they maintained.
Context and Culture
As we noted earlier, what counts as a signif icant level of dis-
tress, impair ment, or r isk of har m depends on the context in
which it arises. That human waste was found in an empty room
at Grey Gardens might indicate abnormal behavior, but the fact
that the plumbing was out of order for a period of time might
provide a reasonable explanation. Of course, knowing that the
human waste was allowed to remain in place after the plumb-
ing was f ixed would probably decide the question of whether the behavior was
abnormal.
In addition, the Beales appeared to have delusions—that people wanted to
break into the house or kidnap them, and that then-President Nixon might have
been responsible for the 1971 “raid” on their house by the town health inspectors
(Wright, 2007). But these delusions aren’t necessarily as farfetched as they might
Using this book’s definition of a psychological
disorder, did either of the Beales have a
disorder? Big Edie exhibited distress that
was inappropriate to her situation; both
women appeared to have an impaired ability
to function. The risk of harm to the women,
however, is less clear-cut.
To
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The History of Abnormal Psychology 7
sound. Their house was broken into in 1968, and,
as relatives of Jackie Kennedy, they had cars with
Secret Service agents posted outside their house
while John F. Kennedy was president.
Behavior that seems inappropriate in one con-
text may make sense in another. Having a psycho-
logical disorder isn’t merely being different—we
wouldn’t say that someone was abnormal simply
because he or she was avant-garde or eccentric or
acted on unusual social, sexual, political, religious,
or other beliefs (American Psychiatric Association,
2013). And as we’ve seen with the Beales, the ef-
fects of context can blur the line between being
dif ferent and having a disorder. Table 1.1 pro-
vides additional information about psychological
disorders.
Culture, too, can play a crucial role in how
mental illness is diagnosed. To psychologists, cul-
ture is the shared norms and values of a society;
these norms and values are explicitly and implicitly
conveyed to members of the society by example and
through the use of reward and punishment. Differ-
ent societies and countries have their own cultures,
each with its own view of what constitutes mental
health and mental illness—even what constitutes
distress and how to communicate that distress. For
example, in some cultures, distress may be con-
veyed by complaints of fatigue or tiredness rather
than by sadness or depressed mood. Some sets of
symptoms that are recognized as disorders in other
parts of the world are not familiar to most Western-
ers. One example, described in Case 1.1, is koro, a
disorder that arises in some people from countries
in Southeast Asia. Someone with koro rapidly de-
velops an intense fear that his penis—or her nipples
and vulva—will retract into the body and possibly cause death (American Psychi-
atric Association, 2013). This disorder may break out in clusters of people, like an
epidemic (Bartholomew, 1998; Sachdev, 1985). Similar genital-shrinking fears have
been reported in India and in West African countries (Dzokoto & Adams, 2005;
Mather, 2005).
CASE 1.1 • FROM TH E OUTSIDE: Cultural Influence on Symptoms
Although most cases of koro appear to resolve quickly, in a minority of cases, symptoms may
persist.
A 41-year-old unmarried, unemployed male from a business family, presented with the
complaints of gradual retraction of penis and scrotum into the abdomen. He had frequent
panic attacks, feeling that the end had come. The symptoms had persisted more than
15 years with a waxing and waning course. During exacerbations he spent most of his time
measuring the penis by a scale and pulling it in order to bring it out of [his] abdomen. He
tied a string around it and attached it to a hook above to prevent its shrinkage during [the]
night. . . . He did not have regular work and was mostly dependent on the family.
(Kar, 2005, p. 34)
How do we define “risk” or “danger” in
different cultural environments? How
does culture impact our understanding of
abnormal behavior?
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TABLE 1.1 • Psychological Disorders: Facts at a Glance
• Psychological disorders are a leading cause of disability and death, ranked second
after heart disease (Murray & Lopez, 1996).
• About half of all Americans will likely develop at least one of 30 common psycho-
logical disorders, such as those related to depression, anxiety, or substance abuse,
over the course of their lives; in half of the cases, symptoms will begin by age 14
(Kessler, Berglund, et al., 2005).
• Those born more recently have a higher likelihood of developing a psychological
disorder than those born earlier (Kessler, Berglund, et al., 2005).
• Within a given year, about 25% of Americans experience a diagnosable or diag-
nosed mental disorder; of these cases, almost one quarter are severe (Kessler, Chiu,
et al., 2005).
• Disadvantaged ethnic groups—Hispanics and Blacks—do not have a higher risk
than others for psychological disorders overall (Breslau et al., 2005).
Culture
The shared norms and values of a society that
are explicitly and implicitly conveyed to its
members by example and through the use of
reward and punishment.
8 C H A P T E R 1
In addition, cultural norms about psy-
chopatholog y are not set in stone but can
shift. Consider that, in 1851, Dr. Samuel
Ca r t w r ig ht of Lou isia na w rote a n essay
in which he declared that slaves’ running
away wa s ev idence of a ser iou s ment a l
d isorder t h at he ca l led “ d r apetom a n ia”
( E a k i n , 2 0 0 0 ) . Mor e r e ce nt l y, homo –
sexualit y was of f icially considered a psy-
cholog ica l d isorder in the Un ited States
until 1973, when it was removed from the
Diagnostic and Statistical Manual of Mental
Disorders (DSM), the manual used by men-
tal health clinicians to classify psychologi-
cal disorders.
L e t ’s e x a m i ne t he b eh av ior of t he
Bea les w ith in their context and cu lture.
Big Ed ie’s father claimed that h is ances-
tor s were prom i nent French Cat hol ics ;
she and her sibl ing s g rew up f inancia l ly
well off. Big Edie was a singer and a per-
former, but, as a product of her time, she
wa s ex pected to m a r r y wel l ( McKen na,
2004). Her father arranged for her to wed
New York lawyer Phelan Beale, from a so-
cially prominent Southern family ( Rakoff,
2002 ). Little Edie was bor n about a year
later, followed by two brothers. Big Edie
was very close to her daughter, even keep-
ing her out of school when Little Edie was
11 and 12, ostensibly for “health reasons.” However, Little Edie was well enough
to go to the movies with her mother ever y day and on a shopping trip to Paris
(Sheehy, 2006).
After she was married, Big Edie continued to sing, to write songs with her
accompanist, and even to record some of those songs. At that time, however, cul-
tural conventions required a woman of Big Edie’s social standing to stop perform-
ing after marr ying, even if such performances generally were limited to social
functions. Big Edie’s need to perform was almost a compulsion, though, and she
would head straight to the piano at family gatherings.
In 1934, when Little Edie was 16, Big Edie and her husband divorced; divorce
back then was much less common and much less socially acceptable than it is today.
This event marked the start of Big Edie’s life as a recluse (Davis, 1969). By 1936,
the house and grounds began to suffer from neglect (Davis, 1996). In 1942, Big
Edie’s husband stopped supporting her financially after she showed up late for their
son’s wedding, dressed inappropriately—another time when Big Edie’s behavior
was unusual for the context and culture. Big Edie’s father set up a trust fund for
her, which provided a small monthly allowance, barely enough to pay for food and
other necessities.
Like her mother, Little Edie was artistically inclined. She aspired to be an actress,
dancer, and poet. In 1946, she left home to live in New York City and work as a
model, but her father disapproved of this, as he had disapproved of his wife’s musical
performances (Sheehy, 2006).
GETTING THE PICTURE
Which photo shows a person more likely to have a psychological disorder based on the
voluntary changes made to his/her skin? Answer: It depends on the cultural context. The
scarring of the man in the left is intentional and common in his West African tribe, and
hence would not be considered a sign of abnormality—but such scarring might be a sign
of something abnormal in some Western cultures. However, cultures shift over time, and
what is abnormal in one time and place may not be in another. For example, ear gauging
(shown on the right) used to be found in African tribes but not in the West, but recently
some young people in Western culture have adopted this practice.
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The History of Abnormal Psychology 9
In 1952, after 6 years of being separated from her daughter, Big Edie became
seriously depressed (Sheehy, 2006), although there is no information about her spe-
cific symptoms. She spent 3 months calling Little Edie daily, begging her to return to
Grey Gardens. Eventually, Little Edie moved back to take care of Big Edie. When she
did, her artistic aspirations became only dreams and fantasies. Grey Gardens vividly
captures Little Edie’s disappointment at the path her life took—becoming a round-
the-clock caretaker to her mother, a disappointed woman herself.
So far, we’ve seen that psychological disorders lead to significant distress, impair-
ment in daily life, and/or risk of harm. We’ve also seen that the determination of a
disorder depends on the culture and context in which these elements occur. A case
could be made that the Beale women did have psychological disorders; let’s consider
each woman in turn. Big Edie exhibited significant distress when alone for more
than a few minutes; her reclusiveness and general lifestyle suggest an impaired abil-
ity to function independently in the world—perhaps to the point where there might
have been a risk of harm to herself or her daughter. Her behavior and experience
appear to satisfy the first two criteria, which is enough to indicate that she had a psy-
chological disorder. Moreover, Big Edie suffered from depression at some point after
Little Edie moved to New York, and she experienced enough distress that she begged
her daughter to return to Grey Gardens.
As for Little Edie, her distress was appropriate for the context and thus would
not meet the first criterion. Her ability to function independently, though, appears to
have been significantly impaired, which also increased the risk of harm to herself and
her mother. It appears that she, too, suffered from a psychological disorder. However,
these conclusions must be tentative—they are based solely on films of the women and
other people’s descriptions and memories of them.
Now that we know what is required to determine whether someone has a
psychological disorder, we’ll spend the rest of this chapter looking at how psychopa-
thology has been explained through the ages, up to the present.
Thinking Like A Clinician
Suppose Pietro was hearing the voice of a deceased relative, and he was from a culture where
such experiences were considered normal—or at least not abnormal. But he was distressed
about hearing the voice, to the point where he was having a hard time doing his job. Should
Pietro be considered to have a psychological disorder? If so, why? If not, why not? What
additional information would you want to help you decide, if you weren’t sure?
Views of Psychological Disorders
Before Science
Psychological disorders have probably been around as long as there have been
humans. In every age, people have tried to answer the fundamental questions of why
mental illness occurs and how to treat it. In this section, we begin at the beginning,
by considering the earliest known explanations of psychological disorders.
Ancient Views of Psychopathology
Throughout history, humans have tried to understand the causes of mental illness
in an effort to counter its detrimental effects. The earliest accounts of abnormal
thoughts, feelings, and behaviors focused on two possible causes: (1) supernatural
forces and (2) an imbalance of substances within the body.
10 C H A P T E R 1
Supernatural Forces
Societies dating as far back as the Stone Age appear to have explained psychologi-
cal disorders in terms of supernatural forces—magical or spiritual in nature (Porter,
2002). Both healers and common folk believed that the mentally ill were possessed
by spirits or demons, and possession was often seen as punishment for some reli-
gious, moral, or other transgression.
In the ancient societies that understood psychological disorders in this way,
treatment often consisted of exorcism—a ritual or ceremony intended to force
the demons to leave the person’s body and restore the person to a normal
state. The healer led the exorcism, which in some cultures consisted of re-
citing incantations, speaking with the spirit, and inflicting physical pain
to induce the spirit to leave the person’s body (Goodwin et al., 1990).
This belief in supernatural forces was common in ancient Egypt and
Mesopotamia and, as we shall see shortly, arose again in the Middle
Ages in Europe and persists today in some cultures. Although it is tempt-
ing to regard such a view of psychopathology and its treatment as barbaric or uncivi-
lized, the healers were simply doing the best they could in trying to understand and
treat devastating impairments.
Imbalance of Substances Within the Body
Throughout histor y, some societies have understood psychological disorders as
arising from imbalances of one or more bodily substances.
Chinese Qi
Healers in China beginning in the 7th century b.c.e. viewed psychological disor-
ders as a form of physical illness, reflecting imbalances in the body and spirit. This
view rests on the belief that all living things have a life force, called qi (pronounced
“chee,” as in cheetah), which flows through the body along 12 channels to the organs.
Illness results when qi is blocked or seriously imbalanced; to this day, this view
underpins aspects of Chinese medicine. Even today, Chinese treatment for various
problems, including some psychological disorders, aims to restore the proper balance
of qi. Practitioners use a number of techniques, including acupuncture and herbal
medicine.
Ancient Greeks and Romans
Like the ancient Chinese, the ancient Greeks viewed mental illness as a form of bodily
illness arising from imbalances (U.S. National Library of Medicine, 2005). Specifi-
cally, mental illness arose through an imbalance of four humors (that is, bodily fluids):
black bile, blood, yellow bile, and phlegm. Each humor corresponded to one of four
basic elements: earth, air, fire, and water. The ancient Greeks believed that differ-
ences in character reflected the relative balance of these humors, and an extreme
imbalance of the humors resulted in illness—including mental illness. Most promi-
nent among the resulting mental disorders were mania (marked by excess uncontrol-
lability, arising from too much of the humors blood and yellow bile) and melancholy
(marked by anguish and dejection, and perhaps hallucinations, arising from too much
black bile). The goal of treatment was to restore the balance of humors through diet,
medicine, or surgery (such as bleeding—letting some blood drain out of the body—if
the person were diagnosed as having too much of the humor blood).
Beginning with the physician Hippocrates (460–377 b.c.e.), the ancient Greeks
emphasized reasoning and rationality in their explanations of natural phenomena,
rejecting supernatural explanations. Hippocrates suggested that the brain—rather
than any other bodily organ—is responsible for mental activity, and that mental
illness arises from abnormalities in the brain (Shaffer & Lazarus, 1952). Today, the
Archaeologists have found evidence of
trephination, the boring of a hole in the skull,
dating as far back as 7,000 years ago. In some
ancient cultures, insanity was thought to arise
from supernatural forces; one explanation for
trephination is that the hole allowed these
supernatural forces to escape. Treatment
for mental illness is usually related to the
prevailing explanation of the cause of the
mental illness.
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The History of Abnormal Psychology 11
term medical model is used to refer to Hippocrates’ view that all illness, including
mental illness, has its basis in biological disturbance. Galen (131–201 c.e.), a Roman
doctor, extended the ideas of the Greeks. Galen proposed that imbalances in humors
produced emotional imbalances—and such emotional problems in turn could lead to
psychological disorders.
Forces of Evil in the Middle Ages and the Renaissance
With the rise of Christianity in Europe, psychopathology came to be attrib-
uted to forces of evil. During the Middle Ages (approximately 500–1400 c.e.),
the Greek emphasis on reason and science lost influence, and madness was
once again thought to result from supernatural forces. However, at this time
mental illness was conceived as a consequence of a battle between good and
evil for the possession of a person’s soul. Prophets and visionaries were be-
lieved to be possessed or inspired by the will of God. For example, French
heroine Joan of Arc reported that she heard the voice of God command
her to lead a French army to drive the British out of France. The French
hailed her as a visionary. In contrast, other men and women who reported
such experiences usually were believed to be possessed by the devil or were
viewed as being punished for their sins. Treatment consisted of attempts to
end the possession: exorcism, torture (with the idea that physical pain would
drive out the evil forces), starvation, and other forms of punishment to the
body. Such inhumane treatment was not undertaken everywhere, though.
As early as the 10th century, Islamic institutions were caring humanely for
those with mental illness (Sarró, 1956).
During the Renaissance (approximately the 1400s through the 1600s),
mental illness continued to be viewed as a result of demonic possession, and
witches were held responsible for a wide variety of ills. Indeed, witches were
blamed for other people’s physical problems and even for societal and envi-
ronmental problems, such as droughts or crop failures. As before, treatment
was primarily focused on ridding the person of demonic forces, in one way
or another.
During this period, people believed that witches put the whole com-
munit y in jeopardy through their evil acts and through their associa-
tion with the devil (White, 1948). The era is notable for its witch hunts,
which were organized efforts to track down people who were believed
to be in league with the devil and to have inflicted possession on other
people (Kemp, 2000). Once found, these “witches” were often burned
alive. The practice of witch burning spread throughout Europe and the American
colonies:
Judges were called upon to pass sentence on witches in great numbers. A French judge
boasted that he had burned 800 women in 16 years on the bench; 600 were burned
during the administration of a bishop in Bamberg. The Inquisition, originally started
by the Church of Rome, was carried along by Protestant Churches in Great Britain
and Germany. In Protestant Geneva 500 persons were burned in the year 1515. Other
countries, where there were Catholic jurists, boasted of as many burnings. In Treves,
7,000 were reported burned during a period of several years.
(Bromberg, 1937, p. 61, quoted in White, 1948, p. 8)
Rationality and Reason in the 18th and 19th Centuries
At the end of the Renaissance, rational thought and reason gained acceptance
again. French philosopher René Descartes proposed that m ind and body are
distinct and that bodily illness arises from abnormalities in the body, whereas
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The almost naked man is being beaten by
priests in order to drive out the devil (the devil
is kneeling in front of another priest). Such
punishments or torture were attempts to
“cure” mental illness, which was believed to
arise from the devil.
12 C H A P T E R 1
mental illness arises from abnormalities in the mind. Similarly, according to the
17th-centur y British philosopher John Locke, insanit y is caused by irrational
thinking, and so could be treated by helping people regain their rational, logical
thought process.
However, the theory that deficits in rationality and reason caused mental ill-
ness did not lead to consistent approaches to treatment. In the Western world, the
mentally ill were treated differently from country to country and decade to decade.
As we see in the following sections, various approaches were tried in an effort to
cope with the mentally ill and with mental illness itself.
Asylums
The Renaissance was a time of widespread innovation and enlight-
ened thinking. For some people, this enlightenment extended to
their view of how to treat those with mental illness—humanely.
Some groups founded asylums, institutions to house and care for
people who were afflicted with mental illness. In general, asylums
were founded by religious orders; the first of this type was opened
in Valencia, Spain, in 1409 (Sarró, 1956). In subsequent decades,
asylums for the mentally ill were built throughout Europe.
Before long, though, cr iminals and others who weren’t
necessarily mentally ill were sent to asylums, and the facilities
became overcrowded. Their residents were then more like in-
mates than patients. At least in some cases, people were sent to
asylums simply to keep them off the street, without any effort to
treat them.
Perhaps the most famous asylum from this era was the Hos-
pital of St. Mary of Bethlehem in London (commonly referred
to as “Bedlam,” which became a word meaning “confusion and
uproar”). In 1547, that institution shifted from being a general
hospital to an asylum used to incarcerate the mad, particularly
those who were poor. Residents were chained to the walls or floor or put in cages
and displayed to a paying public, much like animals in a zoo (Sarró, 1956). Officials
believed that such exhibitions would deter people from indulging in behaviors be-
lieved to lead to mental illness.
Pinel and Mental Treatment
The humane treatment of people with psychological disorders found a great sup-
porter in French physician Phillipe Pinel (1745–1826). He and others transformed the
lives of asylum patients at the Salpêtrière and Bicêtre Hospitals (for women and men,
respectively) in Paris: In 1793, Pinel removed their chains and stopped “treatments”
that involved bleeding, starvation, and physical punishment (Porter, 2002). Pinel and
his colleagues believed that “madness” is a disease; they carefully observed patients
and distinguished between different types of “madness.” Pinel also identified partial
insanity, where the person was irrational with regard to one topic but was other-
wise rational. He believed that such a person could be treated through psychological
means, such as reasoning with him or her, which was one of the first mental treat-
ments for mental disorders.
Moral Treatment
In the 1790s, a group of Quakers in England developed a treatment for mental ill-
ness that was based on their personal and religious belief systems. Mental illness was
seen as a temporary state during which the person was deprived of his or her rea-
son. Moral treatment consisted of providing an environment in which people with
Asylums were initially meant to be humane
settings for those with mental illness. A victim
of their success, asylums became overcrowded
as a result of an influx of criminals and people
with medical illnesses. With overcrowding,
the primary purpose of asylums became
incarceration rather than treatment, as was
true of the Hospital of St. Mary of Bethlehem
(“Bedlam”) in the early 18th century,
illustrated here.
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Asylums
Institutions to house and care for people who
are afflicted with mental illness.
Moral treatment
Treatment of the mentally ill that involved
providing an environment in which people with
mental illness were treated with kindness and
respect and functioned as part of a community.
The History of Abnormal Psychology 13
mental illness were treated with kindness and respect. The “mad” residents lived
out in the country, worked, prayed, rested, and functioned as a community. Over
90% of the residents treated this way for a year recovered (Whitaker, 2002), at least
temporarily.
Moral treatment also began to be used in the United States. Around the time that
Pinel was unchaining the mentally ill in France, Doctor Benjamin Rush (1745–1813),
a physician at the Pennsylvania Hospital in Philadelphia, moved the mentally ill from
filthy basement cells to rooms above ground level, provided them with mattresses
and meals, and treated them with respect.
In the 1840s Dorothea Dix (1802–1887), a schoolteacher who had witnessed
the terrible conditions in the asylums of New England, also began to support moral
treatment. She engaged in lifelong humanitarian efforts to ensure that the mentally
ill were housed separately from criminals and treated humanely, in both public and
private asylums (Viney, 2000). Dix also helped to raise millions of dollars for build-
ing new mental health facilities throughout the United States. Her work is all the
more remarkable because she undertook it at a time when women did not typically
participate in such social projects.
Moral treatment proved popular, and its success had an unintended consequence:
Unlike private asylums, public asylums couldn’t turn away patients, and thus their
population increased tenfold, as the mentally ill were joined by people with epi-
lepsy and others with neurological disorders, as well as many who might otherwise
have gone to jail. As a result, public institutions housing the mentally ill again be-
came overcrowded and underfunded, and moral treatment—or treatments of any
kind—were no longer provided (Porter, 2002). Sedation and management became
the new goals.
Thinking Like A Clinician
Why might explanations of mental illness as arising from supernatural forces have been
popular for so long? How does a given treatment follow from beliefs about the cause of
mental illness? Can you think of at least two specific examples where beliefs about the cause
of mental illness have shaped treatments in different ways?
The Transition to Scientific
Accounts of Psychological
Disorders
Each of the prescientific explanations of psychological disorders proved inadequate.
There is, however, one positive legacy from the prescientific era: The mentally ill
came to be regarded as ill, and so were treated humanely, at least in some places
and some eras. If the Beales had lived in the 18th century or earlier, they might
have ended up in Bedlam on display. If the Beales were diagnosed today, they would
almost certainly receive treatments that would enable them to function more effec-
tively in the world. Let’s now consider the crucial transition from prescientific times
to today.
Freud and the Importance of Unconscious Forces
Sigmund Freud (1856–1939), a Viennese neurologist, played a major role in making
the study of psychological disorders a science. He not only developed new methods
Humanitarian Dorothea Dix worked tirelessly
for humane treatment of the mentally ill in
the United States (Viney, 2000).
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14 C H A P T E R 1
for both diagnosis and treatment (many of which are still in use today) but also pro-
posed a rich and intricate theory, which continues to have massive inf luence on
many clinicians.
Initially Freud, influenced by the French neurologist Jean-Martin Charcot, used
hypnosis with his patients in Vienna. Although he had some success, he found that not
everyone was equally hypnotizable and that patients’ symptoms often returned. This
led Freud to develop another method to help patients with hysteria: free association, a
technique in which patients are encouraged to say whatever thoughts occur to them.
Free association was part of Freud’s treatment that involved talking—often referred
to as the “talking cure”—which rested on his idea that mental disorders in general
arise in part because of unconscious conflicts. His idea was that talking freely would
help a person to reduce his or her unconscious conflicts and so provide some relief
from the psychological disorder.
Psychoanalytic Theory
Freud developed a far-reaching theory of the origins, nature, and treatment of psycho-
pathology based on both his work with patients (who were mostly middle-class and
upper-middle-class women) and his observations about himself. His psychoanalytic
theory (the Greek word psyche means “mind”) proposes that thoughts, feelings, and
behaviors are a result of conscious and unconscious forces continually interacting in
the mind. Psychoanalytic theory also suggests that the mind is organized to function
across three levels of consciousness:
• The conscious consists of thoughts and feelings that are in awareness; this is normal
awareness.
• The preconscious consists of thoughts and feelings that a person does not perceive,
but that can be brought voluntarily into conscious awareness in the future.
• The unconscious includes thoughts and feelings that cannot be perceived or called
into awareness on command, but which have power to influence a person.
According to Freud, people have sexual and aggressive urges from birth onward.
Freud argued that when we find such urges unacceptable, they are banished to our
unconscious, where they inevitably gain strength and eventually demand release.
Unconscious urges can be released as conscious feelings or thoughts, or as
behaviors. Freud believed that abnormal experiences and behaviors arise
from this process. For example, according to psychoanalytic theory, one
woman’s extreme fear of eating dust arose from unconscious sexual im-
pulses related to “ taking in” semen (the dust symbolically represented
semen; Frink, 1921).
Freud (1923/1961) also distinguished three psychological structures of
the mind—the id, the ego, and the superego:
• The id is the seat of sexual and aggressive drives, as well as of the de-
sire for immediate gratification of physical and psychological needs. These
physical needs (such as for food and water) and psychological drives ( sexual
and aggressive) constantly require satisfaction. The id is governed by the
pleasure principle, seeking gratif ication of needs without regard for the
consequences.
• The superego, the seat of a person’s conscience, works to impose moral-
ity. According to Freud, the superego is responsible for feelings of guilt, which
motivate the person to constrain his or her sexual and aggressive urges that demand
immediate gratification. People with an inflexible morality—an overly rigid sense
of right and wrong—are thought to have too strong a superego.
Psychoanalytic theory
The theory that thoughts, feelings, and
behaviors are a result of conscious and
unconscious forces continually interacting in
the mind.
Id
According to Freud, the seat of sexual and
aggressive drives, as well as of the desire
for immediate gratification of physical and
psychological needs.
Superego
According to Freud, the seat of the conscience,
which works to impose morality.
In Freud’s view, mental illness is caused
by unconscious conflicts that express
themselves as psychological symptoms. He
revolutionized treatment of psychological
disorders by listening to what patients had
to say.
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The History of Abnormal Psychology 15
• Meanwhile, the ego tries to mediate the id’s demands for immediate gratification
and the superego’s high standards of morality, as well as the constraints of external
reality. Normally, the ego handles the competing demands well. However, when
the ego is relatively weak, it is less able to manage the conf licts among the id,
superego, and reality, which then cause anxiety and other symptoms.
Figure 1.2 shows how the three mental structures are related to the three
levels of consciousness.
One of Freud ’s last ing cont r ibut ions to the f ield of psychopa-
tholog y—and all of psycholog y, in fact—is his notion of the uncon-
scious, the thoughts and feelings that cannot be perceived or cal led
into awareness on com mand, but which have power to inf luence a
person.
Psychosexual Stages
Freud also identified five distinct stages of development (the oral, anal,
phallic, latency, and genital stages) through which children proceed from
infancy into adulthood. Four of these stages involve particular erogenous
zones, which are areas of the body (the mouth, genitals, and anus) that
can satisfy the id’s urges and drives. Freud called these five stages psy-
chosexual stages because he believed that each erogenous zone demands
some form of gratification and that each stage requires that a person suc-
cessfully complete a key task for healthy psychological development.
All of these stages arise during infancy or childhood, although they may
not be resolved until adulthood, if ever. An unresolved conflict or issue
from an earlier stage, which leaves the person focused on issues related
to that stage, is referred to as a fixation. For example, according to Freud
(1905/1955), people with a fixation at the oral stage use food or alcohol to
alleviate anxiety.
Mental Illness, According to Freud
Freud proposed two general categories of mental illness: neuroses and psycho-
ses. A neurosis is a pattern of thoughts, feelings, or behaviors that expresses
an unresolved conf lict between the ego and the id or between the ego and the
superego.
Freud (1938 ) def ined psychosis a s a brea k f rom rea l it y cha racter ized by
conf lict between the ego’s view of realit y and realit y itself. (Note that this is
not the current conventional def inition of psychosis—an impaired ability to per-
ceive realit y, such as ar ises with hal lucinations—used by most mental health
cl in icians and researcher s, and wh ich we use in the rest of th is tex tbook.)
According to the psychoanalytic view, then, schizophrenia involves a psychosis
because it is an escape from realit y into one’s own internal world ( Dorcus &
Shaffer, 1945).
Freud was also revolutionary in proposing that parents’ interactions with their
child are central in the formation of personality. For instance, parents who are too
strict about toilet training their toddler may inadvertently cause their child to tend to
become fixated at the anal stage.
Defense Mechanisms
In addition to proposing an explanation for how internal psychological conflict arises,
Freud, along with his daughter, the noted psychoanalyst Anna Freud (1895–1982),
suggested how such conflicts are resolved: The ego frequently employs unconscious
Ego
According to Freud, the psychic structure that
is charged with mediating between the id’s
demands for immediate gratification and the
superego’s high standards of morality, as well
as the constraints of external reality.
Psychosexual stages
According to Freud, the sequence of five distinct
stages of development (oral, anal, phallic, latency,
and genital) through which children proceed
from infancy to adulthood; each stage has a key
task that must be completed successfully for
healthy psychological development.
Neurosis
According to psychoanalytic theory, a pattern of
thoughts, feelings, or behaviors that expresses
an unresolved conflict between the ego and the
id or between the ego and the superego.
Conscious
Preconscious
Unconscious
Superego
Ego
Id
FI G U RE 1.2 • Freud’s Iceberg
Metaphor of the Organization of
the Mind Freud proposed that the mind
is made up of three structures: id, ego, and
superego. Each person is aware (conscious) of
some of what is in his or her ego and superego;
some of the preconscious contents of the ego
and the superego can be brought into awareness,
and some of those contents—along with all of
the id—remain unconscious.
16 C H A P T E R 1
defense mechanisms, which work to transform the conflicts in a way that pre-
vents unacceptable thoughts and feelings from reaching consciousness. If successful,
defense mechanisms can decrease anxiety (see Table 1.2).
Psychoanalytic Theory Beyond Freud
Psychoanalytic theory has been modified by Freud’s followers; these variations fall
under the term psychodynamic theory and have attracted many adherents. Psychody-
namic theorists have focused on areas that Freud did not develop fully:
• normal versus abnormal development of the self (Kohut, 1971);
• the contribution of additional sources of motivation, such as feelings of inferiority
(Ansbacher & Ansbacher, 1956);
• the development and work of the ego (Hartmann, 1939);
• the possibility that our species has certain inborn and unconscious archetypes
(an archetype is an abstract, ideal characterization of a person, object, or concept)
that underlie some aspects of motivation ( Jung, 1983).
In addition, Karen Horney (1885–1952) and other psychologists conducted re-
search on the ways that moment-to-moment interactions between child and parent
can contribute to psychological disorders (Horney, 1937; Kernberg, 1986; Sullivan,
1953). This emphasis on the contribution that an infant’s social world can make to
psychopathology is one of the lasting contributions of psychodynamic theory. Treat-
ment based on psychodynamic theory is generally referred to as psychodynamic therapy.
Various modifications of psychodynamic therapy have been developed based on spe-
cific alterations of Freud’s theory.
Evaluating the Contributions of Freud and His Followers
One challenge to psychodynamic theory is that its guiding principles, and those of
its corresponding treatments, rest primarily on subjective interpretations of what pa-
tients say and do. Another challenge is that the theory is not generally testable using
TABLE 1.2 • Common Defense Mechanisms
Defense Mechanism
How the Defense Mechanism
Transforms the Conflict Example
Repression (considered
to be the most important
defense mechanism)
Unintentionally keeping conflict-inducing
thoughts or feelings out of conscious
awareness
You “forget” about the time you saw someone getting mugged
across the street.
Denial
Not acknowledging the conflict-inducing
thoughts or feelings to oneself (and others)
You are addicted to painkillers but won’t admit it, even though
the addiction has caused you to miss work.
Rationalization
Justifying the conflict-inducing thoughts,
feelings, or behaviors with explanations
After a father hits his daughter, he justifies his behavior to
himself by saying it will build her character.
Projection
Ascribing (projecting) the conflict-inducing
thoughts or feelings onto others
Instead of admitting that you don’t like a classmate, you say
the person doesn’t like you.
Reaction formation
Transforming the conflict-inducing thoughts
or feelings into their opposite
Your feelings of attraction to your colleague at work are
transformed into distaste and disgust, and you begin to feel
repulsed by the colleague.
Sublimation
Channeling the conflict-inducing thoughts or
feelings into less-threatening behaviors
When a father’s frustration and anger at his teenage
daughter mount, he channels his feelings by going for a
20-minute run.
Defense mechanisms
Unconscious processes that work to transform
psychological conflict in order to prevent
unacceptable thoughts and feelings from
reaching consciousness.
The History of Abnormal Psychology 17
scientific methodologies. For instance, according to psychodynamic theory, a fear of
eating dust could be due to a sublimation of sexual impulses or a reaction formation
to an unconscious desire to play with fecal matter (see Table 1.2). The problem is
not that there can be more than one hypothesis based on psychodynamic theory, but
rather that there is no evidence and no clear means for obtaining evidence that either
hypothesis (or both) is correct.
Nevertheless, psychodynamic theory rested on a fundamental insight that was
crucial for the development of later theories and treatments: Mental processes are
the internal operations that underlie cognitive and emotional functions (such as per-
ception, memory, and guilt feelings) and most human behavior. In addition, psycho-
dynamic theory’s focus on mental contents—the specific memories, knowledge,
goals, and other material that are stored and processed in the mind—has led to much
fruitful research. Furthermore, the notion that some mental processes and mental
contents are hidden away from consciousness has proven invaluable to understanding
psychopathology.
The Humanist Response
Some psychologists, such as Abraham Maslow (1908–1970), reacted adversely to
Freud’s ideas, especially two notions: (1) that mental processes are mechanistic
(with the same sort of cause-and-effect relations that govern all machines), driven
by sexual and aggressive impulses, and (2) that humans don’t really have free will
because our behavior is in response to unconscious processes. These psychologists
proposed a different view of human nature and mental illness that came to be called
humanistic psychology, which focuses on free will, innate goodness, creativity, and the
self (Maslow, 1968).
Carl Rogers (1902–1987) proposed that symptoms of distress and mental illness
arise when a potential route to personal growth is blocked, as can occur when a
person lacks a coherent and unified sense of self or when there is a mismatch—an
incongruence—between the ideal self (the qualities a person wants to have) and the
real self (the qualities the person actually has) (Rogers, 1942). For example, sup-
pose a woman believes she should always be energetic (ideal self ), but her real self is
someone who is often energetic, but not always. The incongruence between the two
selves can lead her to feel bad about herself, which in turn creates feelings of apathy
and guilt.
Rogers developed client-centered therapy to help people reduce such incongruence
and to help them create solutions to their problems by releasing their “real selves.”
In accordance with this approach of self-empowerment, Rogers (1942) stressed that
his clients were not patients who are seen to be “sick” and lacking in power. Referring
to people as “clients” indicated that they had control over their own lives and were
interested in self-improvement through engagement with mental health services
(Kahn, 1998).
Although the emphasis on self-empowerment has proven useful, the humanist
approach, like al l approaches, fal ls short on its own as a general method for
conceptualizing and treating mental illness. As we shall see, other factors (e.g., bio-
logical and social) must be considered.
Thinking Like A Clinician
Based on what you have read, why do you think Freud’s theory has less influence today than
it once had? Why might certain aspects of psychodynamic theory continue to influence
modern perspectives?
Mental processes
The internal operations that underlie cognitive
and emotional functions (such as perception,
memory, and guilt feelings) and most human
behavior.
Mental contents
The specific material that is stored in the mind
and operated on by mental processes.
18 C H A P T E R 1
Scientific Accounts of
Psychological Disorders
In the early 20th century, advances in science led to an interest in theories of psy-
chological disorders that could be tested rigorously, generating hypotheses that could
be proven or disproven. Several different scientific approaches (and accompanying
theories) that emerged at that time are still with us today; they focus on different
aspects of psychopathology, including behavior, cognition, social interactions, and
biology. These scientific accounts and theories have thrived because studies have
shown that they explain some aspects of mental illness. Let’s examine these modern
approaches to psychopathology and how they could explain Big Edie and Little Edie’s
thoughts, feelings, and behavior.
Behaviorism
All of the views discussed so far focus on forces that affect mental processes and
mental contents. However, some psychologists in the early 20th century took a radi-
cally different perspective and focused only on di-
rectly observable behaviors. Spearheaded by American
psychologists Edward Lee Thorndike (1874–1949),
John B. Watson (1878 –1958 ), and Clark L. Hu l l
(1884 –1952 ), and, most fa mously, B. F. Sk in ner
(1904–1990), behaviorism focuses on understanding
directly observable behaviors rather than unobservable
mental processes and mental contents (Watson, 1931).
The behaviorists’ major contribution to understand-
ing psychopathology was to propose scientifically test-
able mechanisms that may explain how maladaptive
behavior arises (Skinner, 1986, 1987). These psycholo-
gists focused their research on the association between
factors that trigger a behavior and on a behavior and
its consequences; the consequences influence whether
a behavior is likely to recur. For instance, to the extent
that using a drug has pleasurable consequences, a per-
son is more likely to use the drug again.
At about the same time in Russia, Nobel Prize–winning physiologist Ivan Pavlov
(1849–1936) accidentally discovered an association between a reflexive behavior and
the conditions that occur immediately prior to it (that is, its antecedents), an asso-
ciation created by a process sometimes referred to as Pavlovian conditioning (Pavlov,
1936). He studied salivation in dogs, and he noticed that dogs increased their sali-
vation both while they were eating (which he predicted—the increased salivation
when eating is a reflexive behavior) and right before they were fed (which he did not
predict). He soon determined that the dogs began salivating when they heard the
approaching footsteps of the person feeding them. The feeder’s footsteps (a neutral
stimulus) became associated with the stimulus of food in the mouth, thus leading
the dogs to salivate when hearing the sound of footsteps; the dogs’ past association
between the feeder’s footsteps and subsequent food led to a behavior change.
Pavlov investigated the reflexive behavior of salivation, and other researchers
have found that reflexive fear-related behaviors (such as a startle response) can be
conditioned in the same fashion. These findings contributed to the understanding
of how the severe fears and anxieties that are part of many psychological disorders
can arise—how neutral stimuli that have in the past been paired with fear-inducing
The pleasurable feelings that can be induced
by consuming alcohol often serve as
reinforcers, prompting people to engage in the
behavior again (and again, and again).
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Behaviorism
An approach to psychology that focuses on
understanding directly observable behaviors in
order to understand mental illness and other
psychological phenomena.
The History of Abnormal Psychology 19
objects or events can, by themselves, come to induce fear or anxiety. We will con-
sider such conditioning in more detail in Chapter 2.
Among the most important insights of behaviorism, then, is that a person’s
behavior, including maladaptive behavior, can result from learning—from a previ-
ous association with an object, situation, or event. Big Edie appears to have devel-
oped maladaptive behaviors related to a fear of being alone. This may have been
a result of past negative experiences with (and the resulting associations to) being
alone, perhaps by neighborhood boys playing tricks on her when they knew she
was home alone.
Behaviorism ushered in new explanations of—and treatments for—some psy-
chological disorders. The behaviorists’ emphasis on controlled, objective observa-
tion and on the importance of the situation had a deep and lasting impact on the
field of psychopathology. However, researchers also learned that not all psychologi-
cal problems could readily be explained as a result of maladaptive learning. Rather,
mental processes and mental contents are clearly involved in the development and
maintenance of many psychological disorders. This opened the door for cognitive
psychology.
The Cognitive Contribution
Psychodynamic and behaviorist explanations of psychological disorders seemed in-
compatible. Psychodynamic theory emphasized private mental processes and men-
tal contents; behaviorist theories emphasized directly observable behavior. Then,
the late 1950s and early 1960s saw the rise of cognitive psychology, the area of psychol-
ogy that studies mental processes and contents starting from the analogy of infor-
mation processing by a computer. Researchers developed new, behaviorally based
methods to track the course of hidden mental processes and characterize the nature
of mental contents, which began to be demystified. If a mental process operates on
mental contents like a computer program operates on stored data, direct connec-
tions can be made between observable behavior, as well as personal experiences,
and mental events.
Cognitive psychology has contributed to the understanding of psychological dis-
orders by focusing on specific changes in mental processes and mental contents. For
instance, people with anxiety disorders—a category of disorders that involves extreme
fear, panic, and/or avoidance of a feared stimulus—tend to focus their attention in
particular ways, creating a bias in what they expect and remember. In turn, these
biased memories appear to support the “truth” of their inaccurate view about the
danger of the stimulus that elicits their fear. For instance, a man who is very anxious
in social situations may pay excessive attention to whether other people seem to be
looking at him; when people glance in his general direction, he will then notice the
direction of their gaze and infer that they are looking at him. Later, he will remem-
ber that “everyone” was watching him.
Other cognitive explanations of psychological disorders focused on distortions
in the content of people’s thoughts. Psychiatrist Aaron Beck (b. 1921) and psycholo-
gist Albert Ellis (1913–2007) each focused on how people’s irrational and inaccurate
thoughts about themselves and the world can contribute to psychological disorders
(Beck, 1967; Ellis & MacLaren, 1998). For example, people who are depressed often
think very negatively and inaccurately about themselves, the future, and the world.
They often believe that no one will care about them; or, if someone does care, this
person will leave as soon as he or she sees how really inept, ugly, or unlovable the de-
pressed person is. Such thoughts could make anyone depressed! For cognitive thera-
pists, treatment involves shifting, or restructuring, people’s faulty beliefs and irrational
thoughts that led to psychological disorders.
20 C H A P T E R 1
Cognitive therapy might have been appropriate for the Beale women, who had
unusual beliefs. Consider the fact that Little Edie worried about leaving her mother
alone in her room for more than a few minutes because she might come back and
find her mother dead (Graham, 1976). Big Edie also had unusual beliefs. One time,
a big kite was hovering over Grey Gardens and she called the police, concerned that
the kite was a listening device or a bomb (Wright, 2007).
The focus on particular mental processes and mental contents illuminates some
aspects of psychological disorders. But just as behaviorist theories do not fully address
why people develop the particular beliefs and attitudes they have, cognitive theories
do not fully explain why a person’s mental processes and contents are biased in a
particular way. Knowledge about social and neurological factors (i.e., factors that affect
the brain and its functioning) helps to complete the picture.
Social Forces
We can view behavioral and cognitive explanations as psychological: Both refer to
thoughts, feelings, or behaviors of individual people. In addition to these sorts of
factors, we must also consider social factors, which involve more than a single per-
son. There is no unified social explanation for psychological disorders, but various
researchers and theorists in the last half of the 20th century recognized that social
forces affect the emergence and maintenance of mental illness. Many of these social
forces, such as the loss of a relationship, abuse, trauma, neglect, poverty, and discrim-
ination, produce high levels of stress.
One of the social factors that occurs
earliest in life is attachment style, which char-
acterizes the particular way a person relates
to intimate others, and it begins in infancy.
Researchers have delineated four types of
attachment styles in children:
1. Secure attachment. Those who become
upset when thei r mother leaves but
quick ly ca l m down upon her ret ur n
(Ainsworth & Bell, 1970).
2. Resistant/anxious attachment. Those who
become angry when their mother leaves
a nd rem a i n a ng r y upon her ret u r n,
sometimes even hitting her (Ainsworth
& Bell, 1970).
3. Avoidant attachment. Those who had no change in their emotions based on mother’s
presence or absence (Ainsworth & Bell, 1970).
4. Disorganized attachment. Those who exhibit a combination of resistant and
avoidant styles and also appear confused or fearful with their mother (Main &
Solomon, 1986).
Among American children, those with an insecure attachment style (the last three
styles listed above) are more likely to develop symptoms of psychological disorders
(Main & Solomon, 1986; Minde, 2003).
Research on social factors also points to the ways that relationships—and the
social support they provide—can buffer the effects of negative life events ( Hyman
et al., 2003; Swift & Wright, 2000). For example, researchers have found that
healthy relationships can mitigate the effects of a variety of negative events, such
as abuse (during childhood or adulthood), trauma, discrimination, and financial
The type of attachment an infant forms with her parent can have profound implications
later in life. Which photo might illustrate a secure attachment? Although we can’t tell for
sure from one snapshot, children like the one on the right, who are not upset when their
mother is going to leave the room, often show signs of a secure attachment.
GETTING THE PICTURE
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The History of Abnormal Psychology 21
hardship. The opposite is also true: The absence of protective relationships increases
a person’s risk for developing a psychological disorder in the face of a significant
stressor (Dikel et al., 2005). (Note that stressor is the technical term used to refer to
any stimulus that induces stress.)
The Beale women experienced many stressors: financial problems, the dis-
solution of Big Edie’s marriage, and, in later years, social isolation. Their ex-
tended family and their community ostracized them, at least in part because they
were independent-minded and artistic women. In addition, Little Edie endured
her own unique social stresses: Both her parents were excessively controlling.
Her father restricted her artistic pursuits, and Little Edie could scarcely leave her
mother’s room before her mother was calling urgently for her to return; this in-
tense attachment and close physical proximity echo their relationship when Little
Edie was a child.
Like the other factors, social factors do not fully account for how and why psy-
chological disorders arise. For instance, social explanations cannot tell us why, of
people who experience the same circumstances, some will go on to develop a psy-
chological disorder and others won’t.
Biological Explanations
In 1913 it was discovered that one type of mental illness—which was then called gen-
eral paresis, or paralytic dementia—was caused by a sexually transmitted disease, syphi-
lis. The final stage of this disease damages the brain and leads to abrupt changes in
mental processes, including psychotic symptoms (Hayden, 2003). The discovery of a
causal link between syphilis and general paresis heralded a resurgence of the medical
model, the view that psychological disorders have underlying biological causes. Ac-
cording to the medical model, once the biological causes are identified, appropriate
medical treatments can be developed, such as medications. In fact, antibiotics that
treat syphilis also prevent the related mental illness, which was dramatic support for
applying the medical model to at least some psychological disorders.
Since that discovery, scientists have examined genes, neurotransmitters (chemi-
cals that allow brain cells to communicate with each other), and abnormalities in
brain structure and function associated with mental illness.
What biological factors might have contributed to the Beales’ unusual lifestyle
and beliefs? Unfortunately, the documentaries and biographies about the two women
have not addressed this issue, so there is no way to know. All we know is that one of
Big Edie’s brothers was a serious gambler, another died as a result of a drinking prob-
lem, and one of her nieces also battled problems with alcohol; taken together, these
observations might suggest a family history of impulse control problems. We might
be tempted to infer that such tendencies in this family reflect an underlying ge-
netic predisposition, but we must be careful: Families share more than their genes,
and common components of the environment can also contribute to psychological
disorders.
In fact, this is where the medical model reveals its limitations. Explaining psy-
chological disorders simply on the basis of biological factors ultimately strips mental
disorders of the broader context in which they occur—in thinking people who live
in families and societies—and provides a false impression that mental disorders arise
from biological factors alone (Angell, 2011). As we shall see throughout this book,
multiple factors usually contribute to a psychological disorder, and treatments target-
ing only biological factors usually are not the most effective. In the next section we
discuss in greater detail this multiple-perspective approach and the model we will use
throughout this text.
The bacterium Treponema pallidum is
responsible for the sexually transmitted
disease syphilis. Left untreated, syphilis
eventually causes severe brain damage that
in turn gives rise to abrupt changes in mental
processes, including psychotic symptoms.
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22 C H A P T E R 1
The Modern Synthesis of Explanations of
Psychopathology
In the past several decades, researchers and clinicians have increasingly recognized
that psychological disorders cannot be fully explained by any single type of factor or
theory. Two approaches to psychopathology integrate multiple factors: the diathesis–
stress model and the biopsychosocial approach.
The Diathesis–Stress Model
The diathesis–stress model is one way to bring together the various explanations of
how psychological disorders arise. The diathesis–stress model rests on the claim
that a psychological disorder is triggered when a person with a predisposition—a
diathesis—for the particular disorder experiences an environmental event that causes
significant stress (Meehl, 1962; Monroe & Simons, 1991; Rende & Plomin, 1992). Es-
sentially, the idea is that if a person has a predisposition to a psychological disorder, a
particular type of stress may trigger its occurrence. But the same stress would not have
that effect for a person who did not have the predisposition; also, a person who did
have a diathesis for a psychological disorder would be fine if he or she could
avoid those types of high-stress events. Both factors are required.
For example, the diathesis–stress model explains why, if one identical
twin develops depression, the co-twin (the other twin of the pair) also de-
velops depression in less than one quarter of the cases (Lyons et al., 1998).
Because identical twins share virtually 100 % of their genes, a co-twin
should be guaranteed to develop the disorder if genes alone cause it. But
even identical twins experience different types and levels of stress. Their
genes may be virtually identical, but their environments are not; thus, both
twins do not necessarily develop the psychological disorder over time. The
diathesis–stress model is illustrated in Figure 1.3.
A diathesis may be a biological factor, such as a genetic vulnerability to a
disorder, or it may be a psychological factor, such as a cognitive vulnerability
to a disorder, as can occur when irrational or inaccurate negative thoughts
about oneself contribute to depression. The stress is often a social factor,
which can be acute, such as being the victim of a crime, or less intense but
chronic, such as recurring spousal abuse, poverty, or overwork. It is important to
note that not everybody experiences the same social factor in the same way. And
what’s important is not simply the objective circumstance—it’s how a person per-
ceives it. For example, think about roller coasters: For one person, they are great fun;
for another, they are terrifying. Similarly, Big Edie and Little Edie didn’t appear to
mind their isolation and strange lifestyle and may even have enjoyed it; other people,
however, might find living in such circumstances extremely stressful and depressing.
Whether because of learning, biology, or an interaction between them, some people
are more likely to perceive particular events and stimuli as stressors (and therefore to
experience more stress) than others. The diathesis–stress model was the first approach
that integrated existing, but separate, explanations for psychological disorders.
The Biopsychosocial and Neuropsychosocial Approaches
To understand the bases of both diatheses and stress, we need to look more carefully
at the factors that underlie psychological disorders.
Three Types of Factors
Historically, researchers and clinicians grouped the factors that give rise to psy-
chological disorders into three general types: biological (including genetics, the
High
High
Level of stress
Low
Low
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absent
High
Minimal
Diathesis
present
FI G U RE 1.3 • The Diathesis–Stress
Model According to the diathesis–stress
model of depression, people who are more
vulnerable to depression (high diathesis) will
become depressed after experiencing less
stress than people who are less vulnerable
to depression (low or absent diathesis). Put
another way, given the same level of stress,
those who are more vulnerable to depression
will develop more symptoms of depression
than those who are less vulnerable.
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Diathesis–stress model
A model that rests on the idea that a
psychological disorder is triggered when a
person with a predisposition—a diathesis—
for the particular disorder experiences
an environmental event that causes
significant stress.
The History of Abnormal Psychology 23
It’s a snake!
It’s a spear!
It’s a fan!
It’s a wall!
It’s a tree!
It’s a rope!
The whole elephant cannot be described by a
group of blind men if each of them is feeling
only a small part of the animal’s body. In the
same way, past explanations of psychological
disorders that focused on only one or two
factors created an incomplete understanding
of such disorders.
structure and function of the brain, and the function of other bodily systems);
psychological (thoughts, feelings, and behaviors); and, social (social interactions
and the environment in which they occur). The biopsychosocial approach
to understanding psychological disorders rests on identifying these three types
of factors and documenting the ways in which each of them contr ibutes to a
disorder.
The biopsychosocial approach leads researchers and clinicians to look for
ways in which the three t ypes of factors contribute to both the diathesis (the
predisposition) and the stress. For instance, having certain genes (a biological fac-
tor), having biases to perceive certain situations as stressful (a psychological factor),
and living in poverty (a social factor) all can contribute to a diathesis; similarly,
chronic lack of sleep (a biological factor), feeling that one’s job is overwhelming
(a psychological factor), or having a spouse who is abusive (a social factor) can con-
tribute to stress.
However, two problems with the traditional biopsychosocial approach have
become clear. First, the approach does not specifically focus on the organ that
is responsible for cognition and emotion, that al lows us to learn, that guides
behavior, and that underlies all conscious experience—namely, the brain. The
brain not only gives rise to thoughts, feelings, and behaviors, but also mediates
all other biological factors; it both registers events in the body and affects bodily
events.
Second, in the biopsychosocial approach, the factors were often considered in
isolation, as if they were items on a list. Considering the factors in isolation is remi-
niscent of the classic South Asian tale about a group of blind men feeling different
parts of an elephant, each trying to determine what object the animal is. One per-
son feels the trunk, another the legs, another the tusks, and so on,
and each reaches a different conclusion. Even if you combined
all the people’s separate reports, you might
miss the big picture of what an elephant
is: That is, an elephant is more than a
sum of its body parts; the parts come to-
gether to make a dynamic and wondrous
creature.
Researchers are beginning to under-
stand how the three types of factors com-
bine and affect each other. That is, factors
that researchers previously considered to
be independent are now known to inf lu-
ence each other. For example, the way
that parents treat their infant was histori-
cally considered to be exclusively a social
factor—the infant was a receptacle for the
caregiver’s st yle of parenting. However,
more recent research has revealed that par-
enting style is in fact a complex set of interactions between caregiver and infant.
Consider that if the infant frequently fusses, this will elicit a different pattern of re-
sponses from the caregiver than if the infant frequently smiles; if the infant is fussy
and “difficult,” the caregiver might handle him or her with less patience and warmth
than if the infant seems happy and easygoing. And the way the caregiver handles the
infant in turn affects how the infant responds to the caregiver. These early interac-
tions between child and caregiver (a social factor) then contribute to a particular at-
tachment style, which is associated with particular biases in paying attention to and
Biopsychosocial approach
The view that a psychological disorder arises
from the combined influences of three types
of factors—biological, psychological, and
social.
24 C H A P T E R 1
perceiving emotional expressions in faces (psychological factors; Fraley & Shaver,
1997; Maier et al., 2005).
In fact, some researchers who championed the biopsychosocial approach
ack nowledged that ex pla nat ions of psycholog ica l d isorder s depend on the
interactions of biological, psychological, and social factors (Engel, 1977, 1980). But
these researchers did not have the benef it of the recent advances in understand-
ing the brain, and hence were not able to specify the nature of such interactions in
much detail.
These problems led to a revision of the traditional biopsychosocial approach,
to align it better with recent discoveries about the brain and how psychological
and social factors affect brain function. We call this updated version of the clas-
sic approach the neuropsychosocial approach, which is explained in the following
section.
The Neuropsychosocial Approach: Refining the Biopsychosocial Approach
The neuropsychosocial approach has two defining features: the way it character-
izes the factors and the way it characterizes their interactions. As we discuss be-
low, this approach emphasizes the brain rather than the body (hence the neuro- in
its name) and maintains that no factor can be considered in isolation.
Emphasis on the Brain Rather Than the Body in General As psychologists and other
scientists have learned more about the biological factors that contribute to psy-
chological disorders, the primacy of the role of the brain—and even particular
brain structures and functions—in contributing to psychological disorders has
become evident. Ultimately, even such disparate biological factors as genes
and bodily responses (e.g., the increased heart rate associated with anxiety)
are best understood in terms of their relationship with the brain. Because
of the importance of the brain’s influence on all biological functioning
involved in psychological disorders, this book generally uses the term
neurological rather than biological and the term neuropsychosocial rather than
biopsychosocial to refer to the three types of factors that contribute to psycho-
logical disorders.
Emphasis on Feedback Loops Neurological, psychological, and social fac-
tors are usual ly involved simultaneously and are constantly interacting (see
Figure 1.4). These interactions occur through feedback loops: Each factor is af-
fected by the others and also feeds back to affect the other factors. Hence, no
one factor can be understood in isolation, without considering the other factors.
For example, problems in relationships (social factor) can lead people to experi-
ence stress (psychological factor); in turn, when people feel stressed, their brains
cause their bodies to respond with a cascade of events. As you will see throughout
this book, interactions among neurological, psychological, and social factors are
common.
In shor t, the neuropsychosocial approach can al low us to understand
how neurological, psychological, and social factors—which affect and are af-
fected by one another through feedback loops—underlie psychological disorders
(Kendler, 2008).
In the next chapter, we will discuss the neuropsychosocial approach to psycho-
logical disorders in more detail, examining neurological, psychological, and social
factors as well as the feedback loops among them. In that chapter, we will also con-
tinue our evaluation of the Beales and the specific factors that might contribute to
their unusual behavior. In subsequent chapters, we will consider the stories of various
other people.
Neuropsychosocial approach
The view that a psychological disorder arises
from the combined influences of neurological,
psychological, and social factors—which
affect and are affected by one another
through feedback loops.
Social
factors
Neurological
factors
Psychological
factors
FI G U RE 1.4 • The Neuropsychosocial
Approach According to the
neuropsychosocial approach, neurological,
psychological, and social factors interact with
one another via feedback loops to contribute
to the development of psychopathology.
The History of Abnormal Psychology 25
The Three Criteria for Determining
Psychological Disorders
• A psycholog ica l d isorder is a pat ter n
of thoughts, feelings, or behaviors that
causes significant distress, impaired func-
tioning in daily life, and/or risk of harm.
• The distress involved in a psychological
disorder is usually out of proportion to
the situation.
• Impairment in daily life may affect func-
tioning at school, at work, at home, or in
relationships. Moreover, people with a
disorder are impaired to a greater degree
than most people in a similar situation.
A psychosis is a relatively identifiable type
of impairment that includes hallucinations
or delusions.
• A psycholog ica l d isorder may lead to
behaviors that create a significant risk of
harm to the person or to others.
• Mental health clinicians and researchers
recog nize that context and culture in
part determine whether a person’s state
involves significant distress, impairment,
or risk of harm.
Views of Psychological Disorders
Before Science
• The oldest-k nown v iew of psychopa-
thology is that it arose from supernatural
forces, either magical or spiritual. Ancient
and modern Chinese views of psychopa-
thology consider its cause to be blocked or
significantly imbalanced qi. The ancient
Greeks attributed mental illness to an im-
balance of bodily humors. The term medi-
cal model refers to Hippocrates’ view that
illness (including psychological disorders)
results from a biological disturbance.
• The Middle Ages saw a resurgence of the
view that supernatural forces cause psy-
chopathology: Mental illness was viewed
as the result of demonic possession; witch
hunts were frequent. By the end of the
Renaissance, however, the mentally ill
began to be treated more humanely.
• In the years immediately following the
Renaissance, mental illnesses were thought
to arise from irrational thinking, but this ap-
proach did not lead to consistent treatment.
• In the 1790s, Pinel championed humane
treatment for those in asylums in France.
In other European settings, patients were
given moral treatment.
• In the United States, Benjamin Rush ini-
tiated the effort to treat the mentally ill
more humanely; similarly, Dorothea Dix
strove to ensure that the mentally ill were
housed separately f rom cr im ina ls and
treated humanely.
The Transition to Scientific Accounts
of Psychological Disorders
• Freud played a major role in making the
study of psychological disorders a science,
largely by developing new methods for
diagnosis and treatment; he also proposed
an extensive theory of psychopathology.
Freud’s methods included hypnosis and
free association.
• Accord i ng to Freud ’s ps ychoa n a ly t ic
theory, thoughts, feelings, and behaviors
result from conscious and unconscious
forces— such as sex ua l and agg ressive
urges. Moreover, he proposed that the
mind is structured to function across three
levels of consciousness: the conscious, the
preconscious, and the unconscious.
• Freud proposed three psychic structures
in the m ind—id, ego, and superego—
which are continual ly interacting and
negotiating.
• According to Freud, each person passes
through f ive psychosexual stages from
i n f a nc y to adu lthood , of wh ich fou r
involve particular erogenous zones. For
healthy psychological development, each
stage requires the successful completion of
a key task.
• Various forms of psychodynamic therapy
have been proposed, each drawing primar-
ily on a different aspect of psychodynamic
theor y. A drawback of psychodynamic
theory is that it has proven difficult to test
scientifically.
• Humanistic psycholog ists such as Carl
Rogers viewed psychodynam ic theor y
as too mechanistic and opposed to free
w i l l. Rogers proposed that sy mptoms
of distress and mental illness arise when
a potential route to personal growth is
blocked, as can occur when there is in-
congruence between the ideal and real
selves. Rogers developed client-centered
t her apy to decrea se i ncong r uence i n
clients.
Scientific Accounts of Psychological
Disorders
• Psychologists Edward Thorndike, John
Wat son, Cla rk Hu l l, a nd B. F. Sk in-
ner spearheaded behaviorism, focusing
on directly obser vable behaviors rather
than unobservable mental processes and
mental contents. They investigated the
association between a behavior and its
consequence, and proposed scientifically
testable mechanisms to explain how mal-
adaptive behav ior ar ises. Behav ior ism
helps explain how maladaptive behavior
can arise from previous associations with
an object, a situation, or an event.
• Pavlov discovered and investigated what is
sometimes referred to as Pavlovian condi-
tioning—the process whereby a ref lexive
behavior comes to be associated with a stim-
ulus that precedes it. Pavlovian conditioning
helps explain the severe fears and anxieties
that are part of some psychological disorders.
SUMMING UP
Thinking Like A Clinician
Imagine that you are a clinician, and Natasha comes to see you about her depression.
She tells you that she had a “chemical imbalance” a few years ago, which led her to be
depressed then. Based on what you have read, which of the various modern perspectives
was she adopting? What other types of causes could she have used to explain her depres-
sion? How would the two integrationist approaches (diathesis–stress and neuropsychoso-
cial) explain Natasha’s depression? (Hint: Use Figures 1.3 and 1.4 to guide your answers.)
What do the two approaches have in common, and in what ways do they differ from each
other?
26 C H A P T E R 1
More Study Aids
For additional study aids related
to this chapter, including quizzes
to make sure you’ve retained
everything you’ve learned and a
Student Video Activity exploring
early hospital treatments for
severe mental disorders, go to:
www.worthpublishers.com/
launchpad/rkabpsych2e.
Chris Ryan/OJO Images Ltd./Alamy
Abnormal psychology (p. 4)
Psychological disorder (p. 4)
Psychosis (p. 6)
Hallucinations (p. 6)
Delusions (p. 6)
Culture (p. 8)
Asylums (p. 13)
Moral treatment (p. 13)
Psychoanalytic theory (p. 15)
Id (p. 15)
Superego (p. 15)
Ego (p. 16)
Psychosexual stages (p. 16)
Neurosis (p. 16)
Defense mechanisms (p. 17)
Mental processes (p. 18)
Mental contents (p. 18)
Behaviorism (p. 19)
Diathesis–stress model (p. 23)
Biopsychosocial approach (p. 24)
Neuropsychosocial approach (p. 25)
Key Terms
• Cog n it ive ps ycholog y h a s led to t he
scientif ic investigation of menta l pro-
cesses and menta l contents that af fect
how people pay at tent ion to st i mu l i
and develop biases in what they expect
and remember. Such biases in turn can
confirm the inaccurate views that per-
petuate a psychological disorder. Aaron
Beck and A lber t El lis each focused on
how pe ople’s i r r at ion a l a nd i n a cc u –
rate thoughts about themselves and the
world can contr ibute to psycholog ica l
disorders, and each developed a type of
treatment to address the irrational and
inaccurate thoughts.
• Social forces that help explain psycho-
logical disorders include difficulties with
attachment and the role of relationships in
buffering negative life events.
• Psychological disorders cannot be fully
explained by any single t ype of factor
or theor y. One approach to integrating
dif ferent factors is the diathesis– stress
model, wh ich proposes that i f a per-
son ha s a pred isposit ion to a psycho –
logical disorder, stressors may trigger its
occurrence.
• The biopsychosocial approach rests on
the idea that both d iathesis and stress
can be grouped into three types of fac-
tors: biological, psychological, and so-
cial. Recent research allows investigators
to beg in to understand the role of the
brain in psychological disorders and the
feedback loops among the three t ypes
of factors. For these reasons, this book
uses the term neuropsychosocial rather than
biopsychosocial.
The History of Abnormal Psychology 27
29
CHAPTER 2
Understanding
Psychological Disorders:
The Neuropsychosocial
Approach
s we saw in Chapter 1, clearly the Beale women had odd
thoughts and feelings and engaged in unusual behaviors. As
we asked in Chapter 1, were they merely eccentric? Did Big
Edie or Little Edie (or both of them) have a psychological disorder?
Could either of them have had more than one psychological disorder?
If one or both had a disorder, how could we understand why? The
neuropsychosocial approach allows us to consider the factors that lead
someone to develop a psychological disorder, which is known as its
etiology.
Let’s consider the Beale women in terms of the neuropsycho
social approach. First, we can ask about neurological factors: Was some
thing abnormal about their genes or brains? Perhaps their neurons or
neurotransmitters functioned abnormally, and that led to their odd
behavior. Second, we can ask about psychological factors: How might
their thoughts and feelings have motivated them, and what role might
their mental processes have played? And third, we can ask about social
factors, such as their financial circumstances, their family relation
ships, the straitlaced society they were members of, and other cultural
forces affecting them.
Neurological Factors in
Psychological Disorders
Brain Structure and Brain Function
The Genetics of Psychopathology
Feedback Loops in Understanding Genes and
the Environment
Psychological Factors in
Psychological Disorders
Behavior and Learning
Feedback Loops in Understanding Classical
Conditioning and Operant Conditioning
Mental Processes and Mental Contents
Emotion
Social Factors in Psychological Disorders
Family Matters
Community Support
Social Stressors
Culture
A Neuropsychosocial Last Word on
the Beales
Etiology
The factors that lead a person to develop a
psychological disorder.
At Any moment in A dAy of the BeAles’ lives (or any
one’s life, for that matter), all three types of factors are operating:
neurological, psychological, and social. Depending on the state of a
person’s brain (which is affected, for example, by various chemicals
produced by the body), social factors (such as an angry friend or a
stressful job interview) have a greater or lesser impact. This impact
in turn affects psychological factors (the person’s thoughts, feelings,
and behaviors) in different ways. And then the psychological factors
can affect both neurological factors and social factors, continuing the
interaction among these different influences. Thus, considering only
© Sergey Sukhorukov/Kalium/age fotostock. Photo for illustrative purposes only; any individual depicted is a model.
one type of factor would lead to an incomplete understanding of psychological disor
ders. That is why we consider each type of factor—neurological, psychological, and
social—in detail (see Figure 1.4 in Chapter 1). It is important to note, however, that
the neuropsychosocial approach does not focus on each type of factor individually;
rather, we must always consider how the three factors interact and affect one another
via feedback loops.
Neurological Factors in
Psychological Disorders
Big Edie had always been unconventional. She didn’t seem to care what other peo
ple thought of her behavior. And although she loved performing—seemingly to
the point of compulsion—she was a recluse for most of her adult life, seeing almost
no one but her children. How did such a lifestyle arise? And what about Little
Edie’s paranoid beliefs? Could neurological factors account for the odd beliefs and
behaviors of this mother and daughter? In fact, accumulating research indicates
that genes can contribute to the development of disorders by affecting both the
structure and function of the brain (Gottesman, 1991; Greenwood & Kelsoe, 2003;
Hasler et al., 2004).
Neurological factors that contribute to psychological disorders include abnor
malities in the structure of the brain, in the operations of specific chemicals, and in
specific genes. Researchers and clinicians sometimes focus on neurological factors
when they explain psychopathology—noting, for example, that depression is cor
related with abnormal levels of a particular chemical (serotonin) in the brain or that
an irrational fear of spiders develops partly from an overly reactive brain structure
involved in fear (the amygdala; Larson et al., 2006). However, as you know, the
neuropsychosocial approach maintains that explanations based on neurological fac
tors alone rarely provide the whole story. Each thought, feeling, and behavior, as
well as each social experience and the environment in which we live and work, af
fects our neurological functioning. In other words, as noted above, the three types
of factors typically interact with one another through feedback loops. Neurological
factors contribute to psychopathology, but they must be considered in the context of
the other factors.
To understand the role of neurological factors in explanations of psychopathol
ogy, we next consider brain structure and function, neurons and neurotransmitters,
and genetics and the ways that genes interact with the environment.
Brain Structure and Brain Function
The brain is the organ of thinking, feeling, and behavior, and thus it must play a key
role in psychopathology. In the following sections, we start our discussion with the
big picture by considering the overall structure of the brain and its organization into
large systems. Then we turn to increasingly more detailed components, considering
how individual brain cells interact within these systems.
A Quick Tour of the Nervous System
Psychopathology involves deficits in how a person thinks, feels, and behaves. The
brain, of course, is ultimately responsible for all of these functions. Let’s briefly con
sider how different parts of the brain contribute to cognitive and emotional capaci
ties when the brain is structured and functions normally. In later chapters, when we
need to know more to understand a specific psychological disorder, we’ll look more
closely at specific parts of the brain and how they can malfunction.
30 C H A P T E R 2
The Central Nervous System and the Peripheral Nervous System
The central nervous system (CNS) has two parts:
the brain and the spinal cord. The CNS is the seat of
memory and consciousness, as well as perception and
voluntary action (Smith & Kosslyn, 2006). How
ever, the CNS is not the only neurological founda
tion of our internal lives. The peripheral nervous
system (PNS) also plays an important role and is of
particular interest in the study of psychopathology.
The Peripheral Nervous System
Like the CNS, the PNS is divided into two parts,
in this case the sensorysomatic nervous system and
the autonomic nervous system (see Figure 2.1). The
sensory-somatic nervous system is involved in connect
ing the brain to the world, via both the senses (in
puts) and the muscles (outputs). The autonomic nervous system (ANS) is probably of
greater relevance to psychopathology, in part because it plays a key role in how we
respond to stress. The ANS controls many involuntary functions, such as those of the
heart, digestive tract, and blood vessels (Goldstein, 2000; Hugdahl, 2001).
The ANS itself has two major components: the sympathetic nervous system and
the parasympathetic nervous system. The sympathetic nervous system revs you up so that
you can respond to an emergency: It speeds up the heart (providing more blood and
oxygen to the limbs) and dilates the pupils of the eyes (making you more sensitive to
light). The sympathetic system also slows down functions that are not essential in an
emergency, such as those involved in digestion. The result of the sympathetic ner
vous system’s being activated is called the fight-or-flight response (or the stress response,
because it occurs when people experience stress).
The other part of the ANS is the parasympathetic nervous system, which settles
you down after a crisis is over: The parasympathetic nervous system slows the
heart, contracts the pupils, and increases the activity of the digestive tract. The
parasympathetic system typically counteracts the effects of the sym
pathetic nervous system, and psychopathology may arise if it fails to
do so effectively. In fact, dysfunctional activity in the parasympathetic
nervous system has been associated with various psychological prob
lems, such as anxiety disorders, disruptive behavior, and hostility (Pine
et al., 1998).
The Four Brain Lobes
Let’s now focus on one part of the CNS, the brain. As shown in
Figure 2.2, the brain has four major lobes, back to front: occipital lobe,
parietal lobe, temporal lobe, and frontal lobe. The brain is divided into
two hemispheres (or halfspheres), left and right, and each hemisphere
has all four lobes. We start with the back of the brain.
When the eyes are stimulated by light, they send neural impulses
into the brain; the first area to process this information in detail is the
occipital lobe, which is at the very back of the brain. This lobe is entirely
dedicated to the function of vision.
Two major neural pathways lead forward from the occipital lobes.
One extends up into the parietal lobe, at the top, back of the brain. This
lobe processes spatial information, such as the relative location of ob
jects. The parietal lobe also has other functions, including a role in
selfawareness. The second neural pathway from the occipital lobe leads
down to the temporal lobe (so named because it lies under the temple),
FI G U RE 2.1 • The Nervous System
The autonomic nervous system (ANS) is
part of the peripheral nervous system (PNS),
and malfunctioning of the ANS can produce
abnormal responses to stress.
Temporal lobe
Parietal lobeFrontal lobe
Occipital
lobe
FI G U RE 2.2 • The Lobes of the Brain
Sensory-somatic
nervous system
Autonomic
nervous system
Nervous system
Peripheral
nervous system
Sympathetic
nervous system
Parasympathetic
nervous system
Spinal cord Brain
Central
nervous system
Understanding Psychological Disorders: The Neuropsychosocial Approach 31
which stores visual memories, processes auditor y information, and decodes the
meaning of speech; the temporal lobe also contributes to conscious experience. Ab
normal functioning in the temporal lobe can produce intense emotions, such as ela
tion when a person is manic (Gyulai et al., 1997).
Both the parietal lobe and the temporal lobe send information to the frontal lobe,
which is located right behind the forehead. The frontal lobe plays crucial roles in
feeling emotions and using emotional responses in decision making, as well as in
thinking and problem solving more generally; it is also involved in programming ac
tions and controlling body movements. Because these functions are so important to
the vital activities of planning and reasoning, the frontal lobe is sometimes referred to
as the seat of executive functioning; its role is much like that of the head of a successful
company—an executive—who plans the company’s future and formulates responses
to obstacles that arise. Abnormalities in the frontal lobe, and in executive function
ing, are associated with a variety of disorders, including schizophrenia, a psychological
disorder characterized by profoundly unusual and impaired behavior, expression of
emotion, and mental processing (Bellgrove et al., 2006; Morey, Inan, et al., 2005).
The Cortex and Beneath the Cortex
The cerebral cortex is the outer layer of cells on the surface of the brain that
overlays all four of the lobes. Contained in the cerebral cortex is the majority of
the brain’s neurons, the cells
that process in for mat ion re
lated to our physical, mental,
a nd emot ion a l f u nct ion i ng.
Most of the bra i n f u nct ion s
just described are carried out
primarily in the cortex of the
corresponding lobes. But many
important brain functions are
carried out in subcortical areas,
beneath the cortex, as shown
in Figure 2.3.
The limbic system (key parts
of which are shown in the left
half of Figure 2.3) plays a key role in emotions; among its most important compo
nents are the hypothalamus, the hippocampus, and the amygdala:
• The hypothalamus governs bodily functions associated with eating, drinking, and
controlling temperature, and it plays a key role in many aspects of our emotions
and in our experience of pleasure (Swaab, 2003).
• The amygdala is central to producing and perceiving strong emotions, especially
fear (LeDoux, 2000).
• The hippocampus works to store new information in memory of the sort that later
can be voluntarily recalled (Squire, 2004).
In addition to components of the limbic system, other important subcortical struc
tures include the thalamus, the basal ganglia, and the cerebellum. Both physical
abnormalities and abnormal levels of activity in these subcortical brain areas can
contribute to psychological disorders, as we will discuss in later chapters when
relevant.
Neurons
Now that you know essential functions that different parts of the brain perform, it’s
time to discuss how these functions occur. All brain activity depends on neurons,
and malfunctions of neurons often contribute to psychological disorders (Lambert &
Cerebral cortex
The outer layer of cells on the surface of the
brain.
Neurons
Brain cells that process information related to
physical, mental, and emotional functioning.
FI G U RE 2.3 • Key Subcortical
Brain Areas
Hypothalamus
Cerebral
cortex
CerebellumSpinal
cord
Thalamus
Hypothalamus
Amygdala
Hippocampus
32 C H A P T E R 2
Kinsley, 2005). The brain contains numerous types of neurons, which have different
functions, shapes, and sizes. Most neurons interact with other neurons. In some cases,
neurons activate, or act to “turn on,” other neurons; in other cases, neurons inhibit, or
act to “turn off,” other neurons. We can classify neurons into three main types:
• Sensory neurons receive input from the sense organs (eyes, ears, and so on).
• Motor neurons carry output that stimulates muscles and glands.
• Interneurons lie between other neurons—sensory neurons, motor neurons, and/or
other interneurons—and make up most of the neurons in the brain.
Sets of connected neurons that work together to accomplish a basic process, such
as making you recoil when you touch a hot stove, are called brain circuits; sets of
brain circuits are organized into brain systems, which often can involve most of an
entire lobe—or even large portions of several lobes. Many forms of psychopathology
arise because specific brain circuits are not working properly, either alone or as part
of a larger brain system.
To understand brain circuits, consider an analogy to a row of dominoes: When
one domino falls, it causes the next in line to fall, and so on, down the line. Simi
larly, when a neuron within a brain circuit is activated, it in turn activates sequences
of other neurons. However, unlike a domino in a row, the average neuron is con
nected to about 10,000 other neurons—and thus a complex pattern of spreading
activity occurs when a brain circuit is activated, which usually ends up involving
a large brain system. For each input, a brain system produces a specific output—for
instance, an interpretation of the input, an association to it, or a response based on it.
Ultimately, it is the pattern of activated neurons that is triggered—by a sight, smell,
thought, memory, or other event—that gives rise to our cognitive and emotional
lives. A pattern of neurons firing makes us desire that third piece of chocolate cake or
causes us to recoil when a spider saunters out from behind it. Brain systems allow us
to think, feel, and behave.
Psychopathology can arise when neurons fail to communicate appropriately,
leading brain systems to produce incorrect outputs. For example, people with schizo
phrenia appear to have abnormal circuitry in key parts of their frontal lobes (Pantelis
et al., 2003; Vidal et al., 2006). To understand such problems—and possible treat
ments for them—you need to know something about the structure and function of
the neuron and its methods of communication.
The Cell Body
To see how neurons can fail to communicate appropriately,
we must take a closer look at them. Figure 2.4
shows that a neuron has three parts: a receiving
end, a sending end, and a middle part, called
the cell body. When a neuron has been suf
ficiently stimulated (typically by signals
from other neurons), very small holes
in the cell’s outer covering (its “skin”)
open, and the neuron’s internal bal
ance of chemicals changes to the point
where the neuron “fires.” It is this firing
that sends information to other neurons
(Lambert & Kinsley, 2005).
Each neuron registers the sum to tal of inputs, both those that try to stimulate it
to fire and those that try to inhibit it from firing. The neuron, then, balances the two
sorts of inputs against each other and only fires if the stimulating influences substantially
outweigh the inhibiting ones (Kandel et al., 2007). To understand how firing occurs, we
need to look at two other major parts of the neuron: the axon and the dendrites.
Nucleus
Dendrites
(receiving
end)
Myelin
sheath
Terminal buttons
Cell
body
Axon
(sending
end)
Neural impulse
FI G U RE 2.4 • The Neuron
Brain circuits
Sets of connected neurons that work together
to accomplish a basic process.
Brain systems
Sets of brain circuits that work together to
accomplish a complex function.
Understanding Psychological Disorders: The Neuropsychosocial Approach 33
The Axon, Dendrites, and Glial Cells
The axon is the part of the neuron that sends signals to other neurons. The axon is a
long, threadlike structure, some of which is covered by a layer of fatty material, known
as the myelin sheath, that insulates it electrically; the axon includes the terminal but
tons. Although each neuron has only a single axon, it often branches extensively, al
lowing signals to be sent simultaneously to many other neurons ( Shepherd, 1999).
When a neuron has been stimulated to the point that it fires, a wave of chemical
activity moves from the cell body down the axon very quickly. This wave is called an
action potential. When the action potential reaches the end of the axon, it typically
causes chemicals to be released. These chemicals are stored in structures called termi-
nal buttons, and these chemicals affect other neurons, muscles, or glands. If stimula
tion does not cause a neuron to fire when it is supposed to, the circuit of which the
neuron is a part will not function correctly—and psychopathology may result. Let’s
consider why a neuron might not fire when stimulated appropriately.
We’ve seen that neurons fire after they are stimulated, but how are they stimulated?
Two ways: First, they are stimulated at their dendrites, which receive signals from other
neurons. Dendrites, like axons, are highly branched, so a single neuron can receive many
different signals at the same time. Received signals move along the dendrites to the cell
body (Kandel et al., 2007). Second, in some cases, neurons receive inputs directly on
their cell bodies. Such inputs are produced not only by other neurons but also by glial
cells. Glial cells are involved in the “care and feeding” of neurons, and act as a kind of sup
port system (in fact, glial means “glue” in Greek; Lambert & Kinsley, 2005). The brain
has about 10 times as many glial cells as neurons. Researchers have learned that glial cells
do much more than provide support services; they can directly stimulate neurons, and
they play a role in modulating input from other neurons (Parpura & Haydon, 2000).
Given the roles of neurons and glial cells in brain function, it is not surprising
that researchers have found that at least some patients with psychological disorders
(specifically, the sorts of mood disorders we consider in Chapter 5) have abnormally
low numbers of both types of cells. One possible reason for such deficits may be
that stress early in childhood (and even to the mother, prior to a child’s birth) can
disrupt the development of both neurons and glial cells ( Zorumski, 2005).
Chemical Signals
The way neurons communicate is crucial for understanding psychopathology. In many
cases, psychological disorders involve faulty signaling among neurons, and effective med
ications operate by altering the ways in which signals are produced or processed (Kelsey
et al., 2006). Subsequent chapters of this book will describe how particular signaling
problems contribute to some psychological disorders and how certain medications com
pensate for such problems. To understand these problems with chemical signaling, we
now need to consider what happens at the synapse, what neurotransmitters do, the nature
of receptors, and what can go wrong with chemical communication among neurons.
The Synapse
When a neuron fires, chemicals are released at the terminal button. Those chemicals
usually contact another neuron at a synapse, which is the place where the tip of the
axon of one neuron nestles against another neuron (usually at a dendrite) and sends
signals to it. Most of the time, the sending neuron is not physically connected to the
receiving neuron, though. Instead, the chemicals carry the signal across a gap, called
the synaptic cleft, shown in Figure 2.5. Events at the synapses can go awry, which can
underlie a variety of types of psychopathology.
Neurotransmitters
The chemicals that are released by the terminal buttons are called neurotransmit-
ters. It is worth looking briefly at the major neurotransmitters that play roles in
psychological disorders. However, keep in mind that no neurotransmitter works in
Action potential
The wave of chemical activity that moves
from the cell body down the axon when a
neuron fires.
Synapse
The place where the tip of the axon of one
neuron sends signals to another neuron.
Neurotransmitters
Chemicals that are released by the terminal
buttons and cross the synaptic cleft.
34 C H A P T E R 2
isolation and that no psychological disorder can be traced solely
to the function of a single neurotransmitter. Nevertheless, as
shown in Table 2.1, imbalances in some of these substances
have been linked, to some extent, with certain psychological
disorders.
You may have noticed in Table 2.1 that the descriptions of
what the neurotransmitters do are fairly general. There’s a rea
son for this: The effects of neurotransmitters depend in part on
the nature of the receiving neurons. Thus, we must next look
more closely at what’s on the receiving end of these chemi
cal substances. The information in the following section is also
crucial if we are to understand how various drugs work to treat
psychopathology.
Chemical Receptors
A neuron receives chemical signals at its receptors, spe
cialized sites that respond only to specif ic molecules (see
Figure 2.5). Located on the dendrites or on the cell body,
receptors work like locks into which only certain kinds of
keys will f it (Kelsey et al., 2006; Lambert & Kinsley, 2005).
However, instead of literally locking or unlocking the cor
responding receptors, the neurotransmitter molecules bind
to the receptors and af fect them either by exciting them
(mak ing the receiving neuron more l ikely to f ire) or by
inhibiting them (making the receiving neuron less likely
to f ire). We noted earlier that a sending neuron can make
a receiving neuron more or less likely to f ire, and now we see
how these effects occur: The sending neuron releases specif ic
neurotransmitters.
Sending
neuron
Receiving neuron
N
eu
ral im
p
u
lse
Axon of sending
neuron
Terminal button
Sacs containing
neurotransmitter
molecules
Neurotransmitter
molecules crossing
the synaptic cleft
Receptors
Synaptic
cleft
Dendrite of
receiving neuron
Neural impulse
FI G U RE 2.5 • The Synapse
TABLE 2.1 • Major Neurotransmitters, Their Major Functions, and Commonly Associated Disorders
Neurotransmitter Major functions Associated disorders or problems
Dopamine
Reward, motivation, executive function
(in frontal lobes), control of movements
Too little: attention-deficit/hyperactivity disorder
Too much: inappropriate aggression, schizophrenia
Serotonin
Mood, sleep, motivation Too little: depression and obsessive-compulsive disorder
Too much: lack of motivation
Acetylcholine
Storing new information in memory,
fight-or-flight response
Too little: delusions
Too much: spasms, tremors, convulsions
Adrenaline (also called epinephrine)
Attention, fight-or-flight response Too little: depression
Too much: over-arousal, feelings of dread or apprehension
Noradrenaline (also called
norepinephrine)
Attention, fight-or-flight response Too little: distractibility, fatigue, depression
Too much: anxiety disorders, schizophrenia
Glutamate
Registering pain, storing new information
in memory
Too little: schizophrenia
Too much: substance abuse
Gamma-amino butyric acid (GABA)
Inhibits brain activity in specific areas Too little: anxiety, panic disorder (possibly)
Too much: lack of motivation
Endogenous cannabinoids
Emotion, attention, memory, appetite,
control of movements
Too little: chronic pain
Too much: eating disorders, memory impairment, attention
difficulties, schizophrenia (possibly)
Sources: Based on Bressan & Crippa, 2005; Buchsbaum et al., 2006; Eger et al., 2002; Giuffrida et al., 2004; Goddard et al., 2001; Kalivas & Volkow, 2005;Meana et al., 1992; Muller & Schwarz,
2006; Mundo, Richter, et al., 2000; Nemeroff, 1998; Nutt & Lawson, 1992; Rao & Lyketsos, 1998; Wilson & Nicoll, 2001.
Receptors
Specialized sites on dendrites and cell bodies
that respond only to specific molecules.
Understanding Psychological Disorders: The Neuropsychosocial Approach 35
Abnormal Communications Among Neurons
How can communications among neurons at the synaptic cleft go awry, and thereby
lead to psychological disorders? Scientists point to at least three ways in which such
communications can be disrupted.
First, neurons might have too many or too few dendrites or receptors, mak
ing the neurons more or less sensitive, respectively, to even normal amounts of
neurotransmitters in the synaptic cleft (Meana et al., 1992). Second, the sending
neurons might produce too much or too little of a neurotransmitter. Third, the
events after a neuron fires may go awry (Kelsey et al., 2006). In particular, when
a neuron fires and sends neurotransmitter chemicals to another neuron, not all
of these molecules bind to receptors. Rather, some of the molecules linger in the
synaptic cleft and need to be removed. Special chemical processes operate to reup-
take these leftover neurotransmitters, moving them back into the sending neuron.
Sometimes reuptake does not operate correctly, which may contribute to a psycho
logical disorder.
Hormones and the Endocrine System
Hormones are chemicals that are released directly into the bloodstream that acti
vate or alter the activity of neurons. For example, some hormones play a key role
in helping animals respond to stressful situations by altering the functioning of
the ANS (Kandel et al., 2007). However, traumatic events can disrupt this often–
helpful mechanism and contribute to psychological disorders such as depression
(Claes, 2004).
Hormones are produced by glands in the endocrine system, which secretes sub
stances into the bloodstream. Hormones affect various organs throughout the body.
Cortisol is a particularly important hormone, which helps the body to cope with chal
lenges by making more resources available; cortisol is produced by the adrenal glands
(which are located right above the kidneys) and abnormal amounts of cortisol have
been linked to anxiety and depression.
The Genetics of Psychopathology
Researchers knew about the inheritance of traits long before the discovery of DNA
(deoxyribonucleic acid, the long molecule that contains many thousands of genes).
Everyone knows that people “take after” their parents in some ways that have noth
ing to do with learning, and genes are responsible for this resemblance. Genes affect
not only physical traits but also the brain and, through the brain, thinking, feeling,
and behavior; moreover, genes can affect how vulnerable people are to particular
psychological disorders (Plomin et al., 1997, 2003).
In the middle of the 20th centur y, James Watson
and Francis Crick identified genes, which correspond
to segments of DNA that control the production of par
ticular proteins and other substances (see Figure 2.6).
Genes are expressed when the information in them is
used to produce proteins and other substances, which
both produce biological structures (including the parts
of the neurons) and affect biological processes (such as
reputake). For many traits, gene variants— referred to as
alleles—determine how the trait is manifested. The sum
of an organism’s genes is called its genotype. In con
trast, the sum of its observable traits is called its pheno-
type, which results from how the genotype is expressed
in a particular environment.
Gene
DNA molecule
Proteins and other substances
Amino acids
combine to form
codes for
combine to produce
Physical and
psychological traits
FI G U RE 2.6 • DNA
Reuptake
The process of moving leftover
neurotransmitter molecules in the synapse
back into the sending neuron.
Hormones
Chemicals that are released directly into the
bloodstream that activate or alter the activity
of neurons.
Genes
Segments of DNA that control the production
of particular proteins and other substances.
Genotype
The sum of an organism’s genes.
Phenotype
The sum of an organism’s observable traits.
36 C H A P T E R 2
For most traits, many genes work together to cause particular effects. Sets
of genes give r ise to traits, such as height, that are expressed along a contin
uum, and the joint actions of these genes produce complex inheritance (Plo
min et al., 1997). Traits that arise from complex inheritance cannot be linked
to a few distinct genes, but rather emerge from the interactions among the ef
fects of numerous genes. Almost all psychological disorders that have a genetic
component, such as schizophrenia and depression, arise in part through complex
inheritance (Faraone et al., 2001; Plomin et al., 2003).
Behavioral Genetics
Studies that investigate the contributions of genes to mental illness rely on the methods
of behavioral genetics, which is the field that investigates the degree to which the
variability of characteristics in a population arises from genetic versus environmental
factors (Plomin et al., 2003). With regard to psychopathology, behavioral geneticists
consider these questions: What is the role of genetics in causing a particular mental
disorder? What is the role of the environment? And what is the role of interactions
between genes and the environment?
Throughout this book, we discuss the relative contributions of genes and the
environment to the development of specific mental disorders. We must always keep
in mind, however, that any conclusions about the relative contributions of the two
influences are always tied to the specific environment in which the contributions
are measured. To see why, consider the following example (based on Lewontin,
1976). Imagine three situations in which we plant two apple trees of the same
variety, one of which has genes for large apples and one of which has genes for
small apples.
In the first case, we keep the environment the same for the two trees. Unfortunately
for them, however, it is not a very friendly environment: The soil is bad, the trees are
in the shade, and there isn’t much water. Both trees produce small apples. In this case,
the environment overshadows the genetic influence for large apples.
In the second case, the trees are luckier. For both trees, the soil is rich, the
trees are in the sun, and they receive plenty of water. What happens? The tree
with genes for large apples produces larger apples than the tree with genes for small
apples.
In the third case, the tree with genes for large apples is planted in the impover
ished environment, and the tree with genes for small apples is planted in the favorable
environment. Now, the tree that has genes for small apples might produce bigger
apples than the tree with genes for large apples because the environmental conditions
have favored the former and acted against the latter.
As this example makes clear, for trees and other organisms—including humans—
the influence of genes must be described in relation to the environment in which
they function. In other words, genes and environment interact through feedback
loops—and in fact, that’s why the phenotype depends on how genes function in a
specific environment. The same genes can have different effects in different environ
ments. A research finding of a certain degree of genetic influence on a disorder in
one environment does not necessarily have any relationship to the degree of genetic
influence on the disorder in other environments. For example, the fact that genes can
predispose an individual to alcoholism has different effects in the alcoholembracing
culture of France and the alcoholshunning culture of Pakistan.
Heritability
Behavioral genetics characterizes the relative influence of genetic factors in terms
of the heritability of a characteristic. Heritability is an estimate of how much of
the variation in that characteristic within a population (in a specific environment)
Complex inheritance
The transmission of traits that are expressed
along a continuum by the interaction of sets
of genes.
Behavioral genetics
The field that investigates the degree to
which the variability of characteristics in
a population arises from genetic versus
environmental factors.
Heritability
An estimate of how much of the variation in a
characteristic within a population (in a specific
environment) can be attributed to genetics.
Understanding Psychological Disorders: The Neuropsychosocial Approach 37
can be attributed to genetics. For example, the heritability of generalized anxiety
disorder (which is characterized by worry that is not associated with a particular
situation or object, as we will discuss in detail in Chapter 6) is about .32 in citizens
of Western countries (Hettema, Neale, & Kendler, 2001). This means that about
one third of the variation in generalized anxiety disorder in this population is ge
netically determined.
There is no surefire research method for assessing heritability. Many variables
can affect the results. For example, if researchers find a similar prevalence of a men
tal disorder in children and their parents, can they assume genetic inheritance? Not
necessarily; they would have to rule out any effects of the environment that might be
operating. It is difficult to assess “the environment” for a given person. The environ
ment must be understood not in objective terms but rather in terms of how situations
and events are perceived and understood. For instance, for siblings in a given fam
ily, does having divorced parents constitute the same environment? Not exactly: A
child’s age at the time of parents’ divorce can influence how the child experiences the
divorce. A preschooler might believe he or she somehow caused the divorce, whereas
an older child—who is more mature cognitively, emotionally, and socially—is less
likely to make that inference (Allison & Furstenberg, 1989; Hoffman, 1991). Re
searchers can entirely avoid such age effects between siblings by studying twins.
Twin and Adoption Studies
Twin studies compare some characteristic, or set of characteristics, in two groups
of twins, identical and fraternal. Identical twins have basically the same genetic
makeup, because they began life as a single fertilized egg (or zygote) that then
divided to become two embryos. Such twins are monozygotic (mono- means
“one” ). Frater nal t wins beg in life as dif ferent fer tilized eggs, and so are
dizygotic (di- means “two”). Fraternal twins are like any other nonidentical
siblings in terms of their genetic similarity: They have about 50% overlap in
the genes that vary among humans. When researchers compare the charac
teristics of monozygotic twins and dizygotic twins, controlling as much as
possible for the environment, they can attempt to draw conclusions about
the relative contribution of genes to those characteristics in that environ
ment. For instance, such studies have suggested that schizophrenia is about
50 % heritable ( Gottesman, 1991). However, we must be cautious about
such estimates: Not only can identical twins have slightly different genetic
makeups but they also begin to have different experiences before birth—in
fact, one twin is usually heavier and larger at birth because of differences in
the amounts of nutrients the two fetuses receive in the womb (Cheung et al.,
1995; Hollier et al., 1999).
Sometimes researchers try to discover the roles of genes and the environ
ment in mental disorders by conducting adoption studies: They study twins who
were separated at birth and raised in different homes, then compare them to
twins who were raised in the same home. In addition, researchers also study bio
logically unrelated children who were adopted and raised together, then com
pare them to unrelated children who were reared in different homes. But even
in adoption studies, it’s not easy to disentangle the effects of genes and the envi
ronment. The reason is that genetic differences influence the environment—a re
lationship that is characterized by the reciprocal gene–environment model. For instance,
suppose that a pair of twins has genes that lead them to be highstrung and very
active. Even if these twins are raised apart in different environments, their parents
may react similarly to them—trying to keep them calm and out of trouble, which
might mean that they wouldn’t be taken on family outings as often as children who
are less of a handful. The point is that even in different adopted households, genes
It is not easy to sort out the effects of
genetics from those of the environment by
studying identical twins. Each twin has unique
experiences even before he or she is born: One
twin may get fewer nutrients or be exposed to
more toxins while in the mother’s womb; that
is, there can be different environments for the
twins even before birth. Such differences can
result in differences in behavior.
Im
ag
e
S
o
u
rc
e
/G
e
tt
y
I
m
a
g
e
s
Monozygotic twins
Twins who have basically the same genetic
makeup because they began life as a single
fertilized egg (zygote), which then divided
into two embryos; also referred to as identical
twins.
Dizygotic twins
Twins who developed from two fertilized eggs
and so have the same overlap in genes (50%)
as do siblings not conceived at the same time;
also referred to as fraternal twins.
38 C H A P T E R 2
can influence how twins are treated and what they experience. Thus, although
twin and adoption studies can be fascinating, their findings must be interpreted
cautiously.
The problems with twin and adoption studies have led many researchers to take
advantage of recent technological advances in genetics: It is now possible to assess,
inexpensively and quickly (for many genes), whether a particular person has a spe
cific allele of a gene (Schena et al., 1995). Researchers have used such techniques to
attempt to find associations between the presence or absence of specific alleles and
psychological disorders. For example, Rasmussen and colleagues (2006) found that
people who develop schizophrenia relatively late in life tend to have one particular
allele of a certain gene.
Feedback Loops in Understanding Genes
and the Environment
We’ve seen how genes can affect the environment, but—to the surprise of many—
the genes themselves are also affected by the environment, including psychological
and social factors (Slavich & Cole, 2013). We consider the feedback loops between
the environment and the genes in the following two sections.
The Environment Affects the Genes
Many people seem to think of genes as instructions for building the brain and the
body, guiding the construction process and then ceasing to function. For many genes,
this is not so. Even in adulthood, a person’s genes are regulated by the environment
(Hyman & Nestler, 1993). Consider a simple example: Did you ever try to learn
to play piano? If you did, your fingers were probably sore after even a halfhour of
practice. But if you stuck with it, you could play for longer and longer periods with
no discomfort. What happened? Your muscles got stronger. But how? When you
first began, the stress of using your fingers in new ways actually damaged the muscles
(which is why they felt sore). Then, a series of chemical events inside the muscle cells
of your fingers turned on genes in the nuclei of these cells. These genes directed the
cells to produce more proteins, to build up the muscles, which made them stronger.
If you stopped playing for a period of time, those genes would turn off, and the mus
cles would become weaker. This is why your fingers might be sore when you first
resumed playing after having taken a long break.
The point is that some genes are activated, or turned on, as a result of experi
ence, of interacting with the world (Kandel et al., 2007; South & Krueger, 2011).
This is true of genes in the brain that produce neurotransmitters and that cause new
synapses to form. In fact, when you learn something, genes in your brain are turned
on, which causes new connections among neurons to be formed. This is true even
when you learn maladaptive behaviors, which can produce, among other problems, a
phobia—an intense, irrational fear of an object or situation. Moreover, genetic factors
can contribute to a neurological vulnerability for a psychological disorder. For exam
ple, genetic factors can lead a person to be prone to learning maladaptive behaviors.
However, researchers have found that the same genes are associated with a number
of different mental disorders. This probably occurs because these genes affect shared
neural functions that have been disrupted (CrossDisorder Group of the Psychiatric
Genomics Consortium, 2013). It seems likely that if a person inherits genes that can
underlie such fundamental dysfunctions, different environmental stressors can trigger
the dysfunction in different contexts, leading to different disorders.
However, genes are not destiny. More often than not, having specif ic genes
does not determine behavior but rather predisposes a person to be affected by the
SP
N
Understanding Psychological Disorders: The Neuropsychosocial Approach 39
environment in certain ways. That is, genes can predispose a person for a specific
disorder, but those genes may have that effect only when triggered by psychological
or social factors.
The Genes Affect the Environment
We’ve just seen that the environment affects the genes, and we’ve already noted
that the reverse also occurs. Let’s now look in more detail at ways in which the
genes affect the environment. Many researchers (e.g., Plomin et al., 1997; Scarr &
McCartney, 1983) distinguish three ways in which genes affect the environment—
passive interaction, evocative interaction, and active interaction:
1. Passive interaction. The parents’ genes affect the child’s environment—and the
child passively receives these influences. For instance, some parents avoid social
groups because they are shy, which is in part a result of their genes; this means
that their child has relatively few social experiences. The child may not have
inherited the parents’ shy temperament, but the parents’ genes nonetheless act
through the environment to affect the child.
2. Evocative interaction (also called reactive interaction). A person’s inherited traits encour
age other people to behave in particular ways, and hence the person’s social envi
ronment will be affected by his or her genes. For example, if you are very tall and
heavyset, others may respond to you somewhat cautiously—in a way they would
not if you were short and frail. Similarly, others may approach or avoid you (fairly
or not!) in response to your temperament (e.g., shy, calm, highstrung); any spe
cific temperament will appeal to some and not to others. Thus, even your circle of
friends will be somewhat determined by your genes, and those friends will then
affect you in certain ways, depending on their own characteristics.
3. Active interaction. Each of us actively seeks out some environments and avoids
others, and our genes influence which environments feel most comfortable to
us. For example, a person who is sensitive to environmental stimulation might
prefer spending a quiet evening at home curled up with a good book instead of
going to a loud, crowded party at a friend’s house.
The interactions between genes and the environment involve all the factors con
sidered by the neuropsychosocial approach and hence create complex feedback loops.
Once the environment (including social factors, such as one’s choice of friends) has
been influenced by genes, the environment in turn affects the genes (as well as one’s
knowledge, beliefs, attitudes, and so on).
Again, the import of these observations for psychological disorders is clear. Genes
can put a person at risk for a particular psychological disorder, but other factors—
psychological and social—can influence the expression of the genes. And the specific
psychological and social factors that affect a person arise, in part, from that person’s
genes (which affect, for example, aspects of his or her appearance). Thus, even though
genes may make some people vulnerable to specific kinds of mental illness, the path
from genes to illness is neither straight nor inevitable.
Thinking Like A Clinician
Dominic is adopted, and his biological father was an alcoholic; alcoholism has a genetic com-
ponent. Dominic’s adoptive parents are very religious and don’t drink alcohol. Suppose scien-
tists determine that, among alcoholics, a particular brain area has an abnormally high level
of activity of the neurotransmitter dopamine. Further suppose that Dominic has too much
activation of dopamine neurons in this area. Does this mean that his brain is wired like that
of an alcoholic, and he should just resign himself to eventually becoming an alcoholic? How
might psychological and social factors affect dopamine levels?
40 C H A P T E R 2
Psychological Factors in
Psychological Disorders
Both of the Beale women had idiosyncratic ideas and inclinations. For instance,
Little Edie, in talking about World War II, expressed an unusual view about who
should be soldiers and sent off to fight a war—people who are not physically healthy
and hardy. With such people as soldiers, she claimed, the war would be over sooner
(Maysles, 2006). In addition, Big Edie was known to command Little Edie to change
her attire, repeatedly, up to 10 times each day (Maysles, 2006). Psychological factors,
such as learning, can help to account for people’s beliefs and behavior. Could aspects
of Big Edie’s and Little Edie’s views and lifestyle have been learned? And how might
their emotions—such as Big Edie’s fear of being alone or Little Edie’s resentment of
her mother’s control—influence their thoughts and behavior? Let’s examine the role
that previous learning, mental processes and contents, and emotions can play in psy
chological disorders.
Behavior and Learning
As we saw in Chapter 1, psychological disorders involve distress, impaired func
tioning, and/or risk of harm. These three elements can be expressed in behaviors,
such as occurs when people disrupt their daily lives in order to avoid feared stimuli
or when they drink too much alcohol to cope with life’s ups and downs. Many
behaviors related to psychological disorders can be learned. As we shall see, some
psychological disorders can be explained, at least partly, as a consequence of one of
three types of learning: classical conditioning, operant conditioning, and observa
tional learning.
Classical Conditioning
In a landmark study of an 11monthold infant, known as “Little Albert,” John B.
Watson and Rosalie Rayner (1920) demonstrated how to produce a phobia. The
researchers conditioned Little Albert to be afraid of white rats, using the basic
procedure that Pavlov used when he conditioned his dogs (see Chapter 1), except
in this case the reflexive behavior was related to fear rather than salivation. To do
this, they made a very loud sound immediately after a white rat (which was used
as the neutral stimulus) moved into the child’s view; they repeated this procedure
several times. Whenever Little Albert subsequently saw a white rat, he would cry
or exhibit other signs of fear. The process that generated Little Albert’s fear of
white rats is called classical conditioning—a type of learning that occurs when
two stimuli are paired so that a neutral stimulus becomes associated with another
stimulus that elicits a reflexive behavior; classical conditioning is also referred to
(less commonly) as Pavlovian conditioning. By experiencing pairings of the two
stimuli (the white rat and the loud noise in the case of Little Albert), the person
comes to respond to the neutral stimulus alone (the white rat) in the same way that
he or she had responded to the stimulus that elicited the reflexive behavior (the
loud noise).
How, specifically, does classical conditioning occur? Using the lingo of psychol
ogists, the stimulus that reflexively elicits a behavior is called the unconditioned
stimulus (UCS), because it elicits the behavior without prior conditioning. In the
case of Little Albert, the loud noise was the UCS, and the behavior it reflexively elic
ited was a startle response associated with fear. Such a reflexive behavior is called an
unconditioned response (UCR). The neutral stimulus that, when paired with the
UCS, comes to elicit the reflexive behavior is called the conditioned stimulus (CS).
Classical conditioning
A type of learning that occurs when two
stimuli are paired so that a neutral stimulus
becomes associated with another stimulus
that elicits a reflexive behavior; also referred
to as Pavlovian conditioning.
Unconditioned stimulus (UCS)
A stimulus that reflexively elicits a behavior.
Unconditioned response (UCR)
A behavior that is reflexively elicited by a
stimulus.
Conditioned stimulus (CS)
A neutral stimulus that, when paired with an
unconditioned stimulus, comes to elicit the
reflexive behavior.
Understanding Psychological Disorders: The Neuropsychosocial Approach 41
It is called the conditioned stimulus because its ability to elicit the response is condi-
tional on its being paired with a UCS. In Little Albert’s case, the CS was the white
rat. The conditioned response (CR) is the response that comes to be elicited by
the previously neutral stimulus (the CR is basically the same behavior as the UCR,
but the behavior is elicited by the CS). In Little Albert’s case, the CR was the startle
response to the rat alone (and ensuing fearrelated behaviors, such as crying and try
ing to avoid the rat). The process of classical conditioning is illustrated in Figure 2.7.
Although various reflexive behaviors, such as salivation, can be classically con
ditioned (Pavlov, 1927), the ones most important for understanding psychopathol
ogy are those related to emotional responses such as fear and arousal (Davey, 1987;
Schafe & LeDoux, 2004). When emotions and emotionrelated behaviors are clas
sically conditioned, they are referred to as conditioned emotional
responses. People who have the personality characteristic of being gen
erally emotionally reactive—referred to as being high in neuroticism—are
more likely to develop conditioned emotional responses than are people
who do not have this personality characteristic (Bienvenu et al., 2001).
Conditioned responses can also generalize, so that they are elicited
by stimuli that are similar to the conditioned stimulus, a process called
stimulus generalization. For instance, Little Albert became afraid not only of
white rats but also of other white furry things. He even became afraid of a piece of
white cotton! His fear of rats had generalized to similar stimuli.
As we shall see in detail in later chapters, classical conditioning is of interest
to those studying psychological disorders because it helps to explain various types
of anxiety disorders (particularly phobias, such as Little Albert’s phobia), substance
abuse and dependence (Hyman, 2005), and the development of specific types of sex
ual disorders (Domjan et al., 2004).
Operant Conditioning
Operant conditioning is a type of learning in which the likelihood that a behavior
will be repeated depends on the consequences associated with the behavior. Operant
conditioning usually involves voluntary behaviors, whereas classical conditioning usu
ally involves reflexive behaviors. With operant conditioning, when a behavior is fol
lowed by a positive consequence, the behavior is more likely to be repeated. Consider
Big Edie’s behavior of crying out for Little Edie to come back into the room. Little
Edie then returns to the room (a positive consequence), making it more likely that Big
Edie will cry out for Little Edie to return in the future. When a behavior is followed
by a negative consequence, it is less likely to be repeated. For instance, the last time
Big Edie left Grey Gardens was in 1968, when she and her daughter went to a party at
a friend’s house; upon returning home, the Beale women discovered that thieves had
taken $15,000 worth of heirlooms. It seemed to Big Edie that her behavior (leaving the
house) was followed by a negative consequence (the theft), and so she never left again.
Psychologist B. F. Skinner showed that operant conditioning can explain a great
deal of behavior, including abnormal behavior, and operant conditioning can be used
to treat abnormal behaviors (Skinner, 1965). As we shall see throughout this book,
operant conditioning contributes to various psychological disorders, such as depres
sion, anxiety disorders, substance abuse disorder, eating disorders, and problems with
selfregulation in general. Operant conditioning relies on two types of consequences:
reinforcement and punishment; each can be either positive or negative.
Reinforcement
A key element in operant conditioning is reinforcement, the process by which the
consequence of a behavior increases the likelihood of the behavior’s recurrence. The
consequence—an object or event—that makes a behavior more likely in the future
Conditioned response (CR)
A response that comes to be elicited by the
previously neutral stimulus that has become a
conditioned stimulus.
Conditioned emotional responses
Emotions and emotion-related behaviors that
are classically conditioned.
Stimulus generalization
The process whereby responses come to
be elicited by stimuli that are similar to the
conditioned stimulus.
Operant conditioning
A type of learning in which the likelihood that
a behavior will be repeated depends on the
consequences associated with the behavior.
Reinforcement
The process by which the consequence of
a behavior increases the likelihood of the
behavior’s recurrence.
FI G U RE 2.7 • Classical Conditioning
of a Fear: Little Albert
Before Classical Conditioning
UCS
loud noise fear
UCR
Neutral
stimulus
white rat
no
response
During Classical Conditioning
UCS
loud noise
UCR
fear
After Classical Conditioning
CR
fear
(of rats)
CS
white rat
Neutral
stimulus
white rat
42 C H A P T E R 2
is called a reinforcer. In the case of Big Edie’s fear of being alone, the behavior was Big
Edie’s calling out to her daughter to return to her room, and it was followed by a
reinforcer: Little Edie’s return to her mother’s side.
We need to consider two types of reinforcement: positive reinforcement and nega
tive reinforcement. Positive reinforcement occurs when a desired reinforcer is received
after the behavior, which makes the behavior more likely to occur again in the future.
For instance, when someone takes a drug, the chemical properties of the drug may lead
the person to experience a temporarily pleasant state (the reinforcer), which he or she may
want to experience again, thus making the person more likely to take the drug again.
In contrast, negative reinforcement occurs when an aversive or uncomfort
able stimulus is removed after a behavior, which makes that behavior more likely to
be repeated in the future; note that negative, in this instance, does not necessarily
mean “bad.” For example, suppose that a man has a strong fear—a phobia—of dirt.
If his hands get even slightly dirty, he will have the urge to wash them and will be
uncomfortable until he does so. The act of washing his hands is negatively reinforced
by the consequence of removing his discomfort about the dirt, which makes him more
likely to wash his hands again the next time they get a bit dirty. Negative reinforcement
is often confused with punishment; as we see next, however, the two are very different.
Punishment
Positive reinforcement and negative reinforcement both increase the probability of
a behavior’s recurring. In contrast, punishment is a process by which an event or
object that is the consequence of a behavior decreases the likelihood that the behavior
will occur again. Just as there are two types of reinforcement, there are two types of
punishment: positive punishment and negative punishment. Positive punishment
takes place when a behavior is followed by an undesirable consequence, which makes
the behavior less likely to recur. In other words, an undesired stimulus is added in
response to a behavior. For example, imagine that every time a young boy sings along
with a song playing on the radio, his older sister makes fun of him (an undesirable
consequence): In the future, he won’t sing as often when she’s around. That boy has
experienced positive punishment.
Negative punishment occurs when a behavior is followed by the removal of
a pleasant or desired event or circumstance, which decreases the probability of that
Positive reinforcement
The type of reinforcement that occurs when a
desired reinforcer is received after a behavior,
which makes the behavior more likely to occur
again in the future.
Negative reinforcement
The type of reinforcement that occurs when
an aversive or uncomfortable stimulus is
removed after a behavior, which makes that
behavior more likely to be produced again in
the future.
Punishment
The process by which an event or object that
is the consequence of a behavior decreases
the likelihood that the behavior will occur
again.
Positive punishment
The type of punishment that takes place
when a behavior is followed by an undesirable
consequence, which makes the behavior less
likely to recur.
Negative punishment
The type of punishment that takes place when
a behavior is followed by the removal of a
pleasant or desired event or circumstance,
which decreases the probability of that
behavior’s recurrence.
In which photo are the students, at least in theory, receiving positive punishment? Answer: The students in the left photo. School detention is
an attempt at positive punishment: Imposing the consequence of detention on students who exhibit troublesome behaviors should decrease
the likelihood of those behaviors’ occurring in the future.
C
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to
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Understanding Psychological Disorders: The Neuropsychosocial Approach 43
Learned helplessness
The state of “giving up” that arises when an
animal or person is in an aversive situation
where it seems that no action can be
effective.
behavior’s recurrence. Negative punishment
occurs, for example, when a teenager stays
out too late with friends and then her par
ents take away for a week her access to tele
vision (or cell phone, email, use of the car,
or something else she likes). Big Edie’s father
tried to use negative punishment to modify
her behavior: He decreased her monthly al
lowance, repeatedly reduced her inheritance,
and even told her that he was doing this be
cause of her eccentric behavior. His attempts
at negative punishment did not work, how
ever, which indicates that the consequence he
picked—taking away some money—was not
meaningful enough to Big Edie. The four
types of operant conditioning are compared
in Table 2.2.
Receiving frequent punishments or nega
tive criticisms is associated with depression in
some people: Over time, some individuals who
experience such aversive events eventually give
up trying to avoid or escape them and become
depressed. Martin Seligman and his colleagues
suggested that this giving up is learned through operant conditioning (Miller & Selig
man, 1973, 1975). The process appears analogous to what happens to animals in simi
lar circumstances. Consider a classic study by Overmier and Seligman (1967): When
caged dogs were electrically shocked, at first they would respond to the shocks, trying
to escape from them by moving to a different part of the cage. But when they could
not escape the continued shocks, they eventually stopped responding and simply en
dured, huddling on the floor. Even after they were put in a new cage in which they
could easily avoid the shocks by moving, they remained on the floor. This phenom
enon, whether in animals or humans, is called learned helplessness: In an aversive
situation where it seems that no action can be effective, the animal or person stops
trying to escape (Mikulincer, 1994). Learned helplessness is considered to underlie
certain types of depression. For example, sometimes people are emotionally abused—
continually criticized, humiliated, and belittled—and no matter how hard they try to
be “better” (and so prevent the abuse), the emotional abuse continues. When people
in such a situation give up trying, they may become depressed and become vulnerable
to a variety of stressrelated problems.
Feedback Loops in Understanding Classical Conditioning and
Operant Conditioning
Let’s suppose that a student gave a presentation that didn’t go well, and some class
mates snickered during one part (social factor). Let’s also suppose that this student had
an inherited vulnerability (a neurological factor; Stein & Gelernter, 2010) that in
creased his or her risk of developing a conditioned emotional response—in this case,
to making presentations (Mineka & Zinbarg, 1995). And let’s further suppose that the
student developed negative, irrational thoughts about public speaking ( psychological
factor; Abbott & Rapee, 2004; Antony & Barlow, 2002). The three sorts of factors,
fueling each other, can increase the likelihood that the student will develop a social
phobia—an intense fear of public humiliation or embarrassment, accompanied by an
avoidance of social situations likely to elicit this fear.
SP
N
TABLE 2.2 • Four Types of Operant Conditioning
Type of conditioning How it occurs Result Example
Positive
reinforcement
Desired
consequence
is produced by
behavior.
Increased
likelihood of
the behavior
A pleasant effect from drug
use makes drug use more
likely to recur.
Negative
reinforcement
Undesired event
or circumstance
is removed after
behavior.
Increased
likelihood of
the behavior
The uncomfortable feeling of
having dirty hands is relieved
by washing them (which
makes such washing more
likely to recur).
Positive punishment
Undesired
consequence
is produced by
behavior.
Decreased
likelihood of
the behavior
A sister’s humiliating
comment about her brother’s
singing along with the radio
makes future singing in her
presence less likely to recur.
Negative
punishment
Pleasant event
or circumstance
is removed after
behavior.
Decreased
likelihood of
the behavior
Removing a television from
a teenager’s room after he
stays out too late makes
staying out too late less
likely to recur.
44 C H A P T E R 2
Observational Learning
Not all learning involves directly experiencing the associations
that underlie classical and operant conditioning. Observational
learning (also referred to as modeling) results from watching what
happens to others (social factor; Bandura et al., 1961); from our
observations, we learn ways to behave as well as develop ex
pectations about what is likely to occur when we behave the same
way (psychological factor). Observational learning is primarily a
psychological factor: The key is mental processes (who and what be
haviors are paid attention to, how the information is perceived and
interpreted, how motivated the individual is to imitate the behav
ior). However, social factors are also involved, which include who
the model is, his or her status, and his or her relationship to the
observer. For instance, people who have high status or are attrac
tive are more likely to hold our attention—so we are more likely
to model their behavior (Brewer & Wann, 1998).
Through obser vat iona l lear n ing, ch i ld ren can f ig ure out what t y pes of
behavior are acceptable in their family (Thorn & Gilbert, 1998), even if the ob
served behaviors are maladaptive. For example, when children observe parents
managing conflict through violence or by drinking alcohol, they may learn to
use such coping strategies themselves. From a young age, Little Edie spent much
of her time with her mother, and during the 2 years she was kept out of school,
she was with her mother practically day and night. Thus, in her formative years,
Little Edie had ample opportunity to watch her mother’s eccentric behavior and
may have modeled her own eccentric behavior on that of her mother. Further,
observational learning and operant conditioning can work together: When Little
Edie modeled her behavior after her mother’s, she was no doubt reinforced by her
mother.
Mental Processes and Mental Contents
As noted in Chapter 1, both mental processes and mental contents play important
roles in the etiology of psychological disorders. Let’s take a closer look at these two
types of contributing factors.
Mental Processes
We all have biases in our mental processes; hearing the same conversation, we can
differ in what we pay attention to, how we interpret what we hear, and what we re
member. With some psychological disorders, mental processes involved in attention,
perception, and memory may be biased in particular ways:
• Attention results in selecting certain stimuli, including those that may be related to
a disorder (van den Heuvel et al., 2005). Women with an eating disorder, for in
stance, are more likely than women without such a disorder to focus their attention
on the parts of their bodies they consider “ugly” ( Jansen et al., 2005) or on words
related to food (Brooks et al., 2011).
• Perception results in registering and identifying specific stimuli, such as spiders
or particular facial expressions of emotion ( Buhlmann et al., 2006). As one
example of bias in perception, depressed people are less likely than nonde
pressed people to rate neutral or mildly happy faces as “happy” (Surguladze
et al., 2004).
• Memory involves storing, retaining, and accessing stored information, including
that which is emotionally relevant to a particular disorder (Foa et al., 2000).
Observational learning
The process of learning through watching
what happens to others; also referred to as
modeling.
People who are uncomfortable in particular
social situations may leave such situations
as early as possible; this early departure is
negatively reinforced because, once they
leave, they no longer feel uncomfortable. Such
negative reinforcement of social anxiety can
contribute to a psychological disorder called
social phobia—unreasonable anxiety or fear in
social situations.
M
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S
zw
aj
ko
s/
S
w
ig
S
o
ci
a
l
Understanding Psychological Disorders: The Neuropsychosocial Approach 45
Consider the disorder illness anxiety disorder, which is marked by a preoccupation with
bodily sensations, combined with a belief of having a serious illness despite a lack
of medical evidence. People suffering from illness anxiety disorder have a memory
bias: They are better able to remember healthrelated words than non–healthrelated
words (Brown, Kosslyn, et al., 1999), which is not surprising considering that the
disorder involves a preoccupation with illness.
Thus, various mental processes can contribute to psychopathology by influenc
ing what people pay attention to, how they perceive various stimuli, and what they
remember. In turn, these alterations in mental processes influence the content of peo
ple’s thoughts by shifting their awareness of various situations, objects, and stimuli.
Mental Contents
The contents of people’s thoughts can play a role in whether someone
develops a psychological disorder. Psychiatrist Aaron Beck (1967) proposed
that dysfunctional, maladaptive thoughts are the root cause of psychologi
cal problems. These dysfunctional thoughts are cognitive distortions of
reality. An example of a dysfunctional belief is a woman’s conviction that
she is unlovable—that if her boyfriend really knew her, he couldn’t love
her. Cognitive distortions can make a person vulnerable to psychological
disorders and are sometimes referred to as cognitive vulnerabilities (Riskind
& Alloy, 2006). Beck (1967) also argued that recognizing these false and
dysfunctional thoughts and adopting realistic and adaptive thoughts can
reduce psychological problems. Cognitive distortions can be a result of
maladaptive learning from previous experiences. A man with a classically
conditioned fear of rodents, for instance, may come to believe that rodents
are dangerous because of the fear and anxiety he experiences when he’s with
them. Operant conditioning can also give rise to cognitive distortions. For
instance, a child who is repeatedly rejected by her father can grow up to
believe that nobody could love her. In this case, the conditioning could have oc
curred when, every time she tried to hug her father, he turned away. Cognitive
distortions and biased mental processes affect each other. Several common cognitive
distortions are presented in Table 2.3.
People who get anxious about public speaking
often have the dysfunctional belief that
audience members will laugh and jeer; this
belief is a cognitive distortion. This woman is
enjoying herself at a soccer game but laughter
like this is what many people are afraid of
when they think about speaking in public.
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TABLE 2.3 • Cognitive Distortions
Cognitive distortion Definition Example
All-or-nothing thinking Seeing things in black and white You think that if you are not perfect, you are a failure.
Overgeneralization
Seeing a single negative event as part of a never-ending
pattern of such events
While having a bad day, you predict that subsequent days
will also be bad.
Mental filter
Focusing too strongly on negative qualities or events,
to the exclusion of the other qualities or events
Although your overall appearance is fine, you focus
persistently on the bad haircut you recently had.
Disqualifying the positive
Not recognizing or accepting positive experiences or
events, thus emphasizing the negative
After giving a good presentation, you discount the positive
feedback you received and focus only on what you didn’t
like about your performance.
Jumping to conclusions
Making an unsubstantiated negative interpretation of
events
Although there is no evidence for your inference, you
assume that your boss didn’t like your presentation.
Personalization
Seeing yourself as the cause of a negative event when
in fact you were not actually responsible
When your parents fight about finances, you think their
problems are somehow your fault, despite the fact that
their financial troubles weren’t caused by you.
Source: Copyright © 1980 by David D. Burns, M.D. Reprinted by permission of HarperCollins Publishers, William Morrow. For more information see the Permissions section.
Cognitive distortions
Dysfunctional, maladaptive thoughts that
are not accurate reflections of reality and
contribute to psychological disorders.
46 C H A P T E R 2
Mental health professionals need to keep in mind, however, cultural factors that
may contribute to what appear to be maladaptive cognitive distortions but in fact
reflect appropriate social behavior in a patient’s culture. For instance, some cultures,
such as that of Japan, have a social norm of responding to a compliment with a self
deprecating statement. It is only through careful evaluation that a clinician can dis
cern whether such selfdeprecating behavior reflects a patient’s attempt to show good
manners or his or her core maladaptive dysfunctional beliefs about self.
Emotion
Many psychological disorders include problems that involve emotions: not feeling or
expressing enough emotions (such as showing no response to a situation where others
would be joyous or sad), having emotions that are inappropriate or inappropriately
excessive for the situation (such as feeling sad to the point of crying for no appar
ent reason), or having emotions that are difficult to regulate (such as overwhelming
panic) (Aldao & NolenHoeksema, 2010; American Psychiatric Association, 2013).
But what, specifically, are emotions? To psychologists, an emotion is a short
lived experience evoked by a stimulus that produces a mental response, a typical
behavior, and a positive or negative subjective feeling. The stimulus that initiates an
emotion could be physical: It can be a kiss, the positive comments on an essay you
get back from a professor, or the sounds of a tune you listen to on your computer.
Alternatively, the stimulus can occur only in the mind, such as remembering a sad
occasion or tune or imagining your perfect mate.
Mental health clinicians and researchers sometimes use the word affect to refer to
an emotion that is associated with a particular idea or behavior, similar to an attitude.
Affect is also used to describe how emotion is expressed, as when noting that a patient
has inappropriate affect—the patient’s expression of emotion is not appropriate to
what he or she is saying or to the situation. An example is a person laughing at a
funeral or talking about a happy event while looking sad or angry. Flat affect is a lack
of, or considerably diminished, emotional expression, such as occurs when someone
speaks robotically and shows little facial expression. People with some psychological
disorders, such as schizophrenia, frequently display inappropriate or flat affect. Other
people may exhibit labile affect, a pattern in which affect changes very rapidly—too
rapidly. Labile affect may indicate a psychological disorder; for instance, some people
with depression may quickly shift emotions from sad to angry or irritable.
In the film Grey Gardens, Little Edie and her mother often displayed inappropriate
affect, and Little Edie’s emotions were sometimes labile, rapidly changing from anger
to happy excitement to relative calm. For instance, at one point, Big Edie recounts
that when Little Edie had moved to New York City, Big Edie wanted Mr. Beale to
return to Grey Gardens. Little Edie immediately started yelling, “You’re making me
very angry!” (Maysles & Maysles, 1976), even though one moment before she had
been relatively calm, and they were talking about events that had transpired over
20 years earlier.
A mood is a persistent emotion that is not attached to a stimulus. A mood lurks
in the background and influences mental processes, mental contents, and behavior.
For example, when you wake up “on the wrong side of the bed” for no apparent
reason and feel grumpy all day, you are experiencing a type of bad mood. Some psy
chological disorders, such as depression, involve disturbances in mood.
Emotions and Behavior
Emotions and behavior dynamically interact. On the one hand, emotion can change
behavior. People are more likely to participate in activities and behave in ways that are
consistent with their emotions (Bower & Forgas, 2000). For instance, when people
Some disorders are characterized by
inappropriate affect—expressions of emotion
that are inappropriate to the situation. We can
imagine a situation where this young man’s
laughter—which may be just a reaction to a
funny joke—might be a sign of inappropriate
affect if he had just heard bad news.
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Emotion
A short-lived experience evoked by a stimulus
that produces a mental response, a typical
behavior, and a positive or negative subjective
feeling.
Affect
An emotion that is associated with a particular
idea or behavior, similar to an attitude.
Inappropriate affect
An expression of emotion that is not appropriate
to what a person is saying or to the situation.
Flat affect
A lack of, or considerably diminished,
emotional expression, such as occurs when
someone speaks robotically and shows little
facial expression.
Labile affect
Affect that changes inappropriately rapidly.
Mood
A persistent emotion that is not attached to
a stimulus; it exists in the background and
influences mental processes, mental contents,
and behavior.
Understanding Psychological Disorders: The Neuropsychosocial Approach 47
are sad, they tend to hunch their shoulders and listen to slow
music rather than upbeat music; when people are afraid, they
tend to freeze, like a deer caught in the headlights; and when
people are depressed, they often don’t have the inclination or
energy to see friends, which can lead to social isolation. On
the other hand, a change in behavior can lead to a change in
emotion. When people who are depressed make an effort to
see friends or engage in other activities that they used to en
joy, they often become less depressed ( Jacobson et al., 2001).
Emotions, Mental Processes, and Mental
Contents
Emotions affect behavior as well as mental processes and
mental contents. In fact, emotions and moods contribute to
biases in attention, perception, and memory (Demenescu et
al., 2010; MacKay & Ahmetzanov, 2005; Mogg & Bradley, 2005; Yovel & Mineka,
2005). For example, when feeling down, people are more likely to see the world
through “depressed” lenses, to have a negative or pessimistic slant in general; not
only will they find it easier to remember past periods of sadness, but they will also
tend to view the future as hopeless; they will see more reasons to be sad than will
people who aren’t down (Lewis & Critchley, 2003).
The causality also works in the other direction: Mental processes can affect emo
tions. For example, emotions are affected by attributions. That is, we all regularly
try to understand why events in our lives occur, and thus make attributions, assigning
causes for particular occurrences. A person’s mood can be affected by the attribu
tions he or she makes. For instance, college students who tend to attribute negative
events to general, enduring negative qualities about themselves (“I am stupid”) are
more likely to become depressed after a negative event (such as getting a bad grade)
(Metalsky et al., 1993).
Emotional Regulation and Psychological Disorders
Difficulty in regulating emotions and related thoughts and behaviors can lead to
three types of problems (Cicchetti & Toth, 1991; Weisz et al., 1997):
1. Externalizing problems are characterized by too little control of emotion and
related behaviors, such as aggression, and by disruptive behavior. They are called
externalizing problems because their primary effects are on others and/or their
environment; these problems are usually observable to others.
2. Internalizing problems are characterized by negative internal experiences, such as
anxiety, social withdrawal, and depression. Internalizing problems are so named
because their primary effect is on the troubled individual rather than on others;
such problems are generally less observable to others.
3. Other problems include emotional or behavioral problems that do not fit into these
categories. This “other” category includes eating disorders and learning disorders
(Achenbach et al., 1987; Kazdin & Weisz, 1998).
Significant difficulty in regulating emotions can begin in childhood and last through
adulthood, forming the basis for some disorders.
Neurological Bases of Emotion
Emotion is a psychological response, but it is also a neurological response. We can learn
much about the psychological aspects of emotion by considering how it arises from
brain function. For example, research by Richard Davidson and colleagues, conducted
largely by measuring the brain’s electrical activity, have demonstrated that there are
Mental processes can affect emotions, such as
occurs when a person attributes a bad grade
to negative qualities about himself or herself,
which in turn leads to poor mood.
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A
la
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Emotions and behavior have a reciprocal
relationship: Changing behavior can change
emotion, which this depressed person is trying
to do by exercising.
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48 C H A P T E R 2
two general types of human emotions, approach emotions and withdrawal emotions,
each relying on its own system in the brain. Approach emotions are positive emotions,
such as love and happiness, and tend to activate the left frontal lobe more than the
right. Withdrawal emotions are negative emotions, such as fear and sadness, and tend to
activate the right frontal lobe more than the left (Davidson, 1992a, 1992b, 1993, 1998,
2002; Davidson et al., 2000; Lang, 1995). Researchers have also found that people who
generally have more activation in the left frontal lobe tend to be more optimistic than
people who generally have more activation in the right. This is important because de
pression has been associated with relatively less activity in the left frontal lobe (David
son, 1993, 1994, 1998; Davidson et al., 1999). As a result of genetics, learning, or (most
likely) some combination of the two, some people are temperamentally more likely to
experience positive (approach) emotions, whereas others are more likely to experience
negative (withdrawal) emotions (Fox et al., 2005; Rettew & McKee, 2005).
Temperament
Temperament is closely related to emotion: Temperament refers to the aspects of
personality that reflect a person’s typical emotional state and emotional reactivity
(including the speed and strength of reactions to stimuli). Temperament is in large
part innate, and it inf luences behavior in early childhood and even in infancy.
Temperament is of interest in the study of psychological disorders for two reasons
(Nigg, 2006a): First, specific types of temperament may make a person especially
vulnerable to certain psychological disorders, even at an early age. For instance, peo
ple who are temperamentally more emotionally reactive are more likely to develop
psychological disorders related to high levels of anxiety. Second, it is possible that in
some cases a psychological disorder is simply an extreme form of a normal variation
in temperament. For instance, some researchers argue that social phobia is on a con
tinuum with shyness but is an extreme form of it; shyness involves withdrawal emo
tions and lack of sociability, and is viewed as a temperament (Schneider et al., 2002).
The Beale women had unusually reactive temperaments—they reacted strongly
to stimuli. One or the other of them would respond to a neutral or off hand remark
with emotion that was out of proportion: hot anger, bubbling joy, or snapping
irritability. It’s not a coincidence that mother and daughter seemed similar in this
respect. Much evidence indicates that genes contribute strongly to temperament
(Gillespie et al., 2003); in fact, some researchers report that genes account for about
half of the variability in temperament (Oniszcenko et al., 2003). Researchers have
associated some aspects of temperament to specific genes, such as genes that affect
receptors for the neurotransmitter dopamine and a gene involved in serotonin pro
duction, and have shown that these genes can influence depression and problems
controlling impulses (Nomura et al., 2006; Propper & Moore, 2006). Genes that
affect dopamine receptors have also been shown to influence emotional reactiv
ity (Oniszcenko & Dragan, 2005). However, these genes have stronger effects on
children raised in harsh family environments; as we stressed earlier, the effects of
genes need to be considered within the context of specific environments (Roisman &
Fraley, 2006; Saudino, 2005).
C. Robert Cloninger and his colleagues have proposed one particularly influential
theory of temperament, which describes temperament in terms of four dimensions—
novelty seeking, harm avoidance, reward dependence, and persistence—each of
which is associated with a brain system that relies predominantly on a particular
neurotransmitter, as shown in Table 2.4 (Cloninger, 1987b; Cloninger et al., 1993).
In fact, researchers have found associations between genes and these dimensions
of temperament (Gillespie et al., 2003; KeltikangasJärvinen et al., 2006; Rybakowski
et al., 2006). The specific results suggest that temperament arises from the joint
activity of many different genes.
Fear involves a reflexive activation of the
amygdala, not necessarily accompanied by
any cognitive interpretation of the stimulus.
Other emotions, such as guilt, depend on
such interpretation. The ease of treating an
emotional problem may be related to the
nature of the underlying mechanism that gives
rise to the experience of that emotion.
B
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A
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Temperament
The aspects of personality that reflect
a person’s typical emotional state and
emotional reactivity (including the speed and
strength of reactions to stimuli).
Understanding Psychological Disorders: The Neuropsychosocial Approach 49
Maya is depressed; she’s often tearful and feels hopeless about the future and helpless
to change the negative things in her life. Give specific examples of the ways that types
of learning might have influenced her negative expectations of life and led to her current
depression. (It’s okay to speculate here, but be specific.) Based on what you have read,
how can Maya’s thought patterns and emotions lead to her feeling depressed (or make the
depression worse)?
Thinking Like A Clinician
Social Factors in Psychological
Disorders
We exist in a world filled with social forces: our relationships with family, friends,
colleagues, and neighbors; the messages we receive through the media; the norms of
our culture. These social forces help to shape who we become. They can help to pro
tect us from developing psychological disorders, or they can make us more vulnerable
to or exacerbate psychological disorders. Social forces begin to exert their influence
before adulthood, and they can affect each generation differently, as a culture changes
over time. For instance, the more recently an American is born, the more likely he
or she is to develop a psychological disorder ( Kessler, Bergland, et al., 2005), perhaps
because of social trends such as the increased divorce rate, an increased sense of dan
ger, and a diminished sense of local community (Twenge, 2000).
Consider Big Edie and Little Edie. The social factors that influenced them include
their relationships with other members of their family, their financial circumstances,
the prevailing community and cultural standards of appropriate behavior for women—
and the discrimination they encountered. Let’s examine in more detail each type of
social factor—family, community, and culture—as well as the stress they can create.
Family Matters
Certain aspects of family life form the basis for the type of attachment a child has
to the primary caregiver, which influences how a child comes to view himself or
herself and learns what to expect from other people. Other familyrelated social fac
tors include the style of interaction among family members, child maltreatment, and
parental psychological disorders. All of these factors can contribute to the emergence
or persistence of psychological disorders.
TABLE 2.4 • Cloninger’s Four Temperaments
Temperament Description
Hypothesized related
neurotransmitter Associated disorder(s)
Novelty seeking
Searching out novel stimuli and reacting positively
to them; high levels can lead to being impulsive,
avoiding frustration, and easily getting angry
Dopamine With a high level, disorders that involve
impulsive or aggressive behaviors
Harm avoidance
Reacting very negatively to harm and avoiding it
whenever possible
Serotonin With a high level, anxiety disorders
Reward dependence
Degree to which past behaviors that have led to
desired outcomes in the past are repeated
Norepinephrine With a low level (in combination with
high impulsivity), substance use disorders
Persistence
Making continued efforts in the face of
frustration when attempting to accomplish
something.
Possibly dopamine With a low level, attention-deficit/
hyperactivity disorder
50 C H A P T E R 2
Family Interaction Style and Relapse
If family members exhibit hostility, voice unnecessary criticism, or are emotion
ally overinvolved, then the family environment is characterized by high expressed
emotion. Based on what we know of the Beale women, their family environment
would likely be classified as high expressed emotion. Consider these typical com
ments by Big Edie to her daughter: “Well, you made a rotten breakfast,” followed
moments later by, “Everything is perfectly disgusting on account of you” (Maysles &
Maysles, 1976). Big Edie and Little Edie were also clearly overinvolved with each
other: They spent virtually all their waking hours together, participated in all aspects
of each other’s lives, and responded to each other in exaggerated ways.
British researchers found that among people with schizophrenia, those whose
families showed high expressed emotion were more likely to have the disorder recur;
the same association between high expressed emotion and relapse has been found in
other studies in the United States and China (Butzlaff & Hooley, 1998; Yang et al.,
2004). This may be because high expressed emotion is associated with family mem
bers’ belief that the patient has the ability to control his or her symptomatic behav
iors, which sometimes leads the family members to push the patient to change (Miura
et al., 2004). Unfortunately, these exhortations may well backfire: Instead of encour
aging the patient to change, they may produce the sort of stress that makes the disor
der worse! When family members are educated about the patient’s
disorder and taught more productive ways of communicating with
the patient, relapse rates generally decline (Miklowitz, 2004).
High expressed emotion is not associated with relapse in all
cultural or ethnic groups; members of different groups interpret
such emotional expression differently. Among Mexican American
families, for instance, the family member with schizophrenia is
more likely to have a recurrence if the family style is the less com
mon one of being distant and aloof; high expressed emotion is
not related to recurrence ( Lopez et al., 1998). And among African
American families, high expressed emotion is actually associated
with a better outcome ( Rosenfarb et al., 2006). One possible ex
planation is that in African American families, confrontations are
interpreted as signs of honesty (Rogan & Hammer, 1998) and may
signal love and caring.
Child Maltreatment
Child maltreatment comes in various forms—neglect, verbal abuse, physical abuse,
and sexual abuse—and is associated with a higher risk for a variety of psychologi
cal disorders (Cicchetti & Toth, 2005; Green et al., 2010; Naughton et al., in press),
including personality disorders (Battle et al., 2004; Bierer et al., 2003). Child mal
treatment exerts its influence indirectly, through the following:
• An altered bodily and neurological response to stress. For instance, children who have been
maltreated have higher baseline levels of cortisol than do children who have not been
maltreated. Such alteration of the stress response in those who have been maltreated
continues into adulthood (Tarullo & Gunnar, 2006; WattsEnglish et al., 2006).
• Behaviors that are learned as a consequence of the maltreatment. Maltreatment may result
in a type of learned helplessness, so the children are more likely to be victimized as
adults (Renner & Slack, 2006).
• Biases in discriminating and responding to facial expressions. For instance, children who
have been physically abused are more likely to perceive photographs of faces as
conveying anger than are children who have not been physically abused (Pollak
et al., 2000).
Although high expressed emotion is
associated with relapse in a European
American family member with schizophrenia,
this is not true among Mexican Americans;
the likelihood of relapse of a patient with
schizophrenia in a Mexican American family is
higher when family members are emotionally
distant. The family shown here does not
appear to be emotionally distant.
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High expressed emotion
A family interaction style characterized by
hostility, unnecessary criticism, or emotional
overinvolvement.
Understanding Psychological Disorders: The Neuropsychosocial Approach 51
• Difficulties in attachment. Children who have been maltreated are less likely to
develop a secure type of attachment than are children who have not been maltreated
(Baer & Martinez, 2006).
• Increased social isolation. Children who have been physically abused report feeling
more socially isolated than children who have not been physically abused (Elliott
et al., 2005).
However, not everyone who experienced maltreatment as a child develops a psycho
logical disorder (Haskett et al., 2006; Katerndahl et al., 2005).
Parental Psychological Disorders
Another familyrelated factor that may contribute to psychological disorders is the
presence of a psychological disorder in one or both parents (Pilowsky et al., 2006). It is
difficult to pinpoint the specific mechanism responsible for this association, however,
because it could be due to any number—or combination—of factors. For instance, a
parent may transmit a genetic vulnerability for a psychological disorder to a child. Al
ternatively, the specific patterns of interaction between an affected parent and a child
may lead to particular vulnerabilities in learning, mental processes, cognitive distor
tions, emotional regulation, or social interactions—any or all of which can increase the
risk of a psychological disorder as the child grows older (FinziDottan & Karu, 2006).
What is clear is that the association between a parent’s having a psychological dis
order and the increased risk of the child’s later developing a psychological disorder isn’t
solely a result of genetic vulnerability. For instance, when depressed mothers received
treatment, their symptoms improved, and so did their children’s symptoms of anxiety,
depression, and disruptive behaviors. The more positively a mother responded to her
treatment, the less likely her children were to continue to have symptoms (Weissman,
Pilowsky, et al., 2006; Wickramaratne et al., 2011). And consider children of women
who had depressive symptoms: When such children went to preschool, they had fewer
emotional and behavioral problems than did the children who spent their pre
school years at home with their mothers full time (Herba et al., in press.)
Community Support
Social support—the comfort and assistance that an individual receives
through interactions with others—can buffer the stressful events that occur
throughout life (Silver & Teasdale, 2005). Conversely, a lack of social support
can make people more vulnerable to various psychological disorders (Scarpa
et al., 2006). College students who experience high levels of stress, for in
stance, are less likely to be depressed if they have relatively high levels of so
cial support (Pengilly & Dowd, 2000).
The Beale women did not have much social support in their extended
family or community, but they had each other, which clearly played a role
in limiting whatever distress they may have felt about their lifestyle and cir
cumstances. Little Edie noted, “My mother really was the most extraordi
nary member of the family. She was always singing. . . . I was happy to be
alone with mother because we created the sort of life we liked, and it was
very private and beautiful” (Wright, 2007, p. 17). Had the Beale women not
supported each other and shared good times, the symptoms of psychological
disorders that they displayed might have been worse.
Social Stressors
Living in poverty is associated with a higher rate of psychological disorders. Another
social factor associated with psychological disorders is discrimination. Let’s examine
these two factors—socioeconomic status and discrimination—in more detail.
Social support
The comfort and assistance that an individual
receives through interactions with others.
Social support can lessen the detrimental
aftereffects of a stressful event such as an
untimely death. People who do not have such
support have a higher risk of developing a
psychological disorder.
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52 C H A P T E R 2
Socioeconomic Status
Socioeconomic groups are defined in terms of education, income, and occupa
tional level; these indicators are sometimes referred to collectively as socioeconomic
status (SES). People from low SES backgrounds have a higher rate of psychological
disorders than people from higher SES backgrounds (Costello et al., 1996, Mitten
dorferRutz et al., 2004; Ramanathan et al., 2013). Socioeconomic factors may
contribute to the development of psychological disorders in several ways. One the
orized mechanism is through social causation: socioeconomic disadvantages and
stress cause psychological disorders (Freeman, 1994). Specifically, the daily stressors
of urban life, especially as experienced by people in a lower socioeconomic level,
trigger mental illness in those who are vulnerable. For instance, living with in
adequate housing, very limited financial means, and few job opportunities corre
sponds to the stress component of the diathesis–stress model discussed in Chapter 1
(Costello, Compton, et al., 2003). Case 2.1 describes Anna, whose depression was
precipitated by financial stressors.
CASE 2.1 • FROM TH E OUTSIDE: Depression and Social Selection
Anna was a single mother in her 30s when she sought treatment for her depression. At the
time, she was having difficulty getting out of bed and was struggling to maintain order and
basic routines at home for herself and her children. She had separated from her husband
and lost her job 5 years prior to her first visit to the clinic. Since that time she had been
struggling financially. She had a number of part-time jobs to try to make enough money to
keep her family fed and clothed. However, she was often short of funds and felt very wor-
ried and stressed by their straitened [sic] financial situation. She noted she often felt worse
after the summer as she became overwhelmed by the demands of a new school year and
the thought of Christmas. As a result of encountering difficulty finding a permanent full-
time position, her confidence waned, and she feared that she had lost her job skills. She
had recently returned to school to take some business courses to update and extend her
qualifications. . . .
Anna expressed regrets about her divorce. She had not realized at the time what a mas-
sive and difficult journey it would prove to be. She regretted uprooting her children and found
her worries about money very stressful and disconcerting because she had never had to worry
about finances before. Anna was a committed and dedicated mother who, even as she strug-
gled to feed her children, put on a happy face to hide her stress because she did not want to
worry them.
(Watson et al., 2007, pp. 83–84)
Another mechanism that may be responsible for the connection between
psychological disorders and low SES is social selection, the hypothesis that
those who are mentally ill “drift” to a lower socioeconomic level because of their
impairments (Mulvany et al., 2001; Wender et al., 1973). Social selection is some
times referred to as social drift. Research suggests that the relationship between psy
chological disorders and SES cuts both ways: Low SES both contributes to disorders
and is a consequence of having a disorder (Conger & Donnellan, 2007; Fan & Eaton,
2001; Johnson et al., 1999).
A study by Jane Costello and colleagues (Costello, Compton, et al., 2003) tested
the influence of social selection and social causation on psychopathology in children.
These researchers tracked more than 300 Native American children between the
ages of 9 and 13 for 8 years; the children were seen annually. At the start of the study,
over half of the children were living in poverty. Halfway through the study, a casino
opened on the reservation, raising the income of all the Native American families
and pulling one quarter of them above the poverty line. Before the casino opened,
children whose families were below the poverty line had more psychiatric symptoms
than children whose families were above it. After the casino opened, the number of
Social causation hypothesis
The hypothesis that the daily stressors of
urban life, especially as experienced by
people in a lower socioeconomic class,
trigger mental illness in those who are
vulnerable.
Social selection hypothesis
The hypothesis that people who are mentally
ill “drift” to a lower socioeconomic level
because of their impairments; also referred to
as social drift.
Understanding Psychological Disorders: The Neuropsychosocial Approach 53
psychiatric symptoms among children who were no longer living in poverty was the
same as among those who had never lived in poverty. Once the socioeconomic disad
vantages and accompanying family stress were removed, children functioned better,
and their symptoms improved—an outcome that supports the role of social causation
in this setting (Rutter, 2003).
Discrimination, Bullying, and War
Being the object of discrimination is associated with an increased risk of distress and
psychological disorders (Bhui et al., 2005; Chakraborty & McKenzie, 2002; Mays &
Cochran, 2001; Simons et al., 2002). Women,
for example, may experience sexual harass
ment and assault, limitations on their freedom
(such as a prohibition against working outside
the home), or glass ceilings (unstated limits on
social or occupational possibilities). Such ex
periences may lead to increased stress and vul
nerability to psychological disorders. Consider
that sexual harassment of women in the work
place is associated with subsequent increased
alcohol use by those women (Freels et al.,
2005; Rospenda, 2002). Similarly, members of
ethnic, racial, or sexual minority groups may
experience harassment at—or discrimination
in—school, housing, or jobs, which can create
a sense of powerlessness and lead to chronically
higher levels of stress (Bhugra & Ayonrinde,
2001; Mills et al., 2004; Williams & Williams
Morris, 2000), which in turn increases the risk
for developing psychological disorders.
In addition, whereas discrimination involves negative behavior toward someone
because of his or her status as a member of a particular group (based on ethnicity,
race, religion, sexual orientation, or another characteristic), bullying involves nega
tive behavior that may be unrelated to the victim’s membership in an ethnic, racial,
or other group. Research indicates that being a victim of childhood bullying can
contribute to psychological problems in childhood and adulthood (Arseneault et al.,
2008; Copeland et al., 2013; Sourander et al., 2009), and it is particularly likely to
lead to internalizing problems.
Finally, war often inflicts extreme and prolonged stress on soldiers and civilian
victims. How an individual responds to the effects of war is determined by a variety
of factors (discussed at length in Chapter 7), such as proximity to the fighting and
the duration of combat. After mandated extended tours of duty for American soldiers
in Iraq and Afghanistan, at least 20% of returning troops had symptoms of posttrau
matic stress disorder or depression (Tanielian & Jaycox, 2008).
Culture
Every culture promotes an ideal of healthy functioning—of a “normal” personality—
and a notion of unhealthy functioning. These ideals differ somewhat from culture
to culture and can shift over time (DoerfelBaasen & Rauh, 2001). Some cultures,
such as those of many Asian, Latin American, and Middle Eastern countries, are
collectivist, placing a high value on getting along with others; in such cultures, the
goals of the group (family or community) traditionally take precedence over those
of the individual. In contrast, other cultures, such as those of Australia, Canada, the
The stigma and discrimination encountered by
some gays and lesbians can make them—and
others experiencing discrimination—more
vulnerable to psychological disorders (Herek &
Garnets, 2007; Mays & Cochran, 2001).
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54 C H A P T E R 2
United Kingdom, and the United States, are individualist, valuing independence and
autonomy; the goals of the individual take precedence over the goals of the group
(Hui & Triandis, 1986). In either case, if an individual has personality traits that are
different from those valued by the culture, other people’s responses to the person may
lead him or her to feel humiliated and to develop poor selfesteem, which increases
the risk of developing psychological disorders.
In addition, moving from one culture to another often leads people to adopt the
values and behaviors of the new culture, a process that is termed acculturation. This
can be very stressful and can create tension between parents—who moved to the new
culture as adults—and their children, whose formative years were spent in the new
culture. As these children grow up, they may be forced to choose between the values
and views of their parents’ culture and those of the new culture, which can be stress
ful and can make them more likely to develop psychological disorders (Escobar et al.,
2000). However, the degree to which acculturation is stressful and increases the risk
for psychological disorders depends on other factors, such as the degree of difference
in values between the native and new cultures, the reasons for leaving the native
country (for example, traumatic causes for leaving, such as war and famine, can have
strong effects), the change in SES status that results from immigration, and the de
gree of discrimination encountered in the new culture. In the absence of these other
factors, moving to a new culture is not necessarily associated with later psychological
disorders (Kohn, 2002).
Gonsalvo and Bill, roommates, are both first-year college students. Gonsalvo has left his
family and country and moved to another continent to study in the United States; Bill’s
family lives a few hours’ drive away. What social factors may influence whether either young
man develops a psychological disorder during their time at college? Be specific about possible
factors that might lead each man to be vulnerable. What social factors may protect them
from developing a disorder? What additional information would you want to help you answer
these questions, and how might such information affect your predictions?
Thinking Like A Clinician
Which family immigrating to the United States is more likely to experience stressful acculturation? Answer: The family on the left will probably
have a more stressful acculturation; they come from a collectivist culture, with different values. The family on the right comes from an individualist
culture (the Netherlands) that has values more similar to those of the United States.
GETTING THE PICTURE
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Understanding Psychological Disorders: The Neuropsychosocial Approach 55
SUMMING UP
Neurological Factors in Psychological
Disorders
• The nervous system has two major parts:
the central nervous system (CNS), which
is composed of the brain and spinal cord,
and the peripheral nervous system (PNS),
which is composed of the sensorysomatic
nervous system and the autonomic ner
vous system (ANS).
• The A NS cont rols m a ny i nvolunt a r y
functions, such as those of the heart, blood
vessels, and digestive tract. The ANS has
two major components: the sympathetic
nervous system and the parasympathetic
nervous system.
• The bra in is d iv ided into t wo hem i
spheres, left and right; each has four lobes:
occipital lobe (involved in vision), parietal
lobe (e.g., involved in processing spatial
information and selfawareness), tempo
ral lobe (e.g., involved in processing au
ditory information, including speech, and
memory), and frontal lobe (e.g., site of ex
ecutive functioning).
• Subcortical (beneath the cortex) areas of
importance include the limbic system,
which plays a key role in emotions, key
parts of which are the hypothalamus, the
amygdala, and the hippocampus.
• There are three t ypes of neurons: sen
sory neurons, motor neurons, and inter
neurons. Neurons com mun icate w ith
each other to create patterns of activa
tion in brain circuits, which in turn are
organized into large brain systems; these
system s m ay be d isr upted i n ca ses of
psychopathology.
• There are many types of neurotransmit
ters, which play d if ferent roles in the
brain; imbalances of neurotransmitters
can contribute to psychological disorders.
• Hormones, chemicals produced by glands
in the endocrine system, can affect the
functioning of neurons.
• Genes can influence the development of
psychopathology. Heritability is an esti
mate of how much of the variation of a
characteristic across a population, in a spe-
cific environment, is determined by genes.
• Behavioral geneticists may use twin and
adoption studies to determine the relative
influences of genes and environment.
Psychological Factors in
Psychological Disorders
• Three types of learning can contribute to
psychological disorders: classical condition
ing of emotional responses such as fear and
anxiety; operant conditioning of voluntary
behaviors through positive and negative
reinforcement and punishment; and ob
servational learning, which can guide the
observer’s behaviors and expectations.
• Mental processes and mental contents play
important roles in the etiology and main
tenance of psychological disorders.
• Emot iona l d ist urbances contr ibute to
some psychological disorders. Such dis
turbances include not feeling or express
ing emot ions to a nor ma l deg ree and
having difficulty regulating emotions.
• Emotions, behaviors, mental contents,
and menta l processes are of ten inter
twined, and so disturbances in one will
affect the others. Moreover, a person’s
attr ibutions and mood can af fect each
other.
• Emotions involve both a psychological
and a neurological response to a stimulus.
A Neuropsychosocial Last Word
on the Beales
We conclude this chapter by briefly examining how neurological, psychological, and
social factors might have affected each other via feedback loops in the case of Big
Edie and Little Edie. Both women were artistic, unconventional, and independent
(psychological factor), but their social class and the time in which they lived made
their behavior “inappropriate,” leading them to be discriminated against within their
extended family and community (social factor). In turn, the social constraints of
their day prevented them from having jobs or careers, and so they were unable to
support themselves; they were financially dependent on others (social), which created
its own stress (neurological and psychological). These external realities, in turn, may
have heightened their feeling that people were out to get them (psychological factor).
Moreover, it is possible that they had neurological characteristics—such as emotional
reactivity—that predisposed them to behave in certain ways, which in turn evoked
certain responses from others.
We will draw on the neuropsychosocial approach—considering all three types of
factors and their feedback loops—to understand the various psychological disorders dis
cussed in this book. Neurological factors (genetics, brain structure and function, and
bodily responses), psychological factors (learning and behavior, mental processes and
mental contents, and emotions), social factors (social stressors, relationships, family,
culture, and socioeconomic status), and the interactions among these factors all play a
role in explaining psychological disorders.
56 C H A P T E R 2
• Having a particular temperament may
make a person especially vulnerable to
certain psychological disorders, even at an
early age. Evidence indicates that genes
cont r ibute st rong ly to temper a ment ;
however, the effects of genes need to be
considered within the context of specific
environments.
• Temperament is conceived of as having
four dimensions: novelty seeking, harm
avoidance, reward dependence, and per
sistence. Cloninger proposed that each
of these dimensions is associated with the
action of a particular neurotransmitter.
Social Factors in
Psychological Disorders
• Social factors can help protect us from
developing psychological disorders, or
they can make us more vulnerable to or
exacerbate psychological disorders. Such
factors beg in to exer t their in f luence
before adulthood.
• A family’s style of interacting that involves
high expressed emotion can contribute
to relapse in patients with schizophrenia
from particular ethnic or cultural groups.
• Being ma ltreated as a child indirectly
contributes to the development of psy
chological disorders by increasing stress,
teaching maladaptive behaviors, promot
ing biases in discriminating among and
responding to facial expressions, creating
difficulties in attachment, and increasing
social isolation.
• Psycholog ical disorders in parents can
contribute to psychological disorders in
their children, although it is difficult to
pinpoint the specific mechanism through
which this influence occurs.
• Social support can buffer against stress,
and a lack of socia l suppor t can make
people more vulnerable to psychological
disorders.
• Low SES is associated with a higher rate
of psychological disorders; both social
causation and social selection contribute
to this relationship.
• Being the object of discrimination is as
sociated with an increased risk of distress
and psychological disorders.
• Different personality traits and behaviors
are valued in different cultures; thus, ac
culturation can lead to conf lict among
family members, creating stress and a risk
of psychological disorders.
More Study Aids
For additional study aids related
to this chapter, including quizzes
to make sure you’ve retained
everything you’ve learned and a
Student Video Activity exploring
the power a community can have
in treating individuals suffering
from mental illness, go to: www.
worthpublishers.com/launchpad/
rkabpsych2e.
Photodisc
Etiology (p. 29)
Cerebral cortex (p. 32)
Neurons (p. 32)
Brain circuits (p. 33)
Brain systems (p. 33)
Action potential (p. 34)
Synapse (p. 34)
Neurotransmitters (p. 34)
Receptors (p. 35)
Reuptake (p. 36)
Hormones (p. 36)
Genes (p. 36)
Genotype (p. 36)
Phenotype (p. 36)
Complex inheritance (p. 37)
Behavioral genetics (p. 37)
Heritability (p. 37)
Monozygotic twins (p. 38)
Dizygotic twins (p. 38)
Classical conditioning (p. 41)
Unconditioned stimulus (UCS) (p. 41)
Unconditioned response (UCR) (p. 41)
Conditioned stimulus (CS) (p. 41)
Conditioned response (CR) (p. 42)
Conditioned emotional responses (p. 42)
Stimulus generalization p. 42)
Operant conditioning (p. 42)
Reinforcement (p. 42)
Positive reinforcement (p. 43)
Negative reinforcement (p. 43)
Punishment (p. 43)
Positive punishment (p. 43)
Negative punishment (p. 43)
Learned helplessness (p. 44)
Observational learning (p. 45)
Cognitive distortions (p. 46)
Emotion (p. 47)
Affect (p. 47)
Inappropriate affect (p. 47)
Flat affect (p. 47)
Labile affect (p. 47)
Mood (p. 47)
Temperament (p. 49)
High expressed emotion (p. 51)
Social support (p. 52)
Social causation hypothesis (p. 53)
Social selection hypothesis (p. 53)
Key Terms
Understanding Psychological Disorders: The Neuropsychosocial Approach 57
59
CHAPTER 3
Clinical Diagnosis and
Assessment
eannette Walls had an unusual childhood. She and her three
siblings—Lor i, Br ian, and Maureen—had smart, engaging
parents who taught them each to read by the time they were 3,
explained and demonstrated scientific principles to them, instilled a
love of reading and appreciation for the arts, and made their children
each feel that they were special. As Jeannette Walls recounts in her
memoir, The Glass Castle (2005), her father, Rex, was an intelligent
man who was a skilled electrical engineer. Her mother, Rose Mary,
was an artist and had trained to be a teacher. Yet Rex had difficulty
holding onto jobs, and most of the time Rose Mary didn’t have a
paying job. Both parents gave their children enormous freedom to
explore and experiment; they also often left the children to fend for
themselves.
Rex and Rose Mary would uproot and move the family in the
middle of the night, sometimes giving the kids 15 minutes to pack
their things and pile into the car. They’d leave town in order to avoid
bill collectors or child welfare officials, moving to whatever small
town caught Rose Mar y’s and Rex’s fancy. Neither parent spent
much time fulfilling the many daily responsibilities of parenting, such
as preparing meals. For instance, even at the age of 3, if Jeannette was
hungry, she knew not to ask her parents for something to eat but to
make it herself. She figured out how to make hot dogs: put water in a
pot and boil the dogs, standing on a chair by the gas stove in order to
do it. During one stint of hot dog making when she was 3, her dress
caught on fire. She was so severely burned that she was hospitalized
for 6 weeks and had skin grafts. Her hospital stay ended when her
father had a fight with her doctor about whether her bandages should
remain on; her father carried Jeannette from her hospital room in the
middle of the night and out to the car, where her family was waiting
for her. They headed out of town to wherever the road took them;
Jeannette’s scars never properly healed.
Diagnosing Psychological Disorders
Why Diagnose?
A Cautionary Note About Diagnosis
Reliability and Validity in Classifi cation Systems
The Diagnostic and Statistical Manual of
Mental Disorders
The People Who Diagnose Psychological
Disorders
Assessing Psychological Disorders
Assessing Neurological and Other
Biological Factors
Assessing Psychological Factors
Assessing Social Factors
Assessment as an Interactive Process
Diagnosing and Assessing Rose Mary and
Rex Walls?
Andrzej Wojcicki/Science Photo Library/age fotostock. Photo for illustrative purposes only;
any individual depicted is a model.
The family referred To This and oTher laTe nighT moves from one
dusty town to another as doing “the skedaddle.” A few months after taking Jeannette
out of the hospital, the family did the skedaddle again. During Jeannette’s early child-
hood, Rex would get a job as an electrician or an engineer (often making up stories
about previous jobs he’d had or degrees he’d earned). When they left a town, Rex
would explain to the family that they were running from federal investigators who
were chasing him for some unnamed episode in the past; Rose Mary admitted to
the children that frequently they were running from bill collectors. Sometimes they
moved simply because Rex was bored.
Rex and Rose Mary tried to make their tumbleweed life into an adventure for
their children, and they succeeded to some extent when the children were young.
However, the parents’ own problems got in the way of their responsibilities. During
most of Jeannette’s school years, her family was so poor that the children ended up
eating only one meal a day—the lunch leftovers at school that they were able to
scavenge from the trash. When Rex would lose his job, sometimes he’d stay home.
He drew up blueprints for a solar-powered “glass castle” or worked on his design for
a tool that would find gold in rocks. And increasingly during Jeannette’s childhood,
he’d gamble and drink. In what Jeannette describes as his “beer phase,” Rex would
drive fast and sing loudly. When he began to drink the “hard stuff,” Rose Mary
would get frantic because Rex would become angry: He’d beat his wife, throw
furniture around, and yell. Then he’d collapse.
Rose Mary, under duress from her children and the threat of visits from child
welfare officials, tried two different stints of working as a teacher, but she hated it so
much that she had a hard time getting out of bed to get ready for work, and she had
difficulty doing the paperwork required by the job. After a year, Rose Mary refused
to work anymore; she claimed that she needed to put herself first—to paint, sculpt,
and write novels and short stories—even though Rex still was not working and there
was no other regular income.
Did Rex and Rose Mary have psychological disorders? To answer that question,
we must return to the criteria for a psychological disorder that we discussed in
Chapter 1: a pattern of thoughts, feelings, or behavior that lead to distress, impairment
in daily life, and risk of harm, within the context of the culture. Did Rose Mary or
Rex experience significant distress? Remarkably, Jeannette’s account of her family
conveys little sense that her parents were distressed by their situation. What about
impaired functioning? The fact that neither parent was able to hold a job consistently
certainly indicates impairment in daily life.
With regard to risk of harm, Rose Mar y and Rex put themselves and their
children at risk countless times in various ways: They—and their children—regu-
larly went without food (and neither parent was sufficiently motivated to earn
money in order to buy food). Rex repeatedly drove while intoxicated, sometimes
at 90 miles an hour or more. The family members’ physical safety was put at risk
in other ways. One night when Jeannette was 10 years old, she woke up to find
a vagrant sexually groping her. When the children asked their parents to close
the front and back doors at night, their parents refused: “They wouldn’t consider
it. We needed the fresh air, they said, and it was essential that we refuse to sur-
render to fear” (Walls, 2005, p. 103). The parents put themselves at risk of harm
in other ways, including intense fighting. For example, during one fight, Rex
and Rose Mar y went at each other with knives—and then their fighting sud-
denly switched off, and the couple ended up laughing and hugging. Rose Mary
admitted to her children that she was an “ excitement addict,” and her quest for
excitement and Rex’s drinking and related behavior often led the family into
dangerous situations.
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Jeannette Walls
60 C H A P T E R 3
According to Jeannette’s descriptions, then, both Rex and Rose Mary Walls
would seem to have had some t ype of psychopatholog y. On what basis should
you evaluate and classify their behavior? How would a mental health professional
go about identifying their specific psychological problems? How should you go
about determining whether a specific diagnosis is warranted? For mental health
professionals, a diagnosis is the identification of the nature of a disorder (Ameri-
can Psychiatric Association, 2013). A diagnosis is made by assigning a patient’s
symptoms to a specific classification. Classifying a set of symptoms as a disorder
allows you to know more than was initially apparent. Depending on how much
is known about a given disorder, a diagnosis may suggest the disorder’s possible
causes, its course over time, and its possible treatments. In Rex’s case, for ex-
ample, a diagnosis for his pattern of drinking and related behavior would be what
mental health clinicians call alcohol use disorder (which we discuss in more detail
in Chapter 9). Having a diagnosis might allow one to infer why he—and other
people with the same set of symptoms—may have developed the disorder and
whether the symptoms would be likely to shift in frequency or intensit y over
time. Moreover, the diagnosis might indicate that certain t ypes of treatment,
such as those based on behavioral principles (see Chapter 2), might be more ef-
fective than other types of treatment.
A diagnosis is based on information about the patient obtained through in-
terviews, observations, and tests. Such information is part of a clinical assess-
ment—the process of obtaining relevant information and making a judgment
about mental illness based on the information. Clinical assessments often go fur-
ther than providing information needed to make a diagnosis. They also can pro-
vide information about the specific ways in which and the degree to which an
individual is impaired, as well as about areas of functioning that are not impaired.
When we discuss the mental health—or mental illness—of Rex and Rose Mary
Walls, we are trying to approximate a clinical assessment based on the words—and
judgments—of their daughter, Jeannette—someone who knew them intimately.
Rex died at the age of 59. Were he alive today and it were possible to make a
clinical assessment of him and Rose Mary, we would be in a position to determine
with greater confidence whether either of them could be diagnosed with a psycho-
logical disorder.
Diagnosing Psychological Disorders
Rose Mary and Rex Walls created an endurance contest for their growing children.
A typical example was when Lori was diagnosed by the school nurse as severely near-
sighted and in need of glasses. Rose Mary didn’t approve of eyeglasses, commenting,
“If you had weak eyes . . . they needed exercise to get strong” (Walls, 2005, p. 96).
Rose Mary thought that glasses were like crutches.
Rex had unusual beliefs as well. He told his family that he couldn’t find a job in
a coal mining town because the mines were controlled by the unions, which were
controlled by the mob. He said he was nationally blackballed by the electricians’
union in Arizona (where he had previously worked), and in order to get a job in the
mines, he must help reform the United Mine Workers of America. He claimed that
he spent his days investigating that union.
Unusual beliefs may not have been the only factor that motivated Rose Mary
and Rex’s behavior; they also seemed to have a kind of “tunnel vision” that led
them to pay attention to their own needs and desires while being indifferent to
those of their children. When Jeannette was 5 and the family was again mov-
ing, her parents rented a U-Haul truck and placed all four children (including the
Diagnosis
The identification of the nature of a disorder.
Clinical assessment
The process of obtaining relevant information
and making a judgment about mental illness
based on the information.
Clinical Diagnosis and Assessment 61
youngest, Maureen, who was then an infant) and some of the family’s furniture
in the dark, airless, windowless back of the truck for the 14 hours it would take to
get to their next “home.” Rex and Rose Mary instructed the children to remain
quiet in this crypt—which was also without food, water, or toilet facilities—for
the entire journey. The parents also expected the children to keep baby Maureen
silent so that police wouldn’t discover the children in the back: It was illegal to
transport people in the trailer. What explanation did the parents give their children
for locking them up this way? They said that only two people could fit in the front
of the truck.
In order to determine whether Rex and Rose Mary Walls had psychological
disorders, we would have to compare their behavior and psychological functioning to
some standard of normalcy. A diagnostic classification system provides a means of mak-
ing such comparisons. Let’s first examine general issues about classification systems
and diagnosis and then consider the system that is now most commonly used—the
system described in the most recent edition of the Diagnostic and Statistical Manual of
Mental Disorders.
Why Diagnose?
You may have heard that categorizing people is bad: It pigeonholes them and strips
them of their individuality—right? Not necessarily. By categorizing psychological
disorders, clinicians and researchers can know more about a patient’s symptoms
and about how to treat the patient. To be specific, classification systems of mental
disorders provide the following benefits:
• They provide a type of shorthand, which enables clinicians and researchers to use a
small number of words instead of lengthy descriptions.
• They allow clinicians and researchers to group certain abnormal thoughts, feelings,
and behaviors into unique constellations.
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Without a classification system for psychological disorders, the problems that Pete Wentz, Jessica Alba, and Keith Urban appear to have suffered
from—bipolar disorder, obsessive-compulsive disorder, and substance abuse, respectively—would be nameless. Among other purposes, a classification
system allows clinicians to diagnose and treat symptoms more effectively, allows patients to know that they are not alone in their experiences, and
helps researchers to investigate the factors that contribute to psychological disorders and to evaluate treatments.
62 C H A P T E R 3
• A particular diagnosis may convey information—useful for both clinicians and
researchers—about the etiology of the disorder, its course, and indications for its
treatment.
• A diagnosis can indicate that an individual is in need of attention (including
treatment), support, or benefits.
• Some people find great relief in learning that they are not alone in having particular
problems (see Case 3.1).
CASE 3.1 • FROM TH E OUTSIDE: On Being Diagnosed with a Disorder
Sally, an articulate and dynamic 46-year-old woman, came to share her experiences with
our psychiatry class. For much of her adult life, she had suffered from insomnia, panic
attacks, and intense fear. Then, six years ago, a nightmare triggered memories of childhood
sexual abuse and she was finally diagnosed with posttraumatic stress disorder.
Being diagnosed, she told us, was an intense relief.
“All those years, I thought I was just crazy,” she said. “My whole family used to call me
the crazy one. Once, my brother called my mom and asked, ‘So, how’s my crazy sister?’
But all of a sudden I wasn’t crazy any more. It had a name. It had a real reason. I could
finally understand why I felt the way I did,’ she said.”
(Rothman, 1995)
A Cautionary Note About Diagnosis
Having a classification system for mental illness has many advantages, but assigning
the appropriate diagnosis can be challenging. For example, clinicians may be biased
to make—or not make—particular diagnoses for certain groups of people. Patients,
once diagnosed with a disorder, may be stigmatized because of it (Ben-Zeev et al.,
2010). In what follows, we examine the possibilities of bias and stigma in more
detail.
A diagnostic bias is a systematic error in diagnosis (Meehl, 1960). Such a bias
can cause groups of people to receive a particular diagnosis disproportionately, on
the basis of an unrelated factor such as sex, race, or age (Kunen et al., 2005). Stud-
ies of diagnostic bias show, for example, that in the United States, Black patients
are more likely than White patients to be diagnosed with schizophrenia instead
of a mood disorder (Gara et al., 2012; Trierweiler et al., 2005). Black patients are
also prescribed higher doses of medication than are White patients (Strakowski
et al., 1993).
When a mental health clinician is not familiar with the social norms of the
patient’s cultural background, the clinician may misinterpret certain behaviors as
pathological and thus be more likely to diagnose a psychological disorder. So, for
instance, the clinician might view a Caribbean immigrant family’s closeness as
“overinvolvment” rather than as normal for that culture.
Other groups, such as low-income Mexican Americans, may have their mental
illnesses underdiagnosed (Schmaling & Hernandez, 2005). Part of the explanation
for the underdiagnosis may be that the constellation of symptoms experienced by
some Mexican Americans does not fit within the classification system currently used
in North America; another part of the explanation may be language differences be-
tween patient and clinician that make accurate assessment difficult (Kaplan, 2007b;
Villaseñor & Waitzkin, 1999).
Bias is particularly important because when someone is said to have a psycho-
logical disorder, the diagnosis may be seen as a stigmatizing label that influences
how other people—including the mental health clinician—view and treat the per-
son. It may even change how a diagnosed person behaves and feels about himself or
herself (Ben-Zeev et al., 2010; Eriksen & Kress, 2005). Such labels can lead some
Diagnostic bias
A systematic error in diagnosis.
Clinical Diagnosis and Assessment 63
people with a psychological disorder to blame themselves and try to hide their prob-
lems (Corrigan & Watson, 2001; Reinberg, 2011). Feelings of shame may even lead
them to refrain from obtaining treatment (U.S. Department of Health and Human
Services, 1999). Great strides have been made toward destigmatizing mental illness,
although there is still a way to go. One organization devoted to confronting the
stigma of mental illness is the National Alliance for the Mentally Ill (nami.org),
which has a network of advocates—called Stigma Busters—who combat incorrect
and insensitive portrayals of mental illness in the media.
Reliability and Validity in Classification Systems
Classif ication systems are most useful when they are reliable and va lid. If a
classif ication system yields consistent results over time, it is reliable. To un-
derstand what constitutes a reliable classification system, imagine the following
scenario about Rose Mar y Walls: Suppose she decided to see a mental health
clinician because she was sleeping a lot, cr ying ever y day, and had no appetite.
Further, she consented to have her interview with the clinician filmed for other
clinicians to watch. Would every clinician who watched the video clip hear Rose
Mar y’s words and classify her behavior in the same way? Would ever y clinician
diagnose her as having the same disorder? If so, then the classification system
they used would be deemed reliable. But suppose that various clinicians came
up with different diagnoses or were divided about whether Rose Mary even had
a disorder. They might make different judgments about how her behaviors or
symptoms fit into the classification system. If there were significant differences of
opinion about her diagnosis among the clinicians, the classification system they
used probably is not reliable.
Problems concerning reliability in diagnosis can occur when:
• the criteria for disorders are unclear and thus require the clinician to use considerable
judgment about whether symptoms meet the criteria; or
• there is significant overlap among disorders, which can then make it diff icult to
distinguish among them.
However, just because clinicians agree on a diagnosis doesn’t mean that the diagnosis
is correct! For example, in the past, there was considerable agreement about the role
of the devil in producing mental disorders, but we now know that this isn’t a correct
explanation (Wakefield, 2010). Science is not a popularity contest; what the majority
of observers believe at any particular point in time is not necessarily correct. Thus,
another requirement for any classification system is that it needs to be valid. The
categories must characterize what they are supposed to be classifying. Each disorder
should have a unique set of criteria that correctly characterize the disorder.
The reliability and validity of classification systems are important in part be-
cause such systems are often used to study the etiology of a psychological disorder,
its prognosis (the likely course and outcome of the disorder), and whether par-
ticular treatments will be effective. In order to use a classification system in this
way, however, the prevalence of each disorder—the number of people who have
the disorder in a given period of time—must be large enough that researchers are
likely to encounter people with the disorder. (A related term is incidence, which
refers to the total number of new cases of a disorder that are identified in a given
time period.)
In sum, a classification system should be reliable and valid in order to be as useful
as possible for patients, clinicians, and researchers. Next, we’ll examine a commonly
used classification system for psychological disorders—the system in the Diagnostic
and Statistical Manual of Mental Disorders (DSM).
Reliable
A property of classification systems (or
measures) that consistently produce the same
results.
Valid
A property of classification systems (or
measures) that actually characterize what
they are supposed to characterize.
Prognosis
The likely course and outcome of a disorder.
Prevalence
The number of people who have a disorder in
a given period of time.
64 C H A P T E R 3
The Diagnostic and Statistical Manual (DSM)
evolves over time as research and changing
social views lead to changes in the disorders
listed and the criteria for those disorders. DSM
is currently in its fifth edition.
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The Diagnostic and Statistical Manual of Mental Disorders
Suppose that child welfare officials had spoken with Rex and Rose Mary Walls and
required that the parents be evaluated by mental health professionals. How would a
mental health clinician go about determining whether or not either of them had a
disorder? What classification system would the clinician probably use? The classification
system that most clinicians use in the United States is found in the Diagnostic and Sta-
tistical Manual of Mental Disorders, which is currently in its fifth edition. This guide,
published by the American Psychiatric Association (2013), describes the characteristics
of many psychological disorders and identifies criteria—the kinds, number, and dura-
tion of relevant symptoms—for diagnosing each disorder. This classification system is
generally categorical, which means that someone either has a disorder or does not.
A different classification system, used in some parts of the world, is described
in the International Classification of Diseases (ICD). The World Health Organization
(WHO) develops the ICD, with its 11th edition released in 2015. The primary pur-
pose of the ICD is to provide a framework for collecting health statistics worldwide.
Unlike the DSM, however, the ICD includes many diseases and disorders, not just
psychological disorders. In fact, until the sixth edition, the ICD only classified causes
of death. With the sixth edition, the editors added diseases and mental disorders.
Current versions of the mental disorders sections of the ICD and the DSM have been
revised to overlap substantially. Research on prevalence that uses one clas-
sification system is now generally applicable to the other system.
The Evolution of DSM
When the original version of the DSM was published in
1952, it was the first manual to address the needs
of clinicians rather than researchers ( Beutler
& Malik, 2002). At that time, Freud-inspired,
psychodynamic theory was popular, and the DSM
strongly favored the psychodynamic approach in its
classifications. For example, it organized mental illness
according to different types of conflicts among the id,
ego, superego, and reality, as well as different patterns of
defense mechanisms employed (American Psychiatric As-
sociation, 1952). The second edition of the DSM, published
in 1968, had only minor modifications. The first two editions
were criticized for problems with reliability and validity, which
arose in part because their classifications relied on psychody-
namic theory. Clinicians had to draw many inferences about the
specific nature of patients’ problems, including the specific uncon-
scious conflicts that motivated patients’ behavior.
The authors of the third edition (DSM-III), published in 1980,
set out to create a classification system that had better reliability and valid-
ity. Unlike the previous editions, DSM-III:
• did not rest on the psychodynamic theory of psychopathology (or on any
other theory);
• focused more on what can be observed than on what can be inferred;
• listed explicit criteria for each disorder and began to use available research results to
develop those criteria; and
• included a system for clinicians and researchers to record diagnoses as well as
additional information—such as related medical history—that may affect diagnosis,
prognosis, and treatment.
Clinical Diagnosis and Assessment 65
The weaknesses of DSM-III led to DSM-IV, published in 1994, which
specified new disorders and revised the criteria for some of the dis-
orders included in the previous edition. In 2000, the American Psy-
chiatric Association published an expanded version of DSM-IV that
included more current information about each disorder, such as new
information about prevalence, course, issues related to gender and
cultural factors, and comorbidity—the presence of more than one
disorder at the same time in a given patient. This revised edition is
called DSM-IV-TR, where TR stands for “Text Revision.” The list
of disorders and almost all of the criteria in DSM-IV-TR were not
changed, but the text discussion of the disorders was revised. DSM-IV
and DSM-IV-TR defined 17 major categories of psychological prob-
lems, and nearly 300 specific mental disorders.
In 2013, the American Psychiatric Association published the fifth edi-
tion, DSM-5, which includes over 300 disorders (depending on how you
count) across 22 categories, as shown in Table 3.1 (American Psychiatric
Association, 2013). The new edition was intended to address criticisms of
DSM-IV and to incorporate more recent research findings about disorders
that relate to the diagnostic criteria, and into what category they best fall.
However, many have criticized DSM-5 as not addressing the flaws in DSM-
IV and being less based on research than the previous edition (Frances, 2013;
Greenberg, 2013). In fact, the National Institute of Mental Health, which
funded research that used DSM-IV diagnoses to categorize patient’s symp-
toms, will not fund research using DSM-5 diagnoses (Insel, 2013).
The edition number went from Roman numbers (IV) to Arabic
numbers (5) because the mental health professionals in charge of creat-
ing DSM-5 envisioned the fifth edition as “a living document,” with “Web-based
releases” of refinements to the manual over time (5.1, 5.2, and so on; Kupfer, 2012).
However, the idea of a living document with frequent updates has been criticized as
creating confusion for clinicians and problems for researchers
who need to compare results from studies across the updates
(Rosenberg, 2013a).
The Evolution of DSM-5
The jury is still out on whether DSM-5 is an improvement over
the previous edition, DSM-IV-TR. To understand some of the
factors that led to the creation of DSM-5, we will use the ex-
ample of the diagnosis of schizophrenia (see Table 3.2); this dis-
order is discussed in more detail in Chapter 12. The issues raised
in the discussion that follows apply to most DSM-5 disorders.
Subjectivity in Determining Clinical Significance
Various editions of DSM have been criticized because their
criteria require mental health professionals to draw sub-
jective opinions. Consider the symptoms of schizophrenia
in Table 3.2. DSM-5 instructs the clinician to determine
whether, because of these symptoms, the individual’s func-
tioning is “markedly below the level achieved prior to the
onset.” (American Psychiatric Association, 2013, p. 99) Part
of the problem is that this decision, to a certain extent, is
subjective. DSM-5 does not specify what, exactly, markedly
means. Not all professionals would consider the same patient’s
dysfunction marked enough to qualify. These problems are
TABLE 3.1 • The 22 Categories of Mental Disorders
in DSM-5
Neurodevelopmental Disorders
Schizophrenia Spectrum and Other Psychotic Disorders
Bipolar and Related Disorders
Depressive Disorders
Anxiety Disorders
Obsessive-Compulsive and Related Disorders
Trauma- and Stressor-Related Disorders
Dissociative Disorders
Somatic Symptom and Related Disorders
Feeding and Eating Disorders
Elimination Disorders
Sleep–Wake Disorders
Sexual Dysfunctions
Gender Dysphoria
Disruptive, Impulse Control, and Conduct Disorders
Substance-Related and Addictive Disorders
Neurocognitive Disorders
Personality Disordersw
Paraphilic Disorders
Other Mental Disorders
Medication-Induced Movement Disorders and Other Adverse
Effects of Medication
Other Conditions That May Be a Focus of Clinical Attention
Source: Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition,
American Psychiatric Publishing, 2013.
Comorbidity
The presence of more than one disorder at the
same time in a given patient.
TABLE 3.2 • Summary of DSM-5 Diagnostic Criteria for
Schizophrenia
• At least two or more positive symptoms (termed positive because they
indicate the presence of an—extreme or distorted version of—typical
behavior), each present for at least 1 month.
° Delusions: Unusual, persistent and entrenched beliefs.
° Hallucinations: Sensations so vivid they seem real, although they
are not.
° Scrambled speech: Thoughts appear disconnected, sentences are
incoherent and words can be jumbled.
° Significantly disorganized or catatonic behavior: Difficulty with daily
tasks such as planning a meal or daily hygiene and physical immobility.
• Some negative symptoms (termed negative because they indicate the
absence of typical behavior), such as a failure to express or respond to
emotion; slow, empty replies to questions; or an inability to initiate
goal-directed behavior.
• Social and/or work-related dysfunction since the onset of symptoms.
The functioning level since the onset of the symptoms is significantly
below the prior level.
Source: Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition, American
Psychiatric Publishing, 2013.
66 C H A P T E R 3
complicated further if the clinician relies on the patient’s description of his or her
previous level of functioning; the patient’s view of the past may be clouded by the
present symptoms.
In a similar vein, consider the disorders known as adjustment disorders, which are
characterized by a response, such as distress, that is “out of proportion to the severity
or intensity of the stressor” (American Psychiatric Association, 2013, p. 286). The
clinician must determine whether an individual’s response is proportional. How-
ever, different people have different coping styles, and what seems to one clinician
like an excessive response may be deemed normal by another clinician (Narrow &
Kuhl, 2011).
Disorders as Categories, Not Continuous Dimensions
The criteria for disorders in DSM-5 are structured so that someone either has or
does not have a given disorder. It’s analogous to the old adage about pregnancy: A
woman can’t be a little bit pregnant—she either is or isn’t pregnant. But critics argue
that many disorders may exist along continua (continuous gradations), meaning that
patients can have different degrees of a disorder (Kendell & Jablensky, 2003).
Consider, for example, two young men who have had the diagnosis of schizo-
phrenia for 5 years. Aaron has been living with roommates and attending college part
time; Max is living at home, continues to hallucinate and have delusions, and cannot
hold down a volunteer job. (Hallucinations are sensations that are so vivid that the per-
ceived objects or events seem real, although they are not, and delusions are persistent
false beliefs that are held despite evidence that the beliefs are incorrect or exaggerate
reality.) Over the holidays, both men’s symptoms got worse, and both were hospital-
ized briefly. Since being discharged from the hospital, Aaron has had only mild symp-
toms, but Max still can’t function independently, even though he no longer needs
to be in the hospital. The categorical diagnosis of schizophrenia lumps both of these
patients together, but the intensity of their
symptoms suggests that clinicians should
have different expectations, goals, treat-
ments, and prognoses for them. As shown
in Figure 3.1, on a dimensional scale, one
of them is likely to be diagnosed with mild
schizophrenia, whereas the other is likely
to be diagnosed with severe schizophrenia.
To address this general criticism, DSM-5 includes optional dimensional scales for
some disorders; clinicians can rate the severity of symptoms (from mild to severe).
For instance, DSM-5 includes a set of scales to rate each of eight symptoms related
to schizophrenia. However, such ratings are optional and the decision to diagnose a
patient is still categorical (McHugh & Slavney, 2012).
People with Different Symptoms Can Be Diagnosed With the
Same Disorder
For many DSM-5 disorders, including schizophrenia, a person needs to have only
some of the symptoms in order to be diagnosed with the disorder. For example, in
Table 3.2, a person needs to have only two out of the five symptoms. Consider three
people who have been diagnosed with schizophrenia: One has delusions and halluci-
nations. Another has disorganized speech and disorganized behavior but no delusions
or hallucinations. And a third person classified as having schizophrenia has negative
symptoms and delusions, but not disorganized behavior or hallucinations. Taken to-
gether, these three people with schizophrenia display heterogeneous symptoms: The
sets of symptoms are different from each other. Nevertheless, the three people are
classified with the same disorder according to DSM-5. People with different combi-
No symptoms Cutoff for
diagnosis
Many, and/or
severe symptoms
Aaron Max
FI G U RE 3.1 • A Disorder as on
a Continuum If a disorder such as
schizophrenia is best characterized along a
continuum, then two people, Aaron and Max,
diagnosed with schizophrenia but with different
severity or numbers of symptoms, would fall at
different points on the continuum. Aaron has
fewer symptoms and is able to function better
than Max. According to DSM-5, they both have
the same disorder. However, their illnesses have
different courses and prognoses and will likely
require different types of treatment. None of
this information is captured by the categorical
diagnostic system of DSM-5.
Clinical Diagnosis and Assessment 67
nations of symptoms may have developed the disorder in different ways, and different
treatments might be effective. Thus, the DSM-5 diagnostic system may obscure im-
portant differences among types of a given mental disorder ( Malik & Beutler, 2002).
Duration Criteria Are Arbitrary
Each set of criteria for a disorder specifies a minimum amount of time that symptoms
must be present for a patient to qualify for that diagnosis (see the last bullet point in
Table 3.2). However, the particular duration, such as that noted for bipolar disorder
(which requires that the symptoms be present for at least 1 week), is often arbitrary
and not supported by research (Brauser, 2012; Greenberg, 2013).
Some Sets of Criteria Are too Restrictive
Some categories of disorders in DSM-5 include two types of diagnoses that can be
used when a person’s symptoms do not meet the necessary minimum criteria for the
disorder that is the best fit, but the person is nonetheless significantly distressed or
impaired. At least for some categories of disorders in DSM-IV, this type of diagno-
sis (called not otherwise specified in DSM-IV) was the most frequent diagnosis in the
category (Keel et al., 2011). The two types in DSM-5 are Other Specified
(fill in the blank with the category of disorder) and Unspecified . With
the former, the clinician notes why—in what ways—the criteria are not met (e.g.,
the symptoms have not yet been present long enough); with the latter, the clinician
chooses not to specify why the criteria are not met. Thus, people might be diagnosed
with either of these “other” type disorders because their symptoms do not meet the
minimum duration necessary for a diagnosis of a specific disorder; alternatively, they
might be diagnosed with one of these “other” disorders because they don’t have
enough symptoms to meet the criteria for that specific disorder.
Psychological Disorders Are Created to Ensure Payment
With each edition of DSM, the number of disorders increased, reaching over 300
with DSM-5. Does this mean that more types of mental disorders have been dis-
covered and classified? Not necessarily. This increase may, in part, reflect economic
pressures in the mental health care industry (Eriksen & Kress, 2005). Today, in order
for a mental health facility or provider to be paid or a patient to be reimbursed by
health insurance companies, the patient must have symptoms that meet a DSM-5
diagnosis. The more disorders that are included in a new edition of DSM, then, the
more likely it is that a patient’s treatment will be paid for or reimbursed by health
insurance companies. But this does not imply that all of the disorders are valid from
a scientific perspective.
To address the criticism about the growing number of disorders, the authors of
DSM-5 set out to maintain or reduce the total number of disorders. To achieve this
goal, and still add new disorders, in some cases disorders have been consolidated: for
instance, what was a disorder in DSM-IV may now be a subtype of another disorder
in DSM-5. Using such “accounting” methods, the authors of DSM-5 claim to have
achieved their goal while at the same time potentially increased the types of symp-
toms for which health insurance payment may be possible.
Social Factors Are Deemphasized
Perhaps because DSM-5 does not generally address etiological factors (the causes
of a disorder), it does not explicitly recognize social factors that contribute to disor-
ders. DSM-5 states that its diagnoses are not supposed to apply to conflicts that are
mainly between an individual and society but rather to conflicts within an individual
(American Psychiatric Association, 2013). However, this distinction is often difficult
to make (Caplan, 1995). For instance, people can become depressed in response to
a variety of social stressors: after losing their jobs, after they are exposed to system-
atic discrimination, after emigrating from their native country, or after experiencing
other social and societal conflicts.
68 C H A P T E R 3
Social factors are further deemphasized in DSM-5 with the pre-
sumption of neurobiological causes of mental illness, at least with
some categories of disorders, such as neurodevelopmental disorders
and neurocognitive disorders.
Comorbidity Is Common
About half of the people who have been diagnosed with a DSM-
IV disorder have at least one additional disorder; that is, they ex-
hibit comorbidity (Kessler et al., 2005). This will probably be true
with DSM-5 because the criteria for many disorders have not be-
come more stringent (which would reduce the number of people
diagnosed with the disorders); in fact, in some cases, the criteria
in DSM-5 have actually become less stringent, so that they ap-
ply to more people. This high comorbidity raises the question of
whether some disorders in DSM-5 are actually distinct. For in-
stance, half of the people who meet the criteria for major depressive
disorder also have an anxiety disorder (Kessler et al., 2003). Such a high rate of
comorbidity suggests that these two types of DSM-5 disorders often represent dif-
ferent facets of the same underlying problem (Hyman, 2011; Kendler et al., 2011).
This possibility raises questions about validity and makes DSM-5 diagnoses less
useful to clinicians and researchers.
DSM-5 Is Unscientific and Lacks Rigor
The process leading up to the publication of DSM-5 has been criticized on a number
of grounds, some of which stem from a rush to meet a publication deadline that some
argued was set arbitrarily. Criticisms include (Strakowski & Frances, 2012):
• Proposed diagnoses and criteria were not adequately field-tested: Mental health
professionals in various types of settings (e.g., hospitals, clinics) tried using the new
manual to diagnose patients. Unfortunately, these field tests showed disappoint-
ingly low reliability for some disorders (Ghaemi, 2012; Greenberg, 2013). That is,
using the new criteria, mental health clinicians didn’t agree on what diagnosis was
most appropriate for a given patient. After field testing, some of the criteria were
revised, in the hope of increasing reliability, and these new criteria (and wording)
were supposed to have another round of field testing.
• However, the planned final stage of research on the new criteria was cancelled
because of pressure to meet the planned publication deadline. One consequence is
that the wording of the criteria that were tested in earlier phases isn’t the wording in
the final version of DSM-5; problems with reliability and validity of the diagnoses
are thus more likely (Greenberg, 2013).
• Many disorders were proposed as additions to DSM-5, some of which were very
controversial, and others were placed in a section of the manual (equivalent to an ap-
pendix) for disorders that need further study before being accepted into the regular
part of the manual. An example is attenuated psychosis syndrome, which was originally
named psychosis risk syndrome because the diagnosis is for people thought to be at risk
to develop a psychotic disorder. Given the controversial nature of such disorders,
some researchers argued that they should not have been included even in an appendix
because the implications of adding the new disorder, and of deciding its criteria for
further study, were not thought through well enough (Cornblatt & Correll, 2010).
As Allen Frances, organizer of and contributor to several previous DSM editions
(DSM-III, DSM-IV, DSM-IV-TR) noted about DSM-5:
Each change in a DSM is an opportunity for clinical and forensic misuse, with unpre-
dictable and harmful unintended consequences. Changes are also costly to psychiatric
research in direct ways, such as the cost of changing instruments midstream, and even
more importantly in indirect ways, such as the [difficulty comparing research results
One criticism of DSM-5 is that social factors
that contribute to psychological disorders—
such as being laid off from work, which
apparently was the case for this man—are not
incorporated into the diagnosis (Greenberg,
2013). This doesn’t mean to imply that this
man, who was looking for help in Los Angeles,
has a disorder.
©
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Clinical Diagnosis and Assessment 69
for a given disorder using diagnostic criteria that differ across editions]. . . It might be
worth the risks and costs of DSM-5 changes if there were compelling science support-
ing them, but there isn’t.
(Strakowski & Frances, 2012).
Although the criticisms of DSM-5 must be taken seriously, the clinical chapters
of this book (Chapters 5–15) are generally organized according to DSM-5 categories
and criteria. The DSM has been, to date, by far the most widely used classification
system for diagnosing psychological disorders.
The People Who Diagnose Psychological Disorders
Who, exactly, are the mental health professionals who might diagnose Rex or Rose
Mary Walls, or anyone else who might be suffering from a psychological disorder?
As you will see, there are different types of mental health professionals, each with a
different type of training. The type of training can influence the kinds of informa-
tion that clinicians pay particular attention to, what they perceive, and how they
interpret the information. However, regardless of the type of training they receive,
all mental health professionals must be licensed in the state in which they practice (or
board certified, in the case of psychiatrists); licensure indicates that they have been
appropriately trained to diagnose and treat mental disorders.
Clinical Psychologists and Counseling Psychologists
A clinical psychologist generally has a doctoral degree, either a Ph.D. (doctor of
philosophy) or a Psy.D. (doctor of psychology), that is awarded only after several
years of coursework and several years of treating patients while receiving supervision
from experienced clinicians. People training to be clinical psychologists also take
other courses that may include neuropsychology and psychopharmacology. In addi-
tion, clinical psychologists with a Ph.D. will have completed a dissertation—a major,
independent research project. Programs that award a Psy.D. in clinical psychology
place less emphasis on research.
Clinical neuropsychologists are a particular type of clinical psychologist. Clinical
neuropsychologists concentrate on characterizing the effects of brain damage and
neurological diseases (such as Alzheimer’s disease) on thoughts (that is, mental
processes and mental contents), feelings (affect), and behavior. Sometimes, they help
design and conduct rehabilitation programs for patients with brain damage or neuro-
logical disease.
A counseling psychologist might have a Ph.D. from a psychology program
that focuses on counseling or might have an Ed.D. (doctor of education) degree from
a school of education. Training for counseling psychologists is similar to that of clini-
cal psychologists except that counseling psychologists tend to have more training in
vocational testing, career guidance, and multicultural issues, and they generally don’t
receive training in neuropsychology. Counseling psychologists also tend to work
with healthier people, whereas clinical psychologists tend to have more training
in psychopathology and often work with people who have more severe problems
(Cobb et al., 2004; Norcross et al., 1998). The distinction between the two types of
psychologists, however, is less clear-cut than in the past, and both types may perform
similar work in similar settings.
Clinical psychologists and counseling psychologists are trained to perform
research on the nature, diagnosis, and treatment of mental illness. They also both
provide psychotherapy, which involves helping patients better cope with diff icult
experiences, thoughts, feelings, and behavior. Both types of psychologists also learn
how to administer and interpret psychological tests in order to diagnose and treat
psychological problems and disorders more effectively.
Clinical psychologist
A mental health professional who has a
doctoral degree that requires several years
of related coursework and several years of
treating patients while receiving supervision
from experienced clinicians.
Counseling psychologist
A mental health professional who has either a
Ph.D. degree from a psychology program that
focuses on counseling or an Ed.D. degree from
a school of education.
70 C H A P T E R 3
Psychiatrists, Psychiatric Nurses, and General Practitioners
Someone with an M.D. (doctor of medicine) degree can choose to receive further
training in a residency that focuses on mental disorders, becoming a psychiatrist.
A psychiatrist is qualif ied to prescribe medications; psychologists in the United
States, except for appropriately trained psychologists in New Mexico and Louisiana,
currently may not prescribe medications. (Other states are considering allowing
appropriately trained psychologists to prescribe.) But psychiatrists usually have not
been taught how to interpret and understand psychological tests and have not been
required to acquire detailed knowledge of research methods used in the f ield of
psychopathology.
A psychiatric nurse has an M.S.N. (master of science in nursing) degree, plus
a C.S. (clinical specialization) certificate in psychiatric nursing; a psychiatric nurse
may also be certified as a psychiatric nurse practitioner (N.P.). Psychiatric nurses
normally work in a hospital or clinic to provide psychotherapy; in these settings,
they work closely with physicians to administer and monitor patient medications.
Psychiatric nurses are also qualified to provide psychotherapy in private practice and
are permitted in some states to monitor and prescribe medications independently
(Haber et al., 2003).
Although not considered a mental health professional, a general practitioner (GP),
or family doctor (the doctor you may see once a year for a checkup), may inquire
about psychological symptoms, may diagnose a psychological disorder, and may rec-
ommend to patients that they see a mental health professional. Responding to pres-
sure to reduce insurance companies’ medical costs, general practitioners frequently
prescribe medication for some psychological disorders. However, studies have found
that treatment with medication is less effective when prescribed by a family doctor
than when prescribed by psychiatrists, who are specialists in mental disorders and
more familiar with the nuances of such treatment (Lin et al., 2000; Wang et al.,
2005; Wilson et al., 2003).
Mental Health Professionals with Master’s Degrees
In addition to psychiatric nurses, some other mental health professionals have master’s
degrees. Most social workers have an M.S.W. (master of social work) degree and
may have had training to provide psychotherapy to help individuals and families.
Social workers also teach clients how to find and benefit from the appropriate so-
cial services offered in their community. For example, they may help clients to ap-
ply for Medicare or may facilitate home visits
from health care professionals. Most states also
license marriage and family therapists (M.F.T.s),
who have at least a master’s degree and are
trained to provide psychotherapy to couples
and families. Other therapists may have a mas-
ter’s degree (M.A.) in some area of counseling
or clinical psychology, which indicates that
their training consisted of fewer courses and
research experience, and less supervised clini-
cal training than that of their doctoral-level
counterparts. Some counselors may have had
particular training in pastoral counseling, which
provides counseling from a spiritual or faith-
based perspective.
Table 3.3 reviews the different types of
mental health clinicians.
Psychiatrist
A mental health professional who has an M.D.
degree and has completed a residency that
focuses on mental disorders.
Psychiatric nurse
A mental health professional who has an
M.S.N. degree, plus a C.S. certificate in
psychiatric nursing.
Social worker
A mental health professional who has an
M.S.W. degree and may have had training to
provide psychotherapy to help individuals and
families.
TABLE 3.3 • Clinicians Who Diagnose Mental Disorders
Type of clinician Specific title and credentials
Doctoral-level
psychologists
Clinical psychologists (including clinical neuropsychologists)
and counseling psychologists have a Ph.D., Psy.D., or Ed.D.
degree and have advanced training in the treatment of mental
illness.
Medical personnel
Psychiatrists and general practitioners have a M.D. degree;
psychiatrists have had advanced training in the treatment of
mental illness. Psychiatric nurses have a M.S.N. degree and
have advanced training in the treatment of mental illness.
Master’s-level mental
health professionals
Social workers with a master’s degree (M.S.W.), marriage and
family therapists (M.F.T.), and master’s level counselors (M.A.)
are mental health clinicians who have received specific training
in helping people with problems in daily living or with mental
illness. Psychiatric nurses have master’s level training.
Clinical Diagnosis and Assessment 71
Your abnormal psychology class watches a videotape of a clinical interview with Peter, a
man who has been diagnosed with schizophrenia. Your professor has been researching new
criteria for diagnosing schizophrenia and has asked you and your classmates to determine
whether Peter does, in fact, have schizophrenia according to the new criteria. If you and your
classmates disagree with each other about his diagnosis, what might that indicate about the
criteria’s reliability and validity, and what might it indicate about the interview itself?
The professor then asks you to decide whether Peter has schizophrenia as defined by
the DSM-5 criteria. What are some of the advantages and disadvantages of using DSM-5?
Based on what you have read, what factors, other than the specifics of Peter’s symptoms,
might influence your assessment? (Hint: Think of biases.) Should Peter be diagnosed with
schizophrenia, might there be any benefits to him that come with the diagnosis, based on
what you have read? What might be the possible disadvantages for Peter of being diagnosed
with schizophrenia? Be specific in your answers.
Thinking Like A Clinician
Assessing Psychological Disorders
People came to know about Rose Mary and Rex Walls through the eyes of their
daughter, Jeannette. In her memoir, Jeannette reports incidents that seem to be clear
cases of neglect and irresponsible behavior. How might a mental health clinician or
researcher have gone about assessing Rose Mary’s or Rex’s mental health? Although
mental health clinicians might read Jeannette Walls’s memoir, hear her speak about her
parents, or even see brief video clips of Rose Mary Walls, the information conveyed
by those accounts isn’t adequate to make a clinical assessment: Jeannette’s memoir—
and Rose Mary’s brief statements on videotape—portray what Jeannette and the
video directors chose to include; we don’t know about events that were not discussed
or portrayed, and we don’t know how accurate Jeannette’s childhood memories are.
Other people’s accounts of an individual’s mental health generally provide only nar-
row slices of information—brief glimpses as seen from their own points of view, none of
which is that of a mental health clinician in this case. Without use of the formal tools
and techniques of clinical assessment, any conclusions are likely to be speculative.
Were it possible to obtain information about Rose Mary and Rex Walls directly,
what specif ic information would a clinician want to know in order to make a
diagnosis and recommendations for treatment? More generally, what types of infor-
mation are included in a clinical assessment?
A complete clinical assessment can include various types of information regarding
the three main categories that underlie the neuropsychosocial model:
• neurological and other biological factors (i.e., the structure and functioning of brain and
body),
• psychological factors (i.e., behavior, emotion and mood, mental processes and contents,
past and current ability to function), and
• social factors (i.e., the social context of the patient’s problems, the living environment
and community, family history and family functioning, history of the person’s rela-
tionships, and level of financial resources and social support available).
Most types of assessment focus primarily on one type of factor. We’ll consider assess-
ments of each of these main types of factors in the following sections.
Assessing Neurological and Other Biological Factors
In some cases, clinicians assess neurological (and other biological) functioning in
order to determine whether abnormal mental processes and mental contents, affect,
or behaviors arise from a medical problem, such as a brain tumor or abnormal
72 C H A P T E R 3
hormone levels. In other cases, researchers seek to understand neurological and other
biological factors that may be related to a particular disorder because this informa-
tion might provide clues for possible treatments. Although neurological and other
biological factors are not generally part of the DSM criteria for diagnosing mental
disorders, the search for neurological and other biological markers or indicators of
various psychological disorders has proceeded at a rapid pace over the past decade. It
is clearly only a matter of time before these sorts of factors will be part of the standard
diagnostic criteria for many psychological disorders ( Lieberman, 2011).
Assessing Abnormal Brain Structures with X-Rays, CT Scans,
and MRIs
Some psychological disorders, such as schizophrenia, appear to involve abnormali-
ties of the structure of the brain. This is why clinical assessments sometimes make
use of scans of a patient’s brain. Neuroimaging techniques provide images of the brain.
The oldest neuroimaging technique involves taking pictures of a person’s brain
using X-rays. A computer can then analyze these X-ray images and reconstruct a
three-dimensional image of the brain. Computerized axial tomography (CT)
(tomography is from a Greek word for “section”) builds an image of a person’s brain,
slice by slice, creating a CT scan (sometimes called a CAT scan).
A more recent technology, magnetic resonance imaging (MRI), makes
especially sharp images of the brain, which allows more precise diagnoses when brain
abnormalities are subtle. MRI makes use of the magnetic properties of different atoms.
By detecting different atoms and combining the signals into images, MRI can indi-
cate the location of damaged tissue and can reveal particular parts of the brain that are
larger or smaller than normal. For instance, an MRI can reveal the shrinkage of brain
tissue that typically arises with chronic alcoholism (Rosenbloom et al., 2003); had
Rex Walls had an MRI, it might well have shown that his brain had such shrinkage.
CT scans and MRIs can provide amazing images of the structure of the living
brain, which may provide information that can help to diagnose psychological condi-
tions. For example, some people with schizophrenia have larger ventricles (interior,
fluid-filled spaces in the brain) than do people who do not have the disorder (Schnei-
der-Axmann et al., 2006). These larger ventricles may occur, at least in part, because
some of the surrounding brain tissue is smaller than normal (Gaser et al., 2004).
Assessing Brain Function with PET Scans and fMRI
Some mental disorders are associated not with abnormal brain structures (physical
makeup) but rather with abnormal brain functioning (how the brain operates). The brain
can also produce abnormal thoughts, feelings, and behaviors because it functions inap-
propriately. Researchers use different types of brain scans to assess brain functioning.
We’ve just talked about how certain neuroimaging techniques can reveal brain struc-
ture, but how can researchers observe brain functioning? A key fact is that when a part of
the brain is active, more blood (which transports oxygen and nutrients) flows to it, a little
like the way that more electricity flows into a house when more appliances are turned on.
The neurons draw more blood while they are sending and receiving signals than
they do when they are not activated, because the activity increases their need for
oxygen and nutrients. Because neurons in the same area of the brain tend to work
together, specific areas of the brain will have greater blood flow while a person per-
forms particular tasks.
In the field of psychopathology, researchers use functional neuroimaging to iden-
tify brain areas related to specific aspects of a disorder. For example, in one study,
researchers asked participants with social phobia, who were afraid of speaking in pub-
lic, to speak to a group and also to speak in private while their brains were scanned.
People with schizophrenia tend to have
abnormally large ventricles (fluid-filled spaces
in the brain). Compare the two MRI images
above: The ventricles are indicated by the
red arrows.
D
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Schizophrenia
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Computerized axial tomography (CT)
A neuroimaging technique that uses X-rays to
build a three-dimensional image (CT or CAT
scan) of the brain.
Magnetic resonance imaging (MRI)
A neuroimaging technique that creates
especially sharp images of the brain by
measuring the magnetic properties of
atoms in the brain.
Clinical Diagnosis and Assessment 73
Speaking in public activated key parts of the limbic system, particularly the amyg-
dala, more than did speaking in private (Tillfors et al., 2001). As noted in Chapter 2,
the amygdala is involved in strong emotion, particularly fear. This part of the brain
was not activated when people without a social phobia were tested. Other researchers
have reported similar results for other sorts of phobias (Pissiota et al., 2003).
The functional neuroimaging technique used in the study of social phobia just
described was positron emission tomography (PET), one of the most impor-
tant methods for measuring blood flow (or energy consumption) in the brain. PET
requires introducing a very small amount of a radioactive substance into the blood-
stream. While a person performs a task, as active regions of the brain take up more
blood they take up more of the radioactive substance than do less active regions. The
relative amounts of radiation from different areas of the brain are measured and sent
to a computer, which constructs a three-dimensional image of the brain that shows
the levels of activity in the different areas. In PET images, higher radiation (greater
activity) typically is illustrated with brighter colors.
Functional magnetic resonance imaging (f MRI) is currently the most
widely used method for measuring human brain function. When a region of the
brain is activated, it draws blood more quickly than the oxygen carried by the hemo-
globin in the blood can be used. This means that red blood cells with oxygenated he-
moglobin accumulate in the activated region—and this increase is what is measured
in an f MRI scan. Brain regions that are not activated (or are activated less strongly)
when a person is performing a particular task (such as speaking in public or looking
at pictures) draw less blood, and the oxygen carried by the blood gets used up. The
difference in oxygen levels due to brain activity is reflected in the f MRI images.
The advantages of f MRI over PET include the absence of radiation and the abil-
ity to construct brain images showing activation that occurs in just a few seconds.
Disadvantages include the requirement that a participant must lie very still in the
narrow tube of a noisy machine (which some people find uncomfortable).
Neuropsychological Assessment
An assessment of neurological factors may include neuropsychological testing,
which uses behavioral responses to test items in order to draw inferences about brain
functioning. Assessing neuropsychological functioning
allows clinicians and researchers to distinguish the effects
of brain damage from the effects of psychological problems
(for example, disrupted speech can be caused by either of
these). Neuropsychological assessment is also used to deter-
mine whether brain damage is contributing to psychological
problems (for example, frontal lobe damage can disrupt the
ability to inhibit aggressive behavior).
Neuropsychological tests range from those that assess
complex abilities (such as judgment or planning) to those
that assess a relatively specific ability (such as the ability to
recognize faces). Other neuropsychological tests, such as the
Bender Visual-Motor Gestalt Test-II (2nd edition) (Bender,
1963; Brannigan & Decker, 2003), assess more complex
functions. Patients are shown a series of drawings that range
from simple to complex and are asked to reproduce them.
This test assesses the integration of visual and motor func-
tioning, which involves many distinct parts of the brain. The
test may be used to help diagnose various problems, including learning disorders and
memory problems (Brannigan & Decker, 2006).
The Rey Osterrieth Test requires the test-taker
to copy a complex figure, and then draw it from
memory; the test assesses visual perception,
organizational ability, and memory.
R
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Ed
it
Positron emission tomography (PET)
A neuroimaging technique that measures blood
flow (or energy consumption) in the brain and
requires introducing a very small amount of a
radioactive substance into the bloodstream.
Functional magnetic resonance imaging
(fMRI)
A neuroimaging technique that uses MRI to
obtain images of brain functioning, which
reveal the extent to which different brain
areas are activated during particular tasks.
Neuropsychological testing
The employment of assessment techniques
that use behavioral responses to test items
in order to draw inferences about brain
functioning.
74 C H A P T E R 3
Assessing Psychological Factors
During an assessment, clinicians and researchers often seek to identify the ways in
which psychological functioning is disordered and the ways in which it is not. For
instance, a clinical assessment would shed light on the extent to which Rex Walls’s
problems were primarily a result of his drinking or arose from underlying distress or
impairments that may have been masked by his pronounced drinking.
Certain areas of psychological functioning—mental processes and mental
contents, affect, and behavior—are often directly related to DSM-5 criteria for specific
disorders. Further, these areas are frequently the most relevant for determining a
person’s current and future ability to function in daily activities.
Menta l hea lth researchers and clinicians employ a var iet y of assessment
techniques and tools to evaluate psychological functioning, including interviews and
tests of cognitive and personality functioning. Which tools and techniques are used
depends on the purpose of the assessment.
Clinical Interview
An important tool used to assess psychological functioning is the clinical interview, a
meeting between clinician and patient during which the clinician asks questions related to
the patient’s symptoms and functioning. A clinical interview provides two types of infor-
mation: the content of the answers to the interview questions, and the manner in which the
person answered them (Westen & Weinberger, 2004). Questions may focus on symptoms,
general functioning, degree and type of impairment, and the patient’s relevant history. Cli-
nicians generally use three types of interviews: unstructured, structured, or semistructured.
In an unstructured interview, the clinician asks whatever questions he or she deems
appropriate, depending on the patient’s responses. The advantage of an unstructured
interview is that it allows the clinician to pursue topics and issues specific to the patient.
However, different clinicians who use this approach to interview the same patient may
arrive at different diagnoses, because each clinician’s interview may cover different
topics and therefore gather different information. Another problem with unstructured
interviews is that the interviewer may neglect to gather important information about
the context of the problem and the individual’s cultural background.
In a structured interview, conversely, the clinician uses a fixed set of questions to
guide the interview. A structured interview is likely to yield a more reliable diagnosis
because each clinician asks the same set of questions. However, such a diagnosis may
be less valid, because the questions asked may not be relevant to the patient’s particular
symptoms, issues, or concerns (Meyer, 2002b). That is, different clinicians using a
structured interview may agree on the diagnosis, but all of them may be missing the
boat about the nature of the problem and may diagnose the wrong disorder.
A semistructured interview, discussed in more detail later, combines elements of
both of the other types: Specific questions guide the interview, but the clinician also
has the freedom to pose additional questions that may be relevant, depending on the
patient’s answers to the standard questions.
Observation
All types of interviews provide an opportunity for the clinician or researcher to
observe and make inferences about different aspects of a patient:
• Appearance. In addition to obvious aspects of appearance (whether the person has bathed
recently and is dressed appropriately), signs of disorders can sometimes be noted by care-
fully observing subtle aspects of a person’s appearance. For example, patients with the
eating disorder bulimia nervosa (to be discussed in Chapter 10) may regularly induce
vomiting; as a result of repeated vomiting, their parotid glands, located in the cheeks, may
swell and create a somewhat puffy look to the cheeks (similar to a chipmunk’s cheeks).
Clinical interview
A meeting between clinician and patient
during which the clinician asks questions
related to the patient’s symptoms and
functioning.
Clinical Diagnosis and Assessment 75
• Behavior. The patient’s body language, facial expression, movements, and speech
can provide insights into different aspects of psychological functioning:
Emotions. What emotions does the patient convey? The clinician can observe
the patient’s expression of distress (or lack thereof ) and emotional state (upbeat,
“low,” intense, uncontrollable, inappropriate to the situation, or at odds with the
content of what the patient says).
Movement. The patient’s general level of movement—physical restlessness or a
complete lack of movement—may indicate abnormal functioning.
Speech. Clinicians observe the rate and contents of the patient’s speech: Speaking
very quickly may suggest anxiety, mania, or certain kinds of substance abuse;
speaking very slowly may suggest depression or other kinds of substance abuse.
Mental processes. Some behaviors reveal characteristics of mental processes. Do the
patient’s mental processes appear to be unusual or abnormal? Does the patient
appear to be talking to someone who is not in the room, which would suggest
that he or she is having hallucinations? Can the patient remember what the clini-
cian just asked? Does the patient flit from topic to topic, unable to stay focused on
answering a single question?
Behaviors observed during a clinical interview can, in some cases, provide more
information than the patient’s report about the nature of the problem. In other
cases, such observations round out an assessment; it is the patient’s own report of the
problem—its history and related matters—that provides the foundation of the inter-
view. In any case, the clinician must keep in mind that “unusual” behavior should
perhaps be interpreted differently for patients from different cultural backgrounds.
Patient’s Self-Report
Some symptoms cannot be obser ved directly, such as the hallucinations that
characterize schizophrenia, or the worries and fears that characterize some anxiety
disorders. Thus, the patient’s own report of his or her experiences is a crucial part of
the clinical assessment.
At some point in the interview process, the clinician will ask about the patient’s
history—past factors or events that may illuminate the current difficulties—and
the patient will report such information about himself or herself. For example, the
Does how someone look play a role in assessment? If these models were actually clients you saw in
an emergency room, the appearance of which model would likely provide a clinician with important
information to follow up on during an assessment? Answer: Both. The model on the left appears
disheveled, suggesting the possibility of depression or psychosis, whereas the animation of the person
on the right might indicate mania or substance use.
GETTING THE PICTURE
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76 C H A P T E R 3
clinician will ask about current and past psychological or medical problems and about
how the patient understands these problems and possible solutions to them. The cli-
nician will inquire about substance use, sexual or physical abuse or other traumatic
experiences, economic hardships, relationships with family members and others, and
thoughts about suicide. The patient’s answers help the clinician put the patient’s cur-
rent difficulties in context and determine whether his or her psychological
functioning is maladaptive or adaptive, given the environmental circum-
stances (Kirk & Hsieh, 2004).
Some patients, however, intentionally report having symptoms that they
don’t actually have or exaggerate symptoms that they do have, either for material
gain or to avoid unwanted events (such as criminal prosecution); such behavior
is the hallmark of malingering. For instance, a malingering soldier may exag-
gerate his or her anxiety symptoms and claim to have posttraumatic stress dis-
order in order to avoid further combat. Malingering contrasts with factitious
disorder, which occurs when someone intentionally falsely reports or induces
medical or psychological symptoms in order to receive attention. Whereas
both malingering and factitious disorder involve deception— inventing or
exaggerating symptoms—the motivations are different. Unlike those with
malingering, people with factitious disorder do not deceive others about the
symptoms for material gain or to avoid negative events.
Most patients intend to report their current problems and history as accu-
rately as possible. Nevertheless, even honest self-reports are subject to various
biases. Most fundamentally, patients may accurately report what they remem-
ber, but their memory of the frequency, intensity, or duration of their symp-
toms may not be entirely accurate. As we noted in Chapter 2, emotion can
bias what we notice, perceive, and remember.
Another bias that can affect what patients say about their symptoms is
reporting bias—inaccuracies or distortions in a patient’s report because of a
desire to appear in a particular way (Meyer, 2002b). In some cases, patients
may not really know the answer to a question asked in a clinical interview.
For instance, when asked, “Why did you do that? ” they may not have
thought about their motivation before and may not really be aware of what it
was but instead create an answer on the spot (Westen & Weinberger, 2004). In other
cases, people’s psychological functioning is sufficiently impaired that they confuse
their internal world—their memories, fears, beliefs, fantasies, or dreams—with real-
ity, which leads to inaccuracies in self-reports.
Thus, although a patient’s self-report is important, it has limitations. Similarly, when
interviewing children, the clinician must be sensitive to the fact that they may lack
adequate insight and/or the verbal ability to reliably report their mental health status.
Semistructured Interviews
Because clinicians sometimes want to be sure to cover specific ground with their
questions, they may use a semistructured interview format, asking a list of standard
questions but formulating their own follow-up questions. The follow-up questions
are based on patients’ responses to the standard questions. One set of questions that as-
sesses a patient’s mental state at the time of the interview is the mental status exam. In a
mental status exam, the clinician asks the patient to describe the problem, its history,
and the patient’s functioning in different areas of life. Other standard questions in the
mental status exam probe the patient’s ability to reason, to perform simple mathemat-
ical computations, and to assess possible problems in memory and judgment. The cli-
nician uses the patient’s answers to the standard questions to develop hypotheses about
possible diagnoses and difficulties with functioning, and then asks other questions to
obtain additional information. For instance, as part of the mental status exam, patients
Malingering
Intentional false reporting of symptoms or
exaggeration of existing symptoms, either for
material gain or to avoid unwanted events.
Factitious disorder
A psychological disorder marked by the
false reporting or inducing of medical or
psychological symptoms in order to receive
attention.
Some problematic behaviors may be obvious
to a mental health professional while
interacting with a patient. Other behaviors,
which occur infrequently or only in specific
types of environments, such as avoiding
stepping on cracks (which some people with
obsessive-compulsive disorder do) are less
likely to be observed. If the patient doesn’t
view these behaviors as a problem, he or she
may not report them.
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Clinical Diagnosis and Assessment 77
are routinely asked whether they remember their own name, the date and year,
and who is president. If the patient doesn’t remember correctly who the current
president is, the clinician might ask other, more detailed questions involving
different aspects of memory—such as memories of other languages spoken, of
more distant events or important personal events in the recent past—which may
reflect an underlying neurological problem. People from other cultures may an-
swer some of the questions in a mental status exam in unconventional ways, and
clinicians must take care not to infer that “ different” is “abnormal.”
A mental status exam assesses cognitive, emotional, and behavioral func-
tioning broadly, and the standard questions are not designed to obtain specific
information that corresponds to the categories in DSM-5. The interviewer can
arrive at a diagnosis based on answers to both standard and follow-up ques-
tions, but the goal of the mental status exam is more than diagnosis: It creates a
portrait of the individual’s general psychological functioning. The mental sta-
tus exam contrasts with another semistructured interview format, the Structured
Clinical Interview for DSM (SCID; First et al., 1997, 2002). The SCID is gen-
erally used when the interview is part of a research project and is designed to
assist the researcher in diagnosing patients according to DSM criteria.
Clinical interviews provide a wealth of information about the patient’s
symptoms and general functioning, as well as about the context in which the
symptoms arose and continue. However, a thorough clinical interview can be
time-consuming and may not be as reliable and valid as assessment techniques
that utilize tests.
Tests of Psychological Functioning
Many different tests are available to assess various areas of psychological functioning.
Some tests assess a relatively wide range of abilities and areas of functioning (such as
intelligence or general personality characteristics). Other tests assess a narrow range
of abilities, particular areas of functioning, or specific symptoms (such as the ability
to remember new information or the tendency to avoid social gatherings).
Cognitive Assessment
One tool to assess cognitive functioning is an intelligence test. Clinicians typically
use the Wechsler Adult Intelligence Scale, 4th edition (WAIS-IV, revised in 2008), or
the Wechsler Intelligence Scale for Children, 4th edition (WISC-IV, revised in 2003),
depending on the age of the patient. Numerical results of these tests yield an intelligence
quotient (IQ); the average intelligence in a population is set at a score of 100, with
normal intelligence ranging from 85 to 115. IQ scores of 70 to 85 are considered
to be in the borderline range, and scores of 70 and below signify mental impairment.
However, the single intelligence score is not the only important information that the
WAIS-IV and WISC-IV provide. Both of these tests include subtests that assess four
types of abilities:
• verbal comprehension (i.e., the ability to understand verbal information);
• perceptual reasoning (i.e., the ability to reason with nonverbal information);
• working memory (i.e., the ability to maintain awareness and mentally manipulate
new information); and
• processing speed (i.e., the ability to focus attention and quickly utilize information).
In addition, the WAIS-IV and WISC-IV are devised so that the examiner can com-
pare an individual’s responses on each of the subtests to the responses of other peo-
ple of the same age and sex. Information about specific subtests helps the examiner
determine the individual’s pattern of relative strengths and weaknesses in intellectual
functioning.
As part of the mental status exam, patients
are asked whether they know their own
name, the date and year, and who is currently
president. Patients who do not know these
facts may have some type of memory
impairment. Further tests will be done to
determine the specific memory problems,
their cause, and possible treatments.
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78 C H A P T E R 3
Current versions of intelligence tests have been designed to minimize the influ-
ence of cultural factors, in part by excluding test items that might require cultural
knowledge that is unique to one group (and would thus put members of other groups
at a disadvantage) (Kaufman et al., 1995; Poortinga, 1995).
Personality Assessment
Various psychological tests assess different aspects of personality functioning.
Inventories In order to assess general personality functioning, a clinician may use
an inventory—a questionnaire with items pertaining to many different problems and
aspects of personality. An inventory can indicate to a clinician what problems and
disorders might be most likely for a given person. Inventories usually contain test
questions that are sorted into different scales, with each scale assessing a different
facet of personality. The most commonly used inventory is the Minnesota Multiphasic
Personality Inventory, 2nd edition (MMPI-2; Butcher et al., 1989); see Table 3.4 for
TABLE 3.4 • A Sample of MMPI®-2 Scales
Scale Sample Item What Is Assessed
? (Cannot Say)
The score is the number of items
that were unanswered or answered
as both true and false.
An inability or unwillingness to complete the test appropriately,
which could indicate the presence of symptoms that interfere with
concentration.
L (Lie)
Sometimes want to swear (F) Attempts to present himself or herself in a positive way, not
admitting even minor shortcomings.
F (Infrequency)
Something wrong with mind (T) Low scores suggest attempts to try to fake appearing to have “good”
mental health or psychopathology; high scores suggest some type of
psychopathology.
K (Correction)
Often feel useless (F) More subtle attempts to exaggerate “good” mental health or
psychopathology. This scale is also associated with education level—
more educated people score higher than those with less education.
1. Hs (Hypochondriasis) Body tingles (F) An abnormal concern over bodily functioning and imagined illness.
2. D (Depression) Usually happy (F) Symptoms of sadness, poor morale, and hopelessness.
3. Hy (Hysteria)
Often feel very weak (T) A propensity to develop physical symptoms under stress, along with
a lack of awareness and insight about one’s behavior.
4. Pd (Psychopathic Deviate) Am misunderstood (T) General social maladjustment, irresponsibility, or lack of conscience.
5. Mf (Masculinity–Femininity)
Like mechanics magazines
(T for women)
The extent to which the individual has interests, preferences, and
personal sensitivities more similar to those of the opposite sex.
6. Pa (Paranoia)
No enemies who wish me harm (F) Sensitivity to others, suspiciousness, jealousy, and moral self-
righteousness.
7. Pt (Psychasthenia)
Almost always anxious (T) Obsessive and compulsive symptoms, poor concentration, and self-
criticism.
8. Sc (Schizophrenia)
Hear strange things when alone (T) Delusions, hallucinations, bizarre sensory experiences, and poor
social relationships.
9. Ma (Hypomania)
When bored, stir things up (T) Symptoms of hypomania—elated or irritable mood, “fast” thoughts,
impulsiveness, and physical restlessness.
10. Si (Social Introversion) Try to avoid crowds (T) Discomfort in social situations and preference for being alone.
Note: (T) indicates that when the item is marked as true, it contributes to a high score on the scale; (F) indicates that when the item is marked as false, it contributes
to a high score on the scale. The dark green rows above refer to the validity scales, and the light green rows refer to the clinical scales.
Source: Excerpted from the MMPI-2 Booklet of Abbreviated Items. Copyright © 2005 by the Regents of the University of Minnesota. All rights reserved. Used by permission of the University of
Minnesota Press. “MMPI-2” and “Minnesota Multiphasic Personality Inventory 2” are trademarks owned by the Regents of the University of Minnesota.
Clinical Diagnosis and Assessment 79
FI G U RE 3.2 • An MMPI-2 Profile This is the MMPI-2 profile
of a depressed 47-year-old man. His highest clinical scores are on
the D and Pt scales, followed by Pd and Si. People with this profile
typically are significantly depressed, agitated, and anxious. They
may brood about their own deficiencies and have concentration
problems (Greene, 2000).
30
50
70
90
40
60
80
100
110
L F K
Validity scales Clinical scales
A
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sc
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Hs D Hy Pd Mf Pa Pt Sc Ma Si
Projective test
A tool for personality assessment in which the
patient is presented with ambiguous stimuli
(such as inkblots or stick figures) and is asked
to make sense of and explain them.
the scales, and Figure 3.2 for the sample profile. Originally developed in the 1930s
to identify people with mental illness, it was revised in 1989 to include norms of
people from a wider range of racial, ethnic, and other groups and to update specific
items; the scores were recalibrated in 2003, in a form referred to as the MMPI-
2-RF, where the new suffix stands for “Restructured Form.” The MMPI-2 consists
of 567 questions about the respondent’s behavior, emotions, mental processes, men-
tal contents, and other characteristics. The respondent rates each question as being
true or false about himself or herself. Test-takers generally require about 60 to 90
minutes to complete the inventory. (There is also a short form, with 370 items.)
The MMPI-2 has been translated into many languages and is used in many different
countries.
Projective Tests Psychologists may also wish to assess facets of patients’ personali-
ties that are less likely to emerge in a self-report, such as systematic biases in mental
processes. In a projective test, the patient is presented with an ambiguous stimulus
(such as an inkblot or a group of stick figures) and is asked to make sense of and
explain the stimulus. For example, what does the inkblot look like, or what are
the stick figures doing? The idea behind such a test is that the particular structure
a patient imposes on the ambiguous stimulus reveals something about the patient’s
mental processes or mental contents. This is the theory behind the well-known
Rorschach test, which was developed by Herman Rorschach (1884–1922). This test
includes 10 inkblots, one on each of 10 cards. The ambiguity of the shapes permits a
patient to imagine what the shapes resemble. Although the Rorschach test may pro-
vide information about some aspects of a patient’s personality and mental function-
ing, it does not accurately assess most aspects of psychological disorders (Lilienfeld
et al., 2000; Wood et al., 2001).
Another projective test, the Thematic Apperception Test (TAT), uses detailed
black-and-white drawings that often include people. The TAT was developed
by Christiana Morgan and Henr y Murray (1935) and is used to discern motiva-
tions, thoughts, and feelings without having to ask a person directly. The pa-
tient is asked to explain the drawings in various ways: The clinician may ask
the patient what is happening in the picture, what has just happened, what will
happen next, or what the people in the picture might be thinking and feeling.
Like the Rorschach test, the TAT elicits responses that presumably reflect un-
conscious beliefs, desires, fears, or issues (Murray, 1943). Responses on the TAT
may be interpreted freely by the clinician or scored according to a scoring sys-
tem. However, only 3% of clinicians who use the TAT rely on a scoring system
(Pinkerman et al., 1993).
The Rorschach test is a projective test that
consists of inkblots. Patients are asked what
each inkblot—like the one here—looks like.
The Rorschach test is based on the idea that
the test-taker imposes a structure onto the
ambiguous inkblot; the patient’s responses are
thought to reveal something about himself or
herself.
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80 C H A P T E R 3
Assessing Social Factors
Symptoms arise in a context, and part of a thorough clinical assessment is collecting
information about social factors. To some extent, the context helps the clinician or
researcher understand the problems that initiated the assessment: How does the patient
function in his or her home environment? Are there family factors or community fac-
tors that might influence treatment decisions? Is the patient from another culture, and
if so, how might that affect the presentation of his or her symptoms or influence how
the clinician should interpret other information obtained as part of the assessment?
The importance of social and environmental factors in making an assessment
is illustrated by Arthur Kleinman (1988) in examples such as this: If a man has lost
energy because he has contracted malaria, has a poor appetite as a result of anemia
(due to a hookworm infestation), has insomnia as a result of chronic diarrhea, and he
feels hopeless because of his poverty and powerlessness, does the person have depres-
sion? His symptoms meet the criteria for depression (as we shall see in Chapter 5),
but isn’t his distress a result of his health problems and social circumstances and their
consequences? Summing up his experiences as depression might limit our under-
standing of his situation and the best course of treatment.
Family Functioning
As noted in Chapter 2, various aspects of family functioning can affect a
person’s mental health. This was certainly true of the Walls family, where
Rex’s drinking and irresponsibility led Rose Mary to become overwhelmed
and to “shut down”—staying in bed for days and crying. Similarly, their
marriage appeared to have a role in Rex’s drinking problem (Walls, 2005).
In order to assess family functioning, clinicians may interview all
or some family members or ask patients about how the family func-
tions. Some clinicians and researchers try to assess family function-
ing more systematically than through interviews or observations. For
example, the Family Environment Scale (Moos & Moos, 1986) requires
family members to answer a set of questions. Their answers are inte-
grated to create a profile of the family environment—how the family
is organized, different types of control and conflict, family values, and
emotional expressiveness. Such information helps the clinician or re-
searcher to understand the patient within the context of his or her family and identi-
fies possible areas of family functioning that could be improved (Ross & Hill, 2004).
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As part of the Thematic Apperception Test, patients are
asked to describe the motivations, thoughts, and feelings
of people portrayed in various drawings. Some clinicians
consider a patient’s answers to reflect unconscious
beliefs, feelings, and desires.
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The subtle dynamics that develop in a family,
such as one sibling’s feeling that the other is
favored, can have far-reaching implications.
Clinical Diagnosis and Assessment 81
Community
When making a clinical assessment, a clinician should try to learn about the patient’s
community in order to understand what normal functioning is in that environ-
ment. As we saw in Chapter 2, people who have low socioeconomic status (SES) are
more likely to have psychological disorders. These people live in poorer communi-
ties, which tend to have relatively high crime rates—and so they are more likely to
witness a crime, be a victim of crime, or to live in fear. What, then, is “normal”
functioning in this context?
In an effort to understand a patient within his or her social environment, “com-
munity” may be defined loosely; it can refer not only to where the patient lives but
also to where he or she spends a lot of time, such as school or the workplace. Some
jobs and work settings can be particularly stressful or challenging, and a compre-
hensive assessment should take such information about a patient into account. Con-
sider that some work settings place very high demands on employees—high enough
that some may become “burned out” (Aziz, 2004; Lindblom et al., 2006). Symp-
toms of burnout (a psychological condition, though not a psychological disorder in
DSM-5) include feeling chronically mentally and physically tired, dissatisfied, and
performing inefficiently—which resemble symptoms of depression (Maslach, 2003;
Mausner-Dorsch & Eaton, 2000).
The clinician should also assess the patient’s capacity to manage daily life in his
or her community, considering factors such as whether the patient’s psychological
problems interfere with the sources for social support and ability to communicate
his or her needs and interact with others in a relatively normal way. Similarly, the
clinician may be asked to determine whether the patient would benefit from training
to enhance his or her social skills (Combs et al., 2008).
Culture
To assess someone’s reports of distress or impairment, a clinician must understand
the person’s culture. Different cultures have different views about complaining and
how to describe different types of distress or other symptoms, which influence the
amount and type of symptoms people will report to a mental health clinician—
which, in turn, can affect the diagnosis a clinician makes. For instance, White
British teenagers with anorexia nervosa say they are afraid of becoming fat and re-
port being pre occupied with their weight (both symptoms are part of the criteria set
for anorexia); in contrast, British teenagers of South Asian background do not report
these symptoms but are more likely to report a loss of appetite (which is not part
of the criteria set; Tareen et al., 2005). Thus, the reported symptoms of the British
teenagers of South Asian background may not meet enough of the criteria for a
diagnosis of anorexia—although they may still have significant distress, impairment,
or risk of harm.
Such cultural differences may underlie, at least in part, the dramatic differences
in the apparent rates of serious mental illness across countries, shown in Figure 3.3
(WHO World Mental Health Survey Consortium, 2004). (A mental illness was con-
sidered serious if the individual was unable to carry out his or her normal activities
for at least 30 days in the past year.) These rates were based on data gathered in face-
to-face interviews. Notice how much higher the rates are in the United States than
in other developed and developing countries. One explanation for this discrepancy
is that Americans are less inhibited about telling strangers about their psychological
problems. People in other countries might have minimized the frequency or severity
of their symptoms.
To help clinicians assess cultural factors, DSM-5 includes a 16-question Cultural
Formulation Interview. Specifically, responses to this set of questions help clinicians to
Clinicians should inquire about the problems
and strengths of a patient’s community, such
as the presence of violence and the sources for
support. Such information helps us understand
the wider context of the patient’s symptoms,
as well as interventions that might be helpful.
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82 C H A P T E R 3
understand how culture and cultural identity might influence the ways that patients
explain and understand their problems. These factors, in turn, may influence diagno-
sis and treatment (American Psychiatric Association, 2013).
Assessment as an Interactive Process
Mental health researchers and clinicians learn about patients from assessing psycho-
logical and social factors and, to a lesser extent, neurological and other biological
factors. Information about each type of factor should not be considered in isola-
tion but rather should influence how the clinician understands the other types of
information.
Knowledge of psychological factors must be developed in the context of the
patient’s culture. Psychiatrist Paul Linde (2002) recounts his experiences working in
a psychiatric unit in Zimbabwe: The residents of that country generally understand
that bacteria can cause an illness such as pneumonia, but they nonetheless wonder
why the bacteria struck a particular individual at a specific point in time (a question
that contemporary science is just beginning to try to answer). They look to ancestral
spirits for an answer to such a question, even when a particular person is beset with
mental rather than physical symptoms. In Zimbabwe, the first experience of halluci-
nations and delusions is viewed as a sign that the individual is being called to become
a healer, a n’anga, and not as an indicator of mental illness.
Thus, knowledge of the patient’s culture influences how an outside researcher
such as Linde understands the symptoms. When a patient in Zimbabwe claims to be
hearing voices of dead ancestors, Linde undoubtedly interprets this symptom some-
what differently than he would if a White, American-born patient made the same
claim. At the same time, knowledge of a patient’s family history of chronic schizo-
phrenia (which may indicate a neurological factor—genetic, in this case) will also
influence the interpretation of the patient’s symptoms.
0
1
2
3
4
5
6
7
8
100
P
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ce
n
ta
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o
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p
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Un
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S
ta
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Fr
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Be
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Ne
th
er
la
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s
Ja
pa
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Ge
rm
an
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Ita
ly
Sp
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Developed countries
0
1
2
3
4
5
6
7
8
100
P
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ce
n
ta
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f
p
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it
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m
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ta
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d
is
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er
Co
lo
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bi
a
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Le
ba
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M
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ico
Ch
in
a
(S
ha
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ha
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Ch
in
a
(B
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jin
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Ni
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ria
Less-developed countries
FI G U RE 3.3 • Rates of Serious Mental Illness Across Countries From 2001 to 2003, the World Health Organization
conducted surveys to measure the prevalence of serious mental disorders in the populations of various countries. The results revealed
significant differences among countries (WHO World Mental Health Survey Consortium, 2004).
Source: Copyright 2004 by the American Medical Association. For more information, see the Permissions section.
Clinical Diagnosis and Assessment 83
Clearly, the way that each type of factor is assessed can influence how the other types
of factors are assessed. However, comprehensive assessment of all three factors in the same
patient is rarely undertaken. Formal testing beyond a brief questionnaire that the patient
completes independently can be relatively expensive, and often health insurance companies
will not pay for routine assessments; they will pay only for specific assessment procedures
or tests that they have authorized in advance, based on indications of clear need (Eisman
et al., 2000). Beyond an interview, other forms of assessment are most likely to be admin-
istered as part of a legal proceeding (e.g., a custody hearing or sentencing determination)
or as part of a research project related to psychological disorders and their treatment.
Thinking Like A Clinician
Suppose that you have decided to become a mental health professional. What type of
training (and what type of degree) would you obtain, and why?
Now suppose that you are working in an emergency room, assessing possible mental ill-
ness in patients. You have been asked to determine whether a 55-year-old woman, who was
brought in by her son, has a psychological disorder severe enough for her to be hospitalized.
Based on what you have read, if you could use only one assessment method of each type
(neurological, psychological, and social), what methods would you choose, and why?
Diagnosing and Assessing
Rose Mary and Rex Walls?
Now that you know something about diagnosis and assessment, let’s review what we
know—and what we don’t know—about Rose Mary and Rex Walls, starting with
Rex, using the neuropsychosocial approach.
We know that he drank alcohol—regularly and to excess. In fact, he drank
so much and so chronically that when he stopped drinking, he developed delirium
tremens (also known as the DTs)—withdrawal symptoms marked by hallucinations
and shaking. He clearly would have been diagnosed as having alcohol use disorder. (Dis-
orders related to misuse of alcohol and other substances are discussed in Chapter 9.)
We don’t know whether the tall tales he told about himself were delusions or
merely attempts to make himself look good in his own eyes and those of other peo-
ple. Based on Jeannette’s descriptions of her father, it appears that Rex also strove to
be the center of attention. This pattern of self-centered behavior suggests that he may
have had a personality disorder (specifically, what is known as narcissistic personality
disorder, and possibly other personality disorders, discussed in Chapter 14).
What about Rose Mary? Based on Jeannette’s descriptions of her mother’s dif-
ficulties. Rose Mary may have suffered from depression. It is possible, though, that
certain behaviors instead may have been expressions of anger and resentment about
feeling forced to work when her husband was so irresponsible. She was bitter that
she hadn’t become a famous artist and blamed her lack of success on her children.
In addition, given her own preoccupations with her worth as an artist, even as her
children were starving, she may well have had narcissistic personality disorder.
However, again we need to be cautious: No mental health clinician can know
with certainty what, if any, specific disorder Rose Mary or Rex Walls may have had.
We cannot make a direct clinical assessment of neurological, psychological, or social
factors; we can only infer such factors from their daughter’s account, which does not
provide the kind of information needed to make an accurate clinical assessment.
Finally, clinicians and researchers diagnosing and assessing patients must keep in
mind the possibility that symptoms of a psychological disorder can arise from medi-
cal problems. Only after ruling out medical illnesses can a mental health clinician or
researcher have confidence in a diagnosis of a psychological disorder.
84 C H A P T E R 3
Diagnosing Psychological Disorders
• Among other purposes, classification sys-
tems for diagnosis allow (1) patients to
be able to put a name to their experi-
ences and to learn that they are not alone;
(2) clinicians to distinguish “normal” from
“ abnormal” psychological functioning and
to group together similar types of problems;
and (3) researchers to discover the etiology,
course, and effectiveness of treatments for
abnormal psychological functioning.
• Classif ication systems have drawbacks:
(1) They can be subject to diagnostic bias—
perhaps on the basis of the patient’s sex,
race, or ethnicity; and (2) for some people,
being diagnosed with a psychological dis-
order is experienced as stigmatizing, which
changes how the person feels about himself
or herself or is seen by others.
• Classification systems should be both reli-
able and valid.
• The most commonly used classif ication
system in the United States is the Diagnos-
tic and Statistical Manual of Mental Disorders,
presently in its f ifth edition (DSM-5).
The DSM-5 generally does not focus on
etiology but instead focuses on what can
be observed rather than inferred and lists
explicit criteria for each disorder.
• DSM-5 has been criticized on numerous
grounds, including:
° What constitutes clinically significant
distress or impaired functioning is sub-
jective and can var y widely from one
clinician to another.
° Most disorders are classified as categori-
cal rather than as on continua.
° The way the criteria are structured leads
heterogeneous groups to be diagnosed
with the same disorder.
° The duration criteria can be arbitrary and
not necessarily supported by research.
° Many diagnoses have been created in
order to ensure payment from health
insurance providers. Moreover, diagno-
ses have been added for disorders that
clearly are medical problems.
° Social factors that lead or contribute to
psychological disorders are deemphasized.
° There is a high comorbidity rate: Half
the people diagnosed with one disorder
have at least one other disorder.
• Psychological disorders are generally diag-
nosed by clinical and counseling psycholo-
gists, psychiatrists, psychiatric nurses, and
social workers. Other clinicians in a posi-
tion to diagnose psychological disorders
include general practitioners, pastoral coun-
selors, and marriage and family therapists.
Assessing Psychological Disorders
• Neurological and other biological factors
may be assessed using various methods.
Neuroimaging techniques can assess brain
str ucture ( X-rays, computer ized a xial
tomog raphy, and mag net ic resonance
imaging) and brain function (positron emis-
sion tomography and functional magnetic
resonance imaging). Neuropsychological
testing can assess brain functioning.
• Various methods are used to assess psy-
cholog ica l factor s. These include the
clinical interview, observing the patient,
patient self-report, and reports of others
involved in the patient’s life. Specific as-
pects of psychological functioning can be
assessed through tests of cognitive abili-
ties, and personality functioning can be
assessed with inventories, questionnaires,
and projective tests.
• Some techniques used to assess psycholog-
ical factors also can be used to assess social
factors—such as family functioning—as
well as to provide a more detailed portrait
of the patient’s community and culture.
These social factors affect and are affected
by neurological and psychological factors.
SUMMING UP
Diagnosis (p. 61)
Clinical assessment (p. 61)
Diagnostic bias (p. 63)
Reliable (p. 64)
Valid (p. 64)
Prognosis (p. 64)
Prevalence (p. 64)
Comorbidity (p. 66)
Clinical psychologist (p. 70)
Counseling psychologist (p. 70)
Psychiatrist (p. 71)
Psychiatric nurse (p. 71)
Social worker (p. 71)
Computerized axial tomography (CT) (p. 73)
Magnetic resonance imaging (MRI) (p. 73)
Positron emission tomography (PET) (p. 74)
Functional magnetic resonance
imaging (fMRI) (p. 74)
Neuropsychological testing (p. 74)
Clinical interview (p. 75)
Malingering (p. 77)
Factitious disorder (p. 77)
Projective test (p. 80)
Key Terms
More Study Aids
For additional study aids related to this chapter, including
quizzes to make sure you’ve retained everything you’ve
learned and a Student Video Activity exploring how to assess
antisocial behavioral patterns, go to: www.worthpublishers.
com/launchpad/rkabpsych2e.
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Clinical Diagnosis and Assessment 85
87
CHAPTER 4
Research Methods
uppose you are a psychologist at a college counseling cen-
ter. A student, Carlos, comes to the center because he’s been
depressed since his girlfr iend, Liana, broke up with him
5 weeks ago. Liana’s rejection came out of nowhere, as far as Carlos
is concerned. He feels abandoned and alone. He has been spiraling
downward since the breakup, feeling irritable and sad, sleeping a
lot, and without appetite. He was just fired from his on-campus job
because of his poor attitude. He doesn’t care much about his classes or
schoolwork. During your sessions with Carlos, he seems preoccupied
with his relationship with Liana and worries that no other woman
will ever love him.
Carlos is not the only student on campus to have this type of
problem. You’ve noticed that a surprising number of students seeking
help at the counseling center are depressed and have recently broken
up with a boyfriend or a girlfriend. Like Carlos, these students fre-
quently report feeling hurt, rejected, and unlovable. Some even think
about suicide.
You wonder, though, whether the depression that many of these
students are experiencing is a result specifically of their breakups.
Perhaps they were depressed before the breakup—and that contrib-
uted to the failure of the relationship. In Carlos’s case, perhaps his
depression started earlier (although he hadn’t realized it), and Liana
got sick of his being down in the dumps. On the other hand, maybe a
lot of the students would not have become depressed if their relation-
ships had not ended.
How can you determine wHetHer tHe students are
depressed because their relationships ended, or whether their
relationships ended because they were depressed? In this chapter, we
explore specific methods that psychologists use to study psychopa-
thology and its treatment, the challenges associated with the use of
the different research methods, and the ways in which researchers
address those challenges.
Using the Scientific Method to Understand
Abnormality
The Scientifi c Method
Types of Scientifi c Research
Ethical Guidelines for Research
Research Challenges in Understanding
Abnormality
Challenges in Researching Neurological Factors
Challenges in Researching Psychological Factors
Challenges in Researching Social Factors
Researching Treatment
Researching Treatments That Target Neurological
Factors
Researching Treatments That Target
Psychological Factors
Researching Treatments That Target Social
Factors
Paper Boat Creative/Stone/Getty Images. Photo for illustrative purposes only; any individual depicted is a model.
Using the Scientific Method to
Understand Abnormality
Perhaps your observations about depression and relationship breakups are based
simply on a coincidence: People—particularly young people—are frequently be-
ginning and ending relationships, and depression and breakups occur completely
independently of each other. Many of the depressed students coming to the coun-
seling center have had prior bouts of depression. In such cases, a breakup would
not necessarily be the culprit, because those people might have had another bout
of depression regardless. Alternatively, there may be a causal connection between
breaking up and depression—but it could go either way, with either one leading to
the other.
To determine whether the breaking up of a relationship can in fact lead to de-
pression, you would use the scientific method, which is the process of gathering
and interpreting facts that generally consists of the following steps:
1. Collect initial observations
2. Identify a question
3. Develop a hypothesis that might answer the question
4. Collect relevant data to test the hypothesis
5. Develop a theory
6. Test the theory
The Scientific Method
How can the scientific method help researchers learn more about the association be-
tween breakups in relationships and depression or, more generally, about how a psy-
chological disorder such as depression arises?
Collect Initial Observations
The first step in the scientific method is to collect initial observations. Sometimes
the initial observations lead immediately to the next steps, but other times they
lead the researcher to describe the phenomenon more carefully and systematically
by collecting data. Data are methodical observations, which often include numeri-
cal measurements of phenomena. Scientific facts are based on such data. Data about
depression and breakups, for instance, might include responses to a questionnaire
on which people who have recently gone through a breakup rate their moods and
functioning.
Properly collected data can be replicated under identical or nearly identical con-
ditions: Any other researcher, using the same collection method, should obtain a sec-
ond set of data with the same characteristics as the first. For example, if a researcher
at another college’s counseling center gave the same questionnaire about mood and
functioning to a different group of students who’d recently suffered a breakup, that re-
searcher would be trying to replicate the data.
Identify a Question
The process of explaining a set of observations begins by asking a specific ques-
tion. Let’s say that your observations have led you to ask this question: “Why do
some people get depressed after a relationship ends rather than bounce back?” The
question identifies an area where properly conducted research can point toward an
answer.
Scientists often collect quantitative data
(numerical measurements, such as how many
symptoms someone has, the number of weeks
symptoms have been present, or how many
people in the family have similar symptoms).
P
ic
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In
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to
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Scientific method
The process of gathering and interpreting
facts that generally consists of collecting
initial observations, identifying a question,
developing a hypothesis that might answer
the question, collecting relevant data,
developing a theory, and testing the theory.
Data
Methodical observations, which include
numerical measurements of phenomena.
Replication
The process of repeating a study using the
same data collection methods under identical
or nearly identical conditions to obtain data
that should have the same characteristics as
those from the original study.
88 C H A P T E R 4
Develop and Test a Hypothesis
After identifying a question, a researcher forms a hypothesis. A hypothesis is a
preliminary idea that is proposed to answer the question about a set of observa-
tions. Hypotheses are important in part because they direct the researcher to
make specific additional observations (which may include making precise mea-
surements). The most common kinds of hypotheses propose a way to understand
differences in measurements of a variable in different circumstances (such as dif-
ferences in rates of depression when no breakup has occurred versus soon after
a breakup) or to establish a relationship between different variables. Variables are
measurable characteristics of the object or event of interest; for example, mood
(rated on a scale ranging from very positive to very negative) is a variable. For in-
stance, a hypothesis might address which people are likely to get depressed or why
some people are likely to get depressed. Let’s say you develop this hypothesis:
People who suffered a major loss during childhood (such as the death of a parent) are
more likely to get depressed after a relationship ends during adulthood. Your hypothesis
involves two variables: (the presence or absence of ) childhood loss and depression.
After the researcher has a hypothesis, he or she must test it by collecting new
data. If the resulting data are as expected, the hypothesis is supported. But if the data
are inconsistent with the hypothesis, the researcher must think again—and try to
develop a new hypothesis and then test it. And even when the data generally are con-
sistent with the hypothesis, often some aspect of the data were unexpected, which
leads to new hypotheses to be tested.
Develop a Theory
After enough data are collected and hypotheses are confirmed or disconfirmed, the
researcher proposes a theory, which is a principle or set of principles that explains a
set of data. A theory provides an answer to the question identified by the researcher.
For example, you might theorize that depression is particularly likely to arise in adults
after a relationship ends if they, as children, suffered a loss and there was nothing they
could do to control or manage the situation. That is, according to this theory, the
child forms an enduring association between loss and a sense of helplessness, and it is
the feelings of helplessness that produce depression. According to this theory, when
later in life the adult experiences a loss, this triggers the associations to helplessness,
which in turn leads the adult to become depressed.
Test the Theory
The next step of the scientific method is to test the theory by collecting and examining
additional data. The theory leads to predictions, hypotheses that should be confirmed
if a theory is correct. So, for instance, your theory focuses on people who not only had a
significant loss during childhood but also felt that they could not control or manage the
situation. The theory predicts that children who felt particularly helpless after a loss would
be more likely as adults to become depressed after a relationship breaks up. Data can then
be collected to address this specific prediction: In addition to questionnaires about early
loss and mood and functioning, an additional questionnaire might ask about memories of
feeling helpless. You could then test people who did or did not have an uncontrollable loss
during childhood by giving them increasingly difficult puzzles; as a measure of current
feelings of helplessness, you would assess how easily participants give up trying to solve
the puzzles. You would predict that people who experienced a loss as a child would be
more likely to feel—and behave as if they were—helpless currently, and that these people
would become depressed after a relationship breaks up. Many methods can be used to test
the predictions made by a theory, and we’ll see what these are in the following section.
Figure 4.1 provides a summary of the steps of the scientific method.
The scientific method is used to determine
whether a hypothesis—such as the idea
that a relationship’s breaking up can lead
to depression—is correct. The process of
research on psychopathology often begins
with observations that lead to a hypothesis
about either the factors that may contribute
to psychological disorders or the aspects of
treatment that may be particularly helpful.
R
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Hypothesis
A preliminary idea that is proposed to answer
a question about a set of observations.
Theory
A principle or set of principles that explains a
set of data.
Predictions
Hypotheses that should be confirmed if a
theory is correct.
Research Methods 89
Types of Scientific Research
Any individual researcher does not need to go through the entire sequence of steps in
the scientific method to be doing science. Moreover, psychologists may employ differ-
ent research methods when they work on different phases of the sequence and when
they attempt to answer different questions; such methods include experiments, quasi-
experiments, correlational research, case studies, and meta-analysis. As we review the var-
ious research methods, we will point out both their major strengths and their weaknesses.
Conducting Research with Experiments
Ideally, researchers prefer to employ experiments, which are research studies in
which investigators intentionally manipulate one variable at a time and measure the
consequences of such manipulation on one or more other variables.
Independent Variables and Dependent Variables
You probably noticed that the definition of experiments mentioned two kinds of vari-
ables: those that are manipulated and those that then are measured. In an experiment,
researchers manipulate one variable at a time in order to observe possible changes in
another variable. The variable that a researcher manipulates is called the indepen-
dent variable (so named because it is free to change—it is independent). The vari-
able that may change as a result is called the dependent variable (because its value
depends on the independent variable). When the independent variable is changed, the
accompanying changes in the dependent variable are the effect. A researcher might
separately manipulate several independent variables (always keeping all else constant
while a single variable is changed), hoping to discover which ones cause the greatest
effect on the dependent variable.
Of course, researchers could not use an experimental design to investigate the specific
question about helplessness during early loss and subsequent depression after a breakup.
A researcher ethically cannot cause a person to have a major loss during childhood (or to
feel helpless at the time). Participants in an experimental study come as they are—with
particular neurological, psychological, and social histories that can’t be changed.
This is why most of the research on causes of psychological disorders does not use
an experimental design. For ethical reasons as well as practical ones, researchers can-
not alter participants’ genes, subject participants to high levels of stress, cause them to
Identify the
question
Why do some
people get
depressed after
a relationship
ends rather
than bounce
back?
Collect initial
observations
Make observa-
tions, which may
include specific
measurements,
such as
responses to a
questionnaire
rating mood
and functioning
(such data can
be replicated).
Develop and test
a hypothesis
Develop a
theory
Loss during
childhood leads
to a sense of
helplessness,
which in turn
predisposes
people to
become
depressed in
adulthood after
a relationship
breaks up, when
they again feel
helpless.
Test the
theory
Test people who
have just had a
relationship break
up. Assess: 1)
whether they did
or did not have an
uncontrollable
loss during
childhood;
2) current level of
helplessness by
measuring how
easily participants
give up trying to
solve difficult
puzzles; 3) their
level of depression
People who suffered a major
loss during childhood (such
as the death of a parent) are
more likely to get depressed
after a relationship ends
during adulthood.
Participants are people who
have just had a relationship
breakup; they complete a
questionnaire about their
losses in childhood and a
questionnaire about their
current mood and functioning.
FI G U RE 4.1 • Steps of the Scientific Method
Experiments
Research studies in which investigators
intentionally manipulate one variable at a
time, and measure the consequences of such
manipulation on one or more other variables.
Independent variable
A variable that a researcher manipulates.
Dependent variable
A variable that is measured and that may
change its values as a result of manipulating
the independent variable.
90 C H A P T E R 4
have traumatic experiences, or create disruptive family events—all of which would
involve intentionally manipulating independent variables. However, some aspects of
psychopathology can be studied with an experimental design. For instance, Watson
and Rayner’s experiment with Little Albert (1920; see Chapter 2) used an experimen-
tal design to test a theory about the etiology of a phobia. In that study, the independent
variable was whether or not the conditioned (that is, the initially neutral) stimulus had
been paired with an aversive unconditioned stimulus. The dependent variable was the
presence of fear-related behaviors—as measured by Albert’s crying and trying to get
away from the white rat. When the conditioned stimulus (CS) and the unconditioned
stimulus (UCS) had not yet been paired, Albert was not afraid of the rodent. His fear-
related behaviors (the dependent variable) depended on his exposure to the pairing of
CS and UCS. (Note that the ethical guidelines that apply to research today had not yet
been developed at the time of Watson and Rayner’s study with Little Albert.)
Other examples of experimental designs in research on psychopathology include
studies of people who have panic attacks—specific periods of intense dread or fear,
accompanied by physical symptoms of fear; the independent variable is the situation
or condition that may induce a panic attack (which is manipulated by presenting or
removing such a situation or condition), and the dependent variable is the number
of such attacks. Further examples include studies of people who have substance abuse
problems, where the independent variable is the type of cues, or stimuli, that trigger
cravings to take a drug or to drink alcohol, and the dependent variable may be inten-
sity of cravings for the drug or alcohol or physiological measures of arousal.
If an experiment has not been carefully designed, some factors might inadver-
tently affect the variables of interest. These factors are called confounding vari-
ables, also referred to as confounds. For example, suppose that you conducted an
experiment in which the independent variable was the type of movie viewed by two
groups of participants, those who had experienced a loss during childhood and those
who did not. One movie involved the death of a loved one and the other did not
touch on the theme of loss, and the dependent variable was mood. Then suppose that
for the “loss” group, the movie involving loss was always shown immediately after a
serious drama, whereas for the “no loss” group, the movie that did not involve loss
was always shown immediately after a comedy. It could be the type of movie shown
first—drama or comedy—and not differences between the groups that produces the
effects on the dependent variable; thus, the type of film first shown is a confounding
variable. Confounds lead to ambiguous or uncertain results. To minimize the possi-
bility of confounds, a researcher should try to ensure that the experimental manipu-
lation alters only the independent variables (and does not inadvertently affect other
variables, such as the order in which the movies are presented) and that only those
changes in the independent variables affect the dependent variable.
Control Groups and Control Conditions
A common method for ruling out possible effects of confounds in an experiment is to
create a control group. The experimental group (or groups) and the control group are
treated identically throughout the experiment, except that the independent variable is
not manipulated for the control group. For example, say that the participants who
had suffered an early loss and experienced helplessness did in fact have a more negative
mood after watching a movie with the theme of loss. But here’s a potential confound:
Maybe these people are just very sensitive to depressing movies in general, not to themes
of loss specifically. To rule out this possibility, you would control for this factor by test-
ing another group of these people, showing them a depressing movie that has nothing
to do with loss. (This movie should be as similar as possible to the first one in every
way, except that it does not have the theme of loss.) If the finding does not result from
a confounding, then you should find a much larger drop in mood following the movie
Some studies investigating psychopathology
use an experimental design. Here the
independent variable is different types of
music, in major versus minor keys, and the
dependent variable is participants’
self-reported mood after listening to the two
types of music.
b
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ck
w
in
ke
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A
la
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y
Confounding variables
Factors that might inadvertently affect the
variables of interest in an experiment.
Control group
A group of participants in an experiment
for which the independent variable is not
manipulated, but which is otherwise treated
identically to the experimental group.
Research Methods 91
about loss than following the movie that was merely depressing—which would provide
evidence that the theme of loss itself is important.
To use a control group appropriately, it must be as similar as possible to the
experimental group. If the members of a control group differ from members of the ex-
perimental group in terms of age, education, cultural background, temperament, or any
other characteristic, one or more confounding variables has been introduced. Such a con-
found would cloud the interpretation of the results because a difference in the dependent
variable could be attributed to the confound instead of to the relationship you intended
to test. Perhaps the control group responded less strongly to the depressing movie simply
because most of the participants in that group happened to be temperamentally placid.
You can imagine how hard it can be to match a control group perfectly to an
experimental group. This difficulty often leads researchers to match the experimental
group to the most similar possible control group: the experimental group itself! Some-
times, rather than having two separate groups that are treated differently, researchers
have all participants take part in different conditions, or circumstances, which corre-
spond to the different ways that experimental and control groups would be treated in a
study that had both types of groups. For example, the same people could watch a movie
about loss and at a different time watch a movie that is depressing but not about loss.
However, when the same group of people take part in more than one condition, you
need to avoid a confound introduced by the order of presentation of the conditions. For
instance, if the “loss” film was always presented first, it could be that the participants
were more alert during that part of the study and that’s why they responded differently.
To avoid this, you would counterbalance the order of exposure to each condition: Half of
the participants would watch the “loss” film first, and the other half would watch the
“nonloss/depressing” film first. This procedure would ensure that each condition oc-
curred equally often in each place in the order of presentation.
Possible Effects of Bias
The way a study is set up can affect the assignment of participants into groups or
can inappropriately influence the outcome of the experiment. For instance, suppose
that you have two groups: Members of one group see a “loss-and-depressing” film,
and members of the other see a “nonloss-but-depressing” film. When you assign
participants to the groups, you inadvertently assign the people who smile at you to
the “non-loss-but- depressing” group. Whether or not it is conscious (intentional) or
unconscious (unintentional), a tendency or influence that distorts data—which ends
up producing a confound—is called bias. This is why researchers place participants
in groups using random assignment, assigning participants to each group by a pro-
cedure that relies on chance.
Many sorts of biases exist. For example, a particularly important one is sam-
pling bias, which occurs when the participants are not drawn randomly from the
relevant population. Sampling bias needs to be avoided if you want to be able to
generalize (i.e., extrapolate) from the people in your study to the population at large.
This brings us to an important distinction: The population is the complete set of
possible participants (e.g., all rats or all people, or, in certain cases, all people of a
particular age, gender, or race). The sample is the small portion of the population
that is examined in a study.
Internal and External Validity
A study has internal validity if it controls for possible confounding variables. Inter-
nal validity means that variations in the independent variable are in fact responsible
for variations in the dependent variable (or variables, in studies in which more than
one type of measurement is taken) and that the results are not a by-product of other,
extraneous variables.
Bias
A tendency that distorts data.
Random assignment
Assigning participants to each group in a
study using a procedure that relies on chance.
Sampling bias
The distortion that occurs when the
participants in an experiment have not been
drawn randomly from the relevant population
under investigation.
Population
The complete set of possible relevant
participants.
Sample
The small portion of a population that is
examined in a study.
Internal validity
A characteristic of a study that indicates
that it measures what it purports to measure
because it has controlled for confounds.
92 C H A P T E R 4
A study is said to have external
validity when (1) the results gener-
alize from the sample (the particular
participants who were tested) to the
population from which it was drawn
and (2) the conditions used in the study
(such as the particular movies shown)
generalize to similar conditions outside
the study. If a study does not have in-
ternal validity, it cannot have external
validity. In contrast, even if a study has
internal validity (its results are not pro-
duced by confounds), it is not guaran-
teed to have external validity (that its
results apply to other people and other
similar situations).
Quasi-Experimental Design
Ideally, the participants in a study are randomly assigned to groups. But in many cases,
random assignment is not ethical, desirable, or possible. For instance, when trying to
test hypotheses about why a disorder develops, researchers cannot “assign” one group
to have a particular set of genes or brain functioning, a particular way of thinking, a
particular type of traumatic experience, or particular friends or families. Therefore, in
trying to understand possible causes of psychopathology, researchers often use quasi-
experimental designs, which rely on groups that already exist. In fact, the “experiment”
that we have been discussing is—like much research on psychopathology—a quasi-
experiment: As in an experiment, an independent variable was manipulated and a de-
pendent variable was measured, but participants were selected from preexisting groups,
not randomly assigned.
To have made a true experiment, you would need to have assigned participants
randomly to three groups (loss with helplessness, loss without helplessness, and no
loss) during childhood. Obviously, this is undesirable and impossible. But in a quasi-
experimental design, you can sort participants into groups—those who had a child-
hood loss and experienced helplessness, those who had a childhood loss but didn’t
experience helplessness, and those without a childhood loss. Then you might show
people in all three groups a film that involves relationships breaking up. After view-
ing the film, participants in all three groups would rate their mood. Your hypothesis
would be that participants who experienced early loss and helplessness (like Carlos)
will report greater sadness after seeing the film than will those in the other two
groups. With a quasi-experimental design, you still try to control as many variables—
such as age, health, education, and economic level—as you can in order to make the
groups as similar as possible.
Correlational Research
Experiments and quasi-experiments allow researchers to zero in on which vari-
ables cause which effects. In some cases, however, manipulating variables, even in a
quasi-experiment, can be unethical or difficult. When independent variables can’t or
shouldn’t be manipulated, researchers can study the relationships among variables by
looking for a correlation, a relationship between the measurements of two variables
in which a change in the value of one variable is associated with a change in the value
of the other variable. Much of the research on defining and understanding psychopa-
thology is correlational.
Suppose researchers want to know what
the prevalence is in the United States of the
type of depression that results from seasonal
changes in the amount of daylight (sometimes
referred to as seasonal affective disorder).
Researchers in Portland, Oregon, collaborated
on a study with researchers in Boston, New
York, Chicago, and Detroit. Participants in the
study are drawn from those five cities. Do
you see the sampling bias problem? All these
cities are in the northern half of the United
States and therefore have a different number
of daylight hours than does the southern half.
Whatever prevalence rate was calculated
would not reflect the entire United States.
External validity
A characteristic of a study that indicates that
the results generalize from the sample to the
population from which it was drawn and from
the conditions used in the study to relevant
conditions outside the study.
Correlation
The relationship between the measurements
of two variables in which a change in the value
of one variable is associated with a change in
the value of the other variable.
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Research Methods 93
A correlation compares two measurements and
indicates the amount of similarity in their variations; the
stronger the correlation, the more closely related the two
variables are. There are no independent and dependent
variables in correlational research: Nothing is manipulated;
instead, naturally occurring variations among measure-
ments of different variables are compared. These compari-
sons can involve measures from different individuals or
groups, or measures from the same participants at different
times. For example, if your study were correlational, your
two variables of interest might be the extent to which a
child experienced helplessness during a loss (perhaps rated
by relatives who were present at the time or by the person’s
memory of how severe the feeling of helplessness was) and
the number of symptoms of depression experienced as an
adult, after a breakup. Twin studies (discussed in Chapter
2) often involve correlational research.
Correlation Does Not Imply Causation
A major disadvantage of correlational methods is that they only indicate that two vari-
ables are related. A correlation between variables does not demonstrate causation—that is,
it does not mean that either variable caused the other to change. In an experiment or
in a quasi-experiment, the point is to show that changes in the independent variable
cause changes in the dependent variable. In contrast, in a correlational research study,
the point is only to show that the values of two variables are related. For example,
although the degree of helplessness felt during childhood loss and the amount of de-
pression after an adult relationship breaks up may be correlated, the loss experienced
after the breakup may not be the cause of the depression. As discussed earlier, it could
be that depression comes first, and it causes the breakup! Simple correlations do not
control for possible confounding variables.
Measuring a Correlation
The strength of the correlation between any two variables is quantified by a num-
ber called a correlation coefficient (most typically symbolized by r). When this
number is positive, it signifies that the variables change in the same direction; both
variables either increase or decrease in the same general pattern. A positive relationship
is indicated by any correlation coefficient between 0 and 11. When the correlation
coefficient is negative, it signifies that the variables change in opposite directions in
the same general pattern; one goes up while the other goes down. A negative relation-
ship is indicated by a correlation coefficient between 0 and 21. In either case, positive
or negative, the stronger the relationship, the closer the coefficient is to 11 or 21,
which would indicate a perfect correspondence.
If the variables do not have any relationship at all, the correlation coefficient is
0. If you plot two variables on a graph, putting one variable on each axis, you can
see whether or not the variables change together. The closer the data points are to a
straight line that has a slope (either up, for positive correlations, or down for negative
ones), the stronger the correlation. Figure 4.2 illustrates five correlations.
Statistical Significance
Even when variables are completely independent, they might vary in the same pat-
tern simply by chance. In fact, the correlation coefficient between any two randomly
selected sets of data is very seldom exactly 0. A correlation coefficient—or the result
of performing any other statistical test (such as a “t-test,” which assesses the difference
between means)—is statistically significant when it is greater than what would be
Correlation coefficient
A number that quantifies the strength of
the correlation between two variables; the
correlation coefficient is most typically
symbolized by r.
Statistically significant
The condition in which the value of a statistical
test is greater than what would be expected by
chance alone.
Epidemiology
The type of correlational research that
investigates the rate of occurrence, the
possible causes and risk factors, and the
course of diseases or disorders.
©
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A correlational study found that suicide
is more likely to be the cause of death in
high-altitude states, such as Colorado, than
in lower-altitude states (D. Cheng, 2002).
This relationship may arise for a number
of reasons, such as decreased levels of
oxygen from the higher altitude (McCook,
2002), the challenges of mountain living,
differences in the age and education levels
of the populations, or perhaps the fact that
depressed people seek a type of solitude
more often found in high-altitude states.
One possible confound the study did not
control for was the amount of time those
who committed suicide had lived at the
higher altitude: Those who were born in high-
altitude states would have adapted to the
lower oxygen level. Researchers could have
investigated one possible explanation by
examining this variable (McCook, 2002).
94 C H A P T E R 4
expected by chance alone. Statistical significance
is not the same thing as “importance.” It simply
means that the observed result is unlikely to be
a quirk of random variation in the data. Suppose
that, for your participants, you calculated the cor-
relation between age when experiencing a loss
during childhood and symptoms of depression af-
ter an adult breakup, and the result was r 5 20.31.
This means the younger a person was when a loss
occurred, the more symptoms of depression he or
she is likely to have after a breakup as an adult.
However, this relationship may not hold for every
participant. Researchers want to know not only
the correlation coefficient but also the value of p
(which stands for probability) that is associated with
that coefficient; the value of p indicates how likely
it is that the correlation could have arisen due to
chance. For instance, your correlation coefficient
of 20.31 was tied to p , .01. This means that the
probability that the correlation is due to chance is
less than 1 in 100. Similarly, a value of p , .05
means that the probability that the correlation is
due to chance is less than 5 in 100. In fact, p ,
.05 is usually considered the cutoff for statistical
significance. As a rule, the more participants that
were tested, the lower the correlation can be and
be statistically significant.
Using Correlational Methods
Correlational research in psychopathology is de-
signed to discover whether one variable (which
often taps a characteristic of a disorder) is linked
to other var iables (which often tap a symp-
tom or associated factor, such as alterations in
neural activit y, irrational thoughts, or family
functioning). Epidemiology is a type of correla-
tional research that investigates the rate of occur-
rence, the possible causes and risk factors, and the
course of diseases or disorders. Thus, in epidemi-
ological studies of psychopathology, researchers
identify people with one (or more) disorder and
correlate the presence or severity of the disorder
with other variables, such as the age of onset of
the disorder, the number of people in the fam-
ily who have had symptoms of the disorder, or
socioeconomic status.
Note that certain factors (such as having a relative with a disorder) can be risk
factors, which increase the likelihood of developing a disorder. However, by defi-
nition, risk factors are simply that—risks, not destiny. How are such risks identi-
fied? Studies often use correlational data to determine whether people who have a
psychological disorder are different in some way from people who don’t have the
disorder. Some of these studies are longitudinal studies, which are designed to
determine whether a given variable is a risk factor by using data collected from
Longitudinal studies (in studies of
psychopathology)
Research studies that are designed to
determine whether a given variable is a risk
factor by using data collected from the same
participants at various points in time.
x
y
Perfect-positive correlation (1.0)
Moderate-positive correlation (.5)
x
y
x
y
No correlation (0.0)
Moderate-negative correlation (–.5)
x
y
Perfect-negative correlation (–1.0)
x
y
FI G U RE 4.2 • Five Values of Correlation
Research Methods 95
the same participants at multiple points in time. Specifically, such stud-
ies track a group of children or adults over time and observe whether a
disorder develops. The presence or absence of the disorder (or its level of
severity) is then correlated with neurological factors (perhaps information
about brain structure or function or hormone levels), psychological factors
(cognitive or emotional functioning, beliefs, or personality traits), and/
or social factors (family and other intimate relations, school performance,
or socioeconomic status) that typically were assessed at an earlier point in
time. Factors that are significantly correlated with the subsequent emer-
gence of the disorder are taken to signal risk for developing that disorder.
However, because such longitudinal studies are usually correlational, re-
searchers cannot infer causality on the basis of the findings. As with virtually all
correlational studies, many factors can explain differences observed in longitudinal
studies.
Case Studies
Research on psychopathology may also rely on case studies, which focus in detail
on one person and the factors that underlie his or her psychological disorder or dis-
orders. For instance, someone noticed that a young patient had a very bad sore throat
prior to developing symptoms of obsessive-compulsive disorder (OCD)—a disorder that
is characterized by frequent and intrusive unwanted thoughts and behaviors that the
individual feels compelled to engage in (we will say more about this in Chapter 7).
Studies that were inspired by this observation found that OCD may sometimes de-
velop from a particular type of streptococcal infection (Swedo et al., 1998), and even-
tually researchers identified pediatric autoimmune neuropsychiatric disorder associated with
streptococcal infection, or PANDAS (Giulino et al., 2002). PANDAS appears to arise,
at least in part, when antibodies that attack the strep bacteria also attack a part of the
brain known as the basal ganglia. Antibiotics that treat the strep infection (leading
to lower levels of antibodies) end up decreasing the OCD symptoms. The discovery
of PANDAS began from a case study. Case 4.1 discusses a case of a young woman
with autism spectrum disorder—a disorder that is diagnosed in childhood and involves
significant problems with communication and social interactions. (We’ll discuss this
disorder in more detail in Chapter 14.)
Risk factors are usually variables that are
associated—correlated—with the later
emergence of psychological disorders. For
instance, soldiers who fought in the Gulf
War in 1991 were more likely to develop
psychological disorders in the next year than
were soldiers deployed elsewhere during that
time period (Fiedler et al., 2006). However, the
presence of risk factors doesn’t guarantee that
a disorder will develop.
A
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Case studies (in studies of
psychopathology)
A research method that focuses in detail on one
individual and the factors that underlie that
person’s psychological disorder or disorders.
CASE 4.1 • FROM TH E OUTSIDE: Menstruation-Related Exacerbation
of Autism Symptoms
A 19-year-old nonverbal girl [with autism spectrum disorder and severe intellectual dis-
ability (previously called mental retardation)] was referred for treatment of aggression
and SIB [self-injurious behavior]. At onset of menarche at age 12, agitation dramatically
increased. Her mother recorded cyclical behavioral changes along with her menses. Before
each menses, she became withdrawn, apathetic, quiet, irritable, and easily agitated with
increased tantrums and appeared anxious. She also had a cyclical amplification of baseline
autistic behaviors: stereotypies (rocking), sensitivity to changes, and sensitivity to noise.
New-onset cyclical handbiting was so intense that scarring resulted, and cyclical aggres-
sion directed at objects and others occurred several times daily. Teacher reports recorded
and corroborated aggression and SIB that corresponded to the days before the onset of
her menstrual period. Within 1 day of menstrual onset, mood symptoms and SIB abated.
Neither behavioral therapy with positive or negative reinforcement nor treatment with
acetaminophen or ibuprofen yielded improvement. Treatment with paroxetine [Paxil, an
SSRI medication] 20 mg every morning resulted in improvement of premenstrual mood
symptoms and premenstrual exacerbated SIB. On discontinuation of paroxetine on two
distinct occasions, cyclical mood symptoms, aggression, and SIB returned.
(Lee, 2004, p. 1193)
96 C H A P T E R 4
Uses and Limits of Case Studies
A case st udy focuses on a par t icu lar ind iv idua l in deta i l, of ten descr ibing
neurological, psychological, and social factors: Such a study often provides informa-
tion about a person’s medical and family history, as well as his or her culture and the
context of the problem. Mental health professionals use case studies for a variety of
reasons:
• to demonstrate some aspect of diagnosis, etiology, or treatment;
• to provide support for (or evidence against) a particular hypothesis or theory; and
• to train other mental health professionals, who are given case studies and must then
propose diagnoses and appropriate treatments.
Mental health clinicians and researchers must resist the temptation to generalize
from a single case: Don’t assume that the findings from a case study necessarily can
be extended to other similar cases, let alone to the population at large. Sometimes
the findings can be generalized, but sometimes they cannot be; every individual is
unique, and a person’s particular history presents many possible confounding factors.
In addition, if a case study relies on correlations among variables, this method—as
usual—prevents us from drawing conclusions about causality.
Single-Participant Experiments
Case studies are not necessarily limited to describing the values of variables and rela-
tions among them. In some situations, clinicians and researchers can actually perform
experiments with only a single case. For instance, a researcher could treat someone
suspected of having PANDAS-related OCD with antibiotics and determine whether
the OCD symptoms improved. Experiments with only a single case are called
single-participant experiments.
Single-participant experiments may rely on an ABAB design, which is often
used to measure change in target behaviors as a result of some treatment. In many
cases, a single participant receives both conditions: a baseline condition with no
treatment (the first phase A of the ABAB design) and the treatment (phase B of
the ABAB design) (Drotar, 2006). The data for the target behavior in the base-
line phase (A) are compared to the data for that behavior in the next phase (B).
In the second A phase, the treatment in phase B is withdrawn, and researchers
can determine whether, or how quickly, the person’s targeted behavior returns to
baseline (for example, withdrawing behavior modification treatment and observ-
ing what happens with extinction). This second A phase addresses the question
“Will any behavior change from the previous phase persist once treatment is with-
drawn? ” The treatment is then presented again in the second B phase, which es-
sentially should obtain an effect related to the effect the first time the treatment
was presented.
Like case studies, single-participant experiments consider only one individual, so
the results can be specific to that individual and based on neurological, psychological,
or social factors that may not apply to others, or at least not in the same combination.
When researchers publish the results of single-participant experiments, they often
wish to inform clinicians about possible interventions that might work for patients
with the same problem and in similar circumstances.
Meta-Analysis
Despite the best efforts of researchers to minimize confounds, the results of any
one study must be taken with a grain of salt; it’s not clear whether researchers
would obtain comparable results if the study were undertaken in somewhat dif-
ferent circumstances. Moreover, if a study’s results are not statistically significant,
it may simply indicate that not enough participants were tested. Meta-analysis
Single-participant experiments
Experiments with only a single participant.
Meta-analysis
A research method that statistically combines
the results of a number of studies that address
the same question to determine the overall
effect.
Research Methods 97
TABLE 4.1 • Research Methods in Psychopathology
Research method Important feature(s) Drawback(s)
Experimental design
Use of independent and dependent variables and
random assignment allows researchers to infer cause
and effect
Most etiological factors that contribute to psychopathology
cannot be studied with experiments (but experiments are often
used to study the effects of treatment).
Quasi-experiments
Used when it is possible to identify independent
and dependent variables, but random assignment of
participants to groups is not possible; researchers can
still infer cause and effect
Because random assignment isn’t possible, possible
confounds are difficult to eliminate.
Correlational research
Used when it is not possible to manipulate independent
variables such as etiological factors; researchers can
examine relationships between variables
Results indicate only related factors, not causal factors.
Case studies
Often descriptive, but can use various research
methods applied to a single participant
Caution must be exercised in generalizing from the sole
participant to others; there are many possible confounding
factors.
Single-participant
experiments
An experiment with one participant (and so random
assignment isn’t possible); cause and effect can be inferred
Caution must be exercised in generalizing from the sole
participant to others; there are many possible confounding
factors.
Meta-analysis
A statistical analysis that combines the results of a
number of studies that examine the same general
question to determine the overall effect
It is difficult to estimate the number of studies that failed to
find an effect and thus were not published and not included
in the analysis; the studies analyzed are often not of equal
quality but their results are nevertheless weighted equally in
the analysis.
is a research method that statistically combines the results of a number of stud-
ies that address the same question. This strategy can be especially valuable when
some studies show an effect but others do not (Rosenthal, 1991). Because a meta-
analysis increases the size of the overall data set, it can help to determine whether
or not certain variables are related; a meta-analysis can uncover a relationship
that is not apparent in any single study, which considers only a single sample from
a particular population. In many cases, when studies are considered together in a
single meta-analysis, the effect emerges loud and clear. However, a meta-analysis
is only as good as the quality of the studies that go into it; if studies are poorly
designed or conducted, the conclusions from a meta-analysis of them will be
shaky. Table 4.1 provides a summar y of the different research methods we’ve
discussed.
Ethical Guidelines for Research
We’ve mentioned several times that it would not be ethical to conduct certain
kinds of experiments, but how do researchers decide which research studies are
ethical and which are not? To address this question, psychologists have devel-
oped ethical guidelines for research, which are part of the overall ethical code for
psychologists. For instance, before someone participates in a study, the investiga-
tor must provide information describing the study, as outlined in Table 4.2. If
a person decides to participate after reading the information, he or she signs an
informed consent form. By signing, the person acknowledges that he or she under-
stands what is involved in the study and agrees to participate, knowing that he or
she can withdraw from the study at any point (American Psychological Associa-
tion, 2002).
TABLE 4.2 • Information Provided for
Obtaining Informed Consent
When obtaining informed consent from
participants, a researcher must give
participants the following information:
(1) the purpose of the research, expected
duration, and procedures;
(2) their right to decline to participate and
to withdraw from the research once
participation has begun;
(3) the foreseeable consequences of
declining or withdrawing;
(4) reasonably foreseeable factors that may
be expected to influence their willingness
to participate such as potential risks,
discomfort, or adverse effects;
(5) any prospective research benefits;
(6) limits of confidentiality;
(7) incentives for participation; and
(8) whom to contact for questions about
the research and research participants’
rights.
Source: Copyright © American Psychological Association.
For more information, see the Permissions section.
98 C H A P T E R 4
Another ethical guideline for research is that investigators must debrief partici-
pants after a study is over. They must ask each participant about his or her experi-
ence, particularly about any negative aspects of the experience (in part so that the
study can be adjusted to minimize possible negative experiences for future partici-
pants). Investigators must also clear up any misconceptions that the participant may
have about the study (American Psychological Association, 2002).
In addition, agencies that fund research on psychopathology and treatment
require that the study be reviewed and approved by an institutional review board
(IRB) in the setting that hosts the study (e.g., hospital, university, or clinic). The
IRB is composed of scientists, clinicians, and members of the community at large.
The board evaluates each study’s possible risks and benefits, and then decides whether
the study should be approved. This serves as another check on any ethical issues that
might arise while a study is being conducted or afterward.
Thinking Like A Clinician
Dr. Xavier treats people with compulsive gambling; she also conducts research on people with this
disorder. Based on her experience, she believes that people who begin gambling compulsively in
their teens and early 20s have a different type of problem than those who begin gambling com-
pulsively in their 40s or later. What type of research design would you suggest she use (experi-
mental, quasi-experimental, or correlational) to evaluate her hypothesis, and why? What might
be some confounding variables she should try to control? What types of information would you
want to know before generalizing from her results to other people with compulsive gambling?
If a researcher wanted to determine the extent to which being in a bar leads former alcoholics (who have stopped drinking) to relapse, which
of the following designs (conveyed in the corresponding photos) would likely be considered unethical by an IRB—the bartender offers the
participant a non-alcoholic drink (the photo on the left), or the bartender offers the participant an alcoholic drink (the photo on the right)?
Answer: The photo on right: Offering the participant an alcoholic drink rather than soft drink needlessly increases the likelihood that the
participant would relapse and creates too great a risk of harm.
GETTING THE PICTURE
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Research Methods 99
Research Challenges in
Understanding Abnormality
Let’s now examine the hypothesis about the relationship between experiencing a
childhood loss and feeling depressed after a breakup in adulthood. How can we use
the neuropsychosocial approach to understand why breaking up might lead some
people to become depressed?
• We could investigate neurological mechanisms by which early loss, associated with
helplessness, might make people more vulnerable to later depression.
• We could investigate psychological effects resulting from early loss, such as
problems with emotional regulation.
• We could investigate social mechanisms, such as how economic hardships arising
from the early loss created a higher baseline of response to daily stress.
• And, crucially, we could propose ways in which these possible factors might inter-
act with one another. For example, perhaps daily financial stress not only increases
the degree of worrying about money but such worrying in turn changes neuro-
logical functioning as well as social functioning (as preoccupying financial worries
alter social interactions).
Whatever type of factors researchers investigate, each type comes with its own
challenges, which affect the way a study is undertaken and which limit the conclu-
sions that can be drawn from a study’s results (Slavich et al., 2011). In what follows,
we examine the major types of challenges to research on the nature and causes of
abnormality from the neuropsychosocial perspective.
Challenges in Researching Neurological Factors
DSM-5 does not generally consider neurological factors when assigning diagnoses,
but many researchers are exploring the possible role of neurological factors in causing
psychological disorders. In fact, current findings about neurological factors are com-
ing to play an increasingly large role in treatment.
With the exception of genetics, almost all techniques that assess neurological fac-
tors identify abnormalities in the structure or function of the brain. This assessment
is done directly (e.g., with neuroimaging) or indirectly (e.g., with neuropsychologi-
cal testing or measurements of the level of stress hormones in the bloodstream). Such
abnormalities are associated (correlated) with specific disorders or symptoms. For
instance, people with schizophrenia have larger-than-normal ventricles (the fluid-
containing cavities in the brain), and other areas of the brain are correspondingly
smaller (Vita et al., 2006). Like all other correlational studies, the studies that revealed
the enlarged ventricles cannot establish causation; for example, this finding does not
specify whether schizophrenia arises because of the effects of this brain abnormality,
whether schizophrenia creates these abnormalities, or whether some third variable is
responsible for the brain abnormality and for the mental disorder. Another limitation
of research using neuroimaging is that we do not yet have a complete understanding
of what different parts of the brain do. Thus, researchers cannot be sure about the
implications of abnormalities in the structure or the functioning of any specific brain
structure.
Nevertheless, the outlook is encouraging. Researchers do know a considerable
amount about what specific parts of the brain do, and they are learning more every
day. Also, they can use other techniques in combination with neuroimaging to learn
which brain areas may play a role in causing or contributing to certain disorders.
We will have more to say about neuroimaging research in subsequent chapters.
100 C H A P T E R 4
Challenges in Researching Psychological Factors
Scientists who study neurological factors examine the difficulties with the biological
mechanisms that process information or that give rise to emotion. In contrast, scien-
tists who study psychological factors examine specific mental contents, mental pro-
cesses, behaviors, or emotions. Information about psychological factors typically is
obtained from patients’ self-reports, from reports by others close to patients, or from
direct observations.
Biases in Mental Processes That Affect Assessment
Assessing mental contents, emotions, and behaviors via self-report or report by oth-
ers can yield inaccurate information because of biases in what people pay attention
to, remember, and report. Sometimes beliefs, expectations, or habits bias how
participants respond, consciously or unconsciously. For instance, people who have
anxiety disorders are more likely than others to be extremely attentive to stimuli that
might be perceived as a threat (Cloitre et al., 1994; Mogg et al., 2000). In contrast,
people with depression do not have this particular bias but tend to be biased in what
they recall; they are more likely than people who are not depressed to recall unpleas-
ant events (Watkins, 2002; Wisco & Nolen-Hoecksema, 2009). In fact, researchers
have found that people in general are more likely to recall information consistent
with their current mood than information that is inconsistent with their current
mood (referred to as mood-congruent memory bias; Teasdale, 1983).
Research Challenges with Clinical Interviews
Patients’ responses can be affected by
whether they are asked questions by an
inter viewer or receive them in writ-
ing (see Figure 4.3). Consider a study in
which participants were asked questions
about their symptoms of either OCD or
social phobia. When the questions were
first asked by a clinician as part of an in-
terview, participants tended not to report
certain avoidance-related symptoms that
they later did report on a questionnaire.
In contrast, when participants completed
the questionnaire f irst, they reported
these symptoms both on the question-
naire and in the subsequent interview (Dell’Osso et al., 2002).
Moreover, when interviewing family members or friends about a patient’s behavior,
researchers must keep in mind that these people may have their own biases. They may
pay more attention to, and so be more likely to remember, particular aspects of a patient’s
behavior, and they may have their own views about the causes of the patient’s behavior
(Achenbach, 2008; Kirk & Hsieh, 2004). For example, when assessing children, research-
ers sometimes rely heavily on reports from others, such as parents and teachers; however,
these individuals often do not agree on the nature or cause of a child’s problems (De Los
Reyes & Kazdin, 2004).
Research Challenges with Questionnaires
In psychopathology research, administering questionnaires is a relatively inexpen-
sive way to collect a lot of data quickly. However, questionnaires must be designed
carefully in order to avoid various biases. For example, one sort of bias arises when a
FI G U RE 4.3 • How the Question Is
Asked Affects the Answer Patients
may respond differently to a question,
depending on whether they read it or are asked
it by an interviewer (Dell’Osso et al., 2002).
Research Methods 101
range of alternative responses are presented. Some questionnaires provide only two
choices in response to an item (“yes” or “no”), whereas other questionnaires give
participants more than two choices (such as, “all the time,” “frequently,” “some-
times,” “infrequently,” or “never”). With more choices come more opportunities
for bias: Twice a week might be interpreted as frequent by one person and infre-
quent by another. To reduce the effects of such bias, some questionnaires—such as
the Posttraumatic Diagnostic Scale (Foa et al., 1997)—define the frequency choices
in terms of specific numerical values (such as having “frequently” defined as three
times a week).
In addition, the range of values on a scale is important. For example, consider
the findings obtained when people were asked to rate how successful they have
been in life. When asked to respond on a rating scale with numbers from 25 to
15, like this:
not at all
successful
extremely
successful
25 15
34% reported having been highly successful in life. When asked to respond on a scale
with numbers from 0 to 10, like this:
not at all
successful
extremely
successful
0 110
only 13% reported having been highly successful in life (Schwarz et al., 1991).
Response bias is another problem to avoid when designing questionnaires.
Response bias refers to a tendency to respond in a particular way, regardless of
what is being asked by the questions. For instance, some people, and members of
some cultures in general, are more likely to check “agree” than “disagree,” regardless
of the content of the statement ( Javeline, 1999; Welkenhuysen-Gybels et al., 2003).
This type of response bias, called acquiescence, can be reduced by wording half the
items negatively. Thus, if you were interested in assessing self-reported shyness in a
questionnaire, you might include both the item “I often feel shy when meeting new
people” and the item “I don’t usually feel shy when meeting new people,” which is
simply a negative rewording of the first item.
Another type of response bias is social desirability: answering questions in a
way that the respondent thinks makes him or her look good in a way that he or she
thinks is socially desirable, even if the answer is not true. For instance, some people
might not agree with the statement “It is better to be honest, even if others don’t like
you for it.” However, they may think that they should agree and respond accordingly.
In contrast to a social desirability bias, some people answer questions in a way that
they think makes them “look bad” or look worse than they actually are. To com-
pensate for these biases, many personality inventories have a scale that assesses the
participant’s tendency to answer in a socially desirable or falsely symptomatic man-
ner. This scale is then used to adjust (or, in the language of testing, to “correct”) the
scores on the part of the inventory that measures traits.
Challenges in Researching Social Factors
Information obtained from and about people always has a context. For research on
psychopathology, a crucial part of the context is defined by other people. Social fac-
tors arise from and characterize the setting (such as a home, hospital, outpatient clinic,
Response bias
The tendency to respond in a particular way,
regardless of what is being asked by the
question.
Social desirability
A bias toward answering questions in a way
that respondents think makes them appear
socially desirable, even if the responses are
not true.
102 C H A P T E R 4
or university), the people administering the study, and the cultural context writ
large. Challenges to conducting research on social factors that affect psychopathology
include the ways that the presence or behavior of the investigator and the beliefs and
assumptions of a particular culture can influence participants’ responses.
Investigator-Influenced Biases
Like psychological factors, social factors are often assessed by self-report (such as
patient’s reports of financial problems), reports by others (such as family members’
descriptions of family interactions or of a patient’s behavior), and direct observation.
Along with the biases we’ve already mentioned, the social interaction between inves-
tigator and participant can affect these kinds of data.
Experimenter Expectancy Effects
Experimenter expectancy effect refers to the investigator’s intentionally or
unintentionally treating participants in ways that encourage particular types of
responses. The experimenter expectancy effect is slightly misnamed: It applies not
only to experiments but to all psychological investigations in which an investigator
interacts with participants. For instance, suppose that you are interviewing patients
about their symptoms. It’s possible that you might ask certain types of questions
(such as about their social lives) with a particular tone of voice or facial expression,
unintentionally suggesting the type of answer you hope to hear. Participants might,
consciously or unconsciously, try to respond as they think you would like, perhaps
exaggerating certain symptoms a bit. Such a social interaction can undermine the
validity of the study.
To minimize the likelihood of experimenter expectancy effects, researchers often
use a double-blind design: Neither the participants nor the investigator’s assistant
(who has contact with the participants) know the group to which each participant
has been assigned or the predicted results of the study. Moreover, instructions given
to participants or questions asked of them are standardized, so
that all participants are treated in the same way.
Reactivity
Have you ever noticed that you were being watched while you
were doing something? Did you f ind that you behaved some-
what differently simply because you knew that you were be-
ing observed? If so, then you have experienced reactivity—a
behavior change that occurs when one becomes aware of be-
ing observed. When participants in a study know that they are
observed, they may subtly (or not so subtly) change their be-
havior, leading the study to have results that may not be valid.
One way to counter such an effect is to use hidden cameras,
but this may raise ethica l issues—many people (r ight ful ly)
object to being “spied on.”
Cultural Differences in Evaluating Symptoms
Some researchers compare and contrast a given disorder in different cultures,
trying to distinguish universal symptoms from symptoms that are found only in
certain cultures. But assessing psychological and social factors in other cultures
can be challenging. For one thing, many words and concepts do not have ex-
act equivalents across languages, making full translation impossible. And even
when two cultures share a language, the meaning of a word may be different
in each culture. For example, when a comprehensive set of interview questions
was translated into Spanish and administered to residents of Puerto Rico and
Mexico, 67% of the questions had to be changed because the meanings of some
Experimenter expectancy effect
The investigator’s intentionally or
unintentionally treating participants in ways
that encourage particular types of responses.
Double-blind design
A research design in which neither the
participant nor the investigator’s assistant
knows the group to which specific participants
have been assigned or the predicted results of
the study.
Reactivity
A behavior change that occurs when one
becomes aware of being observed.
P
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ew
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Although reactivity may be decreased by
observing participants via video camera, they
can still be aware that they are being observed
by others and modify their behavior accordingly.
Research Methods 103
of the Spanish words were understood differently by the two populations (Kihl-
strom, 2002b).
In addition, members of different cultures may have different response biases.
For instance, the Japanese consider it rude to say, “No,” so we must be suspect of re-
sults from Japanese surveys that require Yes/No responses. Sampling biases may also
vary across cultures. For example, women may be underrepresented in samples from
certain countries in the Middle East.
Thinking Like A Clinician
Suppose you are reading about a psychologist who conducts research that is aimed at better
understanding people who have pyromania—the intense urge to start fires—and why they
start fires. The participants can come from two groups: those who’ve been arrested for arson
and those who have interacted in a chat room for people with urges to start fires. To collect
data, the researcher could either have participants complete an anonymous survey online or
arrange to interview them over the phone. What biases might uniquely affect each method,
and what biases might affect both? How could a researcher try to minimize these biases?
Suppose some participants agree to have their brains scanned while they imagined lighting
fires: How might an investigator use such neuroimaging information?
Researching Treatment
Let’s say that your interest in depression that follows breakups, plus your experiences
at the counseling center helping students like Carlos, have led you to develop a new
short-term treatment. In this treatment, which you have named “grief box therapy,”
you encourage patients to create “grief boxes”—boxes into which they place remind-
ers of their recently ended relationships and objects that symbolize their feelings of
loss and hopelessness. You—and others—will want to know whether your treatment
is effective; is using grief boxes better for treating depression (specifically the sort fol-
lowing a breakup) than doing nothing? Is it better than other treatments?
Research on treatment has challenges above and beyond those we’ve already
discussed for research on psychopathology. And such research faces different chal-
lenges, depending on whether the target of treatment is neurological, psychological,
or social factors.
Researching Treatments That Target Neurological
Factors
Researchers and clinicians want to answer several questions when a new medication
is developed, when an existing medication is used in a new way (to treat different
symptoms), or when a new biomedical procedure is developed:
• Is the new treatment more effective than no treatment?
• If a treatment is effective, is it because of its actual properties (such as a medication’s
particular ingredients) or because of patients’ expectations about what the treat-
ment will do?
• Is the treatment more effective than other treatments currently used for those
symptoms or problems?
• What are the treatment’s side effects, and are they troubling enough that patients
tend to stop the treatment? How does this dropout rate compare to that for the
other treatments?
To assess a treatment, researchers first need to determine what specific vari-
ables should be measured and to define what it means to be “effective.” Research
104 C H A P T E R 4
on treatment frequently relies on an experimental or quasi-experimental design;
in such studies, the independent variables might be the type of treatment, a spe-
cific technique, or type or dose of medication. And the dependent variables (the
things measured) might be any of several variables, such as neural activity, spe-
cific mental contents, behavior, or family functioning. These variables are of-
ten related to the symptoms listed in the DSM-5 criteria for the disorder under
investigation.
Drug Effect or Placebo Effect?
One way to determine whether a treatment is effective is to compare it to no treat-
ment. If people receiving the treatment are better off than those who don’t receive
any treatment, the treatment may have made the difference. But perhaps patients
improve after taking a medication not because of the properties of the medication
itself but because they expect to improve after taking it. In fact, many studies have
confirmed that expecting a treatment to be helpful leads to improvement, even if the
patients don’t receive any actual treatment (Colloca & Miller, 2011; Kirsch, 2010;
Kirsch & Lynn, 1999).
The best way to discover whether a medication is effective is to give a group of
participants a placebo, an inert substance or a procedure that itself has no direct medi-
cal value. Often, a placebo is simply a sugar pill. A positive effect of such a medically
inert substance or procedure is called a placebo effect. If patients who are given a
sugar pill show the same improvement as patients who are given the pill with active
ingredients, then a researcher can infer that the medication itself is not effective and
that its apparent benefit is a result of the placebo effect.
The fact that people who suffer from certain disorders, including depres-
sion, sometimes improve following a placebo treatment (Kirsch, 2010; Kirsch et
al., 2002) does not mean that their problem was imaginar y or that they should
throw away their medication. Rather, it seems that—for some people and for
some disorders—the hope and positive expectations that go along with taking
a medication (or undergoing a procedure) allow the body to mobilize its own
resources to function better (Benedetti, 2009, 2010; Kirsch & Lynn, 1999; Scott
et al., 2008).
Dropouts
On average, more than half of those who begin a treatment that is part of a research
study do not complete the treatment—they drop out of the study (Kazdin, 1994;
West, 2009); this reduction in the number of research participants during a study is
called attrition. When attrition in a research study is different for different demo-
graphic groups (such as men versus women, younger people versus older ones, or
people of different races), researchers can’t easily draw definitive conclusions about
how well the treatment would have worked for members of all the groups (Kendall
et al., 2004; Lambert & Ogles, 2004).
Researching Treatments That Target Psychological
Factors
Many of the research issues that arise with biomedical treatments also arise in research
on treatments that target psychological factors. In addition, as shown in Table 4.3, re-
search on treatments that target psychological factors may be designed to investigate
which aspects of therapy in general, or of particular types of therapy—such as the
grief box therapy—are most helpful. In this section we consider factors that influence
research on treatments.
The placebo effect can be strengthened or
weakened by the outward qualities of the
placebo: Taking more placebo pills generally
has a greater effect; capsules do a better
job than pills; and injections do better than
capsules. And (placebo) pills that are reported
to be more expensive are more effective than
“less expensive” ones (Waber et al., 2008).
©
N
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Placebo effect
A positive effect of a medically inert
substance or procedure.
Attrition
The reduction in the number of participants
during a research study.
Research Methods 105
Common Factors and Specific Factors
Just as placebos can provide relief even though they lack medically beneficial in-
gredients, the ver y act of seeing a therapist or counselor—or even setting up a
meeting with one—may provide relief for some disorders (regardless of the specific
techniques or theoretical approach of the therapist or counselor). Such relief may
result from, at least in part, common factors, which are helpful aspects of therapy
that are shared by virtually all types of psychotherapy. According to results from
numerous studies (Lambert & Ogles, 2004; Wampold, 2010), common factors can
include:
• opportunities to express problems;
• some explanation and understanding of the problems;
• an opportunity to obtain support, feedback, and advice;
• encouragement to take (appropriate) risks and achieve a sense of mastery;
• hope; and
• a positive relationship with the therapist.
Common factors, and certain patient characteristics—such as being motivated
to change (Bohart & Tallman, 2010; Clarkin & Levy, 2004)—can contribute more
to having a positive outcome from therapy than the specific techniques used. If the
grief box therapy were effective, it might be because of such common factors and not
something unique to your particular method.
The existence of common factors creates a challenge for researchers who
are interested in determining the benefits of a particular t ype of treatment or
technique. The characteristics that give rise to these unique benefits of a specific
type of treatment are known as specific factors. For instance, when researching
grief box therapy, you might want to investigate whether the process of creating
the grief box provides benefits above and beyond the common factors that any
therapy provides.
In fact, research has shown that common factors alone may not be sufficient to
produce benefits in therapy for some disorders (Elliott et al., 2004; Kirschenbaum &
Jourdan, 2005; Lambert, 2004); at least for some disorders, specific factors play a
key role in treatment. The leftmost column in Table 4.3 notes specific factors—the
therapy variables—that are the subject of research targeting psychological treatments.
(In subsequent chapters, we will discuss research on treatments for specific disorders;
such studies typically examine specific factors.)
Common factors
Helpful aspects of therapy that are shared by
virtually all types of psychotherapy.
Specific factors
The characteristics of a particular treatment
or technique that lead it to have unique
benefits, above and beyond those conferred
by common factors.
TABLE 4.3 • Treatment-Related Variables
Therapy variables Patient variables Therapist variables
Patient–therapist interaction
variables
• Theoretical orientation
• Specific techniques used
• Level of motivation and ability to
change
• Belief in the ability of treatment to
help
• Community resources available
(social and financial support)
• Preferred style of coping and
relating to others
• Preferred treatment focus: on
symptoms or their meaning
• Personality traits
• Enthusiasm for and belief in the
treatment
• Usual style of interacting (such
as supportive or challenging)
• Treatment focus: on symptoms
or on their meaning
• Empathic ability
• Personality traits
• Experience with the particular
type of treatment
• Structure of the relationship
( therapist as expert vs. therapist
as coach)
• Fit between patient’s and thera-
pist’s personalities
• Fit between patient’s and thera-
pist’s treatment focus (symp-
toms vs. their meaning)
• Sense of alliance between
patient and therapist
106 C H A P T E R 4
Is Therapy Better Than No Treatment?
Researchers have questioned whether people actually improve more by receiv-
ing therapy than they would have improved if they hadn’t received any treatment.
To address this question, researchers randomly assign participants to one of two
groups: “treatment” and “no treatment.” However, participants in the “no treat-
ment” group are often assigned to a waiting list for treatment (which is ethically
preferable to not providing any treatment at all), and thus this group is often called
a wait-list control group (Kendall et al., 2004, Lambert & Bergin, 1994). Researchers
usually assess the dependent variable, such as level of symptoms, in both groups at
the beginning of the study, before treatment begins—this is their baseline assessment.
Then, researchers assess the same variables again after the treatment period (for the
wait-list control group, this means assessing symptom level after the same duration
of time as that over which the treatment group received treatment); this is called the
outcome assessment. Researchers then compare the results of the two groups, and may
also assess the variables at a later follow-up point, called a follow-up assessment (see
Figure 4.4).
Treatment group
Wait-list control group
TIME
Baseline
assessment
Outcome
assessment
Follow-up
assessment
Participants
randomly
assigned
randomly
assigned
FI G U RE 4.4 • Comparing a Treatment Group to a Wait-List Control
Group Participants are randomly assigned to one of two groups, a treatment group and a
wait-list control group (although a study could have more than two groups). Generally, the
dependent variables, such as intensity of symptoms, are assessed before the treatment period
begins, to obtain a baseline. After treatment ends (or after the equivalent number of weeks
for the wait-list control group), the dependent variables are again assessed (and may also be
assessed later for follow-up) and the data from the two groups are compared.
Alternatively, instead of (or in addition to) a “no treatment” or wait-list control
group, researchers may use a placebo control group, the members of which meet with
a “therapist” with the same frequency as the members of the treatment group. The
“placebo therapist” refrains from using any of the active treatment techniques em-
ployed in the treatment group, but patients still receive attention and some level of
support. For a study of your grief box therapy, a placebo control group might consist
of patients who meet with therapists who listen to their concerns or complaints—
without grief boxes, social support, or any other specific interventions.
With either type of control group—wait-list or placebo—the symptoms of mem-
bers of the control group might diminish simply with the passage of time. Thus, the
crucial comparison is not whether people in the treatment group got better but rather
how much more they improved than did the people in the control group.
Researchers have conducted such studies for over half a century. How did they
answer the question of whether therapy works? With a resounding “yes.” Therapy
really does make a difference (Lambert & Ogles, 2004; Wampold, 2010). And, not
surprisingly, treatment shows a larger effect when a treatment group is compared to a
wait-list control group than when a treatment group is compared to a placebo group,
Research Methods 107
which highlights the beneficial effects of common factors (Lambert & Ogles, 2004;
Roth & Fonagy, 2005; Wampold, 2010).
But what does it really mean to say that therapy works? The results must have
clinical significance, which means that they change a person’s life in meaningful, prac-
tical ways. Assessments of clinical significance may be based on the patients’ own
perceptions, on observations of friends and family members of the patients, or on the
therapists’ judgment.
Is One Type of Therapy Generally More Effective Than Another?
With the advent of behavior therapy in the 1960s, some researchers asked whether
one type of therapy is generally more effective than another. The initial results of
such research were surprising: No type of therapy appeared to be more effective
than another. This first generation of research on specific treatments found that, in
general, any type of the treatments of psychological disorders led to better outcomes
than no treatment, and no single treatment was superior to others. The latter find-
ing became referred to as the Dodo bird verdict of psychotherapy (Luborsky et al.,
1975), after the character in the book Alice’s Adventures in Wonderland who states:
“ Everybody has won, and all must have prizes.”
However, by the 1980s, a second generation of such research had begun, and re-
searchers refined the methods and procedures they used to provide therapy and assess
its outcome. Let’s briefly consider key advances in how researchers study the effects
of various psychotherapies.
Randomized Clinical Trials
Different types of therapy are in fact better suited than others for treating different
disorders. This became clear during the second generation of research, which began
with the Treatment of Depression Collaborative Research Program study (TDCRP;
Elkin et al., 1985). This study used a research design analogous to the design used
to measure the effect of a medication on symptoms of a medical disorder; this re-
search design is referred to as a randomized clinical trial (RCT; also referred to
as randomized controlled trial). RCTs have at least two groups—a treatment group and
a control group (usually a placebo control)—and participants are randomly assigned
to the groups (Kendall et al., 2004). RCTs may also involve patients and therapists at
multiple sites in a number of cities.
RCTs are the best way to evaluate therapies because they use the scientif ic
method to identify the specific factors that underlie a beneficial treatment. The inde-
pendent variable is often the type of treatment or technique, as it was in the TDCRP,
but it can be any other variable listed in Table 4.3. The dependent variable is usu-
ally some aspect of patients’ symptoms—such as frequency or intensity—or quality
of life.
RCTs generally require therapists to base their treatments on detailed manu-
als that provide session-by-session guidance and specify techniques to be used with
patients. RCTs provide brief therapy, typically from 6 to 16 sessions. Manual-based
treatment ensures that all therapists who use one particular approach provide similar
therapy that is distinct from other types of therapy (Kendall et al., 2004; Nathan,
Skinstad, & Dolan, 2000).
The TDCRP was designed to compare the benefits of four kinds of treat-
ment for depression given over 16 weeks: interpersonal therapy (IPT, interper-
sonal therapy, a time-limited therapy that focuses on relationships; we will discuss
this treatment in more detail in Chapter 5), cognitive-behavioral therapy (CBT),
the antidepressant medication imipramine (which was widely used at the time
of the study) together with supportive sessions with a psychiatrist, and a pla-
cebo medication together with supportive sessions with a psychiatrist. Various
Randomized clinical trial (RCT)
A research design that has at least two
groups—a treatment group and a control
group (usually a placebo control)—to which
participants are randomly assigned.
Initially, studies designed to test the overall
superiority of one form of psychotherapy over
another did not find any one type of therapy
to be more effective than any other. This
finding has been called the Dodo bird verdict,
in reference to the Dodo bird’s proclamation in
Alice’s Adventures in Wonderland: “Everybody
has won, and all must have prizes.” However,
the Dodo bird verdict was based on research
of particular therapies available at that time,
using less rigorous research methods than are
generally used today (Beutler, 2000).
M
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108 C H A P T E R 4
dependent variables were measured. The main results told an interesting stor y:
At the 18-month follow-up assessment, the CBT group had a larger sustained ef-
fect and fewer relapses, especially compared with the imipramine group (Elkin,
1994; Shea et al., 1992). But when the most severely depressed patients in each
group were compared, IPT and imipramine were found to have been more ef-
fective than CBT (Elkin et al., 1995). However, most important in this study,
the qualit y of the “collaborative bond” between therapist and patient (which
was assessed by independent raters who viewed videotapes of sessions) had an
even stronger influence on treatment outcome than did the t ype of treatment
(Krupnick et al., 1996).
The Importance of Follow-up Assessment
It’s one thing for a type of therapy to have an immediate effect, but another—and
usually more important—thing for it to produce enduring change. The TDCRP
study followed patients for over 18 months after treatment ended, but some stud-
ies—because of f inancial or logistical constraints—do not make any follow-up
assessment. This is unfortunate because one type of treatment may be more ben-
eficial at the end of therapy, but those patients may have a higher rate of relapse a
year later, leaving the patients in another treatment group better off in the long run
( Kendall et al., 2004).
Allegiance Effect
Another issue in RCT research is the allegiance effect, in which studies conducted
by investigators who prefer a particular theoretical orientation tend to obtain data
that support that particular orientation (Luborsky et al., 1999). Specifically, RCT
investigators who support one type of treatment tend to have patients who do better
with that type of treatment, whereas patients in the same study (using the same man-
uals) whose investigators support a different type of treatment tend to do better with
that treatment. This means that even the use of manuals is not enough to control all
types of confounds completely.
Different Therapies for Different Disorders
The bottom line is that a specific type or types of therapy are in general best suited
for treating specific types of disorders. We will discuss which types of therapy are
best for which specific disorders in later chapters of this book. In fact, enough is
now known about the effectiveness of particular types of therapy for particular
disorders that clinicians should have an evidence-based practice; that is, for each pa-
tient, they should pick a treatment or set of techniques that research has shown to
be effective for that patient’s problem. (Such a judgment should also take into ac-
count sociocultural factors, as well as the therapist’s preference for—and training
in—a particular method.)
The Therapy Dose–Response Relationship
Is more treatment related to greater improvement? In other words, is a higher “dose”
of therapy (more sessions) associated with a better “response”? This association be-
tween dose and response is referred to as the dose–response relationship, and
research suggests that the general answer to this question is yes. More sessions are
associated with a better outcome (Hansen, Lambert, & Forman, 2002; Shadish et al.,
2000). In general, patients improve the most during the early phase of treatment
(see Figure 4.5), and they continue to improve, but at diminishing rates, over time
(Lutz et al., 2002). There are individual exceptions to this general pattern; people
with more severe or entrenched problems, such as schizophrenia or personality
disorders, may not show as much benefit in the early stages of therapy but rather may
only improve over a longer period of time.
Should a therapist use aromatherapy—
having patients smell certain plant-based
essential oils—to treat psychological
disorders? Aromatherapy is not an
empirically supported treatment for
psychological disorders (Louis & Kowalski,
2002). This technique is in the realm of
pseudopsychology, where claims are
supported primarily by case studies or poorly
designed studies with few participants, often
without an appropriate control group.
R
u
ss
e
ll
S
ad
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r/
G
e
tt
y
I
m
ag
e
s
Allegiance effect
A pattern in which studies conducted
by investigators who prefer a particular
theoretical orientation tend to obtain data
that supports that particular orientation.
Dose–response relationship
The association between more treatment
(a higher dose) and greater improvement (a
better response).
Research Methods 109
The dose–response relationship is correlational; it does not indicate whether the
increased number of sessions causes the increased response. It is possible that people
who are feeling better during the course of treatment are more eager or more will-
ing to attend additional sessions than those who are not responding as well. If this
were the case, the response would be “causing” the increased dose (increased number
of sessions) (Otto, 2002; Tang & DeRubeis, 1999). Alternatively, both dose and re-
sponse could be affected by some other factor. As noted earlier in this chapter, cor-
relation does not imply causation.
Researching Treatments That Target Social Factors
Research on treatment also may investigate the possible benefits of targeting so-
cial factors or the ways in which treatment may be affected by the larger social
context.
A curious finding invites speculation:
People in the eastern part of the United
States remain in treatment longer than
those in the western part (“Fee, Practice,
and Managed Care Survey,” 2000). This
is merely a correlation. One possible
explanation is that people in the eastern
part have a different definition of
“improvement”; that is, they continue
in treatment until their symptoms
have improved more than those of
their counterparts in the western part
of the country. However, there are other
possible explanations; perhaps you can
think of some.
W
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D
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ty
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G
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y
I
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ag
e
s
FI G U RE 4.5 • The Dose–Response
Relationship Comparing a more
stringent definition of “improvement”
(Figure 4.5a) to a more liberal one
(Figure 4.5b) makes it clear that the exact
criteria for improvement determine the
particular height and shape of the curve for
the dose–response relationship.
Source: Lambert et al., 2001.
(a) Time to recovery
100
90
80
70
60
50
40
P
er
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n
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ie
n
ts
30
20
10
0 5 10 15 20 25
Therapy session
30 35 40 45
(b) Time to improvement
100
90
80
70
60
50
40
P
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n
ta
g
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30
20
10
0 5 10 15 20 25
Therapy session
30 35 40 45
Among 10,000 patients with various
psychological disorders, half attained clinically
significant improvement (that is, recovery)
by the 21st session. Another 25% attained
clinically significant improvement by the 40th
session. However, most people in RCTs, or in
therapy in general, receive far fewer than 40
sessions.
Examining data using a lower standard of
improvement—any positive change that was
stable over time—and including patients who
started out able to function reasonably well
despite their disorder, yields different results:
Half the patients attained this lower standard of
improvement by the 7th session, with another
25% “improved” by the 14th session (Lambert,
Hansen, & Finch, 2001).
110 C H A P T E R 4
Gender and Ethnicity of Patient and Therapist
All types of psychotherapy involve a relationship between two (or more)
people. Therapists and patients may be similar with regard to racial or eth-
nic background and gender, or they may be different. Does such a difference
matter? Research suggests not: Differences between patient and therapist in
ethnicity, gender, and age do not systematically alter how effective therapy is
( Fiorentine & Hillhouse, 1999; Lam & Sue, 2001; Maramba & Hall, 2002).
However, with regard to gender, one study found that women and men
are both less likely to drop out of treatment if they have a female therapist
( Flaherty & Adams, 1998).
Nevertheless, some people prefer a therapist with a similar ethnic or
racial background to their own. For those with a strong preference, such
as some Asian Americans, matching the ethnicity of the patient and thera-
pist may lead to better outcomes ( Sue et al., 1994), and it can result in
lower dropout rates among non-Whites (Fiorentine & Hillhouse, 1999;
Sue et al., 1999).
Research on matching by ethnicity usually involves broad categories,
such as patient and therapist who are both Asian American. However, when
patients prefer a therapist from their own ethnic group, matching them with
a therapist from a broadly similar group may not suffice. A Korean American
patient, for instance, may prefer a Korean American therapist, but if such a
therapist is not available, that patient may not prefer a Chinese American therapist
over a therapist of any other background (Karlsson, 2005).
Culturally Sanctioned Placebo Effects
We’ve seen that placebos can be very powerful. It turns out that different products
and practices may operate as placebos in different cultures. Throughout time and
across cultures, people in the role of healer have used different methods to treat
abnormality—and at least some of these methods may have relied on the placebo
effect. For instance, among the Shona people of Africa, those who have psycho-
logical problems often visit a n’anga (healer), who may recommend herbal rem-
edies or steam baths, or may throw bones to determine the source of a person’s
“ bewitchment.” Once the source is determined, the ill person’s family is told how
to mend community tensions that may have been caused by a family member’s
transgressing in some way (Linde, 2002). These n’anga’s treatments, if effective,
may work because of the placebo effect and the common factors that arise from any
treatment (even a placebo): hope, support, and a framework for understanding the
problem and its resolution.
But members of nonindustrialized societies are not the only ones who are
susceptible to such cultural forces. In Western cultures over the past two de-
cades, people diagnosed with depression who are enrolled in studies to evalu-
ate various medications have responded progressively more strongly to placebos
( Walsh, Seidman, et al., 2002 ). Over that same t wo decades, phar maceutical
companies have increasingly advertised their medications directly to potential
consumers, informing them about the possible benef its of the drugs. It is pos-
sible that the participants in these studies became more likely to believe that
medication will be helpful than were participants 30 years ago, before direct
advertising to consumers. And, in fact, research suggests that expectations that
symptoms will improve may account for the lion’s share of the positive response
to an antidepressant among people w ith depression ( K irsch, 2010 ; K irsch &
Lynn, 1999; Walach & Maidhof, 1999).
Some patients prefer a therapist who shares
their ethnic background, and this common
background may make a patient less likely
to drop out of treatment. However, such
matching does not appear to produce better
treatment outcomes (Beutler et al., 1994;
Garfield, 1994; Lam & Sue, 2001).
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Research Methods 111
Using the Scientific Method to
Understand Abnormality
• Researchers use the scientific method to
understand and study psychopatholog y.
In doing so, they observe relevant phe-
nomena, identif y a question to be an-
swered, develop and test hypotheses that
might answer the question, draw on the
evidence to formulate a reasonable theory,
and test the theory.
• Re s e a rche r s s y s t e m a t ic a l l y m a n ipu –
l a t e one or mor e i nd e p e nd e nt va r i –
a b l e s ( ch a n g i n g o n e a t a t i m e ) a n d
ob ser ve po s s ible ch a n g e s i n t he d e –
p e n d e n t v a r i a b l e ( s ) . R e s e a r c h e r s
note how changes in the independent
variable(s) are accompanied by changes
i n t he dependent va r i able ( s ) . I n a d –
d it ion, re sea rcher s ex a m i ne t he pos-
s i b l e c o n t r i b u t io n o f c o n f o u n d s b y
using control groups or control condi-
tions. To minimize unintentional bias,
t hey r a ndom ly a s sig n pa r t ic ipa nt s to
g roups a nd choose st i mu lu s item s to
m in im ize confound ing s. Exper iments
should have both internal and external
validity.
• When random assignment is not ethical,
desirable, or possible, the researchers may
use a quasi-experimental design.
• Correlational research is used when in-
dependent var iables can not or shou ld
not be manipulated. Such studies allow
researchers to investigate the relationship
between two variables and note whether
a change in one var iable is associated
w ith a change in the other. However,
a correlation does not imply causation;
it only indicates that the two variables
are related.
• Case studies allow clinicians and research-
ers to examine one individual in detail.
However, information from a particular
case may not generalize to others.
• Meta-analysis allows researchers to ag-
gregate the results of a number of related
studies in order to determine the relations
among certain variables.
• Psycholog ists have developed an ethi-
cal code of conduct that lays out guide-
l i nes for resea rch, i nclud i ng that the
research must be approved by an IR B,
informed consent must be obtained from
participants, and participants must be de-
briefed after a study is over.
Research Challenges in
Understanding Abnormality
• Many studies that focus on neurological
factors are correlational and so do not re-
veal how neurological factors may cause
psychological disorders.
• Researchers must take care in phrasing
questions in order to minimize various
types of biases.
• Challenges in studying social factors can
create challenges in studying other types
of factors. Such challenges include exper-
imenter-influenced biases, such as experi-
menter expectancy effects and reactivity.
Researching Treatment
• W hen studying medication, a placebo
effect—rather than a true drug effect—
may influence the results. Attrition rates
can also distort the apparent effects of a
treatment.
• A treatment may be effective because of
common factors, as wel l as because of
SUMMING UP
Ethical Research on Experimental Treatments
Any research on treatment conducted by a psychologist is bound by the ethical guide-
lines for research and usually must be approved by an IRB, discussed earlier in the
chapter. As shown in Table 4.4, research on a new type of treatment—an experimental
treatment such as your grief box therapy—is subject to additional guidelines because
the researchers may not be aware of some of the risks and benefits of the new treat-
ment at the outset of the study.
Thinking Like A Clinician
Based on a survey, County Community College has found that 23% of its first-year students
have anxiety or depression severe enough to meet the DSM-5 criteria. The college would
like to institute a treatment program for these students. In fact, the staff at the counsel-
ing center plans to conduct a research study and offer several different types of treatment:
medication (if appropriate), CBT with an individual therapist, and CBT in group therapy. Stu-
dents can sign up for whichever type of treatment they prefer and can even receive more
than one type of treatment. The results will be recorded and used to guide how treatment is
provided in the future. Is this study a randomized clinical trial? Why or why not? What are
some potential problems with the research design of this study? To learn whether each of
the treatments is helpful to students, what questions should be asked of the students before
and after the study?
TABLE 4.4 • Ethical Guidelines for
Research on Experimental
Treatments
Psychologists conducting research on
experimental treatments must clarify to
participants at the outset of the research:
(1) the experimental nature of the treatment;
(2) the services that will or will not be
available to the control group(s) if
appropriate;
(3) the means by which assignment to
treatment and control groups will be
made;
(4) available treatment alternatives if an
individual does not wish to participate
in the research or wishes to withdraw
once a study has begun; and
(5) compensation for or monetary costs of
participating.
Source: Copyright © American Psychological Association.
For more information, see the Permissions section.
112 C H A P T E R 4
More Study Aids
For additional study aids related
to this chapter, including quizzes
to make sure you’ve retained
everything you’ve learned and a
Student Video Activity exploring
how researchers conducted an
experiment on the placebo effect,
go to: www.worthpublishers.
com/launchpad/rkabpsych2e.
Masterfile
Key Terms
Scientific method (p. 88)
Data (p. 88)
Replication (p. 88)
Hypothesis (p. 89)
Theory (p. 89)
Predictions (p. 89)
Experiments (p. 90)
Independent variable (p. 90)
Dependent variable (p. 90)
Confounding variables (p. 91)
Control group (p. 91)
Bias (p. 92)
Random assignment (p. 92)
Sampling bias (p. 92)
Population (p. 92)
Sample (p. 92)
Internal validity (p. 92)
External validity (p. 93)
Correlation (p. 93)
Correlation coefficient (p. 94)
Statistically significant (p. 94)
Epidemiology (p. 94)
Longitudinal studies (in studies of
psychopathology) (p. 95)
Case studies (in studies of
psychopathology) (p. 96)
Single-participant experiments (p. 97)
Meta-analysis (p. 97)
Response bias (p. 102)
Social desirability (p. 102)
Experimenter expectancy effect (p. 103)
Double-blind design (p. 103)
Reactivity (p. 105)
Placebo effect (p. 105)
Attrition (p. 105)
Common factors (p. 106)
Specific factors (p. 106)
Randomized clinical trial (RCT) (p. 108)
Allegiance effect (p. 109)
Dose–response relationship (p. 109)
specific factors unique to that treatment.
Control groups can allow researchers to
examine specif ic factors and to rule out
possible effects of some confounding vari-
ables. In general, therapy is more help-
ful than no treatment, but some specific
therapies are better than others for some
particular disorders.
• Some studies use a randomized clinical
t r ia l ( RCT ) desig n, wh ich a l lows re –
searchers to investigate the ef f icacy of
specif ic factors or treatments ; a RCT
t ypical ly involves manual-based treat-
m e n t . T h e r e s u l t s o f s u ch r e s e a r ch
g e n e r a l l y s u g g e s t a d o s e – r e s p o n s e
relationship.
• Research on treatments that target so-
cia l factor s revea ls that m atch i ng pa-
t i e n t s a n d t h e r a p i s t s b y e t h n i c i t y,
gender, or age does not systematica l ly
a lter the ef fect iveness of therapy. For
patients with a strong preference, how-
ever, m at ch i n g m ay le ad to a bet t er
outcome.
Research Methods 113
115
CHAPTER 5
Mood Disorders and
Suicide
ay Redfield Jamison, a psychologist who studies mood dis-
orders, is uniquely qualif ied to report and ref lect on such
disorders. Not only has she made mood disorders her area
of professional expertise, but she has also lived with such a disorder.
In her memoir, An Unquiet Mind (1995), Jamison recounts her
experiences. The youngest of three children in a military family, she
and her siblings attended four different elementary schools—some in
foreign countries—by the time she was in 5th grade. She describes
her father, a meteorologist and Air Force officer, as enthusiastic, with
infectious good moods, and impulsive, often giving the children
gifts. However, he also suffered periods when he was immobilized
by depression, and he generally had trouble regulating his emotions.
As we’ll see in this chapter, Jamison herself developed difficulties
regulating her emotions. She recounts that when she was a senior in
high school, her mood became so dark that her thinking
. . . was torturous. I would read the same passage over and over again
only to realize that I had no memory at all for what I had just read.
Each book or poem I picked up was the same way. Incomprehen-
sible . . . I could not begin to follow the material presented in my
classes. . . . It was very frightening . . . [my mind] no longer found
anything interesting or enjoyable or worthwhile. It was incapable of
concentrated thought and turned time and time again to the subject of
death: I was going to die, what difference did anything make? Life’s
run was only a short and meaningless one, why live? . . . I dreaded
having to talk with people, avoided my friends whenever possible. . . .
( Jamison, 1995, pp. 37–38)
Depressive Disorders
Major Depressive Episode
Major Depressive Disorder
Depression in Children and Adolescents
Persistent Depressive Disorder
Understanding Depressive Disorders
Treating Depressive Disorders
Bipolar Disorders
Mood Episodes for Bipolar Disorders
The Two Types of Bipolar Disorder
Cyclothymic Disorder
Understanding Bipolar Disorders
Treating Bipolar Disorders
Suicide
Suicidal Thoughts and Suicide Risks
Understanding Suicide
Preventing Suicide
In thIs passage, Jamison describes problems arising from her
mood, a persistent emotion lurking in the background, regardless of
what is occurring. The general category of psychological disorders
referred to as mood disorders encompasses prolonged and marked
disturbances in mood that affect how people feel, what they believe
and expect, how they think and talk, and how they interact with
others. In any particular year, about 9% of Americans experience a
mood disorder (Centers for Disease Control and Prevention [CDC],
Mood disorders
Psychological disorders characterized by
prolonged and marked disturbances in mood
that affect how people feel, what they believe
and expect, how they think and talk, and how
they interact with others.
Valentin Casarsa/Getty Images. Photo for illustrative purposes only; any individual depicted is a model.
2010a). Mood disorders are among the leading causes of disability worldwide (World
Health Organization [WHO], 2008).
DSM-5 distinguishes between two categories of mood disorders: depressive
disorders and bipolar and related disorders. Depressive disorders are mood disorders
in which someone’s mood is consistently low; in contrast, bipolar disorders are mood
disorders in which a person’s mood is sometimes decidedly upbeat, perhaps to the
point of being manic, and sometimes may be low. Mood disturbances that are part
of depressive disorders and bipolar disorders are not the normal ups and downs that
we all experience; they are more intense and longer lasting than just feeling “blue”
or “happy.”
DSM-5 def ines three t ypes of mood episodes as the foundations of mood
disorders: major depressive episode, manic episode, and hypomanic episode (see Table 5.1).
If a patient experiences different types of mood episodes over time (or a different
mixture of such episodes), his or her diagnosis may change. We will first examine
depressive disorders—what they are and their causes and treatments—and then con-
sider bipolar and related disorders. Once we know more about mood disorders, we’ll
examine what is known about suicide and how to prevent it.
Depressive Disorders
Most people who read Jamison’s description of her senior year in high school would
think that she was depressed during that time. But what, exactly, does it mean to
say that someone is depressed? The diagnoses of depressive disorders are based on the
presence of building blocks, which are episodes of specific types of abnormal mood. For
depressive disorders, the building block that leads to a diagnosis is a major depressive
episode; people whose symptoms have met the criteria for a major depressive episode
(see Table 5.2) are diagnosed with major depressive disorder.
Major Depressive Episode
A major depressive episode (MDE) is characterized by severe depression that
lasts at least 2 weeks. MDE is not itself a diagnosis but a set of symptoms that support
making a diagnosis. Mood (which is a type of affect) is not the only symptom of a
major depressive episode. As noted in Table 5.2, specific types of behavior and cogni-
tion also characterize depression.
Affect: The Mood Symptoms of Depression
During an MDE, a person can feel unremitting sadness, hopelessness, or numbness.
Some people also suffer from a loss of pleasure, referred to as anhedonia, a state in
which activities and intellectual pursuits that were once enjoyable no longer are, or
at least are not nearly as enjoyable as they once were. Someone who liked to go to
the movies, for instance, may no longer find it so interesting or fun and may feel
that it is not worth the effort. Anhedonia can thus lead to social withdrawal. Other
mood-related symptoms of depression include weepiness— crying at the drop of a hat
or for no apparent reason—and decreased sexual interest or desire.
Behavioral and Physical Symptoms of Depression
People who are depressed make more negative comments, make less eye contact, are
less responsive, speak more softly, and speak in shorter sentences than people who are
not depressed (Gotlib & Robinson, 1982; Segrin & Abramson, 1994). Depression may
also be evident behaviorally in one of two ways: psychomotor agitation or psychomotor re-
tardation. Psychomotor agitation is an inability to sit still, evidenced by pacing, hand
TABLE 5.1 • Three Types of Mood
Disorder Episodes
• A major depressive episode involves symp-
toms of depression.
• A manic episode involves elated, irritable,
or euphoric mood (mood that is extremely
positive and may not necessarily be
appropriate to the situation).
• A hypomanic episode involves elated,
irritable, or euphoric mood that is less
distressing or severe than mania and is
different from the person’s nondepressed
state. That is, how a person behaves
during a hypomanic episode is different
from his or her usual state.
Psychologist Kay Redfield Jamison described
being depressed as being intruded on by visual
and auditory images related to death.
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Major depressive episode (MDE)
A mood episode characterized by severe
depression that lasts at least 2 weeks.
Anhedonia
A difficulty or inability to experience pleasure.
Psychomotor agitation
An inability to sit still, evidenced by pacing,
hand wringing, or rubbing or pulling the skin,
clothes, or other objects.
116 C H A P T E R 5
wringing, or rubbing or pulling the skin, clothes, or
other objects. In contrast, psychomotor retardation is
a slowing of motor functions indicated by slowed bodily
movements and speech (in particular, longer pauses in
answering) and lower volume, variety, or amount of
speech. Psychomotor retardation, along with changes in
appetite, weight, and sleep, are classified as vegetative signs
of depression. Sleep changes can involve insomnia or,
less commonly, hypersomnia, which is sleeping more
hours each day than normal. In addition, people who
are depressed may feel less energetic than usual or feel
tired or fatigued even when they don’t physically exert
themselves.
Cognitive Symptoms of Depression
When in the grip of depression, people often feel worth-
less or guilt-ridden, may evaluate themselves negatively
for no objective reason, and tend to ruminate over
their past failings (which they may exaggerate). They
may misinterpret ambiguous statements made by other
people as evidence of their worthlessness. For instance,
a depressed man, Tyrone, might hear a colleague’s ques-
tion “How are you?” as an indication that he is incom-
petent and infer that the colleague is asking the question
because Tyrone’s incompetence is so obvious. Depressed
patients can also feel unwarranted responsibility for neg-
ative events, to the point of having delusions that revolve
around a strong sense of guilt, deserved punishment,
worthlessness, or personal responsibility for problems in
the world. They blame themselves for their depression
and for the fact that they cannot function well. During
a depressive episode, people may also report difficulty
thinking, remembering, concentrating, and making de-
cisions, as author William Styron describes in Case 5.1.
To others, the depressed person may appear distracted.
CASE 5.1 • FROM TH E INSIDE: Major Depressive Episode
Another experience of depression was captured by the writer William Styron in his memoir,
Darkness Visible:
In depression this faith in deliverance, in ultimate restoration, is absent. The pain is
unrelenting, and what makes the condition intolerable is the foreknowledge that no
remedy will come—not in a day, an hour, a month, or a minute. If there is mild relief, one
knows that it is only temporary; more pain will follow. It is hopelessness even more than
pain that crushes the soul. So the decision making of daily life involves not, as in normal
affairs, shifting from one annoying situation to another less annoying—or from discom-
fort to relative comfort, or from boredom to activity—but moving from pain to pain. One
does not abandon, even briefly, one’s bed of nails, but is attached to it wherever one goes.
(Styron, 1990, p. 62)
Note, however, that depression is heterogeneous, which means that people with de-
pression experience these symptoms in different combinations. No single set of symptoms
is shared by all people with depression (Hasler et al., 2004). Moreover, researchers distin-
guish two types of depression: Whereas with typical depression, people develop insomnia,
Psychomotor retardation
A slowing of motor functions indicated by
slowed bodily movements and speech and
lower volume, variety, or amount of speech.
Hypersomnia
Sleeping more hours each day than normal.
TABLE 5.2 • DSM-5 Criteria for Major Depressive Episode
A. Five (or more) of the following symptoms have been present during the same
2-week period and represent a change from previous functioning; at least one of
the symptoms is either (1) depressed mood or (2) loss of interest or pleasure.
Note: Do not include symptoms that are clearly attributable to another medical
condition.
1. Depressed mood most of the day, nearly every day, as indicated by either
subjective report (e.g., feels sad, empty, or hopeless) or observation made
by others (e.g., appears tearful). (Note: In children and adolescents, can be
irritable mood.)
2. Markedly diminished interest or pleasure in all, or almost all, activities most
of the day, nearly every day (as indicated by either subjective account or
observation).
3. Significant weight loss when not dieting or weight gain (e.g., a change of
more than 5% of body weight in a month), or decrease or increase in appetite
nearly every day. (Note: In children, consider failure to make expected weight
gain.)
4. Insomnia or hypersomnia nearly every day.
5. Psychomotor agitation or retardation nearly every day (observable by others;
not merely subjective feelings of restlessness or being slowed down).
6. Fatigue or loss of energy nearly every day.
7. Feelings of worthlessness or excessive or inappropriate guilt (which may be
delusional) nearly every day (not merely self-reproach or guilt about being sick).
8. Diminished ability to think or concentrate, or indecisiveness, nearly every day
(either by subjective account or as observed by others).
9. Recurrent thoughts of death (not just fear of dying), recurrent suicidal
ideation without a specific plan, or a suicide attempt or a specific plan for
committing suicide.
B. The symptoms cause clinically significant distress or impairment in social, occu-
pational, or other important areas of functioning.
C. The episode is not attributable to the physiological effects of a substance or
another medical condition.
Reprinted with permission from the Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition,
(Copyright ©2013). American Psychiatric Association. All Rights Reserved.
Mood Disorders and Suicide 117
lose weight, and their poor mood persists throughout the day,
with atypical depression, people sleep more, gain weight, and
their mood brightens in response to positive events.
The symptoms of MDE develop over days and weeks.
A prodrome is the early symptoms of a disorder or
an episode, and the prodrome of an MDE may include
an xiet y or m ild depressive symptoms that last weeks
to months before fully emerging as a major depressive
episode. An untreated MDE typically lasts approximately
4 months or longer (American Psychiatric Association,
2000). The more severe the depression, the longer the
episode is likely to last (Melartin et al., 2004). About two
thirds of people who have an MDE eventually recover
from the episode completely and return to their previous
level of functioning—referred to as the premorbid level
of functioning. About 20 –30 % of people who have an
MDE find that their symptoms lessen over time, to the
point where they no longer meet the criteria for an MDE, but their depression
doesn’t completely resolve and may persist for years.
What distinguishes depression from simply “having the blues”? One distinguish-
ing feature is the number of symptoms. People who are sad or blue generally have
fewer than five of the symptoms listed in the DSM-5 diagnostic criteria for a major
depressive episode (see Table 5.2). In addition, someone who is truly depressed has
severe symptoms for a relatively long period of time and is unable to function effec-
tively at home, school, or work.
One possible exception is grief—which can mimic most or even all symptoms of
depression. In the previous edition of DSM (DSM-IV), people were not considered
to have an MDE if the symptoms could have occurred because of the loss of a loved
one; this was called the “bereavement exclusion.” With this exclusion, if someone
has symptoms of depression within a couple months after the loss of a loved one
and isn’t suffering from significantly impaired functioning, thoughts of suicide, or
psychotic behavior, that person shouldn’t be considered to have an MDE.
However, in DSM-5 this exception has been removed, and that change is
controversial. On the one hand, those who support removing this exception claim
that bereavement- related depression, unlike grief, is similar to an MDE unrelated to
bereavement (Kendler et al., 2008; Lamb et al., 2010; Zisook et al., 2007). They claim
that the hallmark of grief is waves of loss and emptiness and thoughts of the deceased,
whereas the hallmark of depression is persistent and sad or depressed thoughts that
are not solely focused on one thing. They stress that, left untreated, depression related
to bereavement can be as harmful and debilitating as other forms of depression.
On the other hand, removing the bereavement exclusion may lead to overdi-
agnosis of—and rush to treat with medication or psychotherapy—people who are
merely grieving (Wakefield & First, 2012). Training and careful evaluation are re-
quired to distinguish normal grieving from an MDE (Pies, 2013), but not every
clinician will have that training nor the time to make the careful evaluation. This is
particularly likely for family doctors or internists, who are at the forefront of diag-
nosing and treating depression (Katz, 2012; Montano, 1994).
Major Depressive Disorder
According to DSM-5, once someone’s symptoms meet the criteria for a major
depressive episode, he or she is diagnosed as having major depressive disorder
(MDD)—five or more symptoms of an MDE lasting more than 2 weeks. Moreover,
©
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Normal bereavement has characteristics that
are similar to symptoms of a major depressive
episode: sad thoughts and feelings, problems
concentrating, and changes in appetite and
sleep. However, according to DSM-5, bereaved
people are not generally overcome with
feelings of hopelessness or anhedonia.
Prodrome
Early symptoms of a disorder.
Premorbid
Referring to the period of time prior to a
patient’s illness.
Major depressive disorder (MDD)
A mood disorder marked by five or more
symptoms of an MDE lasting more than
2 weeks.
118 C H A P T E R 5
the clinician specifies whether mixed features characterize the mood
episode— whether the person has some symptoms of mania or hy-
pomania (to be discussed later) but not enough of these sorts of
symptoms to meet the criteria for those mood episodes. The mental
health professional also specifies whether this is the first or a recur-
rent episode. Thus, for example, after Kay Jamison had her first ma-
jor depressive episode, she had the diagnosis of MDD, single episode.
More than half of those who have had a single depressive episode go
on to have at least one additional episode, noted as recurrent depression.
Some people have increasingly frequent episodes over time, others
have clusters of episodes, and still others have isolated depressive
episodes followed by several years without symptoms ( American
Psychiatric Association, 2000; McGrath et al., 2006). DSM-5 al-
lows mental health professionals to rate the patient’s depression as
mild, moderate, or severe.
Major depressive d isorder lead s to lowered product iv it y at work—both
from missing days on the job and from presenteeism, being present but being less
productive than normal (Adler et al., 2006; Druss et al., 2001; Stewart et al.,
2003). For people whose jobs require high levels of cognitive effort, even mild
memory or attentional difficulties may disrupt their ability to function adequately
at work.
Sometimes recurrent depression follows a seasonal pattern, occurring at a
particular time of year. Previously referred to as seasonal affective disorder, this
variant of MDD commonly is characterized by recurrent depressive episodes,
hypersomnia, increased appetite (particularly for carbohydrates), weight gain,
and irritability. These symptoms usually begin in autumn and continue through
the winter months. The symptoms either disappear or are much less severe in
the summer. Sur veys find that approximately 4– 6% of the general population
experiences a winter depression, and the average age of onset is 23 years. The
disorder is four times more common in women than in men (American Psychi-
atric Association, 2000). Winter depression often can be treated effectively with
phototherapy (also called light-box therapy), in which full-spectrum lights are
used as a treatment (Golden et al., 2005).
MDD is common in the United States: Up to 20 % of Americans will ex-
per ience it at some point dur ing their lives (Kessler et al., 2003). The docu-
mented rate of depression in the United States is increasing (Lewinsohn et al.,
1993; Rhode et al., 2013), perhaps because of increased stressors in modern life
or decreased social support; in addition, at least part of this increase may sim-
ply reflect higher reporting rates. Depression is currently associated with more
than $ 30 bil lion of lost productivit y among U.S. workers annual ly ( Stewar t
et al., 2003).
Evidence also suggests that the risk of developing depression is increasing for
each age cohort, a group of people born in a particular range of years. The risk
of developing depression is higher among people born more recently than those
born during earlier parts of the previous centur y. In addition, if someone born
more recently does develop depression, that person probably will first experience
it earlier in life than someone in an older cohort. Table 5.3 provides more facts
about MDD.
In some cases, such as that of Marie Osmond in Case 5.2, depression emerges
during pregnancy or within 4 weeks of giving birth; depression in this context is
designated as having a peripartum onset (Wisner et al., 2013). Those most at risk for
peripartum depression are women who have had recurrent depression before giving
birth (Forty et al., 2006).
Phototherapy
Treatment for depression that uses full-
spectrum lights; also called light-box therapy.
Age cohort
A group of people born in a particular range
of years.
Phototherapy can be helpful to people who
have winter depression. Typically, a person
using phototherapy sits near special lights for
an average of 30 minutes per day.
Although depression can arise after giving
birth, for many women “postpartum”
depression may actually begin during
pregnancy, particularly the latter half, and
persist after the birth.
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Mood Disorders and Suicide 119
CASE 5.2 • FROM TH E INSIDE: Peripartum Onset of Depression
After the birth of her seventh child, Marie Osmond developed peripartum depression:
I’m collapsed in a pile of shoes on my closet floor. . . . I sit with my knees pulled up to my
chest. I barely move. It’s not that I want to be still. I am numb. I can tell I’m crying, but it’s
not like tears I’ve shed before. My eyes feel as though they have moved deep into the back
of my head. There is only hollow space in front of them. Dark, hollow space. I am as empty
as the clothing hanging above me. Despite my outward appearance, I feel like a lifeless form.
I can hear the breathing of my sleeping newborn son in his bassinet next to the bed.
My ten-year-old daughter, Rachael, opens the bedroom door and whispers, “Mom?”
into the room, trying not to wake the baby. Not seeing me, she leaves. She doesn’t even
consider looking in the closet on the floor. Her mother would never be there. She’s right.
This person sitting on the closet floor is nothing like her mother. I can’t believe I’m here
myself. I’m convinced that I’m losing my mind. This is not me.
I feel like I’m playing hide-and-seek from my own life, except that I just want to hide
and never be found. I want to escape my body. I don’t recognize it anymore. I have lost
any resemblance to my former self. I can’t laugh, enjoy food, sleep, concentrate on work,
or even carry on a conversation. I don’t know how to go on feeling like this: the emptiness,
the endless loneliness. Who am I? I can’t go on.
(Osmond et al., 2001)
Depression often occurs along with another disorder. In fact, depression and
anxiety disorders co-occur about 50% of the time. Because of this high comorbidity,
researchers propose that the two types of disorders have a common cause, presently
unknown. In addition, although not common, depression can occur with psychotic
features—hallucinations (e.g., in which a patient can
feel that his or her body is decaying) or delusions (e.g.,
in which the patient believes that he or she is evil and
living in hell).
Depression in Children and
Adolescents
In a given 6-month period, 1–3% of elementary-school
children and 5–8% of teenagers are depressed (Garber &
Horowitz, 2002; Lewinsohn & Essau, 2002). Moreover,
some clinicians and researchers are reporting depres-
sion among preschool children, evidenced by avoidance,
decreased enthusiasm, and increased anhedonia (Luby
et al., 2006). Younger children who are depressed are
not generally considered to be at high risk of develop-
ing depression in adulthood. However, those who first
become depressed as teenagers are considered to be at
high risk for being depressed as adults (Lewinsohn,
Rohde, et al., 1999; Rhode et al., 2013; Weissman,
Wol k, Wick r a m a r at ne, et a l., 1999 ; Weissm a n,
Wickramaratne, et al., 2006). Teenage depression has
far-reaching effects: Depressed teens are more likely
than their nondepressed peers to drop out of school or
to have unplanned pregnancies (Waslick et al., 2002).
Persistent Depressive Disorder
When symptoms of major depressive disorder persist
for a long period of time, the person may be diagnosed
with persistent depressive disorder (dysthymia),
characterized by depressed mood and as few as two
TABLE 5.3 • Major Depressive Disorder Facts at a Glance
Prevalence
• Approximately 10–25% of women and 5–12% of men will develop MDD over
their lifetimes, although some studies find even higher rates (Rhode et al.,
2013). Before puberty, however, boys and girls develop MDD in equal numbers
(Kessler et al., 2003).
• People with different ethnic backgrounds, education levels, incomes, and marital
statuses are generally afflicted equally (Kessler et al., 2003; Weissman et al., 1991).
Comorbidity
• Most people with MDD also have an additional psychological disorder (Rush
et al., 2005), such as an anxiety disorder (Barbee, 1998; Kessler et al., 2003) or
substance use disorder (Rush et al., 2005).
Onset
• MDD can begin at any age, with the average age of onset in the mid-20s, although
people are developing MDD at increasingly younger ages (Rhode et al., 2013).
Course
• Among people who have had a single MDE, approximately 50–65% will go on
to have a second episode (Angst et al., 1999; Solomon et al., 2000).
• Those who have had two episodes have a 70% chance of having a third, and
those who have had three episodes have a 90% chance of having a fourth.
Gender Differences
• Women are approximately twice as likely as men to develop MDD (Kessler, 2003;
Rhode et al., 2013).
• Some women report that depressive symptoms become more severe
premenstrually.
Unless otherwise noted above, the source for information is American Psychiatric Association, 2013.
Persistent depressive disorder (dysthymia)
A depressive disorder that involves as few as
two symptoms of a major depressive episode
but in which the symptoms persist for at least
2 years.
Disruptive mood dysregulation disorder
(DMDD)
A depressive disorder in children characterized
by persistent irritability and frequent episodes
of out-of-control behavior.
120 C H A P T E R 5
other depressive symptoms that last for at least
2 years and that do not recede for longer than
2 months at any time during that period (see
Table 5.4). Note that people can come to
be diagnosed with this disorder if they have
fewer symptoms of depression than necessary
for MDD but have these symptoms for at least
2 years or they have MDD that lasts for at least
2 years (also referred to as chronic depression).
Because symptoms are chronic, people
with persistent depressive disorder often incor-
porate the symptoms into their enduring self-
assessment, seeing themselves as incompetent
or uninteresting. Whereas people with shorter-
lasting MDD see their symptoms as happening
to them, people with persistent depressive dis-
order often view their symptoms as an integral
part of themselves (“This is just how I am”), like
Mr. A, in Case 5.3. Moreover, people with per-
sistent depressive disorder are less likely to ex-
perience the vegetative signs associated with an
MDE (psychomotor retardation and changes in
sleep, appetite, and weight; American Psychiat-
ric Association, 2000). In addition, people who
have persistent depressive disorder are generally
younger than those with MDD. See Table 5.5 for
more facts about persistent depressive disorder.
C U R R E N T C O N T R O V E R S Y
Disruptive Mood Dysregulation
Disorder: Overlabeling of Tantrums?
Disruptive mood dysregulation disorder (DMDD) is
a depressive disorder in children characterized by persistent
irritability and frequent episodes of out-of-control behavior.
It is supposed to be a more accurate description of kids who
have out-of-control rage episodes and were incorrectly labeled
as having bipolar disorder and then were (inappropriately)
treated for that disorder. The criteria for using this diagnosis,
which is brand new in DSM-5, include:
• Severe, recurrent temper outbursts, including verbal or
physical aggression, with a duration or intensity that is out of
proportion to the situation and inconsistent with the child’s
developmental level.
• These outbursts occur at least three times a week, on
average.
• Even between outbursts, mood is persistently irritable or angry.
• This pattern starts between ages 6 and 10, occurs in at least
two settings, continues for at least 1 year without letting up
for 3 months, and is not exclusively the result of another
mental disorder.
On the one hand, just as a diagnosis of bipolar disorder
was overused to describe children with out-of-control rage
episodes, a diagnosis of DMDD might label as mentally ill
children who merely have a lot of tantrums, perhaps simply
as a way to gain attention. Moreover, diagnosing a child with
DMDD might focus on—and lead to treatment of—the child
when the real problem is in the family.
On the other hand, the specifics of the criteria (e.g., severity,
frequency, duration) should prevent diagnosing children who
merely are sometimes grumpy or throw occasional tantrums.
To apply this diagnosis, the child’s irritable mood must be per-
sistent and daily, even when there is no reinforcement (such as
attention) for a tantrum. The rages must occur in at least two
settings (e.g., school and home) and not be an expected re-
sponse to a home or school situation. This diagnosis might lead
to fewer such children being put on bipolar medication because
they will no longer be considered to have bipolar disorder.
CRITI C AL TH I N KI N G Even with narrow criteria designed to
prevent inappropriate diagnosis of bipolar disorder, won’t some
clinicians apply (and overuse) this diagnosis to children who are
merely “difficult” attention seekers? How can we prevent this?
( James Foley, College of Wooster)
TABLE 5.4 • DSM-5 Diagnostic Criteria for Persistent Depressive Disorder
(Dysthymia)
A. Depressed mood for most of the day, for more days than not, as indicated by either sub-
jective account or observation by others, for at least 2 years.
Note: In children and adolescents, mood can be irritable and duration must be at least 1 year.
B. Presence, while depressed, of two (or more) of the following:
1. Poor appetite or overeating.
2. Insomnia or hypersomnia.
3. Low energy or fatigue.
4. Low self-esteem.
5. Poor concentration or difficulty making decisions.
6. Feelings of hopelessness.
C. During the 2-year period (1 year for children and adolescents) of the disturbance, the individu-
al has never been without the symptoms in Criteria A and B for more than 2 months at a time.
D. Criteria for a major depressive disorder may be continuously present for 2 years.
E. There has never been a manic episode or a hypomanic episode, and criteria have never
been met for cyclothymic disorder.
F. The disturbance is not better explained by a persistent schizoaffective disorder, schizo-
phrenia, delusional disorder, or other specified or unspecified schizophrenia spectrum
and other psychotic disorder.
G. The symptoms are not attributable to the physiological effects of a substance (e.g., a drug of
abuse, a medication) or another medical condition (e.g., hypothyroidism).
H. The symptoms cause clinically significant distress of impairment in social, occupational
or other important areas of functioning.
Reprinted with permission from the Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition, (Copyright
©2013). American Psychiatric Association. All Rights Reserved.
Mood Disorders and Suicide 121
CASE 5.3 • FROM TH E INSIDE: Persistent Depressive Disorder
Mr. A, a 28-year-old, single accountant, sought consultation because, he said, “I feel I am
going nowhere with my life.” Problems at work included a recent critical job review because
of low productivity, conflicts with his boss, and poor management skills. His fiancée recently
postponed their wedding because she has doubts about their relationship, especially his
remoteness, critical comments, and lack of interest in sex.
Describing himself as a pessimist who has difficulty experiencing pleasure or happiness,
Mr. A has long felt a sense of hopelessness—of life not being worth living. His mother was
hospitalized with [peripartum] depression after the birth of his younger sister; his father
had a drinking problem. His high school classmates found him gloomy and “not fun.”
Although not troubled by thoughts of suicide nor significant vegetative signs of depression,
Mr. A. does have months when his concentration is impaired, his energy level is lowered, and his
interest in sex wanes. At such times, he withdraws from other people (although he always goes
to work), staying in bed on weekends.
(Adapted from Frances & Ross, 1996, pp. 123–124)
Understanding Depressive Disorders
How do depressive disorders arise? Why do some people, but not others, suffer from
them? Like all other psychological disorders, depressive disorders are best understood
as arising from neurological, psychological, and social factors and the feedback loops
among them. However, we must note that many of the factors that have been identi-
fied are correlational. As you know, correlation does not imply causation. In some
cases, there is evidence for causal factors, but in most cases we cannot know whether
a specific factor gives rise to depression or vice versa—or whether some third factor
gives rise to both.
Neurological Factors
Neurological factors that contribute to depressive disorders can be classified into
three categories: brain systems, neural communication, and genetics. Stress-related
hormones—which underlie a specific kind of neural communication—are particu-
larly important in understanding depressive disorders.
Brain Systems
Studies of depressed people have shown that they have unusually low activity in a
part of the frontal lobe that has direct connections to the amygdala (a brain struc-
ture that is involved in fear and other strong emotions) and to other brain areas
involved in emotion (Kennedy et al., 1997). The frontal lobe plays a key role in
regulating other brain areas, and signals from it can inhibit activity in the amyg-
dala. This finding hints that the depressed brain is not as able as the normal brain
to regulate emotion. Moreover, this part of the frontal lobe has connections to
the brain areas that produce the neurotransmitters dopamine, serotonin, and nor-
epinephrine. Thus, this part of the frontal lobe may be involved in regulating the
amounts of such neurotransmitters. This is important because these substances are
involved in reward and emotion, which again hints that the brains of these people
are not regulating emotion normally. Researchers have refined this general obser-
vation and reported that one aspect of depression—lack of motivated behavior—
is specifically related to reduced activity in the frontal and parietal lobes (Milak
et al., 2005).
Neural Communication
Researchers have long known that the symptoms of depression can be alleviated
by medications that alter the activity of serotonin or norepinephrine (Arana &
Rosenbaum, 2000). Indeed, when this fact was first discovered, some researchers
TABLE 5.5 • Persistent Depressive
Disorder Facts at a Glance
Prevalence
• In a given year, 2% of Americans have
persistent depressive disorder.
Comorbidity
• Compared to people with MDD, those
with persistent depressive disorder are
more likely to have at least one other psy-
chological disorder, particularly an anxiety
disorder or substance use disorder.
Onset
• This disorder tends to emerge earlier than
MDD.
Course
• The course of persistent depressive dis-
order is, by its nature, chronic; symptoms
are less likely to fully resolve than with an
MDE.
Gender Differences
• Boys and girls are equally likely to develop
persistent depressive disorder.
• In adulthood, women are two to three
times more likely than men to develop
persistent depressive disorder.
Source: The source for information is American Psychiatric
Association, 2013.
122 C H A P T E R 5
thought that the puzzle of depression was nearly solved. However, we now know
that the stor y is not so simple: Depression is not caused by too much or too
little of any one specific neurotransmitter. Instead, the disorder arises in part
from complex interactions among numerous neurotransmitters and depends on
how much of each is released into the synapses, how long each neurotransmit-
ter lingers in the synapses, and how the neurotransmitters interact with recep-
tors in other areas of the brain that are involved in the symptoms of depression
( Nemeroff, 1998).
Stress-Related Hormones
The chemical stor y doesn’t end with neurotransmitters. Nemeroff (1998, 2008)
formulated the stress–diathesis model of depression (which is to be distinguished
from the general diathesis–stress model, discussed in Chapter 1). The stress–diathesis
model of depression focuses on a part of the brain involved in the fight-or-flight
response, the hypothalamic–pituitary–adrenal axis (HPA axis). The HPA axis is
particularly important because it governs the production of the hormone cor-
tisol, which is secreted in larger amounts when a person experiences stress (see
Figure 5.1). According to the stress–diathesis model, people with depression have
an excess of cortisol circulating in their blood, which makes their brains prone to
overreacting when they experience stress.
Moreover, th is stress react ion, in t ur n,
alters the serotonin and norepinephr ine
systems, which underlie at least some of
the symptoms of depression. Antidepres-
sant medications can lower people’s corti-
sol levels and also decrease their depressive
symptoms (Deuschle et al., 2003; Werstiuk
et al., 1996).
The stress–diathesis model of depression receives support from several sources
( Nemerof f, 2008). For instance, higher levels of cortisol are associated with
decreases in the size of the hippocampus, which thereby impairs the ability to form
new memories (of the sort that later can be voluntarily recalled) —which in turn
may contribute to the decreased cognitive abilities that characterize depression.
And, in fact, researchers have reported that parts of this brain structure are smaller
in depressed people than in people who are not depressed (Neumeister et al., 2005;
Neumeister et al., 2005), which suggests that stress affects the symptoms of depres-
sion in part by altering levels of cortisol, which in turn impairs the functioning of
the hippocampus.
Genetics
Twin studies show that when one t win of a monozygotic (identical) pair has
MDD, the other twin has a risk of also developing the disorder that is four times
higher than when the twins are dizygotic [(fraternal) (Bowman & Nurnberger,
1993; Kendler et al., 1999a)]. Because monozygotic twins basically share all of
their genes but dizygotic twins share only half of their genes, these results point
to a role for genetics in this disorder. One possibility is that genes influence how
a person responds to stressful events (Costello et al., 2002; Kendler et al., 2005).
If a person is sensitive to stressful events, the sensitivity could lead to increased
HPA axis activation (Hasler et al., 2004), which in turn could contr ibute to
depression.
However, genes are not destiny. The environment clearly plays an important role
in whether a person will develop depression (Hasler et al., 2004; Rice et al., 2002).
Even with identical twins, if one twin is depressed, this does not guarantee that
Stressor
Pituitary activity:
Pituitary releases
adrenocortico-
tropic hormone
(ACTH).
Adrenal glands
release cortisol.
Hypothalamic
activity:
Hypothalamus
releases
corticotropin-
releasing factor
(CRF).
FI G U RE 5.1 • The HPA Axis Stress
activates the hypothalamus, which releases
corticotropin-releasing factor (CRF), which in
turn stimulates the pituitary gland to release
adrenocorticotropic hormone (ACTH), which
then leads the adrenal glands to release
cortisol. According to the stress–diathesis
model of depression, people who become
depressed have high levels of cortisol, which
leads to heightened reactivity to stress and
increased serotonin levels.
Mood Disorders and Suicide 123
the co-twin will also be depressed— despite their having basically the same genes.
Whether a person becomes depressed depends partly on his or her life experiences,
including the presence of hardships and the extent of social support.
Psychological Factors
Particular ways that people think about themselves and events, in concert with
stressful or negative life experiences, are associated with an increased risk of depres-
sion. In the following sections we consider psychological factors that can influence
whether a person develops depression; these factors range from biases in attention to
the effects of different ways of thinking to the results of learning.
Attentional Biases
People who are depressed are more likely to pay attention to sad or angry stimuli.
For instance, they will pay more attention to sad or angry faces than to faces that
display positive emotions (Gotlib, Kasch, et
al., 2004; Gotlib, Krasnoperova, et al., 2004;
Leyman et al., 2007); people who do not
have this psychological disorder spend equal
time looking at faces that express differ-
ent emotions. This attentional bias has also
been found for negative words and scenes, as
well as for remembering depression- related—
versus neutral—stimuli (Caseras et al., 2007;
Gotlib, Kasch, et al., 2004; Mogg et al.,
1995). Such an attentional bias may leave
depressed people more sensitive to other
people’s sad moods and to negative feedback
from others, compounding their depressive
thoughts and feelings.
Dysfunctional Thoughts
As discussed in Chapter 2, Aaron Beck pro-
posed that cognitive distortions are the root cause
of many disorders. Beck (1967) has suggested
that people with depression tend to have
overly negative views about: (1) the world,
(2) the self, and (3) the future, referred to as
the negative triad of depression. These distorted
views can cause and maintain chronically
depressed feelings and depression-related be-
haviors. For instance, a man who doesn’t get
the big raise he hoped for might respond with cognitive distortions that give rise to
dysfunctional thoughts. He might think that he isn’t “successful” because he didn’t
get the raise and therefore that he must be worthless (notice the circular reasoning).
This man is more likely to become depressed than he would be if he didn’t have such
dysfunctional thoughts (Gibb et al., 2007).
Rumination and Attributional Style
While experiencing negative emotions, some people reflect on these emotions and
the events that led to them; during such ruminations, they might say to themselves:
“Why do bad things always happen to me? ” or “Why did they say those hurtful
things about me? Is it something I did?” (Nolen-Hoeksema & Morrow, 1991). Such
ruminative thinking has been linked to depression ( Just & Alloy, 1997; Nolen-
Hoeksema, 2000; Nolen-Hoeksema & Morrow, 1991, 1993).
In contrast to people who are not depressed, depressed people are more likely to
pay attention to which of these two photos? Answer: The photo on the right; paying
attention to sad or angry faces will also make such faces more likely to be remembered
than happy faces.
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124 C H A P T E R 5
People who consistently attribute negative events to their own qualities—
called an internal attributional style—are more likely to become depressed. In one
study, mothers-to-be who had an internal attributional style were more likely to
be depressed 3 months after childbirth than were mothers-to-be who had an
external attributional style—blaming negative events on qualities of others or on the
environment (Peterson & Seligman, 1984). Similarly, college students who tended to
blame themselves (rather than external factors) for negative events were more likely
than those who did not to become depressed after receiving a bad grade (Metalsky
et al., 1993).
Three particular aspects of attributions are related to depression: whether the
attributions are internal or external, stable (enduring causes) or unstable (local, transient
causes), and global (general, overall causes) or specific (particular, precise causes). Peo-
ple who tend to attribute negative events to internal, stable, and global factors have a
negative attributional style. These people not only make negative predictions about the
future (e.g., “Even if I find another girlfriend, she’ll dump me too,” Abramson et al.,
1999) but also are vulnerable to becoming depressed when negative events occur
(Abramson et al., 1978).
In fact, people who consistently make stable and global attributions for negative
events—whether to internal or external causes—are more likely to feel hopeless in
the face of negative events and come to experience hopelessness depression, a form of
depression in which hopelessness is a central element (Abramson et al., 1989).
People with a negative attributional style are likely to attribute which adverse situation to negative and enduring aspects of themselves?
Answer: People in a car accident, because they are more likely to blame the accident on enduring qualities such as poor driving or lack of
attention to the road. In contrast, people who have a negative attributional style are less likely to blame themselves for a natural disaster.
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Learned Helplessness
Hopelessness depression is not always based on incorrect attributions. It can arise
from situations in which undesirable outcomes do occur and the person is helpless
to change the situation, such as may occur when children are subjected to physical
abuse or neglect (Widom et al., 2007). Such circumstances lead to learned helpless-
ness, in which a person gives up trying to change or escape from a negative situation
(Overmier & Seligman, 1967; see Chapter 2 for a more detailed discussion). For
example, people in abusive relationships might become depressed if they feel that
they cannot escape the relationship and that no matter what they do, the situation
will not improve.
Mood Disorders and Suicide 125
Social Factors
Depression is also associated with a variety of social factors, including stressful life
events (including in personal relationships), social exclusion, and social interactions
(which are affected by culture). These social factors can affect whether depression
develops or persists.
Stressful Life Events
In approximately 70% of cases, an MDE occurs after a significant life stressor, such
as getting f ired from a job or losing an important relationship. Such events are
particularly likely to contribute to a first or second depressive episode (Lewinsohn,
Allen, et al., 1999; Tennant, 2002).
It might seem obvious that negative life events can lead to depression, but sepa-
rating possible confounding factors and trying to establish causality have challenged
researchers. For instance, people who are depressed (or have symptoms of depres-
sion) may have difficulty doing their job effectively; they may experience stressors
such as problems with their coworkers and supervisors, job insecurity, or financial
worries. In such cases, the depressive symptoms may cause the stressful life events,
not be caused by them. Alternatively, some people, by virtue of their temperament,
may seek out situations or experiences that are stressful; for example, some soldiers
volunteer to go to the front line (Foley et al., 1996; Lyons et al., 1993). The point
is that the relationship between stressful life events and depression may not be as
straightforward as it might seem.
Social Exclusion
Feeling the chronic sting of social exclusion—being pushed toward the margins of
society—is also associated with depression. For instance, those who are the targets
of prejudice are more likely than others to become depressed. Such groups include
homosexuals who experience community alienation or violence (Mills et al., 2004),
those from lower socioeconomic groups (Field et al., 2006; Henderson et al., 2005;
Inaba et al., 2005), and, in some cases, the elderly (Hybels et al., 2006; Sachs- Ericsson
et al., 2005).
Some studies find that Latinos and African Americans experience more depression
than other ethnic groups in the United States; a closer look at the data, however,
suggests that socioeconomic status, rather than ethnic or racial background per se, is
the variable associated with depression (Bromberger et al., 2004; Gilmer et al., 2005).
Social Interactions
To a certain extent, emotions can be contagious: People can develop depression, sad-
ness, anxiety, or anger by spending time with someone who is already in such a state
(Coyne, 1976; Segrin & Dillard, 1992). For instance, one study
found that roommates developed symptoms of depression after
3 weeks of living with someone who was depressed ( Joiner, 1994),
and other studies find similar results (Haeffel & Hames, in press).
Another factor associated with depression is a person’s attachment
style in infancy, which can affect the way adults typically interact in
their personal relationships (Ainsworth et al., 1978; Bowlby, 1973,
1979). Adults tend to display one of the following three patterns:
1. Secure attachment. Adults with this style generally display a
positive relationship style.
2. Avoidant attachment. Adults with this style are emotionally
distant from others.
3. Anxious-ambivalent attachment. Adults with this style chronically
worry about their relationships.
The quality of the bond between elderly
partners can buffer against the negative effects
of stressful life events (Kraaij & Garnefski, 2002).
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126 C H A P T E R 5
Adults who are characterized by the second and third forms of attachment are more
vulnerable to depression: Those with anxious-ambivalent attachment are the most
likely to experience episodes of depression, followed by those with avoidant attach-
ment. Adults with secure attachment are least likely to do so (Bifulco et al., 2002;
Cooper et al., 1998; Fonagy et al., 1996).
Culture
A person’s culture and context can inf luence how the person experiences and
expresses depressive symptoms (Lam et al., 2005). For instance, in Asian and Latin
cultures, people with depression may not mention mood but may instead talk about
“nerves” or describe headaches. Similarly, depressed people in Zimbabwe tend to
complain about fatigue and headaches (Patel et al., 2001). In contrast, some depressed
people from Middle Eastern cultures may describe problems with their heart, and
depressed Native Americans of the Hopi people may report feeling heartbroken
(American Psychiatric Association, 2000).
The influence of culture doesn’t end with the way symptoms are described. Each
culture—and subculture—also leads its members to take particular symptoms more
or less seriously. For instance, in cultures that have strong prohibitions against sui-
cide, having suicidal thoughts is a key symptom; in cultures that emphasize being
productive at work, having difficulty functioning well at work is considered a key
symptom (Young, 2001).
A particular culture can also be inf luenced by another culture and change
accordingly. Consider that depressed people in China have typically reported mostly
physical symptoms of depression, but these reports are changing as China becomes
increasingly exposed to Western views of depression (Parker et al., 2001).
Gender Difference
In North America, women are about twice as likely as men to be diagnosed with
depression (Marcus et al., 2005), and studies in Europe f ind a similar gender
difference (Angst et al., 2002; Dalgard et al., 2006). Research results indicate that the
gender difference arises at puberty and continues into adulthood (Alloy & Abramson,
2007; Jose & Brown, 2008).
One explanation for the gender difference in rates of depression is that girls’ so-
cialization into female roles can lead them to experience more body dissatisfaction,
which in turn can make them more vulnerable to automatic negative thoughts that
lead to depression (Cyranowski et al., 2000; Nolen-Hoeksema & Girgus, 1994).
Another explanation for this difference focuses on a ruminative response to stress:
Women are more likely than men to mull over a stressful situation, whereas men more
often respond by distracting themselves and taking action (Nolen- Hoeksema, 1987;
Nolen-Hoeksema & Morrow, 1993; Vajk et al., 1997). A ruminative pattern can be
unlearned: College students who learned to use distraction more and rumination less
improved their depressed mood (Nolen-Hoeksema & Morrow, 1993).
An additional consideration is that women may be more likely than men to report
symptoms of depression, perhaps because they are less concerned about appearing
“strong”; thus, women may not necessarily experience more of these symptoms than
men (Sigmon et al., 2005).
Furthermore, biological differences—such as specific female hormonal changes
involved in puberty—may contribute to this gender difference (Halbreich & Kahn,
2001; Steiner et al., 2003). A role for this biological factor is consistent with the
finding that before puberty, boys and girls have similar rates of depression (Cohen
et al., 1993). Additional evidence that hormones inf luence depression is the fact
that women and men have similar rates of the disorder after women have reached
menopause (and hence their levels of female hormone are greatly reduced) (Hyde
et al., 2008).
Mood Disorders and Suicide 127
The different explanations for the gender difference are not mutually exclusive,
and these factors may interact with one another (Hyde et al., 2008). For instance,
girls who enter puberty early are more likely to become depressed (Kaltiala-Heino
et al., 2003), perhaps in part because their early physical development makes them
more likely to be noticed and teased about their changing bodies, which in turn can
lead to dissatisfaction with and rumination about their bodies. Let’s examine more
broadly how feedback loops contribute to depression.
Feedback Loops in Understanding Depressive Disorders
How do neurological, psychological, and social factors interact through feedback
loops to produce depression? As we noted in the section on genetics, some people
are more vulnerable than others to stress. For these people, the HPA axis is highly
responsive to stress (and often the stress is related to social factors). For example,
abuse or neglect at an early age, with accompanying frequent or chronic increase
in the activity of the HPA axis, can lead cortisol-releasing cells to over respond to
any stressor—even a mild one (Nemeroff, 1998). In fact, college students with a
history of MDD reported feeling more tension and responded less well after a stress-
ful cognitive task (one that, unknown to these participants, was impossible to solve)
than college students with no history of MDD (Ilgen & Hutchison, 2005). These
results support the notion that people who are vulnerable to MDD are affected by
stressors differently than are people without such a vulnerability (Hasler et al., 2004).
A cognitive factor that makes a person vulnerable to depression, such as a negative
attributional style, ruminative thinking, or dysfunctional thoughts (all psychological
factors), can amplify the negative effects of a stressor. In fact, such cognitive factors
can lead people to be hypervigilant for stressors or to interpret neutral events as
stressors, which in turn activates the HPA axis. This neurological response then can
lead such people to interact differently with others (social factor)—making less eye
contact, being less responsive, and becoming more withdrawn.
Researchers have identified other ways that neurological, psychological, and social
factors create feedback loops in depression. According to James Coyne’s interactional
theory of depression (Coyne, 1976; Coyne & Downey, 1991; Joiner et al., 1999),
someone who is neurologically vulnerable to depression (perhaps because of genes
or neurotransmitter abnormalities) may, through verbal and nonverbal behaviors
( psychological factor), alienate people who would otherwise be supportive (social
factor; Nolan & Mineka, 1997). For example, researchers have found that depressed
undergraduates are more likely than nondepressed undergraduates to solicit negative
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Girls typically are encouraged to cope with
stressors by ruminating. In contrast, boys
typically are encouraged to use activity
and distraction. This gender difference may
contribute to the higher rate of depression
among women than among men (Nolen-
Hoeksema, 1987, 2001).
128 C H A P T E R 5
information from happy people—which in turn can lead happier people to reject the
depressed questioner (Wenzlaff & Beevers, 1998). And soliciting negative informa-
tion (and similar behaviors) could arise from negative attributions and views about
self and the environment ( psychological factors), which in turn could arise from
group interactions (social factors), such as being teased or ridiculed, or modeling the
behavior of someone else.
In short, people’s psychological characteristics affect how they interpret events
and how they behave, which in turn inf luences how they are treated in social
interactions, which then influences their beliefs about themselves and others (Casbon
et al., 2005). And all this is modulated by whether the person is neurologically
vulnerable to depression. Figure 5.2 illustrates the feedback loops.
stress
diathesis
st
re
ss
di
at
he
si
s
stress
diathesis
NeuroPsychoSocial NeuroPsychoSocial
NeuroPsychoSocial
Mental Processes and
Mental Contents
Attentional biases
Attributions
Rumination
Cognitive distortions
Stressful Life Events
Relationship
problems or loss
Social exclusion
Abuse
Gender/Culture
Discrimination
Socioeconomic hardship
Symptom expression
Family
Insecure
attachment
Behavior
Learned
helplessness
Affect
Depressed
Brain Systems
Frontal lobes
Hippocampus
Amygdala
HPA axis
Neural Communication
Serotonin
Norepinephrine
Dopamine
Cortisol
Genetics
Inherited
vulnerability
for depressive
disorders
FI G U RE 5.2 • Feedback Loops
in Understanding Depressive
Disorders
Mood Disorders and Suicide 129
Treating Depressive Disorders
Different treatments target different factors that contribute to depression. However,
successful treatment of any one factor will affect the others. For example, improving
disrupted brain functioning will alter a person’s thoughts, mood, and behavior, and
interactions with others.
Targeting Neurological Factors
In treating depressive disorders, clinicians rely on two major types of treatment that
directly target neurological factors: medication and brain stimulation.
Medication
Several types of medications are commonly prescribed for depression, but it can
take weeks for one of these medications to improve depressed mood. Antidepressant
medications include the following:
• Selective serotonin reupta ke in h ibitors ( SSR Is), such a s f luoxetine
( Prozac), paroxetine ( Paxil), and sertraline (Zoloft). SSRIs slow the reuptake
of serotonin from synapses. Because these antidepressants affect only certain
receptors, they have fewer side effects than other types of antidepressant medi-
cations, which can make people less likely to stop tak ing them (Anderson,
2000 ; Beasley et a l., 2000 ). However, SSRIs are the on ly t y pe of antide-
pressant to have the side ef fect of decreased sexual interest, which can lead
some patients to stop taking them (Brambilla et al., 2005). Many patients also
f ind that the same dose of an SSRI br ings less benef it over time (A rana &
Rosenbaum, 2000).
• Tricyclic antidepressants (TCAs), such as amitriptyline (Elavil). TCAs are named
after the three rings of atoms in their molecular structure. These medications have
been used since the 1950s to treat depression and, until SSRIs became available,
were the most common medication to treat this disorder. TCAs are generally as
effective as Prozac for depression (Agency for Health Care Policy and Research,
1999). The side effects of TCAs differ from those of SSRIs: The most common
side effects include low blood pressure, blurred vision, dry mouth, and constipation
(Arana & Rosenbaum, 2000).
• Monoamine oxidase inhibitors (MAOIs), such as phenelzine (Nardil).
Some neurotransmitters, such as serotonin, dopamine, and norepinephrine, are
classified as monoamines; monoamine oxidase is a naturally produced enzyme
that breaks down monoamines in the synapse. MAOIs inhibit this chemical
breakdown, so the net effect is to increase the amount of neurotransmitter in
the synapse. MAOIs are more effective for treating atypical depression (Cipriani
et al., 2007) than typical depression. An MAOI is now available as a skin patch,
which avoids absorption via the gastrointestinal tract; this method reduces the
medical risks of oral MAOIs, including potentially fatal blood pressure changes
that are associated with eating tyramine-rich foods such as cheese and wine
( Patkar et al., 2006).
SSRIs have been the most popular antidepressants, in part because they have the
fewest side effects. By 2004, however, mental health professionals and laypeople were
raising concerns about whether SSRI use was associated with increased suicide rates.
Studies comparing SSRIs to other antidepressants did, in fact, find a greater risk for
suicidal thoughts and suicide attempts in children and adolescents taking such medi-
cations (Martinez et al., 2005); these findings led to a warning label indicating that
the medications may increase the risk of suicide in children who take them and that
the children should be closely monitored for suicidal thoughts or behaviors or for an
increase in depressive symptoms. Since the warning label was mandated, additional
research suggests that the benefits of SSRI antidepressants for youngsters outweigh
Selective serotonin reuptake
inhibitors (SSRIs)
Medications that slow the reuptake of
serotonin from synapses.
Tricyclic antidepressants (TCAs)
Older antidepressants named after the three
rings of atoms in their molecular structure.
Monoamine oxidase inhibitors (MAOIs)
Antidepressant medications that increase the
amount of monoamine neurotransmitter in
synapses.
130 C H A P T E R 5
any risk of suicide, although people taking them should continue to be carefully
monitored (Bridge et al., 2007).
Some newer antidepressants, such as venlafaxine ( Ef fexor) and duloxetine
( Cymbalta), affect neurons that respond both to serotonin and norepinephrine;
such medications are sometimes referred to as serotonin/
norepinephrine reuptake inhibitors (SNR Is). Other new
antidepressants af fect noradrenaline (the alter native
term for norepinephrine) and serotonin and are referred
to as noradrenergic and specific serotonergic antidepressants
(NaSSAs, where Na stands for “noradrenergic” ). The
antidepressant mirtazapine (Remeron) is a NaSSA. These
new medications can help some patients who do not
respond to the earlier medications.
Some people with depression who do not want to
take prescription medication have successfully used an
extract from a flower ing plant called St. John’s wort
(Hypericum perforatum). Results of meta-analytic studies
comparing St. John’s wort to prescription antidepres-
sants and placebos indicate that the herbal medication
can help patients with m ild to moderate depression,
and sometimes—but less commonly—even those with
severe depression ( Linde et a l., 20 05 ; Linde et a l.,
2008). Patients taking St. John’s wort report fewer side effects than do patients
tak ing prescr iption medications (Linde et al., 2008 ); the most com mon side
effect is dry mouth or dizziness.
Brain Stimulation: ECT and TMS
When patients with depression are not helped by medication or by other commonly
employed treatments, they may receive electroconvulsive therapy (ECT), which
consists of electrical pulses that are sent into the brain to cause a controlled brain
seizure. This seizure may reduce or eliminate the symptoms of certain psychological
disorders, most notably some forms of depression. ECT may be used when a patient:
(1) has severe depression that has not improved significantly with either medication
or psychotherapy, (2) cannot take medication because of side effects or other medi-
cal reasons, or (3) has a psychotic depression (depression with psychotic features) that
does not respond to medication (Fink, 2001; Lam et al., 1999).
In the ECT procedure, electrical pulses are delivered via electrodes placed
on the scalp. Just before ECT treatment, the patient receives a muscle relaxant,
and the treatment occurs while the patient is under anesthesia. Because of the
risks associated with anesthesia, ECT is performed in a hospital and may require
a hospital stay. ECT for depression is usually administered 2 to 3 times a week
over several weeks, for a total of 6 to 12 sessions (Shapira et al., 1998; Vieweg
& Shawcross, 1998). Depressive symptoms typically decrease a few weeks after
the treatment begins, although scientists don’t yet understand exactly how ECT
provides relief (Pagnin et al., 2004). Some people receiving ECT suffer memory
loss for events that occurred during a brief period of time before the procedure
(Semkovska & McLoughlin, 2010).
Depressed patients who did not respond to antidepressants commonly relapse
after receiving ECT: At least half of these patients experience another episode of
depression over the following 2 years (Gagne et al., 2000; Sackheim et al., 2001).
To minimize the risk of a relapse, patients usually begin taking antidepressant medi-
cation after ECT ends.
St. John’s wort, shown here as the plant and
in capsule form, may reduce mild to moderate
depression but may not be as effective as
antidepressant medication for those with
severe MDD (Linde et al., 2005).
V
a
le
ri
e
G
il
e
s/
S
ci
e
n
ce
S
o
u
rc
e
D
o
n
F
a
rr
a
ll
/G
e
tt
y
I
m
ag
e
s
Electroconvulsive therapy (ECT)
A procedure that sends electrical pulses into
the brain to cause a controlled brain seizure, in
an effort to reduce or eliminate the symptoms
of certain psychological disorders.
Mood Disorders and Suicide 131
Some patients with depression benefit from transcranial magnetic stimula-
tion. In contrast to ECT, which relies on electrical impulses, transcranial
magnetic stimulation (TMS) uses sequences of short, strong magnetic
pulses sent into the brain via a coil placed on the scalp. Each pulse lasts only
100–200 microseconds. TMS has varying effects on the brain, depending
on the exact location of the coil and the frequency of the pulses, and
researchers are still working to understand how the magnetic field affects
brain chemistry and brain activity (George et al., 1999; Wassermann et al.,
2008). In some encouraging studies, about half of the depressed patients
who did not improve with medication were treated successfully enough
with TMS that they did not need to receive ECT (Epstein et al., 1998;
Figiel et al., 1998; Klein et al., 1999). Nevertheless, ECT generally is more
effective than TMS (Slotema et al., 2010), but TMS is easier to adminis-
ter and causes fewer side effects than ECT. However, unlike with ECT,
researchers have yet to establish definitive guidelines for TMS that govern
critical features of the treatment, such as the positioning of the coils that
deliver magnetic pulses and how often the treatment should be administered
(Holtzheimer & Avery, 2005). In 2008, the Federal Drug Administration
approved TMS as a treatment for depression to be used when medication
treatments have failed.
Targeting Psychological Factors
Biomedical treatments are not the only treatments available for depression.
A variety of treatments are designed to alter psychological factors—changing
the patient’s behaviors, thoughts, and feelings.
Behavioral Therapy and Methods
Behavior therapy rests on two ideas: (1) Maladaptive behaviors stem from previous
learning, and (2) new learning can allow patients to develop more adaptive behav-
iors, which in turn can change cognitions and emotions. Behavioral methods focus
on identifying depressive behaviors and then changing them; such methods focus on
the ABCs of an unwanted behavior pattern:
• the antecedents of the behavior (the stimuli that trigger the behavior),
• the behavior itself, and
• the consequences of the behavior (which may reinforce the behavior).
For instance, being socially isolated or avoiding daily activities can lead to depressive
thoughts and feelings or can help maintain them (Emmelkamp, 1994). Changing these
behaviors can, in turn, increase the opportunities to receive positive reinforcement
(Lewinsohn, 1974).
Specific techniques to change such behaviors are collectively referred to as behav-
ioral activation (Gortner et al., 1998). These techniques include self-monitoring (keep-
ing logs of activities, thoughts, or behaviors), scheduling daily activities that lead to
pleasure or a sense of mastery, and identifying and decreasing avoidant behaviors.
Behavioral activation may also include problem solving—identifying obstacles that
interfere with achieving a goal and then developing solutions to circumvent or elimi-
nate those obstacles. For instance, a depressed college student may feel overwhelmed
at the thought of asking for an extension for an overdue paper. The student and
therapist work together to solve the problem of how to go about asking for the exten-
sion; they come up with a realistic timetable to complete the paper and discuss how
to talk with the professor.
Behavioral activation techniques may initially be aversive to a person with
depression because they require more energy than the person feels able to summon;
Transcranial magnetic stimulation (TMS)
A procedure that sends sequences of short,
strong magnetic pulses into the brain via
a coil placed on the scalp, which is used to
reduce or eliminate the symptoms of certain
psychological disorders.
Behavior therapy
The form of treatment that rests on the
ideas that: (1) maladaptive behaviors stem
from previous learning, and (2) new learning
can allow patients to develop more adaptive
behaviors, which in turn can change cognitions
and emotions.
Transcranial magnetic stimulation is a
relatively recent technique that has some
advantages over ECT for treating depression.
Jo
e
S
o
n
g
e
r/
A
L.
co
m
/L
a
n
d
o
v
132 C H A P T E R 5
however, mood improves in the long term. In fact, behavioral activation is superior
to cognitive therapy techniques in treating both moderate and severe depression
(Dimidjian et al., 2006).
Cognitive Therapy and Methods
In cont r a st to behav ior ther apy, cog n it ive therapy rest s on these idea s :
(1) Mental contents—in particular, conscious thoughts—influence a person’s
feelings and behavior; (2) irrational thoughts and incorrect beliefs contribute
to mood and behavior problems; and (3) correcting such thoughts and beliefs,
sometimes referred to as cognitive restructuring, leads to more rational thoughts
and accurate beliefs and therefore will lead to better mood and more adaptive
behavior.
The methods of cognitive therapy often require patients to collect data to
assess the accuracy of their beliefs, which are often irrational and untrue (Hollon &
Beck, 1994). This process can relieve some patients’ depression and can prevent
or minimize further episodes of depression (Teasdale & Barnard, 1993; Teasdale
et al., 2002).
Consider Kay Jamison: She felt that she was a burden to her friends and family
and that they would all be better off if she were dead. In cognitive therapy, the
therapist would explore the accuracy of these beliefs: Why did she think she was
a burden? What evidence did she have to support this conclusion? How might
friends or family react if she told them that they’d be better off if she were dead?
A cognitive therapist might even suggest that she talk to them about her beliefs
and listen to their responses to determine whether her beliefs were accurate.
Most likely, her friends and family would not agree that they’d be better off if she
were dead.
Cognitive-Behavior Therapy
Although cognitive and behavior therapies began separately, their approaches are
complementary and are frequently combined; when methods from cognitive and
behavior therapies are implemented in the same treatment, it is called cognitive-
behavior therapy (CBT). CBT, particularly when it includes behavioral activation,
is often about as successful as medication (Sava et al., 2009; Spielmans et al., 2011,
TADS Team, 2007). In some ways, CBT may be better than medication. For
example, the side effects of medication may lead patients to stop taking it: Various
studies have found that about 75% of patients either stop taking their antidepressant
medication within the first 3 months or take less than an optimal dose (Mitchell,
2007). And when patients stop taking medication, a high proportion of them relapse.
Furthermore, even when medication is successful, research suggests that people at
risk for further episodes should continue to take the medication for the rest of their
lives to prevent relapses (Hirschfield et al., 1997). In contrast, the beneficial effects of
CBT can persist after treatment ends (Hollon et al., 2005); CBT is an alternative that
need not be administered for life.
As usual, CBT and medication can be used together. In fact, studies have shown
that a combination of CBT and medication is more effective than medication alone—
even for severely depressed adolescents and adults (TADS Team, 2007; Thase et al.,
1997). In addition, after treatment with antidepressants has ended, a patient’s residual
symptoms of depression can be reduced through CBT; this supplemental CBT can
reduce the relapse rate (Fava et al., 1998a, 1998b).
Targeting Social Factors
Treatment for depression can also directly target a social factor—personal relation-
ships. Such treatment is designed to increase the patient’s positive interactions with
others and minimize the negative interactions.
Cognitive therapy
The form of treatment that rests on the
ideas that: (1) mental contents influence
feelings and behavior; (2) irrational thoughts
and incorrect beliefs lead to psychological
problems; and (3) correcting such thoughts
and beliefs will therefore lead to better mood
and more adaptive behavior.
Cognitive-behavior therapy (CBT)
The form of treatment that combines
methods from cognitive and behavior
therapies.
Mood Disorders and Suicide 133
Interpersonal Therapy
Interpersonal therapy (IPT) emphasizes the links between mood and events in
a patient’s recent and current relationships (Klerman et al.,
1984). The theory underlying IPT is that symptoms of psy-
chological disorders such as depression become exacerbated
when a patient’s relationships aren’t functioning well. The
goal of IPT is thus to improve the patient’s skills in relation-
ships so that they become more satisfying; as relationships
improve, so do the patient’s thoughts and feelings, and the
symptom of depression lessen. IPT addresses four general as-
pects of relationships, generally in about 16 sessions:
• a deficiency in social skills or communication skills, which
results in unsatisfying social relationships;
• persistent, significant conflicts in a relationship;
• grief about a loss; and
• changes in interpersonal roles (for example, a partner with
a new job may have become less emotionally available).
IPT is effective in a wide range of circumstances and settings (Cuijpers et al.,
2011). For example, in an innovative study of depressed people in 30 Ugandan rural
villages, researchers randomly assigned depressed residents from 15 villages to group
IPT, consisting of 16 weeks of 90-minute sessions. The depressed residents from the
other 15 villages received no treatment (the control group). Those who received
group IPT had a significant decrease in their depressive symptoms (and were better
able to provide for their families and participate in community activities) than those
in the control group (Bolton et al., 2003).
IPT has also successfully reduced the occurrence of peripartum depression in
pregnant women at high risk for the disorder (Zlotnick et al., 2006). In addition
to alleviating depressive symptoms, occasional additional “maintenance” sessions of
IPT—either alone or in combination with CBT—may prevent relapse (Frank et al.,
2007; Klein et al., 2004).
Systems Therapy: A Focus on the Family
A family’s functioning also may be a target of treatment; this usually occurs when a fam-
ily member’s depression is related either to a maladaptive pattern of interaction within the
family or to a conflict that arose within the family. For example, conflicts— particularly
over values—may arise within families that have immigrated to the United States;
immigrant parents and their children who grow up in the United States may experience
tension because what the parents want for their children conflicts with what the chil-
dren (as they become adults) want for themselves. Immigrant parents from Mexico, for
instance, may want to be very involved in their children’s lives, just as they would be in
their native hometown. But their children, growing up in the United States, may come
to resent what the children perceive as their parents’ intrusive and controlling behavior
(compared to the parents of their non-immigrant peers) (Santisteban et al., 2002). The
parents, in turn, may think that their children are rejecting both their Mexican heritage
and the parents themselves. Caught between two cultures—the old and the new—and
wanting to maintain aspects of their heritage but also feel “American,” the resulting
conflict can contribute to depression (Hovey, 1998, 2000).
Such problems in families may be treated with systems therapy, which is designed to
change the communication or behavior patterns of one or more family members. Ac-
cording to this approach, the family is a system that strives to maintain homeostasis, a state
of equilibrium, so that change in one member affects other family members. Systems
therapy is guided by the view that when one member changes (perhaps through therapy),
Interpersonal therapy seeks to improve
patients’ relationships and thereby alleviate
depression.
S
p
e
n
ce
r
G
ra
n
t/
P
h
o
to
E
d
it
Interpersonal therapy (IPT)
The form of treatment that is intended to
improve the patient’s skills in relationships so
that they become more satisfying.
134 C H A P T E R 5
change is forced on the rest of the system (Bowen, 1978; Minuchin, 1974). To a family
systems therapist, the “patient” is the family; systems therapy focuses on communication
and power within the family. The symptoms of a particular family member are under-
stood to be a result of that person’s intentional or unintentional attempts to maintain or
change a pattern within the family or to convey a message to family members.
Feedback Loops in Treating Depressive Disorders
The goals of any treatment for depressive disorders are ultimately the same:
• to reduce symptoms of distress and depressed mood as well as negative or unrealistic
thoughts about the self (psychological factors),
• to reduce problems related to social interactions—such as social withdrawal—and
to make social interactions more satisfying and less stressful (social factors), and
• to correct imbalances in the brain associated with some of the symptoms, such as by
normalizing neurotransmitter functioning or hormone levels (neurological factors).
Treatments that target one type of factor also affect other factors. CBT, for in-
stance, not only can reduce psychological symptoms but can also change brain activity
(Goldapple et al., 2004), improve physical symptoms (including disrupted sleep, appetite,
and psychomotor symptoms), and improve social relations. Moreover, medication for
depression works both through its effects on neurological functioning and through the
placebo effect (see Chapter 4 for a discussion about the placebo effect). Thus, a depressed
patient’s beliefs (psychological factor) can account for much of the effect of antidepressant
medication. Figure 5.3 illustrates the various treatments discussed, the targets of treat-
ments for depressive disorders, and the feedback loops that arise with successful treatment.
Note that Figure 5.3 lists the various types of treatment for depressive disorders,
sorted into the three types of factors; in two cases, we go one step further and list
SP
N
Treatments Targeting
Neurological Factors
Treatments Targeting
Psychological Factors
Treatments Targeting
Social Factors
Changes neural
activity
Changes thoughts,
feelings, and
behaviors
Changes social
interaction
Decreases family
conflict
Medication: SSRIs,
SNRIs, TCAs, MAOIs
ECT
TMS
IPT
Family systems
therapy
CBT: Behavioral
activation, cognitive
restructuring
FI G U RE 5.3 • Feedback Loops in
Treating Depressive Disorders
Mood Disorders and Suicide 135
specific types of drugs and specific CBT methods. Why are we specific with only
these two forms of treatment? Because these forms of treatment have been studied the
most extensively, and hence more is known about which specific medications and CBT
methods are most likely to reduce symptoms and improve quality of life. Rigorous
studies of other types of treatments are less common, and hence less is known about the
specific methods that are most likely to be effective. You will find this same disparity
in knowledge reflected in subsequent figures that illustrate feedback loops of treatments
for other disorders (most of these types of figures can be found on the book’s website).
Now that we’ve discussed depressive disorders, let’s look back at what we know
about Kay Jamison thus far and see whether MDD is the diagnosis that best fits her
symptoms. She experienced depressed moods, anhedonia, fatigue, and feelings of
worthlessness. She also had recurrent thoughts of death, as well as difficulty con-
centrating. Taken together, these symptoms seem to meet the criteria for MDD.
However, she also has symptoms that may support the diagnosis of another mood
disorder. We examine those building blocks in the following section.
Suppose that a friend began to sleep through morning classes, seemed uninterested in going
out and doing things, and became quiet and withdrawn. What could you conclude or not
conclude based on these observations? If you were concerned that these were symptoms
of depression, what other symptoms would you look for? If your friend’s symptoms did not
appear to meet the criteria for an MDE, what could you conclude or not conclude? If your
friend was, in fact, suffering from depression, how might the three types of factors explain
the depressive episode? What treatments might be appropriate?
Thinking Like A Clinician
Bipolar Disorders
After receiving her Ph.D. in psychology and joining the faculty of the Department
of Psychiatry at UCLA, Kay Jamison went to a garden party for faculty. The man
who would later become her psychiatrist was there, and years later they discussed
the party. Jamison’s memory of the party was that she was confident and alluring; in
contrast, he remembered her as:
. . . dressed in a remarkably provocative way, totally unlike the conservative manner
in which he had seen me dressed over the preceding year. I had on much more
makeup than usual and seemed, to him, to be frenetic and far too talkative. He says
he remembers having thought to himself, Kay looks manic. I, on the other hand, had
thought I was splendid. (p. 71)
The other set of mood disorders is bipolar disorders—in which a person’s mood
is often persistently and abnormally upbeat or shifts inappropriately from upbeat to
markedly down. (Bipolar disorders were previously referred to as manic-depressive
illness or simply manic depression.) Jamison’s behavior at the garden party indicates the
opposite of depression—mania.
Mood Episodes for Bipolar Disorders
Diagnoses of bipolar disorders are based on three types of mood episodes. These
three types are major depressive episode (which underlies MDD), manic episode, and
hypomanic episode. The patterns of a person’s particular mood episodes determines not
only the diagnosis but also the treatment and prognosis.
Manic Episode
The hallmark of a manic episode, such as the one Jamison apparently had when at
the garden party, is a discrete period of at least 1 week of abnormally increased energy
Bipolar disorders
Mood disorders in which a person’s mood is
often persistently and abnormally upbeat
or shifts inappropriately from upbeat to
markedly down.
136 C H A P T E R 5
or activity and abnormally euphoric feelings, intense irritability, or an expansive mood.
During an expansive mood, the person exhibits unceasing, indiscriminate enthusi-
asm for interpersonal or sexual interactions or for projects. The expansive mood and
related behaviors contrast with the person’s usual state. For instance, a normally shy
person may have extensive intimate conversations with strangers in public places dur-
ing a manic episode. For some, though, the predominant mood during a manic epi-
sode may be irritability. Alternatively, during a manic episode, a person’s mood can
shift between abnormal and persistent euphoria and irritability, as it did for Jamison:
When you’re high, it’s tremendous. The ideas and feelings are fast and frequent like
shooting stars, and you follow them until you find better and brighter ones. Shyness
goes, the right words and gestures are suddenly there, the power to captivate others
a felt certainty . . . Sensuality is pervasive and the desire to seduce and be seduced ir-
resistible. Feelings of ease, intensity, power, well-being, financial omnipotence, and
euphoria pervade one’s marrow. But, somewhere, this changes. The fast ideas are far
too fast, and there are far too many; overwhelming confusion replaces clarity. Memory
goes. Humor and absorption on friends’ faces are replaced by fear and concerns. Ev-
erything previously moving with the grain is now against—you are irritable, angry,
frightened, uncontrollable, and enmeshed totally in the blackest caves of the mind . . .
It will never end, for madness carves its own reality.
(1995, p. 67)
Table 5.6 lists the criteria for a manic episode.
As noted in Table 5.6, during a manic episode, a person may begin projects that
he or she doesn’t have the special knowledge or training to complete; for instance, the
person might try to install a dishwasher, despite knowing nothing about plumbing.
Moreover, when manic, some people are uncritically grandiose—often believing them-
selves to have superior abilities or a special relationship to political or entertainment
figures; these beliefs may reach delusional proportions, to the point where a person may
stalk a celebrity, believing that he or she is destined to marry that famous person.
Manic episode
A period of at least 1 week characterized
by abnormally increased energy or activity
and abnormal and persistent euphoria or
expansive mood or irritability.
Expansive mood
A mood that involves unceasing,
indiscriminate enthusiasm for interpersonal or
sexual interactions or for projects.
TABLE 5.6 • DSM-5 Criteria for Manic Episode
A. A distinct period of abnormally and persistently elevated, expansive, or irritable mood and
abnormally and persistently increased goal-directed activity or energy, lasting at least 1 week
and present most of the day, nearly every day (or any duration if hospitalization is necessary).
B. During the period of mood disturbance and increased energy or activity, three (or more)
of the following symptoms (four if the mood is only irritable) are present to a significant
degree and represent a noticeable change from usual behavior:
1. Inflated self-esteem or grandiosity.
2. Decreased need for sleep (e.g., feels rested after only 3 hours of sleep).
3. More talkative than usual or pressure to keep talking.
4. Flight of ideas or subjective experience that thoughts are racing.
5. Distractibility (i.e., attention too easily drawn to unimportant or irrelevant external
stimuli), as reported or observed.
6. Increase in goal-directed activity (either socially, at work or school, or sexually) or
psychomotor agitation (i.e., purposeless non-goal-directed activity).
7. Excessive involvement in activities that have a high potential for painful consequences (e.g.,
engaging in unrestrained buying sprees, sexual indiscretions, or foolish business investments).
C. The mood disturbance is sufficiently severe to cause marked impairment in social or occu-
pational functioning or to necessitate hospitalization to prevent harm to self or others, or
there are psychotic features.
D. The episode is not attributable to the physiological effects of a substance (e.g., a drug of
abuse, a medication, other treatment) or to another medical condition.
Reprinted with permission from the Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition, (Copyright
©2013). American Psychiatric Association. All Rights Reserved.
Mood Disorders and Suicide 137
Du r i ng a m a n ic episode, a per son need s much less
sleep—so much less that he or she may be able to go days
without it, or sleep only a few hours nightly, yet not feel
tired. Similarly, when manic, the affected person may speak
rapidly or loudly and may be diff icult to interrupt; he or
she may talk nonstop for hours on end, not letting any-
one else get a word in edgewise. Moreover, when manic,
the person rarely sits still (Cassano et al., 2009). Another
sy mptom of man ia is a f light of ideas—thoughts that
race faster than they can be said. When speaking while in
this state of mind, the person may f lit from topic to topic;
f light of ideas has commonly been described by patients as
something like watching two or three television programs
simultaneously.
D u r i n g a m a n ic e pi s o d e, t he per s on m ay a l s o b e
h ig h ly d ist r act ible a nd u n able to screen out i r releva nt
details in the environment or in conversations. Another symptom of a manic
episode is excessive plann ing of, and par t icipat ion in, mu lt iple act iv it ies. A
col lege student w ith this symptom m ight par ticipate in eight time-intensive
ex t racur r icu lar act iv it ies, includ ing a theat r ica l product ion, a musica l per –
for mance, a communit y ser vice group, and a leadership position in a campus
politica l g roup. The expansiveness, unwar ranted optim ism, g randiosit y, and
poor judgment of a manic episode can lead to the reck less pursuit of pleasur-
able act iv it ies, such a s spend ing sprees or unusua l sex ua l behav ior ( such a s
inf idelit y or indiscr im inate sexua l encounters w ith strangers). These activi-
t ies of ten lead to adverse consequences : cred it card debt f rom the spend ing
sprees or sexually transmitted diseases, including HIV, from unpro-
tected sex.
People who have had a manic episode report afterward that they
felt as if their senses were sharper during the episode—that their ability
to smell or hear was better. People often don’t recognize that they’re ill
during a manic phase; this was the case with Jamison, who, for many
years, resisted getting treatment.
Typically, a manic episode begins suddenly, with symptoms escalat-
ing rapidly over a few days; symptoms can last from a few weeks to several
months. Compared to an MDE, a manic episode is briefer and ends more
abruptly.
Hypomanic Episode
The last t y pe of mood episode associated w ith bipolar d isorders is
a hypomanic episode, which has the same cr iter ia as a manic episode,
w ith t wo sig n i f ica nt d i f ferences : The sy mptom s (1) don’t i mpa i r
functioning, require hospitalization, or have psychotic features; and
(2 ) they last a m in imum of 4 days, not 1 week. Hy poman ia rarely
includes the f light of ideas that bedevils someone in the grips of ma-
nia (American Psychiatric Association, 2013). In contrast to the gran-
diose thoughts people have about themselves during manic episodes,
dur ing hy pom an ic episodes people are uncr it ica l ly sel f- con f ident
but not grandiose. When hypomanic, some people may be more ef-
f icient and creat ive than they t y pica l ly are (A mer ican Psych iat r ic
Association, 2013). Dur ing a hypomanic episode, people may tend
to talk loudly and rapidly, but, unlike when people are manic, it is possible to
interrupt them.
Manic episodes can lead to the reckless
pursuit of pleasurable activities, including
uncharacteristic risqué or indiscriminant
sexual behavior.
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During a hypomanic episode, which is less
impairing than a manic episode, a person may go
on spending sprees or make foolish investments.
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Flight of ideas
Thoughts that race faster than they can be said.
138 C H A P T E R 5
The Two Types of Bipolar Disorder
The presence of different types of mood episodes leads to different diagnoses.
According to DSM-5, there are two types of bipolar disorder: bipolar I disorder and
bipolar II disorder. Another disorder— cyclothymia (discussed shortly)—is charac-
terized by symptoms of hypomania and depression that do not meet the criteria for
either of the two types of bipolar disorder.
The presence of manic symptoms—but not a manic episode—is the common el-
ement of the two types of bipolar disorder. The types differ in the severity of the
manic symptoms. To receive the diagnosis of the more severe bipolar I disorder, a per-
son must have a manic episode; an MDE may also occur with bipolar I. Thus, just as
an MDE automatically leads to a diagnosis of MDD, having a manic episode auto-
matically leads to a diagnosis of bipolar I. Writer and actor Carrie Fisher, who suffers
from bipolar disorder I, describes her experience in Case 5.4.
CASE 5.4 • FROM TH E INSIDE: Bipolar Disorder
“I never shut up,” she says of the times her mania would start to take over. “I could be brilliant.
I never had to look long for a word, a thought, a connection, a joke, anything.” Such heady
feelings never lasted, though.
“I’d keep people on the phone for eight hours. When my mania is going strong, it’s sort of a
clear path. You know, I’m flying high up onto the mountain, but it starts going too fast.”
“I stop being able to connect. My sentences don’t make sense. I’m not tracking anymore and
I can’t sleep and I’m not reliable.”
(Staba, 2004)
In contrast, to be diagnosed with bipolar II disorder, a person must alternate
between hypomanic episodes and MDEs (see Table 5.7); bipolar II can be thought
of as less severe because of the absence of manic episodes; however, the unpredict-
able changes in mood and the depressive episodes can impair a person’s functioning.
Table 5.8 provides additional facts about bipolar disorders.
Are people with bipolar disorders more creative?
Although actress, author, and screenwriter Carrie
Fisher has a bipolar disorder, many people with
such a disorder are not exceptionally creative, and
many creative people do not have such a disorder.
Research suggests that the two variables—the
presence of bipolar disorder and creativity—may
be unrelated (Rothenberg, 2001).
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Rapid cycling (of moods)
Having four or more episodes that meet the
criteria for any type of mood episode within
1 year.
Both types of bipolar disorder can include rapid cycling of moods, defined as
having four or more of any type of mood episode within 1 year (American Psychiatric
Association, 2013). Rapid cycling is most common with bipolar II disorder and in women
(Papadimitriou et al., 2005). Rapid cycling of either type of bipolar disorder is associated
with difficulty finding an effective treatment (Ozcan et al., 2006). As with MDD, people
with bipolar disorders may experience psychotic symptoms. People of different races and
ethnicities are equally likely to be afflicted with bipolar disorders, just as with depres-
sion. Some mental health clinicians, however, tend to diagnose schizophrenia instead of a
bipolar disorder when evaluating Black patients (Neighbors et al., 2003).
From Jamison’s descriptions, some of her experiences, such as those at the faculty
garden party, appear to have been manic episodes. Because she had at least one manic
episode, Jamison would be diagnosed with bipolar I disorder, thus changing from the
tentative diagnosis of MDD proposed earlier in the chapter.
TABLE 5.7 • DSM-5 Diagnostic Criteria for Bipolar II Disorder
• Presence (or history) of at least one major depressive episode (MDE)
• Presence (or history) of at least one hypomanic episode
• No history of manic episodes
• These symptoms (either the depression or the cycling between the depression and the
hypomania) are creating problems with functioning or significant distress.
Source: Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition, American Psychiatric Publishing, 2013.
Mood Disorders and Suicide 139
Cyclothymic disorder
A mood disorder characterized by chronic,
fluctuating mood disturbance with numerous
periods of hypomanic symptoms alternating
with depressive symptoms, each of which
does not meet the criteria for its respective
mood episodes.
TABLE 5.8 • Bipolar Disorders Facts at a Glance
Prevalence
• Between 0.4% and 1.6% of Americans suffer from bipolar I disorder; worldwide the prevalence is 0.6% (Merikangas et al., 2011).
• Approximately 0.5–1% of Americans will develop bipolar II disorder in their lifetimes (Merikangas et al., 2007); worldwide the prevalence is 0.4%
(Merikangas et al., 2011).
Onset
• Both men and women begin to have symptoms of bipolar I and II disorder by age 20, on average, although the symptoms do not necessarily
include full-blown manic attacks.
Comorbidity
• Up to 75% of those with any bipolar disorder are also diagnosed with another mental disorder, such as anxiety disorders and eating disorders
(Merikangas et al., 2011).
Course
• People who have had one manic episode have a 90% chance of having at least one further manic episode.
• Bipolar II disorder typically has a more chronic, though less severe, course than bipolar I disorder (Judd et al., 2003).
• People with either type of bipolar disorder have MDEs that are more severe and lead to more lost work days than do people with depressive
disorders (Kessler, Akiskal, et al., 2006).
• Between 5 and 15% of people with bipolar II will have a manic episode at some point, thereby changing the diagnosis to bipolar I.
Gender Differences
• Bipolar I disorder is equally common among males and females; research indicates that bipolar II disorder may be more common among females
than among males.
• Almost half of men with bipolar I disorder have their first full-blown manic episode by age 25; in contrast, only one third of women have their first
manic episode by that age ( Kennedy et al., 2005).
• In males, the number of manic episodes (or hypomanic, in the case of bipolar II disorder) often equals or exceeds the number of MDEs, whereas in
women, MDEs predominate (Altshuler et al., 2010).
• For women, having a bipolar disorder boosts the risk of developing mood episodes (of any kind) immediately after giving birth; women are also
more likely to have rapid mood cycling.
Cultural Differences
• In one international study, the United States has the highest rate of bipolar disorders, with up to 4.4% of Americans having the disorder in their
lifetimes (Merikangas et al., 2011).
Source: Unless otherwise noted, the source for information is American Psychiatric Association, 2013.
Cyclothymic Disorder
Just as persistent depressive disorder is a more chronic but typically less intense version
of MDD, cyclothymia is a more chronic but less intense version of bipolar II disorder.
The main feature of cyclothymic disorder is a chronic, fluctuating mood disturbance
with numerous periods of hypomanic symptoms that alternate with depressive symp-
toms, each of which does not meet the criteria for its respective mood episodes. These
symptoms have been present for at least half of the time within a 2-year period and
have not completely disappeared for more than 2 consecutive months (see Table 5.9).
Cyclothymia has a lifetime prevalence of 0.4–1.0% and affects men and women equally
often (American Psychiatric Association, 2013). Some people may function particularly
well during the hypomanic periods of cyclothymic disorder but be impaired during
depressive periods; this diagnosis is given only if the person’s depressed mood leads
him or her to be distressed or impaired. Thus, someone with cyclothymic disorder
may feel upbeat and energetic when having symptoms of hypomania and may begin
several projects at work or complete projects ahead of schedule. However, when having
140 C H A P T E R 5
symptoms of depression, he or she may have difficulty concentrating or mustering the
energy to work on the projects and so may fall behind on the deadlines.
Cyclothymia usually unfolds slowly during early adolescence or young adulthood,
and it has a chronic course, as Mr. F’s history reveals (see Case 5.5). Approximately
15–50% of people with cyclothymia go on to develop bipolar disorder (American
Psychiatric Association, 2013).
CASE 5.5 • FROM TH E OUTSIDE: Cyclothymic Disorder
At his girlfriend’s insistence, Mr. F., a 27-year-old single man, goes for a psychiatric evaluation. Mr. F.
reports that he is excessively energetic, unable to sleep, and irritable, and he isn’t satisfied with
the humdrum nature of his work and personal life. He is often dissatisfied and irritable for periods
of time ranging from a few days to a few weeks. These periods alternate with longer periods of
feeling dejected, hopeless, worn out, and wanting to die; his moods can shift up to 20–30 times
each year, and he describes himself as on an “emotional roller-coaster” and has been for as long
as he can remember. He twice impulsively tried to commit suicide with alcohol and sleeping pills,
although he has never had prominent vegetative symptoms, nor has he had psychotic symptoms.
(Adapted from Frances & Ross, 1996, p. 140)
Because Jamison had both MDEs and manic episodes, her
symptoms do not meet the criteria for cyclothymic disorder.
Figure 5.4 identif ies the various mood episodes and the corre-
sponding mood disorders.
Understanding Bipolar Disorders
Kay Jamison made her professional life into a quest to understand
mood disorders and why some people develop them. In the fol-
lowing sections we examine what is known about bipolar disorders
using the neuropsychosocial approach.
Neurological Factors
As with depressive disorders, both distinctive brain functioning
and genetics are associated with bipolar disorders.
Brain Systems
One hint about a neurological factor that may contribute to bipolar
disorders is the finding that the amygdala is enlarged in people who
have been diagnosed with a bipolar disorder (Altshuler et al., 1998).
This finding is pertinent because the amygdala is involved in ex-
pressing emotion, as well as in governing mood and accessing emo-
tional memories (LeDoux, 1996). Researchers have also found that
the amygdala is more active in people who are experiencing a manic
Manic episode
(current or in the past)
Hypomanic episode (current or in
the past, plus at least one MDE)
MDE only
(current or in the past)
Periods of hypomanic symptoms
alternating with periods of
depressive symptoms, over 2 years
At least three symptoms of an
MDE for at least 2 years duration
Bipolar I disorder*
Bipolar II disorder*
Major depressive disorder
(specify single
episode or recurrent)
Cyclothymic disorder
Persistent depressive
disorder (dysthymia)
MDE = Major depressive episode
FI G U RE 5.4 • Differential Diagnosis
of Mood Disorders
* According to DSM-5, once this diagnosis is made, the clinician should also note what
type of mood episode is current or most recent.
TABLE 5.9 • DSM-5 Diagnostic Criteria for Cyclothymic Disorder
A. For at least 2 years (at least 1 year in children and adolescents) there have been numerous periods with hypomanic symptoms that do not meet
criteria for a hypomanic episode and numerous periods with depressive symptoms that do not meet criteria for a major depressive episode.
B. During the above 2-year period (1 year in children and adolescents), the hypomanic and depressive periods have been present for at least half the
time and the individual has not been without the symptoms for more than 2 months at a time.
C. Criteria for a major depressive, manic, or hypomanic episode have never been met.
D. The symptoms in Criterion A are not better explained by schizoaffective disorder, schizophrenia, schizophreniform disorder, delusional disorder, or
other specified or unspecified schizophrenia spectrum or other psychotic disorder.
E. The symptoms are not attributable to the physiological effects of a substance (e.g., a drug of abuse, a medication, other treatment) or to another
medical condition.
F. The symptoms cause clinically significant distress or impairment in social, occupational, or other important areas of functioning.
Reprinted with permission from the Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition, (Copyright ©2013). American Psychiatric Association. All Rights Reserved.
Mood Disorders and Suicide 141
episode than it is in a control group of people who are not manic (Altshuler et al., 2005).
The more reactive the amygdala, the more readily it triggers strong emotional reactions—
and hence the fact that it is especially active during a manic episode makes sense.
Neural Communication
As we’ve discussed earlier in this chapter and in Chapter 2, imbalances in the levels of
certain chemicals in the brain can contribute to psychological disorders. There’s rea-
son to believe that serotonin (Goodwin & Jamison, 1990) and norepinephrine have
roles in bipolar disorders. For example, treatment with lithium (discussed shortly)
not only lowers norepinephrine levels but also reduces the symptoms of a bipolar
disorder (Rosenbaum, Arana, et al., 2005). Serotonin is an inhibitory neurotrans-
mitter, and low levels of it have been associated with depression (Mundo, Walker,
et al., 2000). However, glitches in neural communication contribute to psychological
disorders in complex ways; the problem rarely (if ever) is limited to an imbalance
of a single substance but rather typically involves complex interactions among sub-
stances. In fact, researchers have also reported that the left frontal lobes of patients
with mania produce too much of the excitatory neurotransmitter glutamate (Michael
et al., 2003), so at least three neurotransmitters—serotonin, norepinephrine, and glu-
tamate—are involved in bipolar disorders.
Genetics
Twin and adoption studies suggest that genes influence who will develop bipolar disor-
ders. If one monozygotic twin has a bipolar disorder, the co-twin has a 40–70% chance
of developing the disorder; if one dizygotic twin has the disorder, the co-twin has only
about a 5% chance of developing the disorder, which is still over twice the prevalence
in the population (Fridman et al., 2003; Kieseppä et al., 2004; McGuffin et al., 2003).
In general, if you have a first-degree relative who has bipolar disorder, you have a
4–24% risk of developing the disorder (American Psychiatric Association, 2013).
Depressive disorders and bipolar disorders—even though they now are considered
distinct disorders—in fact may be different manifestations of the same genetic vul-
nerability. When a dizygotic twin has a bipolar disorder, the other twin has an 80%
chance of developing any mood disorder (MDD, persistent depressive disorder, a bi-
polar disorder, or cyclothymia) (Karkowski & Kendler, 1997; McGuffin et al., 2003;
Vehmanen et al., 1995). Given such findings, it’s not surprising that Jamison had
many relatives (on her father’s side) who had mood disorders. However, research-
ers do not yet know how specific genes contribute to an inherited vulnerability for
mood disorders.
Psychological Factors: Thoughts and Attributions
Most research on the contribution of psychological factors to bipolar disorders
f ocuses on cognitive distortions and automatic negative thoughts, which not only
are common among people with depression but also plague people with a bipolar
disorder during MDEs. In fact, research suggests that when depressed, people with
either MDD or a bipolar disorder have a similar internal attributional style for nega-
tive events (Lyon et al., 1999; Scott et al., 2000). Mirroring these results, people with
cyclothymia or persistent depressive disorder have a similar negative attributional
style (Alloy et al., 1999).
In addition, even after a manic episode is completely resolved, up to one third of peo-
ple may have residual cognitive deficits, ranging from difficulties with attention, learning,
and memory to problems with executive functioning (planning and decision making)
and problem solving (Kolur et al., 2006; Thompson et al., 2005; Zubieta et al., 2001).
Moreover, the more mood episodes a person has, the more severe these deficits tend to
be. Researchers propose that the persistent cognitive deficits associated with mania should
become part of the diagnostic criteria for bipolar disorders, in addition to criteria on
mood-related behaviors (Phillips & Frank, 2006).
142 C H A P T E R 5
Social Factors: Social and Environmental Stressors
Social factors such as starting a new job or moving to a different city can also affect the
course of bipolar disorders (Goodwin & Jamison, 1990; Malkoff-Schwartz et al., 1998).
Stress appears to be part of the process that
leads to a first episode ( Kessing et al., 2004);
people who develop a bipolar disorder of-
ten experience significant stressors in their
lives before their f irst episode ( Goodwin
& Ghaemi, 1998; Tsuchiya, Agerbo, et al.,
2005). Stress can also worsen the course of
the disorder ( Johnson & Miller, 1997). In
addition, stress—in particular, family-related
stress—may contribute to relapse; people
who live with family members who are crit-
ical of them are more likely to relapse than
those whose family members are not critical
(Honig et al., 1997; Miklowitz et al., 1988).
Social factors can also have indirect ef-
fects, such as occurs when a new job dis-
rupts a person’s sleep pattern, which in turn
triggers neurological factors that can lead to a mood episode.
Feedback Loops in Understanding Bipolar Disorders
Bipolar disorders have a clear genetic and neurological basis, but feedback loops nev-
ertheless operate among the neurological, psychological, and social factors associated
with these disorders. Consider the effects of sleep deprivation. It may directly or indi-
rectly affect neurological functioning, making the person more vulnerable to a manic
or depressive episode. Moreover, like people with depression, people with a bipolar
disorder tend to have an attributional style (psychological factor) that may make them
more vulnerable to becoming depressed. In turn, their attributional style may affect
how these people interact with others (social factor), such as in the way they respond
to problems in relationships. Even after a mood episode is over, residual problems with
cognitive functioning—which affect problem solving, planning, or decision making—
can adversely influence the work and social life of a person with a bipolar disorder.
We can now understand Jamison’s bipolar disorder as arising from a confluence
of neuropsychosocial factors and feedback loops. Her family history provided a strong
genetic component to her illness, which has a clear neurological basis (neurological
factors). Her struggle against recognizing that she had an illness (psychological
factors) meant that she didn’t do as good a job as she could have done in protecting
herself from overwork (social factor), making her more vulnerable to a mood episode.
Treating Bipolar Disorders
As with depressive disorders, treatment for bipolar disorders can directly target any of the
three types of factors—neurological, psychological, and social. Keep in mind, though,
that the effects of any successful treatment extend to all the types of factors. Jamison
describes the subtle ways that feedback loops operated on her disorder and treatment:
My temperament, moods, and illness clearly, and deeply, affected the relationships I
had with others and the fabric of my work. But my moods were themselves power-
fully shaped by the same relationships and work. The challenge was in learning to
understand the complexity of this mutual beholdenness and in learning to distinguish
the roles of [the medication] lithium, will, and insight in getting well and in leading a
meaningful life. It was the task and gift of psychotherapy.
(1995, p. 88)
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Mood Disorders and Suicide 143
Targeting Neurological Factors: Medication
People d iag nosed w ith a bipolar d isorder usua l ly take some t ype of mood
stabilizer—a medication that minimizes mood swings—for the rest of their lives.
(The term mood stabilizer is sometimes used more broadly to include medications that
decrease impulsive behavior and violent aggression.) Mood stabilizers can reduce
recurrences of both manic and depressive episodes (Arana & Rosenbaum, 2000).
The oldest mood stabilizer is lithium; technically the medication is called lithium
carbonate, a type of salt. Jamison describes her response to the drug: “I took [lithium]
faithfully and found that life was a much stabler and more predictable place than I
had ever reckoned. My moods were still intense and my temperament rather quick to
the boil, but I could make plans with far more certainty and the periods of absolute
blackness were fewer and less extreme” (1995, p. 153). Lithium apparently affects
several different neurotransmitters (Lenox & Hahn, 2000) and thereby alters the
inner workings of neurons (Friedrich, 2005). However, too high a dose of lithium
can produce severe side effects, including coordination problems, vomiting, muscular
weakness, blurred vision, and ringing in the ears; thus, patients must have their blood
levels of lithium checked regularly to ensure that they are taking an appropriate
dosage (Arana & Rosenbaum, 2000).
Lithium is not an effective treatment for all patients. In fact, up to half of patients
who are prescribed lithium either cannot tolerate the side effects or do not show
significant improvement, especially patients who have rapid cycling (Burgess et al.,
2001; Keck & McElroy, 2003; Montgomery et al., 2001). In such cases, other mood
stabilizers may help to prevent extreme mood shifts, especially recurring manic
episodes. These include antiepileptic medications (also called anticonvulsants) such as
divalproex ( Depakote), carbamazepine (Tegretol), lamotrigine (Lamictal), and gabapentin
(Neurontin).
Some people with bipolar disorders stop taking mood stabilizers not because of
the common side effects (such as thirst, frequent urination, and diarrhea) but rather
because the medication does what it’s supposed to do—evens out their moods (Arana
& Rosenbaum, 2000; Rosa et al., 2007). Some of these people report that they miss
aspects of their manic episodes and feel that the medication blunts their emotions.
Mood stabilizers aren’t the only medications given for bipolar disorders. Patients
with a bipolar disorder may be given antidepressant medication for depression, but
such medications can induce mania and so should be taken along with a mood
stabilizer; in addition, patients with a bipolar disorder who take antidepressant medi-
cation should take it for as brief a period as possible (Rosenbaum, Arana, et al., 2005).
For a manic episode, the person may be given an antipsychotic medication such as
olanzapine ( Zyprexa) or aripiprazole (Abilify) or a high dose of a benzodiazepine—a
class of medications commonly known as tranquilizers (Keck et al., 2009; Yildiz
et al., 2011).
Despite the number of medications available to treat bipolar disorders, mood epi-
sodes still recur; in one study, half of the participants developed a subsequent mood
episode within 2 years of recovery from an earlier episode (Perlis, Ostacher, et al., 2006).
Targeting Psychological Factors: Thoughts, Moods, and Relapse
Prevention
Medication can be an effective component of treatment for bipolar disorders, but
often it isn’t the only component. Treatment that targets psychological factors focuses
on helping patients develop patterns of thought and behavior that minimize the risk
of relapse (Fava, Bartolucci, et al., 2001; Jones, 2004; Scott & Gutierrez, 2004). CBT
can help patients stick with their medication schedules, develop better sleeping strate-
gies, and recognize early signs of mood episodes, such as needing less sleep (Frank
et al., 2005; Miklowitz, 2008; Miklowitz et al., 2007).
Mood stabilizer
A category of medication that minimizes
mood swings.
Lithium
The oldest mood stabilizer.
144 C H A P T E R 5
Other treatments that target social factors focus on the family: educating family
members about bipolar disorder and providing emergency counseling during crises
(Miklowitz et al., 2000, 2003, 2007). Also, family therapy that leads family mem-
bers to be less critical of the patient can reduce relapses (Honig et al., 1997). Another
treatment with a social focus is group therapy or a self-help group, either of which
can decrease the sense of isolation or shame that people with a bipolar disorder may
experience; group members support each other as they try to make positive changes.
Feedback Loops in Treating Bipolar Disorder
Both Jamison and her psychiatrist understood that treatment could affect multi-
ple factors. She recognized that medication might help her, but she had to want to
take the medication. Similarly, she recognized that psychotherapy alone could not
prevent her mood episodes. She needed them both.
We have seen that successful treatments for bipolar disorders can address multiple
factors—for example, CBT can result in more consistent medication use, and IPSRT
can reduce the frequency of events that might trigger relapse. Successful treatment
can also affect interpersonal relationships, leading patients to interact differently with
others, develop a more regular schedule, and come to view themselves differently.
Moreover, such therapy leads patients to change the attributions they make about
events and even change how reliably they take medication for the disorder.
O N L I N E
SP
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For someone making use of interpersonal social and rhythm therapy, which of the wakeup times shown in the photos
would be best on a weekend, assuming that the person wakes up at 6:00 a.m. during the week? Answer: 6:00 a.m.
(the photo on the left); keeping a regular sleep–wake schedule 7 days per week can help reduce the risk of relapse.
GETTING THE PICTURE
©
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Targeting Social Factors: Interacting with Others
Treatments that target social factors are designed to help patients minimize disruptions
in their social patterns and develop strategies for better social interactions (Lam et al.,
2000), which can reduce the rate of relapse. One such treatment, adapted from IPT,
is called interpersonal and social rhythm therapy (IPSRT; Frank et al., 1999). As in IPT,
IPSRT sessions focus on identifying themes of social stressors, such as a relationship
conflict that arises because partners have different expectations of the relationship.
Treatment can then focus on developing effective ways for the patient to minimize
such social stressors. In addition, IPSRT focuses on the timing of events (such as ar-
ranging weekend activities so that the patient wakes up at the same time each morn-
ing and goes to sleep at the same time each night—weekend and weekday), increasing
overall regularity in daily life (such as having meals at relatively fixed times during
the day), and helping the patient want to maintain regularity. IPSRT plus medication
is more effective than medication alone (Miklowitz, 2008; Miklowitz et al., 2007).
Mood Disorders and Suicide 145
Jamison’s treatment involved interactions among the factors: Her therapy helped
her to recognize and accept her illness and encouraged her to take care of herself
more appropriately (psychological and social factors), including sticking with a daily
regimen of lithium (neurological factor). Furthermore, the successful lithium treat-
ment allowed her to have better relationships with others (social factor), which led to
a positive change in how she saw herself (psychological factor).
You get in touch with a friend from high school who tells you that she recently had experiences
that you realize are symptoms of hypomania. What are two possible DSM-5 diagnoses that might
apply to her? (Be specific.) What will determine which diagnosis is most appropriate? What are a
few of the symptoms that are hallmarks of hypomania? What would be the difference in symp-
toms if your friend instead experienced a manic episode? Would her diagnosis change or stay the
same? Explain. What would be the most appropriate ways to treat bipolar disorders?
Thinking Like A Clinician
Suicide
On more than one occasion, Kay Jamison seriously contemplated suicide. One day,
when deeply depressed, she did more than think about it—she attempted suicide. She
was seeking relief from her pain and for the pain she felt she was inflicting on her
family and friends:
In a perverse linking with my mind I thought that . . . I was doing the only fair
thing for the people I cared about; it was also the only sensible thing to do for
myself. One would put an animal to death for far less suffering.
(p. 115)
When Jamison attempted suicide, she was already receiving treatment for
her disorder; in contrast, a majority of people who die by suicide have
an untreated mental disorder, most commonly depression. Jamison’s at-
tempt was foiled. She later describes being grateful that she continued liv-
ing. The hopelessness that she had felt went away, and she was able to enjoy
life again.
Suicidal Thoughts and Suicide Risks
In the United States and Canada, suicide is ranked 10th among causes of death
(CDC, 2010a; Statistics Canada, 2005). Approximately 32,000 people die by suicide
each year in the United States (CDC, 2005), which constitutes about 1% of all deaths
per year (McIntosh, 2003). Worldwide, suicide is the second most frequent cause of
death among women under 45 years old (tuberculosis ranks first), and it is the fourth
most frequent cause among men under 45 (after road accidents, tuberculosis, and vio-
lence; WHO, 1999). Table 5.10 lists more facts about suicide.
Thinking About, Planning, and Attempting Suicide
When suffering from a mood disorder, people may have thoughts of death or
thoughts about committing suicide, known as suicidal ideation (Rihmer, 2007).
But suicidal ideation does not necessarily indicate the presence of a psychological
disorder or an actual suicide risk. Approximately 10–18% of the general popula-
tion—including both those with and without disorders—has at some point had sui-
cidal thoughts (Weissman, Bland, et al., 1999). One study found that 6% of people
who were healthy and had never been depressed occasionally thought about suicide
(Farmer et al., 2001). Suicidal thoughts may range from believing that others would
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Past research suggested that suicide rates
peak in the spring for both men and women,
with another peak in the autumn for women
(Meares et al., 1981). However, more recent
research suggests that such a relationship
may be weakening over time (Yip et al., 1998,
2000, 2006), perhaps because the effects of
seasonal differences are minimized by modern
artificial environments (Simkins et al., 2003).
Suicidal ideation
Thoughts of suicide.
146 C H A P T E R 5
be better off if the person were dead (which Jamison had) to specific plans to commit
suicide.
Approximately 30% of those who have thoughts of suicide have also conceived
of a plan (Kessler, Borges, et al., 1999). Even having a plan does not by itself indicate
that a person is at risk for suicide. However, certain behaviors can suggest serious sui-
cidal intent and can serve as warning signs (Packman et al., 2004):
• giving away possessions,
• saying goodbye to friends or family members,
• talking about death or suicide generally or about specific plans to commit suicide,
• threatening to commit suicide, and
• rehearsing a plan for suicide.
Not everyone who plans or is about to commit suicide displays such warning signs.
For some people, suicidal thoughts or plans do turn into actions. Certain
methods of suicide are more lethal than others, and the more lethal the method,
the more likely it is that the suicide attempt will result in death or serious medical
problems. For instance, shooting, hanging, and jumping from a high place are
more lethal than taking pills and cutting a vein. In the latter situations, the per-
son often has at least a few minutes to seek help after having acted. Some people
may be very ambivalent about suicide and so may attempt suicide with a less lethal
method or try to ensure that they are found by others before any lasting damage
is done. Unfortunately, these suicide attempts may still end in death because the
help the person had anticipated may not materialize. Other people who attempt sui-
cide do not appear to be ambivalent; they may or may not display warning signs
TABLE 5.10 • Suicide Facts at a Glance
Prevalence
• Approximately 1.3% of all deaths in the United States are considered to be suicides—more
than 32,000 people annually (CDC, 2005).
• Worldwide, the elderly (65 and older) are three times as likely to commit suicide as are those
under 25 years old (WHO, 1999).
• In the United States, suicide is most likely to occur among the middle aged (45–54),
particularly White men; young people (under 26) are the next most likely to commit suicide
(CDC, 2000, 2005, 2013; Miniño et al., 2002).
• From 1950 to 1995, worldwide suicide rates increased by 60%, particularly among young
men (WHO, 1999), making it the third leading cause of death for teenagers, particularly
males (Waters, 2000).
Gender Differences
• Worldwide, women are more likely to attempt suicide than are men (Nock et al., 2008).
• In the United States, although women are more likely to attempt suicide, men are four times
more likely to die from an attempt (CDC, 2005).
Cultural Differences
• Hanging is the most common method of suicide worldwide, but guns are the most common
method in the United States (particularly among men), undoubtedly because access to them
is easier than in other countries (De Leo, 2002a; Moscicki, 1995; Romero & Wintemute, 2002).
• Internationally, Eastern European countries, as a region, have the highest rates of suicide;
examples are Belarus (41.5 per 100,000) and Lithuania (51.6 per 100,000). Latin American
countries tend to have the lowest rates; examples are Paraguay (4.2 per 100,000) and
Colombia (4.5 per 100,000) (WHO, 2002).
Mood Disorders and Suicide 147
but will follow through unless someone or something inter venes
(Maris, 2002).
Not all acts associated with suicide—such as certain t ypes of
sk in cutting—are, in fact, suicide attempts. Such deliberate but
non letha l sel f-ha r m i ng is somet i mes refer red to a s parasuicidal
behavior. People may harm themselves without any suicidal impulse
because they feel numb or because such self-har m ing behaviors
al low them to “feel something” (Linehan, 1981). A lter natively,
some people deliberately harm themselves to elicit particular reac-
tions from others. Parasuicidal behavior is discussed in more detail
in Chapter 13.
Risk and Protective Factors for Suicide
The risk of suicide is higher for people who have a psychological
disorder—whether officially diagnosed or not—than for those who do
not have a disorder. The three most common types of disorders among
those who commit suicide are (Brown et al., 2000; Duberstein & Con-
well, 1997; Isometsä, 2000; Moscicki, 2001):
• major depressive disorder (50%),
• personality disorders (40%), and
• substance-related disorders (up to 50% of those who commit suicide
are intoxicated by alcohol at the time of their death).
People who com m it suicide may have more than one of these
disorders. Recognizing that people with disorders other than mood
disorders may contemplate suicide, DSM-5 includes a question about
suicidal ideation in its cross-cutting symptoms assessment (described in
Chapter 3) (American Psychiatric Association, 2013).
Substance use or abuse plays a pivotal role in many suicide attempts
because drugs and alcohol can cloud a person’s judgment and ability to
reason. A history of being impulsive is another significant risk factor
for suicide (Sánchez, 2001). Impulsive people may not exhibit warning
signs of serious suicidal intent.
Beyond the presence of specific psychological disorders or impulsivity, another
strong predictor of completed suicide is a history of past suicide attempts (Moscicki,
1997; Oquendo et al., 2007). Specifically, people who previously made serious
attempts are more likely subsequently to die by suicide than are those who did not
make serious attempts (Ivarsson et al., 1998; Stephens et al., 1999). Additional risk
factors are listed in Table 5.11. Those at risk may benefit from early evaluation and
treatment.
One group at increased risk for suicide is gays and lesbians, particularly during
adolescence (Ramafedi, 1999). The increased risk, however, stems primarily from
the social exclusion and discrimination experienced by these people ( Igartua et al.,
2003). Among homosexuals, suicide is most likely during the period when dis-
closing their homosexuality to immediate family members (Igartua et al., 2003).
In addition, military personnel in certain settings are at high risk for committing
suicide, probably because of the strain on family relationships caused by long and
repeated tours of duty, combat-related stress, substance abuse, and legal and financial
problems.
Despite such risks, most people who are depressed or have thoughts of suicide
do not actually try to kill themselves. Even when in the blackest suicidal despair,
specific factors can reduce the risk of a suicide attempt: receiving support from family
and friends, holding religious or cultural beliefs that discourage suicide, and getting
Researchers have examined suicide notes to
evaluate what leads some people to try to
kill themselves. Any conclusions drawn from
such data, however, are limited. Fewer than
40% of the people who commit suicide leave
notes, and there may be important differences
between those who leave notes and those
who don’t (Leenaars, 1988; O’Connor et al.,
1999). Moreover, suicide notes are subject
to various self-report biases, including the
desire to leave a particular impression and to
elicit a particular reaction from the readers
(Leenaars, 2003).
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prompt and appropriate treatment for any depression or substance abuse. Additional
protective factors are listed in Table 5.11.
Understanding Suicide
To understand why some people commit suicide, we now turn to examine relevant
neurological, psychological, and social factors and their feedback loops.
Neurological Factors
Because the main risk factors for suicide are associated with depression and impulsiv-
ity (as well as past suicide attempts), it is difficult to identify neurological factors that
uniquely contribute to suicide as distinct from factors that contribute to depression
TABLE 5.11 • Risk and Protective Factors for Suicide
Risk Factors
• Mental disorder associated with suicidal behavior (e.g., depression, substance abuse, or
personality disorder)
• Feeling hopeless
• Being male (in the United States)
• Prior suicidal behavior (suicide threats, suicide attempts)
• Specific behaviors that suggest suicide planning (giving away possessions, saying goodbye
to friends, talking about death or suicide, talking about specific plans to commit suicide,
rehearsing a suicidal act, and/or accumulating medications)
• Family history of suicidal behavior
• Chronic impulsivity or aggression and low stress tolerance
• Poor coping and problem-solving skills
• Poor judgment and rigid, distorted thinking
• Major life stressors (physical or sexual assault, threats against life, diagnosis of serious medical
problem, dissolution of a significant relationship, or sexual identity issues)
• Breakdown of support systems or social isolation
• Changes in mental status (acute deterioration in mental functioning, onset of major mental
illness, extreme anxiety, paranoia, or severe depression)
• Unsatisfying relationship history (never married, separated, divorced, or lack of significant
relationships)
• Poor work history (spotty work history or chronic unemployment)
• Childhood abuse
• History of violent behavior
Protective Factors
• Married (or having a significant relationship)
•
Employed or involved in a structured program (educational or vocational training program)
• Presence of a support system (family, friends, church, and/or social clubs)
• Having children who are under 18 years of age
• Constructive use of leisure time (enjoyable activities)
• General purpose for living (including religious conviction)
• Involved in mental health treatment
• Effective problem-solving skills
Source: Adapted from Sánchez, 2001, Appendix A.
Mood Disorders and Suicide 149
and impulsivity. Nevertheless, neurological factors that contribute to suicide per se
are beginning to be identified.
Guided by the f inding that mood disorders ref lect, at least in part, levels of
the neurotransmitter serotonin, Bielau and colleagues (2005) reported a sugges-
tive trend: People who committed suicide tended to have fewer neurons in the part
of the brain that produces serotonin than did people who died of other causes. In
addition, researchers have found that people who commit suicide may have had fewer
serotonin receptors in their brains (Boldrini et al., 2005). Notably, impulsivity is also
associated with low serotonin levels.
Suicide seems to “run in families” (Correa et al., 2004), but it is difficult to
discern a specific role of genes in influencing people to commit suicide. Depression
has a genetic component, which may account for the higher rates of suicide among
both twins in monozygotic pairs (13%) compared to dizygotic pairs (,1%) (Zalsman
et al., 2002).
Psychological Factors: Hopelessness and Impulsivity
A number of the risk factors in Table 5.11 are psychological factors, such as poor
coping skills (e.g., behaving impulsively) and poor problem-solving skills (e.g.,
difficult y identif ying obstacles that inter fere with meeting goals or failing to
develop ways to work around obstacles), distorted and rigid thinking (thought
patterns associated with depression), and hopelessness. Hopelessness, with its
bleak thoughts of the future, is especially associated with suicide (Beck et al.,
1985, 1990).
Social Factors: Alienation and
Cultural Stress
Suicide rates vary across countries (De Leo, 2002a;
Vijayakumar et al., 2005; WHO, 1999), which
suggests that social and cultural factors affect these
rates. In some developing countries, the presence
or history of a psychological disorder poses less of a
risk for suicide than it does in developed countries
(Vijayakumar et al., 2005).
One important social factor that influences sui-
cidal behavior is religion. Countries where the citizens
are more religious tend to have lower suicide rates than
do countries where citizens are less religious. Coun-
tries with a large Muslim population are among those
with the lowest suicide rates in the world, followed by
countries with a large Roman Catholic population; the
tenets of both of these religions forbid suicide (De Leo,
2002a; Simpson & Conklin, 1989).
Feedback Loops in Understanding Suicide
Suicide can best be understood as arising from the confluence of neurological,
psychological, and social factors. A neurological vulnerability, such as abnormal
neurotransmitter functioning, serves as the backdrop. Add to that the psychological
factors: depression or feelings of hopelessness, beliefs about suicide, poor coping
skills, and perhaps impulsive or violent personality traits. In turn, these factors
affect, and are affected by, social and cultural forces—such as economic reali-
ties, wars, cultural beliefs and norms about suicide, religion, stressful life events,
and social support. The dynamic balance among all these factors can influence a
SP
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Cultural norms and customs can influence
suicide rates. Among the Yuit Eskimos of
St. Lawrence, when someone requests suicide
three times, relatives are supposed to help
the person kill himself or herself (Leighton
& Hughes, 1955). In contrast, among the Tiv
of Nigeria, suicide reportedly never occurs
(Evans & Farberow, 1988). Such cultural norms
about suicide can affect a person’s beliefs and
expectations about suicide.
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person’s suicidal ideation, plans, and behavior (Sánchez,
2001; Wenzel et al., 2009).
Preventing Suicide
Su icide prevent ion ef for t s can focus on i m med iate
safety or longer-term prevention.
Crisis Intervention
For a person who is actively suicidal, the first aim of sui-
cide prevention is to make sure that the person is safe.
After this, crisis intervention helps the person see past the
hopelessness and rigidity that pervades his or her think-
ing, identifies whatever stressors have brought the person
to this point, helps him or her develop new solutions to
the problems, and enhances his or her ability to cope.
In addition, a clinician tries to discover whether the person is depressed or
abusing substances; if so, these problems, which may lead to suicidal thoughts or
behaviors, should be treated (Reifman & Windle, 1995). Because most people who
die by suicide had untreated depression, treatment for depression that targets psycho-
logical factors—typically CBT—can play a key role in suicide prevention. Medica-
tions may also be prescribed to reduce depressive symptoms.
Long-Term Prevention
Ideally, long-term prevention programs decrease risk factors and increase protective
factors, which should decrease the suicide rate. Thus, programs to prevent child abuse,
to provide affordable access to mental health care (and so make it easier to obtain
treatment for psychological disorders, in particular depression), to decrease substance
abuse, and to increase employment may all help prevent suicides in the long term.
Part of the national suicide prevention plan in the United States is to increase
awareness about suicide (Satcher, 1999), both among people who may feel suicidal
and among the friends and family of someone feeling suicidal. The hope is that sui-
cidal people will receive appropriate help before they commit suicide (see Table 5.12).
TABLE 5.12 • Suicide Prevention: What to Do
What can you do if someone you know seems to be suicidal? According to the National
Institute of Mental Health (Goldsmith et al., 2002):
• don’t leave the person alone;
• get help by calling 911 or other trained emergency professionals;
• try to make sure that potential means for committing suicide, such as firearms or poisons,
are not easily accessible; and
• let the person know that you are concerned and try not to be judgmental.
If you, or someone you know, are at risk for suicide, the following organizations can help:
• National Suicide Prevention Lifeline
Phone: 800-273-TALK (8255). This will connect you with a crisis center in your area.
Website: www.suicidepreventionlifeline.org
• American Foundation for Suicide Prevention
Phone: 212-363-3500
Website: www.afsp.org
• Suicide Prevention Resource Center
Phone: 617-438-7772
Website: www.sprc.org
In 2012 the number of suicides among
U.S. Army soldiers was greater than in
previous years, having risen sharply since
2005 (Williams, 2012). The Army’s suicide
prevention efforts include hiring additional
mental health providers and instituting a
program to teach junior Army leaders how
to recognize signs of suicide intention in
their troops and how to then intervene
(Tyson, 2008).
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Mood Disorders and Suicide 151
Based on what you have learned about suicide, explain Kay Jamison’s suicide attempt in terms
of the three types of factors. Identify how the neurological, psychological and social factors
might have influenced each other via feedback loops. From what you know of her, what were
Jamison’s risk and protective factors?
Thinking Like A Clinician
Depressive Disorders
• A major depressive episode (MDE) is a mood
episode upon which a diagnosis of major de-
pressive disorder (MDD) is based. Symptoms
of an MDE can arise in three areas: affect,
behavior, and cognition. Most people who
have an MDE return to their premorbid
level of functioning after the episode, but
some people will have symptoms that do not
completely resolve, even after several years.
• Depression is becom i ng i ncrea si ng ly
prevalent in younger cohorts. Depression
a n d a n x i e t y d i s o r d e r s h a ve a h i g h
comorbidity—around 50%.
• MDD may arise with psychotic features.
• In some cases, depression is related to
pregnancy and giving birth (peripartum
onset) or to seasonal changes in light.
• A d i a g no s i s of per s i st ent depre s s ive
disorder requires fewer symptoms than
does a diagnosis of MDD; however, the
symptoms of persistent depressive disorder
must persist for at least 2 years.
• Neurological factors related to depression
include low levels of activity in the frontal
lobes, and abnormal functioning of various
neurotransmitters (dopamine, serotonin, and
norepinephrine). The stress–diathesis model
of depression highlights the role of increased
activity of the HPA axis and of excess cor-
tisol in the blood. Genes can play a role in
depression, perhaps by inf luencing how a
person responds to stressful events, which in
turn affects the activity of the HPA axis.
• Psychological factors that are associated
with depression include a bias toward pay-
ing attention to negative stimuli, dysfunc-
tional thoughts, rumination, a negative
attributional style, and learned helplessness.
• Socia l factors that are associated w ith
depression include stressful life events,
social exclusion, and problems with social
interactions or relationships. Culture and
gender can influence the specific ways that
symptoms of depression are expressed.
• Neurological, psychological, and social fac-
tors can affect each other through feedback
loops, as outlined by the stress–diathesis
model and Coyne’s interactional theory
of depression. According to the stress–
diathesis model, abuse or neglect during
childhood (a stressor) and increased activ-
ity in the HPA axis can lead to overreactive
cortisol-releasing cells (a diathesis), which
respond strongly to even mild stressors.
Psychological factors can create a cognitive
vulnerability to depression, which in turn
can amplify the negative effects of a stressor
and change social interactions. Coyne’s
theory proposes that among neurologically
vulnerable people, their depression-related
behav ior s m ay a l ienate other people,
producing social stressors.
• Biomedical treatments that target neu-
rological factors for depressive disorders
are medications (SSRIs, TCAs, MAOIs,
SNRIs, NaSSAs) and St. John’s wort, and
brain stimulation (ECT or TMS).
• Treat ment s for depression that t arget
p s yc h o l o g i c a l f a c t o r s i n c l u d e C B T
(particularly with behavioral activation).
• Treat ment s t h at t a rget soc ia l f actor s
include IPT and systems therapy.
Bipolar Disorders
• The three t ypes of mood episode that
u nderl ie bipol a r d i sorder s a re m ajor
depressive episode (MDE), manic episode,
and hypomanic episode. Symptoms of
a m a n ic episode i nclude g ra nd iosit y,
pressured speech, flight of ideas, distract-
ibilit y, poor judgment, decreased need
for sleep, and psychomotor agitation. A
hypomanic episode involves mood that is
persistently elated, irritable, or euphoric;
unlike other mood episodes, hypomanic
episodes do not impair functioning.
• There are two types of bipolar disorder:
Bipolar I disorder—usually more severe—
requires only a manic episode; an MDE
may occur but is not necessar y for this
diagnosis. Bipolar II disorder requires
a lter n at i n g hy pom a n ic epi sode s a nd
MDEs and no history of manic episodes.
Cyclothymic disorder is a more chronic
but less i nten se ver sion of bipol a r II
disorder.
• Neurological factors that are associated
w i t h b i p o l a r d i s o r d e r s i n c l u d e a n
en l a rged a nd more act ive a mygd a l a.
Norepinephrine, serotonin, and glutamate
are also involved. Bipolar disorders are
influenced by genetic factors, which may
affect mood disorders in general.
• Psychological factors that are associated
with bipolar disorders include the cog-
nitive distortions and negative thinking
associated with depression.
• Social factors that are associated with bipo-
lar disorders include disruptive life changes
and social and environmental stressors.
The different factors create feedback loops
that can lead to a bipolar disorder or make
the patient more likely to relapse.
• Tr e a t m e n t s t h a t t a r g e t n e u r o l o g i –
cal factors include medications that act
as mood stabilizers, such as lithium and
anticonvulsants. When manic, patients
may receive an antipsychotic medication or
a benzodiazepine. Patients with a bipolar
disorder who have MDEs may receive an
antidepressant along with a mood stabilizer.
• Treat ment t h at t a rget s ps ycholog ica l
factors—particularly CBT—helps patients
recognize warning signs of mood episodes,
develop better sleeping strategies, and,
when appropriate, stay on medication.
• Treat ment s t h at t a rget soc ia l f actor s
include interpersonal and social rhythm
therapy (IPSRT), fam i ly therapy, and
group therapy or a self-help group.
Suicide
• Suicide is ranked 10th among causes of
death in North America. Having thoughts
of suicide or making a plan to carry it out
may indicate a risk for suicide; certain
behavioral changes (such as giving away
possessions) may indicate a more serious
risk. However, not everyone who attempts
or commits suicide displays warning signs.
In addition, certain types of self-harm may
be parasuicidal behaviors rather than sui-
cide attempts. The presence of certain psy-
chological disorders, such as MDD, and a
SUMMING UP
152 C H A P T E R 5
More Study Aids
For additional study aids related
to this chapter, including quizzes
to make sure you’ve retained
everything you’ve learned
and a Student Video Activity
exploring one man’s struggle with
persistent depressive disorder,
go to: www.worthpublishers.
com/launchpad/rkabpsych2e.
Photodisc
Mood disorders (p. 115)
Major depressive episode (MDE) (p. 116)
Anhedonia (p. 116)
Psychomotor agitation (p. 116)
Psychomotor retardation (p. 117)
Hypersomnia (p. 117)
Prodrome (p. 118)
Premorbid (p. 118)
Major depressive disorder (MDD) (p. 118)
Phototherapy (p. 119)
Age cohort (p. 119)
Persistent depressive disorder (dysthymia)
(p. 120)
Disruptive mood dysregulation disorder
(DMDD) (p. 120)
Selective serotonin reuptake inhibitors (SSRIs)
(p. 130)
Tricyclic antidepressants (TCAs) (p. 130)
Monoamine oxidase inhibitors (MAOIs) (p. 130)
Electroconvulsive therapy (ECT) (p. 131)
Transcranial magnetic stimulation (TMS) (p. 132)
Behavior therapy (p. 132)
Cognitive therapy (p. 133)
Cognitive-behavior therapy (CBT) (p. 133)
Interpersonal therapy (IPT) (p. 134)
Bipolar disorders (p. 136)
Manic episode (p. 137)
Expansive mood (p. 137)
Flight of ideas (p. 138)
Rapid cycling (of moods) (p. 139)
Cyclothymic disorder (p. 140)
Mood stabilizer (p. 144)
Lithium (p. 144)
Suicidal ideation (p. 146)
history of previous serious suicide attempts
increase a person’s risk for suicide.
• Neurological factors that are associated
with suicide include altered serotonin
act iv it y and a genet ic pred isposit ion.
Psycholog ica l r isk f actor s for su icide
include poor coping and problem-solving
skills, distorted and rigid thinking, and
a sense of hopelessness. Var iat ions in
suicide rates across countries point to a
relationship between social factors and
suicide.
• Crisis intervention efforts to prevent sui-
cide first ensure that the suicidal person is
safe and then help the person see past the
hopelessness and rigidity that pervade his
or her thinking. Longer-term suicide pre-
vention may also help the patient to iden-
tify the stressors that led him or her to feel
suicidal and develop new solutions to the
problems.
Key Terms
Mood Disorders and Suicide 153
155
CHAPTER 6
Anxiety Disorders
arl Campbell, born in 1955, gained fame as a National Football
League (NFL) running back from 1978 to 1985. Campbell
was such an outstanding athlete that he was voted most valu-
able player for each of his f irst 3 years in the NFL. He was later
inducted into the Football Hall of Fame and went on to achieve in
other areas of life: He became a food manufacturer, restaurateur, and
businessman.
Campbell possessed remarkable talents and abilities and an
unusually strong drive to achieve. But he also suffered from symp-
toms of anxiety disorders. Anxiety disorders involve significant fear,
agitation, and nervousness and can impair functioning in any or all
spheres of life, including school, work, and interpersonal relation-
ships. Campbell developed such severe anxiety symptoms that he
became unable to work effectively.
In thIs chapter, we discuss six types of anxiety disorders that
are described in DSM-5: generalized anxiety disorder, panic disorder,
agoraphobia, social anxiety disorder, specif ic phobia, and separa-
tion anxiety disorder. We’ll start with a general discussion of what
anxiety is and identify some of the common features of the different
anxiety disorders. In the process, we’ll examine how Earl Campbell
responded to and handled his anxieties.
Common Features of
Anxiety Disorders
Earl Campbell played high school football and, after graduating,
became a star running back on the Universit y of Texas–Austin
football team. From there, he went on to play for the Houston Oilers
in the NFL. At age 24, he married Reuna, a woman from his home-
town whom he had been dating for 10 years. Five years later, they
had their first child, and 2 years after that, at the age of 31, Campbell
retired from football.
Common Features of Anxiety Disorders
What Is Anxiety?
The Fight-or-Flight Response Gone Awry
Comorbidity of Anxiety Disorders
Generalized Anxiety Disorder
What Is Generalized Anxiety Disorder?
Understanding Generalized Anxiety Disorder
Treating Generalized Anxiety Disorder
Panic Disorder and Agoraphobia
The Panic Attack—A Key Ingredient of Panic
Disorder
What Is Panic Disorder?
What Is Agoraphobia?
Understanding Panic Disorder and Agoraphobia
Treating Panic Disorder and Agoraphobia
Social Anxiety Disorder (Social Phobia)
What Is Social Anxiety Disorder?
Understanding Social Anxiety Disorder
Treating Social Anxiety Disorder
Specific Phobia
What Is Specifi c Phobia?
Specifi cs About Specifi c Phobia
Understanding Specifi c Phobia
Treating Specifi c Phobia
Separation Anxiety Disorder
What Is Separation Anxiety Disorder?
Understanding and Treating Separation Anxiety
Disorder
Follow-up on Earl Campbell
© BURGER/PHANIE/age fotostock. Photo for illustrative purposes only; any individual depicted is a model.
Campbell went on to work for the University of Texas–Austin as a goodwill
ambassador, representing the school at various functions, and helping student-athletes
commit to their studies. One day, as Campbell was driving from Austin to Dallas, he
stopped at a traffic light and had an unusual experience:
Out of the blue, my heart started racing. I felt my chest. Then I broke into a cold
sweat, began hyperventilating, and became convinced I was having a heart attack.
The people in the car next to mine seemed totally unaware that anything was wrong.
My heart just kept racing. I couldn’t stop it. I was going to die. How could I stop it? It
was getting worse. I was dying! The driver behind me started blowing his horn. The
light had turned green. I needed help. I couldn’t get out of the car. “God help me!”
I prayed. Then it stopped—just like that, my heart stopped racing. I put my hand to
my heart again. It felt normal. My hands and arms were covered with a cold clammy
sweat. I wiped the perspiration from my face and look[ed] at myself in the rearview
mirror. For the first time in my life, I caught sight of a frightened Earl Campbell and
I didn’t like it. . . .
(Campbell & Ruane, 1999, pp. 83–84)
Not only did Campbell have frightening bodily sensations, but he also developed wor-
ries about “the little details that most people don’t even think about. They weigh on
me and tie up my mind. I am continually inundated with intrusive thoughts related
to everything I say or do. Do I look okay? Am I walking right? Did I do this right?
That right? Why is everyone looking at me? Is it because I’m Earl Campbell, or is
it because there’s something wrong with me?” (Campbell & Ruane, 1999, p. 199).
Campbell’s experiences involve anxiety.
What Is Anxiety?
Like the term depression, the words anxiety and anxious are used in everyday speech.
But what do mental health professionals and researchers mean when they use these
terms? Anxiety refers to a sense of agitation or nervousness, which is often focused
on an upcoming potential danger.
We all feel afraid and anxious from time to time. These feelings can be adaptive,
signaling the presence of a dangerous stimulus, which in turn leads us to be more
alert—which then heightens our senses. For instance, if you are walking alone down
a dark, quiet street late at night, you might feel anxious, which makes you alert; you
might then be able to hear particularly well or be more sensitive to another person’s
presence behind you. Such heightened senses can be adaptive on a dark street. Should
you hear or sense someone, you may choose to head quickly to a well-lit and busier
street. Similarly, a moderate level of anxiety before a test or presentation can enhance
your performance (Deshpande & Kawane, 1982)—and, in fact, the absence of anxi-
ety can lead to lackluster performance, even if you know the material well. Thus,
feeling afraid or anxious can be normal and adaptive.
Extreme anxiety, however, is a persistent, vague sense of dread or foreboding
even when not in the presence of a feared stimulus (such as a snake or a plane trip).
An anxiety disorder involves fear, extreme anxiety, intense arousal, and extreme
attempts to avoid stimuli that lead to fear and anxiety. These emotions, or the efforts
to avoid experiencing them, can create a high level of distress, which can interfere
with normal functioning.
The Fight-or-Flight Response Gone Awry
Campbell describes some of the frightening physical sensations he experienced in
this way: “Visualize yourself just sitting back in a chair, relaxing. Suddenly, your
heart starts racing as if you had just run a hundred-yard dash. You break into a cold
sweat. You have trouble breathing. You feel there is nothing you can do to stop all
In his 30s, former NFL player Earl Campbell
suddenly developed symptoms of anxiety—
racing heart and trouble breathing—which
frightened him, as they would most people.
A
P
P
h
o
to
Anxiety
A sense of agitation or nervousness, which
is often focused on an upcoming possible
danger.
Anxiety disorder
A category of psychological disorders in which
the primary symptoms involve fear, extreme
anxiety, intense arousal, and/or extreme
attempts to avoid stimuli that lead to fear and
anxiety.
156 C H A P T E R 6
of these things from happening” (Campbell & Ruane, 1999, p. i). Campbell was
describing the effects of the fight-or-flight response, also called the stress response
(see Chapter 2), which occurs when a person perceives a threat. Suppose you think
you see a mugger lurking on a dark doorstep as you are hurrying home, alone, late at
night. Your brain and body respond as if you must either fight or take flight, primar-
ily by activating the sympathetic branch of the autonomic nervous system. The stress
response prepares your body to exert physical energy for an action, either fighting the
threat or running away from it. It does not matter whether there is an actual threat.
Your body automatically responds because you perceive a threat. Your body responds
in a number of ways, most notably by:
• increasing your heart rate and breathing rate (in order to provide more oxygen to
your muscles and brain),
• increasing the sweat on your palms (a small amount, which helps you grip better—
yet not so much as to make your palms become slippery), and
• dilating your pupils (in order to let in more light and help you to see better).
Your body responds this way even to threats that do not require a lot of physical
energy, such as—for many people—speaking in front of a group (or even thinking
about speaking in front of them) or taking a pop quiz. In such cases, your body gets
prepared, but most of the physical preparations aren’t really necessary.
This f ight-or-f light (stress) response underlies the fear and anxiety involved
in almost all anxiety disorders. Some people have an overactive stress response—
they have higher levels of arousal during this response. Other people may not have
an overactive stress response, but they may misinterpret their arousal during this
response and attribute the bodily sensations to a physical ailment. They might, for
instance, interpret an increased heart rate as a heart attack. In either case, some peo-
ple come to feel afraid or anxious about the physical sensations of the fight-or-flight
response or the conditions that seem to have caused it. When their arousal feels as if
it is getting out of control, they may start to feel panic, which is an extreme sense
(or fear) of imminent doom, together with an extreme stress response ( Bouton et al.,
2001) —what Campbell experienced sitting in his car at a stoplight. Some people
who become panicked develop a phobia, which is an exaggerated fear of an object
or a situation, together with an extreme avoidance of that object or situation. Such
avoidance can interfere with everyday life. For instance, at one point, Campbell
avoided crowded rooms because he thought that they might bring on the uncomfort-
able physical sensations he’d experienced.
Significant anxiety and phobias are not unusual or rare. In the United States,
anxiety disorders are the most common kind of mental disorder (Barlow, 2002a);
approximately 15% of people will have some type of anxiety disorder in their life-
times (Somers et al., 2006). Women are twice as likely as men to be diagnosed with
an anxiety disorder (Somers et al., 2006). Some explanations of this gender difference
rest on biological factors, such as the hormonal shifts that occur during a woman’s
childbearing years (Ginsberg, 2004); the possible role of hormones is consistent with
the fact that the gender difference in anxiety disorders coincides with the onset of
puberty (as is the case with depression; see Chapter 5). Other explanations for the
gender difference rest on cultural factors (Pigott, 1999): Unlike Campbell, many
men tend to be reluctant to acknowledge symptoms of anxiety because they fear that
admitting such feelings might undercut the masculine image they project to others.
Comorbidity of Anxiety Disorders
As you’ll see throughout this text, symptoms of anxiety or avoidance may occur in
many psychological disorders, including mood disorders (Chapter 5), body dysmorphic
Fight-or-flight response
The automatic neurological and bodily
response to a perceived threat; also called the
stress response.
Panic
An extreme sense (or fear) of imminent doom,
together with an extreme stress response.
Phobia
An exaggerated fear of an object or a
situation, together with an extreme avoidance
of the object or situation.
Anxiety Disorders 157
disorder (Chapter 7), and anorexia nervosa (Chapter 10). Clinicians
must determine whether the anxiety and avoidance symptoms
are the primary cause of the disturbance or a by-product of
another type of problem. In the case of anorexia ner vosa, for
example, when someone gets anxious about eating high-calorie
foods, the anxiet y is secondary to larger concerns about food,
weight, and appearance.
Anxiety and depression often occur together; approximately
50% of people with an anxiety disorder are also depressed (Brown
et al., 2001). Researchers and clinicians are trying to discover
why there is such high comorbidity between anxiety disorders
and depression. Some researchers have proposed a three-part
model of anxiety and depression that specifies the ways in which
the two kinds of disorders overlap and the ways in which they
are distinct (Clark & Watson, 1991; Mineka, Watson, & Clark,
1998). This model has been supported by research ( Joiner, 1996;
Olino et al., 2008). The three parts of the model are depicted
in Figure 6.1. Another disorder that commonly co-occurs with
an anxiety disorder is substance use disorder, and approximately 10–25% of people
who have anxiety disorders also abuse alcohol (Bibb & Chambless, 1986; Otto
et al., 1992).
Thinking Like A Clinician
What is the difference between fear and anxiety? Why (or when) might the fight-or-flight
response become a problem? If people can have symptoms of anxiety when they have other
types of disorders, what determines whether an anxiety disorder should be the diagnosis?
Generalized Anxiety Disorder
Earl Campbell became a worrier—even during the best of times:
On a day when life seems absolutely wonderful—say, a beautiful fall Saturday or
Sunday when I’m watching one of my boys play football—I’ll often be overcome by
the fear that it will all come to an end somehow. It’s just too good. Something bad is
going to ruin it for me. This past year was the most difficult one I’ve had. . . . Tyler [his
son] was in the fifth grade, and I worried the entire year. I was in the fifth grade when
my father died, and I thought my fate was sealed. I was scared I would die and my boys
would have to go through life without a father, the way I did.
(Campbell & Ruane, 1999, p. 204)
Worrying is a normal part of life, and some people worry more than others. But how
much is “too much” worrying?
What Is Generalized Anxiety Disorder?
Generalized anxiety disorder (GAD) is characterized by excessive and per-
sistent worr y and anxiety about a number of events or activities (which are not
solely the focus of another disorder, such as worrying about having a panic attack)
(see Table 6.1; American Psychiatric Association, 2013). For people suffering
from GAD, the worry and anxiety focus primarily on family, finances, work, and
illness (Sanderson & Barlow, 1990), and—given the actual extent of the prob-
lem with family, finances, work, or illness—the person’s worries are excessive
Physiological
hyperarousal
General
distress
(high level
of negative
emotions)
Anxiety Depression
Lack of
enjoyment
(low level
of positive
emotions)
FI G U RE 6.1 • Tripartite Model of
Anxiety and Depression Anxiety
and depression have in common a high level
of negative emotions, but each has unique
elements: Anxiety generally involves a very
high level of physiological arousal, whereas
depression involves a low level of positive
emotions.
Generalized anxiety disorder (GAD)
An anxiety disorder characterized by
uncontrollable worry and anxiety about a
number of events or activities, which are not
solely the result of another disorder.
People with phobias, such as musicians with
performance anxiety (stage fright), may use
alcohol to relieve their anxiety symptoms.
However, using alcohol in this way can lead to
alcoholism, as was the case in the early days
of Sheryl Crow’s career.
Fr
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158 C H A P T E R 6
(as determined by the mental health clinician). Earl Campbell worried mostly
about family and illness; other people may worry about minor matters (Craske et
al., 1989). In contrast to most other people, people with GAD worry even when
things are going well. Moreover, their worries intrude into their awareness when
they are trying to focus on other thoughts, and they lead people to feel on edge
or have muscle tension (American Psychiatric Association, 2013). Like A. H.,
discussed in Case 6.1, people with GAD feel a chronic, low level of anxiety or
worry about many things. Moreover, the fact that they constantly worry in itself
causes them distress.
CASE 6.1 • FROM TH E OUTSIDE: Generalized Anxiety Disorder
A. H. was a 39-year-old divorced mother of two (son aged 12, daughter aged 7) who worked
as a bank manager. However, she had become concerned about her ability to concentrate
on and remember information while at work. A. H. had made some “financially disastrous”
mistakes and was now—at the suggestion of her supervisor—taking some vacation time to
“get her head together.” Because of her concentration and memory problems, it had been
taking her longer to complete her work, so she had been arriving at work 30 minutes early
each day, and she often took work home. She reported being unable to relax, even outside
of work, and at work it was hard to make decisions because she ruminated endlessly (“Is
this the right decision, or should I do that?”) and hence tried to avoid making decisions alto-
gether. Her concentration and memory problems were worst when she was worried about
some aspect of life, which was most of the time. She reported that 75% of her waking life
each day was spent in a state of anxiety and worry. In addition to worrying about her per-
formance at work, she worried about her children’s well-being (whether they had been hurt
or killed while out playing in the neighborhood). She also worried about her relationships
with men and minor things such as getting to work on time, keeping her house clean, and
maintaining regular contact with friends and family. A. H. recognized that her fears were
both excessive and uncontrollable, but she couldn’t dismiss any worry that came to mind.
She was irritable, had insomnia, had frequent muscle tension and headaches, and felt gener-
ally on edge.
(Adapted from Brown & Barlow, 1997, pp. 1–3)
Because the symptoms are chronic (lasting at least 6 months) and because many
people with GAD can usually function adequately in some areas of their daily lives,
they come to see their worrying and anxiety as a part of themselves, not as a disorder.
However, the intrusive worr ying can lead to problems in work and social life.
See Table 6.2 for more facts about GAD.
A s noted i n Table 6.2 , GA D a nd depre s sion h ave a n ex t remely h ig h
comorbidity. Among people who have both disorders at the same time, only 27%
eventually experience remission, compared to 48% of those who have only GAD
and 41% of those who have only depression (Schoevers et al., 2005). People with
both disorders are also likely to have had their symptoms arise at a younger age,
to have more severe symptoms of each disorder, and to function less well than
those who have only one of the two disorders (Moffitt et al., 2007; Zimmerman &
Chelminski, 2003). The high comorbidity also suggests that GAD and depression
may reflect different facets of the same underlying problem, which is rooted in dis-
tress, worry, and the continued intrusion of negative thoughts (Ruscio et al., 2011;
Schoevers et al., 2003).
Understanding Generalized Anxiety Disorder
GA D can be best understood by using the neuropsychosocial approach to ex-
amine its etiology—by considering neurological, psychological, and social factors
and the feedback loops among them. Each type of factor, by itself, seems to be
TABLE 6.1 • DSM-5 Diagnostic Criteria
for Generalized Anxiety Disorder
(GAD)
A. Excessive anxiety and worry
(apprehensive expectation), occurring
more days than not for at least 6 months,
about a number of events or activities
(such as work or school performance).
B. The individual finds it difficult to control
the worry.
C. The anxiety and worry are associated
with three (or more) of the following
six symptoms (with at least some
symptoms having been present for more
days than not for the past 6 months):
Note: Only one item is required in
children.
1. Restlessness or feeling keyed up or
on edge.
2. Being easily fatigued.
3. Difficulty concentrating or mind
going blank.
4. Irritability.
5. Muscle tension.
6. Sleep disturbance (difficulty falling
or staying asleep, or restless,
unsatisfying sleep).
D. The anxiety, worry, or physical symptoms
cause clinically significant distress or
impairment in social, occupational, or
other important areas of functioning.
E. The disturbance is not attributable to the
physiological effects of a substance (e.g.,
a drug of abuse, a medication) or another
medical condition (e.g., hyperthyroidism).
F. The disturbance is not better explained
by another mental disorder (e.g., anxiety
or worry about having panic attacks in
panic disorder, negative evaluation in
social anxiety disorder [social phobia],
contamination or other obsessions
in obsessive-compulsive disorder,
separation from attachment figures in
separation anxiety disorder, reminders
of traumatic events in posttraumatic
stress disorder, gaining weight in anorexia
nervosa, physical complaints in somatic
symptom disorder, perceived appearance
flaws in body dysmorphic disorder, having
a serious illness in illness anxiety disorder,
or the content of delusional beliefs in
schizophrenia or delusional disorder).
Reprinted with permission from the Diagnostic and
Statistical Manual of Mental Disorders, Fifth Edition,
(Copyright ©2013). American Psychiatric Association. All
Rights Reserved.
Anxiety Disorders 159
necessar y but not sufficient to give rise to this dis-
order. It may be best to conceive of neurological and
psychological factors as setting the stage, and social
factors as triggering the symptoms.
Neurological Factors
The parasympathetic nervous system appears to play a
special role in GAD, a complex mix of neurotransmit-
ters is involved in the disorder, and genetics can predis-
pose someone to develop GAD.
Brain Systems
Un l i ke mo st ot her t y pe s of a n x iet y d i sord er s ,
GA D isn’t associated with the cranked-up sympa-
thet ic ner vous system act iv it y that underl ies the
f ight-or-f light response (Marten et al., 1993). In-
stead, GA D is a ssociated w ith decrea sed a rousa l
that ar ises from an unusually responsive parasym-
pathetic nervous system. The parasympathetic ner-
vous system tends to cause ef fects opposite those
caused by the sympathetic ner vous system. So, for
instance, heightened parasympathetic activity slows
heart rate, stimulates digestion and the bladder, and
causes pupils to contract (Barlow, 2002a). When a
person w ith GA D perceives a threaten ing stimu-
lus, his or her subsequent worr y temporarily reduces
arousa l ( Borkovec & Hu, 1990 ), suppresses nega-
tive emotions (see Figure 6.1), and produces muscle
tension (Barlow, 2002a; Pluess et al., 2009). These
facts are in stark contrast to Earl Campbell’s symptoms, which suggest that he
did not have GAD.
Neural Communication
Although the frontal lobes of patients with GAD are normal in size, the dopamine
in the frontal lobes of these patients does not function normally (Stein, Westenberg,
& Liebowitz, 2002 ). In fact, numerous studies suggest that a wide range of
neurotransmitters, including gamma-aminobutyric acid (GABA), serotonin, and
norepinephrine, may not function properly in people with GAD (Nutt, 2001). These
neurotransmitters affect, among other things, people’s response to reward, their
motivation, and how effectively they can pay attention to stimuli and events.
Genetics
Studies of the genetics of GA D have produced solid evidence that GA D has a
genetic component, and the disorder is equally heritable for men and women
( Hettema, Prescott, & Kend ler, 20 01). However, if one fam i ly member has
GAD, other family members are likely to have GAD or depression, which sug-
gests a com mon underlying genetic vulnerabilit y (Gor wood, 2004 ; Kend ler
et al., 2007).
Psychological Factors: Hypervigilance and the Illusion of Control
Psychological factors that contribute to GAD generally involve three characteristic
modes of thinking and behaving:
1. People with GA D pay a lot of attention to stimuli in their environment,
searching for possible threats. This heightened search for threats is called
hypervigilance.
TABLE 6.2 • Generalized Anxiety Disorder Facts at a Glance
Prevalence
• Approximately 9% of people will develop GAD in their lifetime.
Comorbidity
• GAD occurs very frequently with depression, with up to 80% of those having
GAD also experiencing depression at some point (Judd et al., 1998).
Onset
• Approximately half the people with GAD develop the disorder before the age of 30.
Course
• People diagnosed with GAD report that they have felt nervous and anxious all
their lives.
• Once someone has GAD, its course is likely to be chronic, with symptoms fluc-
tuating in response to stress.
Gender Differences
• Twice as many women as men are diagnosed with GAD.
Cultural Differences
• The content of the worries of people with GAD is shaped by their culture, their
personal experiences, and the environment in which they live. Some people
worry about catastrophic events, such as natural disasters; others worry about
human-caused calamities, such as nuclear war or terrorist acts.
Source: Unless otherwise noted, the source for information is American Psychiatric Association, 2013
A construction forewoman talks with a
member of her crew. If one of her employees
were to have GAD, he might be hypervigilant
for possible threats in his environment—for
example, constantly scanning the boss’s face
for possible signs of displeasure or glancing at
the figure in the background to make sure he
wasn’t a threat.
D
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Hypervigilance
A heightened search for threats.
160 C H A P T E R 6
2. People with GAD typically feel that their worries
are out of control and that they can’t stop or alter the
pattern of their thoughts, no matter what they do.
3. The mere act of worrying prevents anxiety from
becoming panic (Craske, 1999), and thus the act of
worrying is negatively reinforcing (Borkovec, 1994a;
Borkovec et al., 1999). The worrying does not help
the person to cope with the problem at hand, but it
does give him or her the illusion of coping, which
temporarily decreases anxiety about the perceived
threat. Some people think that if they worry, they
are actively addressing a problem. But they are not—
worrying is not the same thing as effective problem
solving; the original concern isn’t reduced by the
worrying, and it remains a problem, along with the
additional problem of chronic worrying.
Social Factors: Stressors
Stressful life events—such as a death in the family, friction in a close relationship, or
trouble on the job—can trigger symptoms of GAD in someone who is neurologically
and psychologically vulnerable to developing it. For people who develop GAD after
age 40, the disorder often arises after the person experiences a significant stressor.
GAD also appears to be related more directly to relationships. People with GAD
may experience increased stress if they view themselves as having serious problems in
relationships. Increased stress, in turn, can lead to distress and negative emotions that
can be difficult to manage and regulate (Mennin et al., 2004).
Feedback Loops in Understanding Generalized Anxiety Disorder
Stressful life experiences (typically social factors) can trigger the onset of GAD, but
most people who experience stressful periods in their lives—even extreme stress—never
develop this disorder. Moreover, people who develop GAD often report that they were
afraid and avoidant as children (American Psychiatric Association, 2013), which may be
explained by abnormal neurological functioning. However, such abnormal functioning
in childhood could arise from genes, might develop in childhood because of early life
experiences, or could be caused by some combination of the two. To develop GAD,
a person probably must have abnormal neurological functioning (which may reflect
abnormal levels of GABA or another neurotransmitter), have learned certain kinds
of worry-related behaviors such as hypervigilance for threats, and have experienced a
highly stressful event or set of events such as a death in the family. Any one of these
alone—and probably any two of these—will not cause GAD.
Treating Generalized Anxiety Disorder
Treatment for GAD can target neurological, psychological, or social factors, but
neurological or psychological factors are the predominant focus of treatments. As
usual, interventions targeting any one type of factor have ripple effects that in turn
alter the other types of factors.
Targeting Neurological Factors: Medication
The antianxiety medication buspirone (Buspar) effectively reduces the symptoms of GAD,
probably by decreasing serotonin release. Serotonin facilitates changes in the amygdala
that underlie learning to fear objects or situations (Huang & Kandel, 2007); thus, reduc-
ing serotonin may impair learning to fear or worry about specific objects or situations.
SP
N
O N L I N E
The content of the worries of people with
GAD is influenced by their culture and the
types of catastrophic events most likely to
occur in their locale. Those who live along
the Gulf Coast of the United States may
worry about hurricanes; those who reside in
California may worry about earthquakes; and
those who reside in the Midwest may worry
about tornadoes.
©
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Anxiety Disorders 161
Most people with GAD are also depressed, but buspirone only helps anxiety
symptoms (Davidson, 2001). In contrast, the serotonin/norepinephrine reuptake
inhibitor (SNRI) venlafaxine (Effexor) and certain selective serotonin reuptake
inhibitors (SSRIs), such as paroxetine (Paxil) and escitalopram (Lexapro), appear to
relieve both anxiety and depressive symptoms (Baldwin & Polkinghorn, 2005;
Davidson, 2001). This is why an SNRI is considered the “first-line medication” for
people with both GAD and depression, meaning that it is the medication that clini-
cians try first with these patients (unless there is a reason not to use it).
Targeting Psychological Factors
Psychological treatments for GAD generally have several aims:
• to increase the person’s sense of control over thoughts and worries,
• to allow the person to assess more accurately how likely and dangerous perceived
threats actually are, and
• to decrease muscle tension.
Psychotherapy for GAD generally consists of behavioral and cognitive methods,
which can successfully decrease symptoms (Cottraux, 2004; Durham et al., 2003;
Hanrahan et al., 2013).
Behavioral Methods
Behavioral methods to treat GAD focus on three main areas (Barlow, 2002a):
• awareness and control of breathing,
• awareness and control of muscle tension and relaxation, and
• elimination, reduction, or prevention of worries and behaviors associated with worries.
Breathing retraining requires patients to become aware of their breathing and to try
to control it by taking deep, relaxing breaths. Such breathing can help induce relax-
ation and provide a sense of coping—of doing something positive in response to worry.
Similarly, muscle relaxation training requires patients to become aware of early signs
of muscle tension, a symptom of GAD in some people, and then to relax those muscles.
Patients can learn how to identify tense muscles and then relax them
through standard relaxation techniques or biofeedback, a technique
in which a person is trained to bring normally involuntary or uncon-
scious bodily activity, such as heart rate or muscle tension, under vol-
untary control. Typically, electrodes are attached to a targeted muscle
or group of muscles, and the patient can see on a monitor or hear from
a speaker signals that indicate whether the monitored muscles are
tense or relaxed. This feedback helps the patient learn how to detect
and reduce the tension, eventually without relying on the feedback.
A common treatment for anxiety disorders, including GAD, is based
on the principle of habituation: The emotional response to a stimulus
that elicits fear or anxiety is reduced by exposing the patient to the stimu-
lus repeatedly. The technique of exposure involves such repeated contact
with the (feared or arousing) stimulus in a controlled setting, and usually
in a gradual way, bringing about habituation. Exposure, and therefore
habituation, to fear- or anxiety-related stimuli does not normally occur outside of therapy
because people avoid the object or situation, thereby making exposure (and habituation)
unlikely. In exposure-based treatment, the patient first creates a hierarchy of feared events,
arranging them from least to most feared, and then begins the exposure process by having
contact with the least-feared item on the hierarchy. With GAD, that might be addressing
worries about possibly bouncing a check (lower in the hierarchy) to worries that if a spouse
is late it is because he or she was in a car accident. With sustained exposure, the symptoms
Biofeedback
A technique in which a person is trained to
bring normally involuntary or unconscious
bodily activity, such as heart rate or muscle
tension, under voluntary control.
Habituation
The process by which the emotional response
to a stimulus that elicits fear or anxiety
is reduced by exposing the patient to the
stimulus repeatedly.
Exposure
A behavioral technique that involves repeated
contact with a feared or arousing stimulus in a
controlled setting, bringing about habituation.
This woman is learning how to control
the muscle tension in her face through
biofeedback.
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162 C H A P T E R 6
diminish within 20 to 30 minutes or less; that is, habituation to the fear- or anxiety-
inducing stimuli occurs. Over multiple sessions, this process is repeated with items higher
in the hierarchy (i.e., those that are more feared), until all items no longer elicit significant
symptoms. Patients in therapy can experience exposure in three ways:
• imaginal exposure, which relies on forming mental images of the stimulus;
• virtual reality exposure, which consists of exposure to a computer-generated (often
very realistic) representation of the stimulus; and
• in vivo exposure, which is direct exposure to the actual stimulus.
People with GAD often develop behaviors that are associated with their worries.
For instance, a patient who worries that “something bad” may happen to her family may
call home several times each day. By calling home and finding out that everyone is fine,
she temporarily reduces her anxiety, thus (negatively) reinforcing the calling behavior.
People with GAD do not naturally habituate to such anxiety; as they worry about one
set of concerns, they get increasingly anxious until they shift the focus of their worry to
another set of concerns, never becoming habituated to any specific set of concerns.
Using exposure to treat GAD, patients are asked to think about only one
specific worry (this is the exposure) and to imagine their worst possible fears about
the subject of that worry, such as the possible deaths of family members. Patients
are asked to think about their worry continuously for about 30 minutes. After this
half-hour of exposure, patients then list their rational responses to the worst out-
comes they imagined. Patients’ anxiety and level of worry should decrease both over
the course of the session and across sessions. When patients can think about one set of
concerns without much worry or anxiety, they move on to use the same procedure
with another set of concerns (see Figure 6.2, on the next page).
Cognitive Methods
Cognitive methods for treating GAD focus on first helping patients to identify the
thought patterns that are associated with their worries and anxieties and then helping
them to use cognitive restructuring and other methods to prevent these thought
patterns from spiraling out of control. The methods can also decrease the intensity
of patients’ responses to their thought patterns, so that they are less likely to develop
symptoms. Specific cognitive methods include the following:
• Psychoeducation, which is the process of educating patients about research findings
and therapy procedures relevant to their situation. For patients with GAD, this
means educating them about the nature of worrying and GAD symptoms and
about available treatment options and their possible advantages and disadvantages.
• Meditation, which helps patients learn to “let go” of thoughts and reduce the time spent
thinking about worries (Evans et al., 2008; Lehrer & Woolfolk, 1994; Miller et al., 1995).
• Self-monitoring, which helps patients become aware of cues that lead to anxiety
and worry. For instance, patients may be asked to complete a daily log about their
worries, identifying events or stimuli that lead them to worry more or worry less.
• Problem solving, which involves teaching the patient to think about worries in very
specific terms—rather than global ones—so that they can be addressed through
cognitive restructuring.
• Cognitive restructuring, which involves helping patients learn to identify and shift
automatic, irrational thoughts related to worries (see the third panel in Figure 6.2).
Targeting Social Factors
The neuropsychosocial approach leads us to notice whether certain kinds of
treatments are available for particular disorders. For instance, at present, there are
very few treatments for GAD that specifically target social factors, and none of them
have been successful enough to summarize here.
In vivo exposure
A behavioral therapy method that consists
of direct exposure to a feared or avoided
situation or stimulus.
Psychoeducation
The process of educating patients about
research findings and therapy procedures
relevant to their situation.
Anxiety Disorders 163
Feedback Loops in Treating Generalized Anxiety Disorder
W hen behaviora l methods and cog nitive methods are successful, the person
develops a sense of master y of and control over worries and anxiety (which de-
creases the worries and anxiety even further), and social interactions reinforce
new behaviors. Similarly, medication directly targets neurological factors, which
in turn reduces the person’s worries and anxiety; he or she becomes less preoc-
cupied with these concerns, which increases the ability to focus at work and in
relationships.
Did Earl Campbell develop GAD? Although his worries may seem excessive and
uncontrollable at times, they do not appear to have had the effects necessary for the
O N L I N E
SP
N
I’d like you to worry
about only a single concern. Let’s
start with your worry that when your wife
is late, it’s because she’s been in a car
accident—that she’s slumped
unconcious over the steering wheel.
Let’s try to stay focused only
on that worry.
Okay…
When I think about my wife being
late and possibly in an accident,
after a while I feel anxious.
Are there alternative
explanations for why your wife
might be late other than some
tragedy has befallen her?
Hmm… I suppose she could have
gotten stuck in traffic and didn’t
want to take her eyes off the road
to call me. Or she could be driving
around looking for a parking
place.
Okay, I can think about my wife
being late and not get so anxious. If
I start to worry about her being late
because of an accident, I can
remind myself about alternative
reasons why she’s late. I am ready
to go to the next worry.
FI G U RE 6.2 • Worry Exposure
Worry exposure first involves evoking a particular worry
as vividly as possible and trying to imagine the worst-
case scenario related to that worry.
The patient then tries to stay focused on the single
worry for about a half-hour; the patient should
habituate to the anxiety caused by the worry.
Once the patient has habituated somewhat to the worry,
the patient and therapist generate possible rational
alternatives to the worst-case scenario.
After the patient has habituated to and developed a
rational response to a particular worry, he or she is ready
go through the same process with a new, specific worry.
164 C H A P T E R 6
diagnosis, such as muscle tension, irritability, or difficulty sleeping. Any irritability
or sleep problems he had are better explained as symptoms of another anxiety
disorder—panic disorder, which we discuss in the following section.
Thinking Like A Clinician
Based on what you have read, what differentiates a “worrywart”—someone who worries a
lot—from someone with GAD? If having GAD is distressing, why don’t patients simply stop
worrying? What factors maintain the disorder? If someone you know with GAD asked you for
advice about what kind of treatment to get, what would you recommend (based on what you
have read) and why?
Panic Disorder and Agoraphobia
Earl Campbell’s uncomfortable episodes of anxiety didn’t stop:
The second night we were in the [new] house, I had my third episode. It felt just like
the second one had. I was lying in bed watching television, and Reuna was sound
asleep next to me. I was tr ying to relax and not think about my problem, but my
problem was all I could think about. All of a sudden, my heart went crazy—pounding,
pounding harder and harder. I thought it was going to leap right out of my chest. I sat
up, struggling to regain my composure. It got worse. I couldn’t breathe again.
(Campbell & Ruane, 1999, p. 92)
Campbell again thought he was having a heart attack and that his life was ending. He
was not; instead, Campbell was having a panic attack. A panic attack is a specific
period of intense fear or discomfort, accompanied by physical symptoms, such as a
pounding heart, shortness of breath, shakiness, and sweating, or cognitive symptoms,
such as a fear of losing control.
The Panic Attack—A Key Ingredient of Panic Disorder
Some of the physical symptoms of a panic attack may resemble those associated with
a heart attack—heart palpitations, shortness of breath, chest pain, and a feeling of
choking or being smothered (see Table 6.3), which is why Earl Campbell mistook
his panic attacks for heart attacks. In fact, emergency room staff have learned to look
for evidence of a panic attack when a patient who purportedly has had a heart attack
arrives. During a panic attack, the symptoms generally begin quickly, peak after a
few minutes, and disappear within an hour.
In some cases, panic attacks are cued—that is, associated with particular objects,
situations, or sensations. Although panic attacks are occasionally cued by a particular
external stimulus (such as seeing a snake), they are more frequently cued by situations
that are associated with internal sensations similar to panic, such as breaking out into
a sweat (when overheated). In other cases, panic attacks are uncued—that is, spontane-
ous and feel as though they come out of the blue—and are not associated with a par-
ticular object or situation. Panic attacks can occur at any time, even while sleeping
(referred to as nocturnal panic attacks, which Campbell experienced). Infrequent panic
attacks are not unusual; they affect 30% of adults at some point in their lives.
Recurrent panic attacks may interfere with daily life (for example, if they occur
on a bus or at work) and may cause the person to leave the situation to return home or
seek medical help. The symptoms of a panic attack are so unpleasant that people who
suffer from this disorder may try to prevent another attack by avoiding environments
and activities that increase their heart rates (hot places, crowded rooms, elevators,
exercise, sex, mass transportation, or sporting events). They might even avoid leaving
home (Bouton et al., 2001).
TABLE 6.3 • DSM-5 Criteria for a
Panic Attack
A discrete period of intense fear or
discomfort, in which at least four of the
following symptoms develop abruptly and
reach a peak within minutes:
• palpitations, pounding heart, or accelerated
heart rate
• sweating
• trembling or shaking
• sensations of shortness of breath or
smothering
• feeling of choking
• chest pain or discomfort
• nausea or abdominal distress
• feeling dizzy, unsteady, lightheaded, or
faint
• chills or heat sensations
• paresthesias (numbness or tingling
sensations)
• derealization (feelings of unreality) or
depersonalization (being detached from
oneself)
• fear of losing control or going crazy
• fear of dying
Reprinted with permission from the Diagnostic and
Statistical Manual of Mental Disorders, Fifth Edition,
(Copyright ©2013). American Psychiatric Association. All
Rights Reserved.
Panic attack
A specific period of intense fear or discomfort,
accompanied by physical symptoms, such
as a pounding heart, shortness of breath,
shakiness, and sweating, or cognitive
symptoms, such as a fear of losing control.
Anxiety Disorders 165
What Is Panic Disorder?
Campbell describes panic disorder: “. . . the fear of having another panic
attack, because the last thing in the world you want to face is one
more of those horrible, frightening experiences. And the last thing
you want to accept is the idea of living the rest of your life with panic.
This condition caused me to shut myself up in the my house, where
I would sit in the dark, frustrated, crying, afraid to go out. At one
point, I even considered suicide” (Campbell & Ruane, 1999, p. ii).
To mental health clinicians, panic disorder is marked by fre-
quent, unexpected panic attacks, along with worry about further
attacks or their consequences (such as potentially losing control) and
restrictions of behavior in order to prevent such attacks, lasting at
least 1 month (see Table 6.4). Note, however, that having panic at-
tacks doesn’t necessarily indicate a panic disorder. Panic attacks are
distinguished from panic disorder by the frequency and unpredict-
ability of the attacks and the person’s reaction to the attacks. Re-
search suggests that among people with panic disorder, panic attacks aren’t as out of the
blue as they feel: Changes in breathing and heart rate occur over 30 minutes before the
onset of a panic attack (Meuret et al., 2011). Table 6.5 lists additional facts about panic
disorder, and Case 6.2 provides a glimpse of a woman who suffers from panic attacks.
CASE 6.2 • FROM TH E OUTSIDE: Panic Disorder
S was a 28-year-old married woman with two children, aged 3 and 5 years. S had experienced
her first panic attack approximately 1 year prior to the time of the initial assessment. Her fa-
ther had died 3 months before her first panic attack; his death was unexpected, the result of
a stroke. In addition to grieving for her father, S became extremely concerned about the pos-
sibility of herself having a stroke. S reported [that before her father’s death, she’d never had
a panic attack nor been concerned about her health.] Apparently, the loss of her father pro-
duced an abrupt change in the focus of her attention, and a cycle of anxiety began [which led
to a heightened] awareness of the imminence of her own death, given that “nothing in life
was predictable.” . . . S became increasingly aware of different bodily sensations. Following
her first panic attack, S was highly vigilant for tingling sensations in her scalp, pain around
her eyes, and numbness in her arms and legs. She interpreted all of these symptoms as in-
dicative of impending stroke. Moreover, because her concerns became more generalized, she
began to fear any signs of impending panic, such as shortness of breath and palpitations.
Her concerns led to significant changes in her lifestyle [and she avoided] unstructured
time in the event she might dwell on “how she felt” and, by so doing, panic. . . . S felt that
her life revolved around preventing the experience of panic and stroke.
(Craske et al., 2000, pp. 45–46)
People who suffer from panic attacks may
try to prevent another attack by avoiding
crowded environments such as commuter
trains or public transportation altogether.
Some may even avoid leaving their homes.
C
h
ip
E
a
st
/R
e
u
te
rs
/L
a
n
d
o
v
Panic disorder
An anxiety disorder characterized by frequent,
unexpected panic attacks, along with fear of
further attacks and possible restrictions of
behavior in order to prevent such attacks.
TABLE 6.4 • DSM-5 Diagnostic Criteria for Panic Disorder
A. Recurrent unexpected panic attacks.
B. At least one of the attacks has been followed by 1 month (or more) of one or both of the following:
1. Persistent concern or worry about additional panic attacks or their consequences (e.g., losing control, having a heart attack, “going crazy”).
2. A significant maladaptive change in behavior related to the attacks (e.g., behaviors designed to avoid having panic attacks, such as avoidance of
exercise or unfamiliar situations).
C. The disturbance is not attributable to the physiological effects of a substance (e.g., a drug of abuse, a medication) or another medical condition
(e.g., hyperthyroidism, cardiopulmonary disorders).
D. The disturbance is not better explained by another mental disorder (e.g., the panic attacks do not occur only in response to feared social
situations, as in social anxiety disorder; in response to circumscribed phobic objects or situations, as in specific phobia; in response to obsessions,
as in obsessive-compulsive disorder; in response to reminders of traumatic events, as in posttraumatic stress disorder; or in response to
separation from attachment figures, as in separation anxiety disorder).
Reprinted with permission from the Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition, (Copyright ©2013). American Psychiatric Association. All Rights Reserved.
166 C H A P T E R 6
Symptoms of panic disorder are similar across
cultures, but in some cultures the symptoms focus
on fear of magic or witchcraft (American Psychiat-
ric Association, 2000); in other cultures, the physical
symptoms may be expressed differently. For exam-
ple, among Cambodian refugees, symptoms of panic
disorder include a fear that “wind-and-blood pres-
sure” (referred to as wind overload) may increase to
the point of bursting the neck area, and patients may
complain of a sore neck, along with headache, blurry
vision, and dizziness (Hinton et al., 2001).
In some cultures, people experience symptoms
that are similar—but not identical—to the classic
symptoms of a panic attack. In the Caribbean, Puerto
Rico, and some areas of Latin America, an anxiety-
related problem called ataque de nervios can occur,
usually in women. The most common symptoms are
uncontrollable screaming and crying attacks, together
with palpitations, shaking, and numbness. An ataque
de nervios differs from a panic attack not only in the
specif ic symptoms experienced but also because it
usually is triggered by a specific upsetting event, such
as a funeral or a family conflict. Panic attacks that are
part of panic disorder tend not to have such an obvi-
ous situational trigger. Furthermore, people who have
had an ataque de nervios are usually not worried about
recurrences (Guarnaccia, 1997b; Salmán et al., 1997).
Panic disorder, as well as ataque de nervios and
other anxiety disorders, is diagnosed at least twice
as often in women as in men (American Psychiatric
Association, 2013). A cultural explanation for this
gender difference is that men may be less likely to
report symptoms of anxiety or panic because they perceive them as inconsistent with
how men are “supposed” to behave in their culture ( Ginsburg & Silverman, 2000).
In short, panic disorder has a core of common symptoms across the world,
centering on frequent, unexpected panic attacks and fear of further attacks, but
culture does affect the specifics.
What Is Agoraphobia?
After Campbell’s first panic attack, he refused to go out:
I knew I could not set foot outside my house. Until I learned what was wrong with
me, the only place I would go was to a doctor’s office or a hospital. . . . Reuna thought
that was part of my problem. I was shutting myself off from the world. . . . What if I
had another attack? What if it happened while I was in church? Or while I was walking
down the aisle of a crowded grocery store? What would I do? How could I deal with
the humiliation that such a loss of control would bring?
(Campbell & Ruane, 1999, pp. 93–94)
Campbell had developed agoraphobia.
Agoraphobia (which literally means “fear of the marketplace”) refers to the
persistent avoidance of situations that might trigger panic symptoms or from which
escape would be difficult or help would not be available. For these reasons, public
transportation, tunnels, bridges, crowded places, or even being home alone are
typically avoided or entered with difficulty by people with agoraphobia.
TABLE 6.5 • Panic Disorder Facts at a Glance
Prevalence
• Up to 3% of people worldwide will experience panic disorder at some point in their
lives (Somers et al., 2006). However, 30% of people will experience at least one panic
attack in their lives. Up to 60% of people seen by cardiologists have panic disorder.
Comorbidity
• About 80% of people with panic disorder will have an additional disorder (Ozkan &
Altindag, 2005). The three disorders mostly commonly associated with panic dis-
order are depression (up to 65% of cases), agoraphobia (up to 50% of cases), and
substance abuse (up to 30% of cases) (Keller & Hanks, 1994; Magee et al., 1996).
• Approximately 15–30% of those with panic disorder also have social anxiety disorder
or GAD, and 2–20% have some other type of anxiety disorder (Goisman et al., 1995).
Onset
• Panic disorder is most likely to arise during young adulthood.
Course
• The frequency of panic attacks varies from person to person: some people get
panic attacks once a week for months, others have attacks every day for a week.
• The frequency of panic attacks can vary over time.
Gender Differences
• Women are two times more likely than men to be diagnosed with panic disorder.
Cultural Differences
• Symptoms of panic disorder are generally similar across cultures, although people
in some cultures may experience or explain the symptoms differently, such as
“wind overload” among the Khmer (Hinton et al., 2002, 2003).
Source: Unless otherwise noted, information in the table is from American Psychiatric Association, 2013.
Agoraphobia
An anxiety disorder characterized by persistent
avoidance of situations that might trigger
panic symptoms or from which help would be
difficult to obtain.
Anxiety Disorders 167
About half of the people with agoraphobia also have panic disorder, and most of
the other half experience panic symptoms (but the symptoms are not strong or frequent
enough to meet the criteria for panic disorder); a patient with agoraphobia can also be
diagnosed with panic disorder if he or she has symptoms that meet the criteria for panic
disorder. The avoidance that is a part of agoraphobia is typically a (maladaptive) attempt
not to enter situations that could lead to panic symptoms. These people avoid situations
in which they fear they might panic or lose control of themselves. However, people who
only avoid particular kinds of stimuli (only bridges or only parties) are not diagnosed
with agoraphobia, which is a more general pattern of avoiding many kinds of environ-
ments or situations. Table 6.6 lists the criteria for agoraphobia. Table 6.7 lists additional
facts about agoraphobia, Shirley B., in Case 6.3, suffered from symptoms of agoraphobia.
CASE 6.3 • FROM TH E OUTSIDE: Agoraphobia
“The Story of an Agoraphobic” by Shirley B.:
There isn’t much I can say about how I became agoraphobic. I just slipped a little day
by day. . . . My daughter Nadeen was always by my side on those rare occasions when
I ventured outside, forced to leave my home when I needed medical attention. In the past
my fear kept me at home with all sorts of physical pains and ailments, as horrific as the
pain was, the pain of facing the outside world was greater. When I had two abscessed
teeth and my jaw was swollen to twice its normal size I was in such excruci ating pain that
I had to go to the dentist. So with my legs wobbling, my heart pounding, my hands sweat-
ing, and my throat choking, to the dentist I went. After examining my x-rays, the dentist
said he wouldn’t be able to do anything with my teeth because they were so infected, he
prescribed medication for the pain and infection and said that I must return in ten days,
not in two years. I felt as though those ten days were a countdown to my own execution.
Each day passed at lightning speed—like a clock ticking away. The fear grew stronger and
stronger. I had to walk around with my hand on my heart to keep it from jumping so hard,
as if I were pledging allegiance, which I was—to my fears and phobia. I asked God to please
give me strength to go back to the dentist. When the day came, I knew that my prepara-
tions would take me a little over four hours. I had to leave time, not just to bathe and
dress, but to debate with myself about going.
(Anxiety Disorders Association of America)
People with extreme agoraphobia cannot function normally in daily life.
Some are totally housebound, too crippled by anxiety and fear to go to work, the
supermarket, or the doctor. Others with agoraphobia are able to function better than
Shirley B. and can enter many situations without triggering panic or marked fear or
anxiety. Relying on a friend or family member, often referred to as a “safe” person
(for Shirley it was her daughter Nadeen), can help the sufferer enter feared situations
that otherwise might be avoided.
People with agoraphobia who also have panic symptoms or panic attacks avoid
situations that are associated with past panic; thus, they do not have the opportunity
to learn that they can be in such situations and not have a panic attack.
Understanding Panic Disorder and Agoraphobia
“I still don’t know what triggers a panic attack, but I can tell anyone reading this who
has never experienced one that it is a devastating experience. . . . An attack may hit
me on a day when I’m feeling relaxed and happy. That’s when I think, ‘Why me?’
‘Why today?’” (Campbell & Ruane, 1999, p. 151). The neuropsychosocial approach
allows us to address Campbell’s question about why panic disorder and agoraphobia
occur and are maintained. Because agoraphobia typically develops as a way to avoid
panic symptoms, in what follows we will focus more on panic disorder. Each type of
factor makes an important and unique contribution.
TABLE 6.6 • DSM-5 Diagnostic Criteria
for Agoraphobia
A. Marked fear or anxiety about two (or
more) of the following five situations:
1. Using public transportation (e.g.,
automobiles, buses, trains, ships, planes).
2. Being in open spaces (e.g., parking
lots, marketplaces, bridges).
3. Being in enclosed places (e.g., shops,
theaters, cinemas).
4. Standing in line or being in a crowd.
5. Being outside of the home alone.
B. The individual fears or avoids these
situations because of thoughts that
escape might be difficult or help
might not be available in the event of
developing panic-like symptoms or
other incapacitating or embarrassing
symptoms (e.g., fear of falling in the
elderly; fear of incontinence).
C. The agoraphobic situations almost
always provoke fear or anxiety.
D. The agoraphobic situations are actively
avoided, require the presence of a
companion, or are endured with intense
fear or anxiety.
E. The fear or anxiety is out of proportion
to the actual danger posed by the
agoraphobic situations and to the
sociocultural context.
F. The fear, anxiety, or avoidance is
persistent, typically lasting for 6 months
or more.
G. The fear, anxiety or avoidance causes
clinically significant distress or
impairment in social, occupational or
other important areas of functioning.
H. If another medical condition (e.g.,
inflammatory bowel disease, Parkinson’s
disease) is present, the fear, anxiety or
avoidance is clearly excessive.
I. The fear, anxiety or avoidance is not
better explained by the symptoms of
another mental disorder—for example,
the symptoms are not confined to
specific phobia, situational type; do not
involve only social situations (as in social
anxiety disorder); and are not related
exclusively to obsessions (as in obsessive-
compulsive disorder); perceived defects
or flaws in physical appearance (as in
body dysmorphic disorder), reminders
of traumatic events (as in posttraumatic
stress disorder), or fear of separation (as
in separation anxiety disorder).
Reprinted with permission from the Diagnostic and Statistical
Manual of Mental Disorders, Fifth Edition, (Copyright ©2013).
American Psychiatric Association. All Rights Reserved.
168 C H A P T E R 6
Neurological Factors
Brain systems, neural communication, and genetics con-
tribute to panic disorder and agoraphobia. Specifically,
these three types of neurological factors appear to give
rise to a heightened sensitivity to breathing changes.
Brain Systems
One key to explaining panic attacks came after research-
ers discovered that they could induce such attacks in the
laboratory. Patients who had had panic attacks volunteered
to hyperventilate (that is, to breathe in rapid, short pants,
decreasing carbon dioxide levels in the blood), which trig-
gered panic attacks. Moreover, researchers found that in-
jections of some medically safe substances, such as sodium
lactate (a salt produced in sweat) and caffeine, also produced
attacks—but only in people who have panic disorder (Nutt
& Lawson, 1992; Pitts & McClure, 1967). Why do these
substances induce panic attacks? One possibility is that the
brains of people who experience panic attacks have a low
threshold for detecting decreased oxygen in the blood,
which triggers a brain mechanism that warns us when we
are suffocating (Beck et al., 1999; Papp et al., 1993, 1997).
As predicted by this theory, patients with panic disorder
cannot hold their breath as long as control participants can
(Asmundson & Stein, 1994). When triggered, the neural
mechanism not only produces panic but also leads to hy-
perventilation and a strong sense of needing to escape.
Neural Communication
Researchers also have been investigating the role of neu-
rotransmitters in giving rise to panic disorder. One key
neurotransmitter is norepinephrine, too much of which is apparently produced in
people who have anxiety disorders (Nutt & Lawson, 1992). The locus coeruleus is a
small structure in the brainstem that produces norepinephrine, and some researchers
have theorized that it is too sensitive in people with panic disorder (Gorman et al.,
1989)—and thus may produce too much norepinephrine. The locus coeruleus and
norepinephrine are important because they are central to the body’s “alarm system,”
which causes the fight-or-flight response (including faster breathing, increased heart
rate, and sweating), which often occurs at times of panic.
Finally, we note that SSRIs can reduce the frequency and intensity of panic
attacks (DeVane, 1997); SSRIs reduce the effects of serotonin, which affects the locus
coeruleus in complex ways (Bell & Nutt, 1998).
Genetics
Genetic factors appear to play a role in the emergence of panic disorder. In fact, first-
degree biological relatives of people with panic disorder are up to eight times more
likely to develop the disorder than are control participants, and up to 20 times more
likely to do so if the relative developed it before 20 years of age (Crowe et al., 1983;
Torgersen, 1983; van den Heuvel et al., 2000). Twin studies have yielded similar
results by examining concordance rates; a concordance rate is the probability that
both twins will have a characteristic or disorder, given that one of them has it. The
concordance rate in pairs of female identical (monozygotic) twins is approximately
24%, in contrast to 11% for pairs of fraternal (dizygotic) twins (Kendler et al., 1993).
Thus, the more genes in common, the higher the concordance rates.
Concordance rate
The probability that both twins will have a
characteristic or disorder, given that one of
them has it.
TABLE 6.7 • Agoraphobia Facts at a Glance
Prevalence
• Up to 2% of people worldwide will develop agoraphobia at some point in
their lives (Somers et al., 2006).
Comorbidity
• About half of people with agoraphobia will also have another anxiety disorder
(including panic disorder), the symptoms of which predate the agoraphobia.
• Depression and substance use disorders are also common comorbid disorders,
but unlike with other anxiety disorders, these disorders tend to emerge after
the agoraphobia.
Onset
• Two-thirds of people with agoraphobia develop it before age 35.
• About half of people with agoraphobia report having had panic attacks or
panic disorder before developing agoraphobia.
Course
• Agoraphobia is a chronic mental disorder, persisting over time unless treated.
• More than one-third of people with this disorder are completely housebound.
Gender Differences
• Women are twice as likely as men to be diagnosed with agoraphobia.
Cultural Differences
• People with agoraphobia in Hong Kong also have a fear of being a burden to
others or making others worry (Hui et al., 2012).
Source: Unless otherwise noted, information in the table is from American Psychiatric Association, 2013.
Anxiety Disorders 169
Psychological Factors
Not all cases of panic disorder are related to a person’s threshold for detecting
suffocation; some cases of panic disorder arise from learning. Thus, behavioral and
cognitive theories can also help us understand how panic disorder and agoraphobia
arise and are perpetuated: People come to associate certain stimuli with the sensations
of panic and then develop maladaptive beliefs and behaviors with regard to those
stimuli and the sensations that are related to anxiety and panic.
Learning: An Alarm Going Off
Learning theory offers one possible explanation for at least some cases of panic
disorder. Initially, a person may have had a first panic attack in response to a
stressful or dangerous life event (a true alarm). This experience produces condi-
tioning, whereby the initial bodily sensations of panic (such as increased heart
rate or sweaty palms) become false alarms associated with panic attacks. As the
normal sensations that are part of the fight-or-flight response come to be as-
sociated with subsequent panic attacks, the bodily sensations of arousal them-
selves come to elicit panic attacks (learned alarms). The person then develops a
fear of fear—a fear that the arousal symptoms of fear will lead to a panic attack
(Goldstein & Chambless, 1978), much as S did in Case 6.2. After developing
this fear of fear, the person tries to avoid behaviors or situations where such
sensations might occur (Mowrer, 1947; White & Barlow, 2002).
Cognitive Explanations: Catastrophic Thinking and Anxiety Sensitivity
Cognitive theories, which focus on how a person interprets and then responds to alarm
signals from the body, offer other possible reasons why panic disorder could arise.
People with panic disorder may misinterpret normal bodily sensations as indicat-
ing catastrophic effects (Salkovskis, 1988), which is referred to as catastrophic thinking.
Catastrophic thinking can arise in part from anxiety sensitivity, which is a tendency to
fear bodily sensations that are related to anxiety along with the belief that such sensa-
tions indicate that harmful consequences will follow (McNally, 1994; Reiss, 1991;
Schmidt et al., 1997). For example, a person with high anxiety sensitivity is likely to
believe—or fear—that an irregular heartbeat indicates a heart problem or that short-
ness of breath signals being suffocated. People with high anxiety sensitivity tend to
know what has caused their bodily symptoms—for instance, that exercise caused a
faster heart rate—but they become afraid anyway, believing that danger is indicated,
even if it is not an immediate danger (Bouton et al., 2001; Brown et al., 2003).
Social Factors: Stressors, a Sign of the Times, and “Safe People”
Evidence suggests that social stressors contribute to panic disorder: People with panic
disorder tend to have had a higher-than-average number of such
stressful events during childhood and adolescence (Horesh et al.,
1997). Moreover, 80% of people with panic disorder reported
that the disorder developed after a stressful life event.
In addition, cultural factors can influence whether people de-
velop panic disorder, perhaps through culture’s influence on per-
sonality traits. For example, over the past five decades, increasing
numbers of Americans have developed the personality trait of
anxiety-proneness (Spielberger & Rickman, 1990). The average
child today scores higher on measures of this trait than did chil-
dren who received psychiatric diagnoses in the 1950s (Twenge,
2000)! The higher baseline level of anxiety in the United States
may be a result of greater dangers in the environment—such as
higher crime rates, new threats of terrorism, and new concerns
about food safety—or greater media exposure of such dangers.
People whose hearts sometimes beat too
quickly can be treated with a device implanted
under the skin that shocks the heart, which
causes it to beat at a normal speed again.
However, the shocks can be uncomfortable and
alarming. Research suggests that people who
receive more frequent and intense shocks are
more likely to develop panic disorder, which
arises as a conditioned fear in response to the
automatic shocks (Godemann et al., 2001).
D
r.
P
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a
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S
ci
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n
ce
S
o
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rc
e
Researchers have shown that the mental
stressors of basic military training are more
challenging to people with preexisting anxiety
sensitivity than they are to others.
R
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170 C H A P T E R 6
Social factors are also often related to the ways patients cope with agora-
phobia. As with GAD, the presence of a close relative or friend—a “safe person”
or companion—can help the patient temporarily cope with agoraphobia. In this
case, the presence of a safe person can decrease catastrophic thinking and panick-
ing, as well as the sufferer’s arousal. Although a safe person can make it possible
for the patient with agoraphobia to go into situations that he or she wouldn’t
enter alone, reliance on a safe person can end up perpetuating the disorder: By
venturing into anxiety-inducing situations only when a safe person is around, the
patient never habituates to the anxiety symptoms experienced when alone and in
the situation.
Feedback Loops in Understanding Panic Disorder and
Agoraphobia
Cognitive explanations of panic disorder can help show how a few panic attacks
can progress to panic disorder, but not everyone who has panic attacks develops
panic disorder. It is only when neurological and psychological factors interact with
bodily states that panic disorder develops (Bouton et al., 2001). For example, a
man’s argument with his wife (social factor) might arouse his anger and increase
his breathing rate. Breathing faster results in a lower carbon dioxide level in the
blood, which then leads the blood vessels to constrict—which means less oxygen
throughout the brain and body (neurological factor); the ensuing physical sensa-
tions (such as light-headedness) may be misinterpreted (psychological factor) as
the early stages of suffocation, leading the man to panic (Coplan et al., 1998).
This is how such physical changes can serve as a false alarm (Beck, 1976). After
many false alarms, the associated sensations may become learned alarms and trigger
panic in the absence of a social stressor (Barlow, 1988). Also, this man may become
hypervigilant for alarm signals of panic attacks, leading to anticipatory anxiety.
In turn, this anxiety increases activity in his sympathetic nervous system, which
causes the breathing and heart rate changes that he feared. In this way, the man
may trigger his own panic attack. Figure 6.3, on the next page, illustrates these
three factors and their feedback loops.
Treating Panic Disorder and Agoraphobia
Earl Campbell received treatment for his panic disorder—medication, cognitive-
behavior therapy (CBT), and social support—which targeted all three types of
neuropsychosocial factors. Treatment for agoraphobia also addresses panic symptoms
because fear of having panic symptoms drives sufferers to narrow their lives.
Targeting Neurological Factors: Medication
To treat panic disorder, a psychiatrist or another type of health care provider licensed
to prescribe medication may recommend an antidepressant or a benzodiazepine.
Benzodiazepines are prescribed as a short-term remedy; the benzodiazepines
alprazolam (Xanax) and clonazepam (Klonapin) affect the targeted symptoms within
36 hours, and they need not be taken regularly. One of these drugs might be
prescribed during a short but especially stressful period. Side effects of benzodiaz-
epines include drowsiness and slowed reaction times, and patients can suffer with-
drawal or need to take increasingly larger doses when these drugs are taken for an
extended period of time. For these reasons, antidepressants such as an SNRI, an
SSRI, or TCAs ( tricyclic antidepressants), such as clomipramine ( Anafranil), are better
long-term medications and are now considered “first-line” medications for panic
disorder (Batelaan et al., 2012). However, these medications can take up to 10 days
SP
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Anxiety Disorders 171
to have an effect (Kasper & Resinger, 2001). After Campbell’s panic attacks were
diagnosed, he initially relied on such medications as his sole treatment; like most
people, though, when he stopped taking the medication or forgot to take a pill, his
symptoms returned. Such recurrences motivated him to make use of other types of
treatments.
Targeting Psychological Factors
CBT is the first-line treatment for panic disorder because it has the most endur-
ing beneficial effects of any treatment (Cloos, 2005; DiMauro et al., 2013). Effec-
tive CBT methods can emphasize either the behavioral or the cognitive aspects of
change.
Mental Processes and
Mental Contents
Catastrophic thinking
Anxiety sensitivity
Misinterpretation of
bodily sensations
Hypervigilance
Affect
Fear of fear
Behavior
Learning of false
alarms
Avoidance of
triggering stimuli
Stressful Life Events
Stressful events,
particularly during
childhood
Gender/Culture
Increasing anxiety-
proneness in
more recent birth
cohorts
Family
Reliance on a safe
person perpetuates
the disorder
Genetics
Inherited
tendency to
be anxious
Neural Communication
NeuroPsychoSocial
Norepinephrine
Serotonin
Brain Systems
Locus coeruleus
NeuroPsychoSocial NeuroPsychoSocial
FI G U RE 6.3 • Feedback Loops in
Understanding Panic Disorder
and Agoraphobia
172 C H A P T E R 6
Behavioral Methods: Relaxation Training, Breathing Retraining, and
Exposure
For people with panic disorder, any bodily arousal can lead to a f ight-or-f light
response. Therapists may teach patients breathing retraining and rela xation
techniques, which stop the progression from bodily arousal to panic attack and
increase a sense of control over bodily sensations. Campbell reported how he learned
to take “long deep breaths and relax my body completely when panic struck. . . .
I somehow had to convince myself that the attack was not really happening. I had to
fight it off by relaxing myself ” (Campbell & Ruane, 1999, p. 119).
Other behavioral methods include exposure. To decrease a patient’s
reaction to bodily sensations associated with panic, behavioral therapists may
use interoceptive exposure: They have the patient intentionally elicit the
bodily sensations associated with panic so that he or she can habituate to
those sensations and not respond with fear. During exposure to interoceptive
cues, patients are asked to behave in ways that induce the long-feared sensa-
tion, such as spinning around to the point of dizziness or intentionally hy-
perventilating (see Table 6.8 for a more extensive list). Within approximately
30 minutes, the bodily arousal subsides. This procedure allows patients to
learn that the bodily sensations pass and no harm befalls them. For people
with agoraphobia symptoms, exposure addresses the patient’s tendency to
avoid activities and situations associated with panic attacks (such as exercise
or crowded theaters, respectively).
Cognitive Methods: Psychoeducation and Cognitive Restructuring
Cognitive methods for panic disorder help the patient recognize misappraisals
of bodily symptoms and learn to correct mistaken inferences about such
symptoms. First, psychoeducation for people with panic disorder involves
This man might just be casually spinning in
his office chair, but this same action is part
of interoceptive exposure: The therapist
intentionally tries to elicit from the patient
the bodily sensations associated with panic
so that he or she can habituate to those
sensations and not respond with fear.
Dizziness, for example, is associated with
panic, so a therapist may have a patient
repeatedly spin around to experience,
and thus habituate to, dizziness in a safe,
controlled environment.
A
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Interoceptive exposure
A behavioral therapy method in which
patients intentionally elicit the bodily
sensations associated with panic so that they
can habituate to those sensations and not
respond with fear.
People receiving interoceptive exposure
perform each of the exercises listed in
this table for the indicated duration; such
exercises are likely to elicit sensations
typically associated with panic. After
each exercise, they rate how intense the
sensations were, their level of anxiety while
doing the exercise, and how similar the
sensations were to panic symptoms.
TABLE 6.8 • Interoceptive Exposure Exercises for Treatment of Panic Disorder
Exercise
Duration
(seconds)
Sensation
intensity (0–8)
Anxiety
(0–8)
Similarity
(0–8)
Shake head from side
to side
30
Place head between legs
and then lift
30
Run on spot 60
Hold breath
30, or as long as
possible
Completely tense body
muscles
60, or as long as
possible
Spin in swivel chair 60
Hyperventilate 60
Breathe through narrow
straw
120
Stare at spot on wall or
own mirror image
90
Source: Craske & Barlow, 1993, Table 1.4, p. 36. For more information see the Permissions section.
Anxiety Disorders 173
helping them understand both how their physical sensations are symptoms of panic—
not of a heart attack or some other harmful medical situation—and the role of cata-
strophic thinking. Campbell read a pamphlet about panic disorder that described his
symptoms perfectly. Having learned about the disorder in this way, he was better
able to handle future panic attacks: “One of the most important things I have learned
about my panic disorder over the years is that although my heart may be racing and I
may feel like I’m having a heart attack, I know that I’m not. And I know it’s going to
stop” (Campbell & Ruane, 1999, p. 204).
Second, cognitive restructuring is then used to transform the patient’s initial
frightened thoughts of a medical crisis into more realistic thoughts, identifying
the symptoms of panic, which may be uncomfortable but do not indicate dan-
ger (Beck et al., 1979). For instance, a therapist may help a patient identify the
automatic negative thought about bodily arousal (“I won’t be able to breathe . . .
I’ll pass out”) and then challenges the patient about the belief: Was the patient truly
unable to breathe, or was breathing only difficult? Has the patient fainted before?
In this way, each of the patient’s automatic negative thoughts related to panic sen-
sations are challenged and thereby reduced. Learning to interpret correctly both
internal and external events can play a key role in preventing panic attacks that
occur when a person experiences symptoms of suffocation (Clark, 1986; Taylor &
Rachman, 1994).
Targeting Social Factors: Group and Couples Therapy
T her apy g roups (eit her sel f-help or conduc ted by a t her api st) t h at foc u s
specif ically on panic disorder and agoraphobia can be a helpful component of
a treatment program (Galassi et al., 2007). Meeting with others who have sim-
ilar diff iculties and shar ing exper iences can help to decrease a patient’s sense
of isolation and shame. Moreover, couples therapy or fam ily therapy may be
appropriate when a partner or other family member has been the safe person;
as the patient gets better, he or she may rely less on that person, which can af-
fect their relationship. In some cases, the patient’s increasing independence is
satisfying for everyone; but if the safe person has found satisfaction in tending to
the patient, the patient’s increased independence can be a stressful transition for
that person.
Feedback Loops in Treating Panic Disorder and Agoraphobia
Because agoraphobia f requent ly co-occur s w ith pan ic d isorder, we d iscuss
treatments for both here. Invariably, medication—which changes neurological
functioning—stops being beneficial when the patient stops taking it. The positive
changes in neural communication and brain activity and the associated changes
in thoughts, feelings, and behaviors do not endure; the symptoms of panic dis-
order return. However, for some patients, medication is a valuable first step, pro-
viding enough relief from symptoms that these patients are motivated to obtain
CBT, which can change their reactions (psychological factor) to perceived bodily
sensations ( neurological factor). When a patient receives both medication and
CBT, the medication should be at a low enough dose that the patient can still feel
the sensations that led to panic in the past (Taylor, 2000). In fact, the dose should
be gradually decreased so that the patient can experience enough anxiety to be
increasingly able to make use of cognitive-behavioral methods. It is the CBT
that leads to enduring changes. Successful treatment will probably lead the pa-
tient, especially if he or she also has agoraphobia, to become more independent—
which in turn can change the person’s relationships, particularly with their safe
people (social factor). These factors and their feedback loops are summarized in
Figure 6.4.
SP
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is
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a
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ie
/S
u
p
e
rs
to
ck
These women may just be affectionately
crossing the street, but a person with
agoraphobia may rely on a friend or family
member, often referred to as a “safe” person,
who can help the sufferer enter feared
situations that otherwise might be avoided.
174 C H A P T E R 6
Thinking Like A Clinician
All you know about Fiona is that she has had about 10 panic attack s. Is this enough
information to determine whether she has panic disorder? If it is, does she have the
disorder? If this isn’t enough information, what else would you want to know, and why?
Now suppose that Fiona star t s missing Monday classes because of panic attack s on
those days. She also stops going to par ties on weekends because she had a couple of
panic attacks at parties. Would you change or maintain your answer about whether she
has panic disorder? Why or why not? Suppose Fiona does have panic disorder. Explain
how she might have developed the disorder. By the end of the semester, Fiona no longer
goes out of her apartment for fear of getting a panic attack. What might be appropriate
treatments for Fiona?
Social Anxiety Disorder
(Social Phobia)
As Earl Campbell’s anxiety increased, he became concerned about what other peo-
ple might think of him if they knew about his problem. As noted earlier, he was
very aware of when people were looking at him. He also avoided crowds. Could
Campbell have developed social anxiety disorder?
Changes neural
activity
Treatments Targeting
Neurological Factors
Medication: SSRIs,
SNRIs, TCAs,
benzodiazepines
Treatments Targeting
Psychological Factors
CBT: Breathing
retraining, relaxation,
interoceptive
exposure, exposure to
agoraphobia-related
stimuli,
psychoeducation,
cognitive restructuring
Changes thoughts,
feelings, and
behaviors
Decreases shame and
isolation
Increases family
members’ support
Treatments Targeting
Social Factors
Group therapy
Couples or family
therapy
FI G U RE 6.4 • Feedback Loops in Treating Panic Disorder and Agoraphobia
Anxiety Disorders 175
What Is Social Anxiety Disorder?
Social anxiety disorder, also called social phobia, is an intense fear of or anxiety
about being scrutinized by others when in social situations, (see Table 6.9; American
Psychiatric Association, 2013). Such social situations fall into three types: social in-
teractions (such as a conversation); being observed (such as when eating or using pub-
lic restrooms); and performing (such as giving a speech). People with social anxiety
disorder may avoid making eye contact and avoid their feared social situations when-
ever possible. As noted in Table 6.9, a DSM-5 criterion is that the fear or anxiety is
disproportional to the danger actually posed.
When a social situation cannot be avoided and must be endured, the person with
social anxiety disorder experiences fear or anxiety, sometimes including symptoms of
upset stomach, diarrhea, sweating, muscle tension, and heart palpitations. DSM-5 dis-
tinguishes between a social phobia that is limited to specific social performances where
the person is the center of attention—such as making a presentation—and a more gen-
eralized social phobia, which leads a person to fear and avoid all social situations, as
does Rachel in Case 6.4. Table 6.10 lists additional facts about social anxiety disorder.
CASE 6.4 • FROM TH E OUTSIDE: Social Anxiety Disorder
Rachel was a twenty-six-year-old woman who worked as an assistant manager of a small
bookstore. [She sought treatment] for her intense anxiety about her upcoming wedding.
Rachel wasn’t afraid of being married (i.e., the commitment, living with her spouse, etc.);
she was terrified of the wedding itself. The idea of being on display in front of such a large
audience was almost unthinkable. In fact, she had postponed her wedding on two previous
occasions because of her performance fears. . . .
She reported being shy from the time she was very young. When she was in high school,
her anxiety around people had become increasingly intense and had affected her school life.
She was convinced that her classmates would find her dull or boring or that they would notice
her anxiety and assume that she was incompetent. Typically, she avoided doing oral reports
at school and didn’t take any classes where she felt her performance might be observed or
judged by her classmates (e.g., gym). On a few occasions, she even went out of her way to
obtain special permission to hand in a written essay instead of doing an oral report.
Throughout college, Rachel had difficulty making new friends. Although people liked
her company and often invited her to parties and other social events, she rarely accepted.
She had a long list of excuses to get out of socializing with other people. She was comfort-
able only with her family and several longtime friends but aside from those, she tended to
avoid significant contact with other people.
(Antony & Swinson, 2000b, pp. 5–6)
People who have social anxiety disorder also tend to be very sensitive to criti-
cism and rejection and to worry about not living up to the perceived expectations
of others. Thus, they often dread being evaluated or taking tests, and they may not
perform up to their potential at school or work. Their diminished performance chal-
lenges their self-esteem, increasing their anxiety during subsequent performances or
tests. Similarly, achievement at work may suffer because they avoid social situations
that are important for advancement on the job, such as making presentations. People
with social anxiety disorder are less likely to marry or have a partner than people
who do not have this disorder.
Sometimes, a clinician or researcher cannot easily distinguish whether a person’s
symptoms indicate that he or she has social anxiety or agoraphobia. However, there
are two key features that distinguish these disorders:
1. People with social anxiety disorder fear other people’s scrutiny.
2. People with social anxiety disorder rarely have panic attacks when alone.
In contrast, people who have agoraphobia do not exhibit these features.
Social anxiety disorder
An anxiety disorder characterized by intense
fear of public humiliation or embarrassment;
also called social phobia.
TABLE 6.9 • DSM-5 Diagnostic Criteria
for Social Anxiety Disorder
A. Marked fear or anxiety about one or more
social situations in which the individual
is exposed to possible scrutiny by others.
Examples include social interactions (e.g.,
having a conversation, meeting unfamiliar
people), being observed (e.g., eating or
drinking), and performing in front of
others (e.g., giving a speech).
Note: In children, the anxiety must
occur in peer settings and not just during
interactions with adults.
B. The individual fears that he or she will
act in a way or show anxiety symptoms
that will be negatively evaluated (i.e.,
will be humiliating or embarrassing; will
lead to rejection or offend others).
C. The social situations almost always
provoke fear or anxiety.
Note: In children, the fear or anxiety
may be expressed by crying, tantrums,
freezing, clinging, shrinking, or falling to
speak in social situations.
D. The social situations are avoided or
endured with intense fear or anxiety.
E. The fear or anxiety is out of proportion
to the actual threat posed by the social
situation and to the sociocultural context.
F. The fear, anxiety, or avoidance is persistent,
typically lasting for 6 months or more.
G. The fear, anxiety, or avoidance causes
clinically significant distress or
impairment in social, occupational, or
other important areas of functioning.
H. The fear, anxiety or avoidance is not
attributable to the physiological effects
of a substance (e.g., a drug of abuse, a
medication) or another medical condition.
I. The fear, anxiety or avoidance is not
better explained by the symptoms of
another mental disorder, such as panic
disorder, body dysmorphic disorder, or
autism spectrum disorder.
J. If another medical condition
(e.g., Parkinson’s disease, obesity,
disfigurement from burns or injury) is
present, the fear, anxiety or avoidance is
clearly unrelated or is excessive.
Reprinted with permission from the Diagnostic and Statistical
Manual of Mental Disorders, Fifth Edition, (Copyright ©2013).
American Psychiatric Association. All Rights Reserved.
176 C H A P T E R 6
TABLE 6.10 • Social Anxiety Disorder Facts at a Glance
Prevalence
• Social anxiety disorder is one of the most common anxiety disorders, with prevalence estimates ranging from 3% to 13%.
• A fear of public speaking or public performance is the most common symptom, followed by a fear of talking to strangers or meeting new people.
Comorbidity
• Among those with social anxiety disorder, over half will also have one other psychological disorder at some point in their lives, and 27% will have
three or more disorders during their lives (Chartier et al., 2003). Approximately 20–44% will have a mood disorder (Chartier et al., 2003; Roth &
Fonagy, 2005).
Onset
• Most people with social anxiety disorder were shy as children, and they developed the disorder during childhood, with broader symptoms gener-
ally appearing during adolescence.
Course
• Social anxiety disorder may develop gradually or it may begin suddenly after a humiliating or stressful social experience.
• Symptoms typically are chronic, although they may lessen for some adolescents as they enter adulthood.
• Only half the people with this disorder seek treatment for it—usually after 15 years of symptoms.
• For some people, symptoms can improve over the course of time.
Gender Differences
• Social anxiety disorder is approximately twice as common in females as in males.
Cultural Differences
• Culture can influence the specific form of social anxiety disorder symptoms; for instance, in Japan, some people with social anxiety disorder may
fear that their body odor will offend others (Dinnel et al., 2002), whereas people with social anxiety disorder in Hong Kong are more likely to be
afraid of talking to people who have a higher social status (Lee et al., 2009).
Source: Unless otherwise noted, information in the table is from American Psychiatric Association, 2013.
Understanding Social Anxiety Disorder
Because of the very nature of this disorder, social factors are prominent contributors
to it. Neveretheless, as we’ll see, all three types of factors play a role and contributed
to Campbell’s problems.
Neurological Factors
Why does social anxiety disorder exist at all? Evolutionary psychologists speculate that
social anxiety disorder may have its origins in behaviors of animals that are lower on
a dominance hierarchy: Less powerful animals fear aggressive action from those more
dominant and therefore behave submissively toward them. It is possible that social
phobias arise when this innate mechanism becomes too sensitive or otherwise responds
improperly (Hofmann et al., 2002). Key facts about the brains of people with social
anxiety disorder are consistent with this conjecture, as we see in the following section.
Brain Systems and Neural Communication
Social anxiety disorder involves fear, and researchers have shown repeatedly that
the amygdala is strongly activated when animals—including humans—are afraid
(Rosen & Donley, 2006). Thus, it’s no surprise that the amygdala is more strongly
activated when people with social anxiety disorder see faces with negative expres-
sions (such as anger) than when they see happy faces and that this difference is greater
than observed in control participants who do not have the disorder (Del Casale et al.,
2012; Phan et al., 2006). Indeed, the more symptoms of social anxiety disorder a
What is your amygdala doing when you see
this negative facial expression? The amygdalae
of people with social anxiety disorder are
more active when seeing negative facial
expressions, such as this one here, compared
to people without the disorder.
Jo
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a
th
a
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Anxiety Disorders 177
person has, the more strongly the amygdala is activated when the person views faces
with negative expressions.
In addition, neurotransmitters may function abnormally in people who have so-
cial anxiety disorder (Li, Lindenberger, & Sikström, 2001). In particular, researchers
have found that patients with social anxiety disorder show less activation in brain
areas that rely on dopamine than do control participants. Furthermore, people with
social anxiety disorder have too little serotonin, which may suggest why SSRIs have
sometimes helped these patients (Gorman & Kent, 1999; Lykouras, 1999).
Genetics
As is the norm for anxiety disorders, social anxiety disorder appears to arise from
both genetic factors and environmental factors (Mathew et al., 2001; Stein, Jang, &
Livesly, 2002). The heritability of social anxiety disorder is about 37% on average
(Beatty et al., 2002; Fyer, 2000; Li et al., 2001; Neale et al., 1994).
We noted earlier that some people with social anxiety disorder were extremely
shy as children; they had what is called a shy temperament, or behavioral inhibition
(Biederman et al., 2001; Kagan, 1989), which has a genetic component. These
patients cannot really be said to have developed a phobia, since they always had a basic
level of discomfort in particular social situations (Coupland, 2001).
Which one of these children is more likely to be diagnosed with social anxiety disorder as an
adult? Answer: The child on the right, who seems shy and may have a behaviorally inhibited
temperament.
GETTING THE PICTURE
Y
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ll
o
w
D
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g
P
ro
d
u
ct
io
n
s/
G
e
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I
m
ag
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s
©
P
ic
tu
re
P
a
rt
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e
rs
/A
la
m
y
Psychological Factors
Three types of psychological factors influence the emergence and maintenance of
social anxiety disorder: cognitive biases and distortions, classical conditioning, and
operant conditioning.
Cognitive Biases and Distortions
People who have social anxiety disorder have particular biases in attention and mem-
ory (Ledley & Heimberg, 2006; Lundh & Öst, 1996; Wenzel & Cochran, 2006).
In particular, people with social anxiety disorder tend to pay more attention to—and
hence better remember—faces that they perceive as critical, which in turn feeds into
their fears about being evaluated.
178 C H A P T E R 6
Similarly, cognitive distortions about the world can lead people with social anxi-
ety disorder to see it as a very dangerous place; they then become chronically hy-
pervigilant for potential social threats and negative evaluations by others (Beck &
Emery, 1985; Joorman & Gotlib, 2006; Rapee & Heimberg, 1997). People with so-
cial anxiety disorder also use distorted emotional reasoning as proof that they will be
judged negatively: They evaluate the impression they made on others based on how
anxious they became during the interaction, regardless of what actually transpired.
Furthermore, people with social anxiety disorder interpret ambiguous cues as nega-
tive, which becomes proof that they were correct in their concerns. For instance, an
anxious woman giving a talk may interpret the fact that some audience members in
the front row are leaning forward in their seats during her talk as proof that they are
“waiting for me to falter or make a jerk out of myself ” rather than that they might be
leaning in to hear her better or might be stretching their backs.
Classical and Operant Conditioning
In some cases, classical conditioning can contribute to the development of social
anxiety disorder: A social situation (the conditioned stimulus) becomes paired with
a negative social experience (such as public humiliation) to produce a conditioned
emotional response (Mineka & Zinbarg, 1995). The conditioned response (fear or
anxiety) may generalize to other, or even all, types of social situations.
Operant conditioning principles apply to social anxiety disorder as well: Like a
person with agoraphobia, a person with social anxiety disorder might avoid social
situations in order to decrease the probability of an uncomfortable experience.
The avoidant behavior does decrease anxiety and is thus reinforced (Mowrer, 1939).
Campbell’s avoidance of crowds does not appear to have been related to social anxi-
ety but rather to his attempting to avoid places where he might have a panic attack.
Social Factors
Extreme overprotection by parents is associated with childhood anxi-
ety (Hudson & Rapee, 2001; Wiborg & Dahl, 1997); such overprotec-
tion may lead children to avoid certain situations to cope with their
anxiety (Barrett et al., 1996).
In addition, different cultures emphasize different concerns about
social interactions, and these concerns influence the specific nature of
social anxiety disorder. For example, in certain Asian cultures, such as
those of Korea and Japan, a person with social anxiety disorder may be
especially afraid of offending others; in particular, he or she may fear
that his or her body odor or blushing will be offensive. In Japan, this
fear is known as taijin kyofusho (Dinnel et al., 2002; Guarnaccia, 1997a).
This contrasts with a fear among North Americans and Europeans
of being humiliated by something they say or do (Lee & Oh, 1999).
This difference in type of social fears is consistent with the collectivist
orientation of Asian countries compared to the individualist orientation
of Western countries (Norasakkunit et al., 2012). The results from one study suggest
that social phobias are becoming more common over time, and a higher proportion of
people in more recent birth cohorts will develop the disorder (Heimberg et al., 2000).
Feedback Loops in Understanding Social Anxiety Disorder
A genetic or other neurological vulnerability, such as a shy temperament, can predispose
people to developing social anxiety disorder (Bienvenu et al., 2007). The neurological
vulnerability both contributes to and is affected by distorted thinking and conditioning
to social situations (psychological factors). In addition, the anxiety and cognitive distor-
tions may be triggered by a negative social event (social factor) and are then perpetuated
SP
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Culture can influence the nature of the
symptoms of social anxiety disorder. In Korea,
for example, social fears called taijin kyofusho
involve the possibility of offending others,
perhaps through body odor or blushing. The
social anxieties of Westerners, in contrast,
involve fears of being humiliated by their own
actions.
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Anxiety Disorders 179
by negative self-evaluations and avoidance of the feared social interactions (Antony &
Barlow, 2002). Based on these psychological factors, people with social anxiety disorder
may interact with others in ways that lead other people to rebuff them (Taylor & Alden,
2006), confirming their own negative view of themselves and of social interactions.
Treating Social Anxiety Disorder
Various forms of treatment are effective for social anxiety disorder; although these
treatments typically target a single type of factor, as usual, they indirectly affect the
other types of factors.
Targeting Neurological Factors: Medication
For people whose social fears are limited to periodic per formances—such as
a business presentation, a class presentation, or an onstage per for mance — a
beta-blocker, such as propranolol (Inderal), is the medication of choice (Rosenbaum
et al., 2005). Beta-blockers bind to some of the brain’s receptors for epinephrine
and norepinephrine and hence make these receptors less sensitive. Both of these
neurotransmitters are released during the fight-or-flight response. Thus, if the person
perceives a “threat” and more epinephrine or norepinephrine is released as part of
the fight-or-flight response, he or she will not experience its physical effects, such as
increased heart rate, as strongly after taking a beta-blocker.
For those whose social anxiety arises in a wider and more frequent set of cir-
cumstances, the medication of choice is the SSRI paroxetine (Paxil) or sertraline
(Zoloft). Other SSRIs and SNRIs, such as venlafaxine (Effexor) and nefazodone (Ser-
zone), and NaSSAs, such as mirtazapine (Remeron), can also help treat social anxi-
ety disorder (Rivas-Vazques, 2001; Van der Linden, Stein, & van Balkom, 2000).
These medications affect the amygdala and the locus coeruleus, decreasing their
activation. As with panic disorder, medication may be effective in treating social
anxiety disorder in the short run (Federoff & Taylor, 2001), but symptoms gener-
ally return when medication is discontinued; thus, CBT is often also appropriate.
Targeting Psychological Factors: Exposure and
Cognitive Restructuring
The cognitive aspects of CBT help people to identify irrational thoughts about social
situations, develop more realistic thoughts and expectations, and test predictions
about the consequences of engaging in specific behaviors (Antony & Barlow, 2002;
Which photo best captures the type of situation that would be part of exposure treatment for social fears
about public speaking? Answer: The photo on the left.
GETTING THE PICTURE
©
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180 C H A P T E R 6
Clark et al., 2006). In addition, the behavioral method of exposure can be very
effective in treating people with social anxiety disorder: When people put themselves
in social situations in order to habituate to their anxiety symptoms, their anxiety
diminishes (Taylor, 1996).
Targeting Social Factors: Group Interactions
Because the anxiety symptoms relate to social interactions, group therapy is the
preferred mode of exposure treatment. Such therapy immerses people in the very type
of experience that is associated with anxiety. Cognitive-behavioral group therapy uses ex-
posure and cognitive restructuring in a group setting. This setting allows patients to
try out their new skills immediately (Heimberg et al., 1990, 1998). Moreover, the
exposure involved in group therapy helps to extinguish the conditioned bodily arousal
(learned alarm) that arises in social situations. Cognitive-behavioral group therapy is as
effective as medication (Davidson et al., 2004) and has the added benefit that the posi-
tive effects continue after treatment ends (Aderka et al., 2011; Furukawa et al., 2013).
In addition to therapy groups, there are self-help organizations for people who
are afraid of speaking in public, such as Toastmasters, which give people an oppor-
tunity to practice making both spontaneous speeches and planned ones. (For more
information, go to www.toastmasters.org.)
Feedback Loops in Treating Social Anxiety Disorder
Research indicates that CBT has effects on the brain that are comparable to those
of some medications; both sorts of treatments actually reduce the activity in certain
key brain areas. For example, one study investigated two kinds of treatments with
participants who had untreated social anxiety disorder (Furmark et al., 2002). The
study began by scanning the participants’ brains as they performed a public speaking
task—which made them all anxious. Each participant was then randomly assigned to
one of three groups: After the first scan, members of one group received the SSRI
citalopram, members of another received CBT, and members of the third group were
placed on a waiting list.
Nine weeks after the f irst scan, patients in the two treatment groups had
improved by the same amount; however, patients in the waiting list group had not
improved. At this point, all participants received a second brain scan, again while they
performed the public speaking task. Comparison of the before and after brain scans
revealed that a host of brain areas had less activity after treatment, particularly those
involved in fear (and related emotions) and memory. Specifically, the amygdala, the
hippocampus, and related areas were activated less strongly during the second scan,
and the activation decreased comparably for the participants in the two treatment
groups. The patients who responded best to treatment showed the greatest decrease
in activation. And perhaps most striking, 1 year later the people who had the greatest
reduction in activation from the first scan to the second scan were the most improved
clinically. This means that the brain scans indicated how well the treatment worked
for people with social anxiety disorder.
However, when medication is discontinued, symptoms of social anxiety disorder
often recur. Such relapse is less likely after CBT. From a neuropsychosocial approach,
CBT changes the way a patient thinks about and behaves in social situations (psycho-
logical factors). Viewing these situations more realistically and with less anxiety means
that the patient does not get as physically aroused (neurological factor). This lowered
arousal, along with positive or neutral expectations about the previously feared social
situations, leads the patient to enter more willingly into a social situation (social factor),
with less negative expectations. When such social experiences are positive, the patient
feels increasing mastery (psychological factor) and less arousal (neurological factor) and
perhaps receives reinforcement from others (social factor) for these changes.
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Anxiety Disorders 181
Specific Phobia
Another type of anxiety disorder—one that does not seem to apply to Campbell—is
specific phobia. To understand why this diagnosis would not apply to him, we need to
learn what specific phobia is.
What Is Specific Phobia?
What distinguishes normal fear and avoidance of an object or situation from its “ab-
normal” counterpart? DSM-5 describes the central element of specific phobia as a
marked anxiety or fear of a specific situation or object that is disproportional to the
actual danger posed (see Table 6.11; American Psychiatric Association, 2013). A per-
son with a specific phobia works hard to avoid the feared stimulus, often significantly
restricting his or her activity in the process (see Case 6.5). A person with an elevator
phobia, for example, will choose to walk up many flights of stairs rather than take the
elevator. A specific phobia you might recognize include claustrophobia (fear of small
spaces), arachnophobia (spiders), hydrophobia (water), and acrophobia (heights).
CASE 6.5 • FROM THE OUTSIDE: A Specific Phobia (Hydrophobia)
Kevin described an experience in which he almost drowned when he was 11. He and his
parents were swimming in the Gulf of Mexico, in a place where there were underwater
canyons with currents that would often pull a swimmer out to sea. He remembered the
experience very distinctly. He was standing in water up to his neck, trying to see where his
parents were. Suddenly, a large wave hit him and dragged him into one of the underwater
canyons. Fortunately, someone on shore saw what had happened and rescued him. After
the experience, he became very much afraid of the ocean, and the fear generalized to
lakes, rivers, and large swimming pools. He avoided them all.
(McMullin, 1986, p. 165)
DSM-5 lists five types or categories of specific phobia: animal, natural environment,
blood-injection-injury, situational, and “other” (American Psychiatric Association, 2013):
• The animal type of specific phobia pertains to an extreme fear or avoidance of a kind
of animal; commonly feared animals include snakes and spiders. Symptoms of the
animal type of specific phobia usually emerge in childhood. People with a phobia
for one kind of animal often also have a phobia for another kind of animal.
• The natural environment type of specific phobia typically focuses on heights, water, or
storms. Phobias about the natural environment typically emerge during childhood.
• The blood-injection-injury type of specific phobia produces a strong response to seeing
blood, having injections, sustaining bodily injuries, or watching surgery. This type
of phobia runs in families and emerges in early childhood. A unique response of this
specific phobia involves first an increased arousal, then a rapid decrease in heart rate
and blood pressure, which often causes fainting. Among people with this type of
phobia, over half report having fainted in response to a feared stimulus (Öst, 1992).
Specific phobia
An anxiety disorder characterized by excessive
or unreasonable anxiety about or fear related
to a specific situation or object.
Nick loved his job—he was a programmer, and he worked from home. The thing he loved
most about his job was that he didn’t have to deal with people all day. However, his company
was recently bought by a larger firm that wants Nick to start working in the central office a
few days a week. His new boss tells him he’ll have to attend several weekly meetings. Nick
gets anxious about these changes. What determines whether Nick has social anxiety disor-
der or is just shy and nervous about the work changes? Explain your answer. If Nick gets so
anxious that he can’t attend the meetings, what would be an appropriate treatment for him?
Thinking Like A Clinician
TABLE 6.11 • DSM-5 Diagnostic
Criteria for Specific Phobia
A. Marked fear or anxiety about a specific
object or situation (e.g., flying, heights,
animals, receiving an injection, seeing
blood).
Note: In children, the fear or anxiety
may be expressed by crying, tantrums,
freezing, or clinging.
B. The phobic object or situation almost
always provokes immediate fear or
anxiety.
C. The phobic object or situation is actively
avoided or endured with intense fear or
anxiety.
D. The fear or anxiety is out of proportion
to the actual danger posed by the
specific object or situation and to the
sociocultural context.
E. The fear, anxiety, or avoidance is persistent,
typically lasting for 6 months or more.
F. The fear, anxiety, or avoidance causes
clinically significant distress or
impairment in social, occupational, or
other important areas of functioning.
G. The disturbance is not better explained
by the symptoms of another mental
disorder, including fear, anxiety and
avoidance of situations associated
with panic-like symptoms or other
incapacitating symptoms (as in
agoraphobia); objects or situations
related to obsessions (as in obsessive-
compulsive disorder); separation from
home or attachment figures (as in
separation anxiety disorder); or social
situations (as in social anxiety disorder).
Reprinted with permission from the Diagnostic and
Statistical Manual of Mental Disorders, Fifth Edition,
(Copyright ©2013). American Psychiatric Association. All
Rights Reserved.
182 C H A P T E R 6
• A situational type of specific phobia involves a fear of a particular situation, such as
being in an airplane, elevator, or other enclosed space, or of driving a car. Some
people develop this type of phobia in childhood, but in general it has a later onset,
often in the mid-20s. People with this type of phobia tend to experience more
panic attacks than do people with other types of specific phobia (Lipsitz et al.,
2002). Situational phobia has a gender ratio, age of onset, and family history similar
to those of panic disorder or agoraphobia.
• Other type of specific phobia includes any such phobia that does not fall into the
other four categories. Examples of specif ic phobias that would be classif ied as
“other” are a fear of costumed characters (such as clowns at a circus) and a phobic
avoidance of situations that may lead to choking or vomiting.
Specifics About Specific Phobia
As noted in Table 6.12, the majority of people who
have one sort of specific phobia are likely to have at
least one more. This high comorbidity among types of
specific phobia has led some researchers to suggest that,
like social anxiety disorder, specific phobia may take
two forms: a focused type that is limited to a specific
stimulus and a more generalized type that involves fear
of various stimuli (Stinson et al., 2007).
The unrea l istic fears and extreme an x iet y of
a specific phobia occur in the presence of the feared
stimulus but may even occur when simply thinking
about it. Often, people with a specific phobia fear that
something bad will happen as a result of contact with
the stimulus: “What if I get stuck in the tunnel, and
it cracks open and floods?” “What if the spider bites
me, and I get a deadly disease? ” People may also be
afraid of the consequences of their reaction to the pho-
bic stimulus, such as losing control of themselves or
not being able to get help: “What if I faint or have a
heart attack while I’m in the tunnel?” or, “What if I
mess my pants after the spider bites me?” In this sense,
the fear of somehow losing control is similar to that in
panic disorder (Horwath et al., 1993).
There is a ver y long l ist of st imu l i to wh ich
people have developed phobias (see www. phobialist
.com), but people do not seem to develop specif ic
phobias toward all kinds of stimuli; for example, a
phobia of flowers is extremely unusual. Humans, like
other animals, have a natural readiness for certain
stimuli to produce certain conditioned responses.
This preparedness means that less learning from experience is needed to produce the
conditioning (Öhman et al., 1976). Some psychologists (Menzies & Parker, 2001;
Öhman, 1986) propose that such preparedness has an evolutionar y advantage:
People are more readily afraid of objects or situations that could lead to death,
such as being too close to the edge of a cliff (and falling off ) or being bitten by a
poisonous snake or spider. According to this view, those among our early ancestors
who were afraid of these stimuli and avoided them were more likely to survive and
reproduce—and thus passed on genes that led their descendants to be prepared to
fear these stimuli.
TABLE 6.12 • Specific Phobia Facts at a Glance
Prevalence
• Approximately 10% of Americans will experience in their lifetime a fear severe
enough to meet the criteria for specific phobia (Stinson et al., 2007).
Comorbidity
• Only a quarter of those with a diagnosis of specific phobia have a single specific
phobia; 50% have three or more phobias. In addition, the more phobias a per-
son has, the more likely he or she is to have another type of anxiety disorder
(Curtis et al., 1998; Stinson et al., 2007).
Onset
• There are different ages of onset for the various types of specific phobia,
although they typically begin in childhood; the average age is approximately
10 years (Stinson et al., 2007).
• Specific phobia that arises after trauma can occur at any age.
Course
• Specific phobia that arises during childhood and persists through adulthood is
less likely to improve without treatment.
Gender Differences
• Twice as many women are diagnosed with specific phobia as men, although this
ratio varies across type of specific phobia (Stinson et al., 2007).
Cultural Differences
• The prevalence rates of the various types of specific phobia vary across countries,
suggesting that cultural factors, such as the likelihood of coming into contact with
various stimuli, affect the form that specific phobia takes (Chambers et al., 1986).
Source: Unless otherwise noted, information in the table is from American Psychiatric Association, 2013.
Anxiety Disorders 183
Understanding Specific Phobia
As we see in the following sections, neurological and psychological
factors appear to contribute to specific phobia more heavily than do
social factors.
Neurological Factors
Researchers are making good headway in understanding the neuro-
logical factors that underlie specific phobia.
Brain Systems and Neural Communication
Perhaps not surprisingly, our old friend the amygdala is again impli-
cated in an anxiety disorder. In fact, the amygdala appears to have
a hair-trigger in patients with specific phobia. For example, in one
f MRI study, patients who were phobic of spiders and control partici-
pants were asked to match geometric figures. In this study, the trick
was that in the background behind each figure—which was completely irrelevant
to the task of matching the f igures—was a picture of either a spider or a mush-
room (because no one in the study was afraid of mushrooms). Even in this task,
where the participants were not paying attention to the background pictures, the
amygdala of the patients with the phobia was more strongly activated in response
to the spiders than the mushrooms; this was not true for the control participants
(Straube et al., 2006).
In addition, the sort of anxiety evoked by specif ic phobia is associated with
too little of the inhibitor y neurotransmitter GABA (File et al., 1999). When a
benzodiazepine (such as diazepam, or Valium) binds to the appropriate receptors, it
facilitates the functioning of GABA—and the drug thereby ultimately produces a
calming effect.
Genetics
Researchers have discovered that some genes predispose people to develop a
particular specific phobia, whereas other genes predispose people to develop some
sort of specific phobia but do not affect which particular type it will be (Kendler
et al., 2001; Lichtenstein & Annas, 2000). According to one theory, genetic dif-
ferences may cause parts of the brain related to fear (in particular, the amygdala) to
be too reactive to specific stimuli; that is, the amygdala is “prepared” to overreact
to a specific stimulus, which leads to a specific phobia of that stimulus. In addition,
some people’s brains may generally be more prepared in this way than others’, and
so they are more likely to develop a specific phobia although not any particular one
(LeDoux, 1996).
Furthermore, genes do not have equal effects for all types of specific phobia:
The different types of specific phobia appear to be influenced to different degrees by
genetics and the environment (see Figure 6.5 for the heritabilities of types of specific
phobia). However, genetics cannot be all there is to it: If it were, then when one
identical twin has specific phobia, so would the other twin, but this is not always the
case. As we’ve noted before, the genes predispose, but rarely determine. Rather, cer-
tain environmental events are necessary to trigger the disorder. For example, family
environment has proven to be an important risk factor for specific phobia (Kendler
et al., 2001).
The sum of the research findings about neurological factors suggests that par-
ticular life experiences can lead to a particular specific phobia for people who—
through genes or other life experiences—are neurologically vulnerable (Antony
& Barlow, 2002).
Although many people fear some kind of
animal, such as spiders or snakes, the fear
and avoidance of that type of animal do not
constitute a specific phobia unless they cause
marked distress or significantly interfere with
normal functioning.
N
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100
90
80
70
60
50
40
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20
Blood-
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Animal
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Situational
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FI G U RE 6.5 • Heritabilities of
Specific Phobia
Source: From Kendler, Karkowski, & Prescott, 1999b.
Copyright 1999 by Cambridge University Press.
184 C H A P T E R 6
Psychological Factors
Life experiences always have their impact via how a person perceives and inter-
prets them. Thus, psychological factors play a key role in whether a person will
develop a specific phobia. Three primar y psychological factors contribute to a
specific phobia: a tendency to overestimate the probability of a negative event’s
occurring based on contact with the feared stimuli, classical conditioning, and
operant conditioning.
Faulty Estimations
Similarly to what we saw with social anxiety disorder, people
who have a specific phobia have a particular cognitive bias—
they believe strongly that something bad will happen when they
encounter the feared stimulus (Tomarken et al., 1989). They
also overestimate the probability that an unpleasant event, such
as falling from a high place or an airplane’s crashing into a tall
building, will occur (Pauli et al., 1998). People who have a spe-
cific phobia may also have perceptual distortions related to their
feared stimulus. For example, a person with a spider phobia
may perceive that a spider is moving straight toward him or her
when it isn’t (Riskind et al., 1995).
Conditioning: Classical and Operant
From a learning perspective, classical conditioning and operant
conditioning could account for the development and maintenance of a specific pho-
bia. Watson and Rayner’s conditioning of Little Albert’s fear of rats was the first ex-
perimental induction of a classically conditioned phobia (see Chapter 2). However,
some recent research has questioned the importance of classical conditioning in the
development of specific phobia. In studies of people with a phobia of water, heights,
or spiders, researchers usually have not found evidence that classical conditioning
played the role that had been predicted (Menzies & Clarke, 1993a, 1993b, 1995a,
1995b; Poulton et al., 1999). Further evidence for a limited role of classical condi-
tioning comes from everyday observations: Many people experience the pairing of
conditioned and unconditioned stimuli but do not become phobic.
Regardless of the extent of the role of classical conditioning, operant condition-
ing clearly plays a key role in maintaining a specific phobia: By avoiding the feared
stimulus, a person can decrease the fear and anxiety that he or she would experience
in the presence of it, which reinforces the avoidance.
Social Factors: Modeling and Culture
Sometimes, simply seeing other people being afraid of a particular stimulus is enough
to make the observer become afraid of that stimulus (Mineka et al., 1984). For
example, if as a young child, you saw your older cousin become agitated and anxious
when a dog approached, you might well learn to do the same. Similarly, repeated
warnings about the dangers of a stimulus can increase the risk of developing a specific
phobia of that stimulus (Antony & Barlow, 2002).
Modeling is not the only way that culture can exert an effect on the content of
specific phobia. Consider the fact that people in India are twice as likely as people in
England to have a phobia of animals, darkness, or bad weather but are only half as
likely to have social anxiety disorder or agoraphobia (Chambers et al., 1986). One
explanation for this finding is that people in India are apt to spend more time at
home than their English counterparts, so they have less opportunity to encounter
feared social situations. Similarly, dangerous and predatory animals are more likely to
roam free in India than in England.
People with specific phobia may have
perceptional distortions that heighten their
fears. For instance, someone with a fear of
flying may misperceive the normal downward
tilt of a plane during landing as a greater tilt
than it is and think the plane is about to crash.
©
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Anxiety Disorders 185
Feedback Loops in Understanding Specific Phobia
A person may be neurologically vulnerable to developing a specific phobia in part
because of his or her genes, which may make his or her amygdala “prepared” to
react too strongly to certain stimuli. Through observing others’ fear of a specific
stimulus (social factor), the person can become afraid and develop faulty cogni-
tions, which can lead to distorted thinking and the conditioning of false alarms
to the feared stimulus (psychological factors). And, once the person begins to
avoid the stimulus, the avoidance behavior is negatively reinforced. This behavior
in turn affects not only the person’s beliefs but also his or her social interactions
(social factors).
Treating Specific Phobia
Treatment for specif ic phobia generally targets one type of factor, although the
beneficial changes affect all the factors.
Targeting Neurological Factors: Medication
Medication, such as a benzodiazepine, may be prescribed for a specific phobia (alone
or in combination with CBT), but this is generally not recommended. Medication
is usually unnecessary because CBT treatment—even a single session—is highly
effective in treating a specific phobia (Ellison & McCarter, 2002).
Targeting Psychological Factors
If you had to choose an anxiety disorder to have, specific phobia probably should be
your choice. This is the anxiety disorder most treatable by CBT, with up to 90% last-
ing improvement rates even after only one session (Gitin et al., 1996; Öst, Salkovskis,
& Hellström, 1991).
Behavioral Method: Exposure
The behavioral method of graded exposure has proven effective in treating specific
phobia ( Vansteenwegen et al., 2007), and is considered a first-line treatment.
With this method, the patient and therapist progress through an individual-
ized hierarchy of anxiety-producing stimuli or events as fast as the patient can
tolerate; this process is like that used in exposure treatment for social anxiet y
discussed earlier in the chapter, but in this case substituting the specific feared
stimulus for the feared social situation or interaction. Moreover, recent research
on treating phobias with exposure suggests that virtual reality exposure works as
well as in vivo exposure, at least for certain phobias (Pull, 2005), such as of flying
and heights (Coelho et al., 2009; Emmelkamp et al., 2001, 2002), and this tech-
nique is part of many treatment programs for fear of flying.
Cognitive Methods
Cognitive methods for treating a specific phobia are similar to those used to treat
other anxiety disorders, such as panic disorder, agoraphobia, and social anxiety
disorder. The therapist and patient identify illogical thoughts pertaining to the
feared stimulus, and the therapist helps highlight discrepant information and chal-
lenges the patient to see the irrationality of his or her thoughts and expectations.
Table 6.13 provides an example of thoughts that someone with claustrophobia—a
fear of enclosed spaces—might have.
In addition, group CBT may be appropriate for some kinds of phobias, such
as fear of flying or of spiders (Rothbaum et al., 2006; Van Gerwen et al., 2006).
However, unlike group CBT for social anxiety disorder, group treatment for specific
phobia does not directly target social factors; rather, group CBT is a cost- effective
way to teach patients behavioral and cognitive methods to overcome their fears.
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186 C H A P T E R 6
Targeting Social Factors: A Limited Role for Observational
Learning
Observational learning may play a role in the development of a specific phobia, but to
many researchers’ surprise, seeing others model how to interact normally with the feared
stimulus generally is not an effective treatment for specific phobia. Perhaps observational
learning is not effective because patients’ cognitive distortions are powerful enough to
negate any positive effects modeling might provide. For instance, someone with a spider
phobia who observes someone else handling a spider might think, “Well, that person
isn’t harmed by the spider, but there’s no guarantee that I’ll be so lucky!”
Feedback Loops in Treating Specific Phobia
When treatment is effective in creating lasting change in one type of factor, it causes
changes in the other factors. Consider dental phobia and its treatment. Over 16% of
people between the ages of 18 and 26 have significant dental anxiety, according to one
survey (Locker et al., 2001). One study examined the effect of a single session of CBT
on dental phobia (Thom et al., 2000). The treatment group was given stress manage-
ment training and imaginal exposure to dental surgery 1 week prior to the surgery;
these patients were asked to review the stress management techniques and visualize
dental surgery daily during the intervening week. Another group of people with den-
tal phobia was only given a benzodiazepine 30 minutes before surgery. A third group
was given nothing; this was the control group. Both types of treatment led to less
anxiety during the dental surgery than was reported by the control group. However,
those in the CBT group continued to maintain and show further improvement at a
2-month follow-up: 70% of them went on to have subsequent dental work, whereas
only 20% of those in the benzodiazepine group and 10% of the control group did so.
The neuropsychosocial approach leads us to consider how the factors and their
feedback loops interact to treat such a specific phobia: The medication, although tem-
porarily decreasing anxiety (neurological factor), did not lead to sustained change
either in brain functioning or in thoughts about dental procedures. The CBT, in con-
trast, targeted psychological factors and also led to changes in a neurological factor—
brain functioning associated with decreased anxiety and arousal related to dental
surgery. In turn, these changes led to social changes—additional dental work. And
the added dental visits presumably led to better health, which in turn affected the
participants’ view of themselves and their interactions with others. Indeed, if the visits
had cosmetic effects (such as a nicer smile), their social benefits would be even more
evident. Such feedback loops underlie the treatment of all types of specific phobia.
O N L I N E
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TABLE 6.13 • Fearful Thoughts Related to Claustrophobia
• Many closed-in places, e.g., elevators, small rooms, do not have enough air.
• I will faint.
• If I go into a closed-in space, e.g., elevator or cave, I will not be able to get out.
• I will not be able to cope if I get stuck in a closed-in place.
• If I get too nervous, I may hurt myself.
• I will embarrass myself.
• I will lose control.
• I cannot think straight in enclosed places.
• I will go crazy.
• I will die.
Source: Antony, Craske, & Barlow, 1995, p. 105. For more information see the Permissions section.
Anxiety Disorders 187
Thinking Like A Clinician
Iqbal is horribly afraid of tarantulas, refusing to enter insect houses at zoos. Do you need
any more information before determining whether Iqbal has a specific phobia of tarantulas?
If so, what would you need to know? If not, do you think he has a specific phobia? Explain.
How might Iqbal have developed his fear of tarantulas? What factors are likely to have been
involved in its emergence and maintenance? Suppose Iqbal decides that he wants to “get
rid of” his fear of tarantulas. What treatments are likely to be effective, and what are the
advantages and disadvantages of each?
Separation Anxiety Disorder
Separation anxiety disorder is characterized by excessive anxiety about separa-
tion from home or from someone to whom the person is strongly attached. This
disorder occurs most commonly in children but can also affect adults. In what fol-
lows, we examine separation anxiety disorder in detail and then turn to its causes and
treatment.
What Is Separation Anxiety Disorder?
During different phases of development, an infant or a toddler will normally become
distressed on separating (or even thinking about separating) from a parent. (In this
section the word parent refers to the person from whom the child fears separation; that
person may be the mother, father, some other family member, caretaker, or another
person involved in the child’s life.) An adult may become distressed about leaving his
or her partner the morning after a big fight, or if the partner is sick. To qualify for a
diagnosis of separation anxiety disorder, the anxiety, distress, or impaired function-
ing must be excessive and typically is exhibited over a period of at least 6 months for
adults (see Table 6.14).
Separation anxiety disorder
A disorder that typically arises in childhood
and is characterized by excessive anxiety
about separation from home or from someone
to whom the person is strongly attached.
TABLE 6.14 • DSM-5 Diagnostic Criteria for Separation Anxiety Disorder
A. Developmentally inappropriate and excessive fear or anxiety concerning separation from those to whom the individual is attached, as evidenced
by at least three of the following:
1. Recurrent excessive distress when anticipating or experiencing separation from home or from major attachment figures.
2. Persistent and excessive worry about losing major attachment figures or about possible harm to them, such as illness, injury, disasters, or
death.
3. Persistent and excessive worry about experiencing an untoward event (e.g., getting lost, being kidnapped, having an accident, becoming ill)
that causes separation from a major attachment figure.
4. Persistent reluctance or refusal to go out, away from home, to school, to work, or elsewhere because of fear of separation.
5. Persistent and excessive fear of or reluctance about being alone or without major attachment figures at home or in other settings.
6. Persistent reluctance or refusal to sleep away from home or to go to sleep without being near a major attachment figure.
7. Repeated nightmares involving the theme of separation.
8. Repeated complaints of physical symptoms (e.g., headaches, stomachaches, nausea, vomiting) when separation from major attachment figures
occurs or is anticipated.
B. The fear, anxiety, or avoidance is persistent, lasting at least 4 weeks in children and adolescents and typically 6 months or more in adults.
C. The disturbance causes clinically significant distress or impairment in social, academic, occupational, or other important areas of functioning.
D. The disturbance is not better explained by another mental disorder, such as refusing to leave home because of excessive resistance to change
in autism spectrum disorder; delusions or hallucinations concerning separation in psychotic disorders; refusal to go outside without a trusted
companion in agoraphobia; worries about ill health or other harm befalling significant others in generalized anxiety disorder; or concerns about
having an illness in illness anxiety disorder.
Reprinted with permission from the Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition, (Copyright ©2013). American Psychiatric Association. All Rights Reserved.
188 C H A P T E R 6
Separation anxiety is more than a child’s
getting upset about temporarily saying goodbye
to a parent. Children with separation anxiety
disorder may become so homesick when away
from home that activities—such as a sleepover at
a friend’s or a stay at overnight camp—are inter-
rupted in order to return home. Or these chil-
dren may want to know the parent’s whereabouts
at all times, using a cell phone to make frequent
contact dur ing any physical separation. And
when away from the parent, they may also have
physical symptoms of anxiety: dizziness, stom-
achaches, nausea and vomiting, and feeling faint
(American Psychiatric Association, 2013).
Some children with separation anxiety dis-
order fear that they will get permanently “lost”
from their parents, and their dreams have similar
themes. And like people with agoraphobia, they
may be unable to leave the house alone (at an age
when it would be appropriate to do so) or even
to be in their room alone. Such children often
try to stay within a few feet of the parent, mov-
ing from room to room as the parent moves from
room to room. At bedtime, they may be unable
to fall asleep unless someone else is in the room with them, and during the night,
they may crawl into bed with parents or a sibling. If parents lock their bedroom door
at night, the child may sleep on the floor right outside the door. If children with this
disorder are separated from their parent, they may have persistent fantasies about
reuniting. Also, like people with generalized anxiety disorder, they may have recur-
rent fears about harm befalling their parent or themselves, as JC did, in Case 6.6.
Table 6.15 lists additional facts about separation anxiety disorder.
CASE 6.6 • FROM TH E OUTSIDE: Separation Anxiety Disorder
JC is a 9-year-old boy who lives with his mother and attends the third grade, where he is an
A student. During the last 2 weeks, he has refused to go to school and has missed 6 school
days. He is awake almost all night worrying about going to school. As the start of the school
day approaches, he cries and screams that he cannot go, chews holes in his shirt, pulls his
hair, digs at his face, punches the wall, throws himself on the floor, and experiences head-
aches, stomachaches, and vomiting. If he attends school, he is less anxious until bedtime. As
his separation anxiety has increased, he has become gloomy, has stopped reading for fun,
and frequently worries about his mother’s tachycardia [rapid heart rate].
JC was seen once by a psychiatrist at age 3 years for problems with separation anxiety.
He did well in preschool and kindergarten. He was seen at a community mental health
center during the first grade for school refusal, but did well again during the second grade.
In addition to having recurrent symptoms of separation anxiety disorder, he is phobic of
dogs, avoids speaking and writing in public, and has symptoms of generalized anxiety
disorder and obsessive-compulsive disorder. His mother has a history of panic disorder.
(Hanna, Fischer, & Fluent, 2006, pp. 56–57)
Adults who have this disorder may worry about the loss of a loved one through
an accident or illness or may not be able to fall sleep away from home unless the
loved one is with them. The diagnosis of separation anxiety disorder is only made
when another disorder, such as agoraphobia or generalized anxiety disorder, does not
better account for the symptoms.
This little girl might just be looking for
something in the laundry basket, but a child
with separation anxiety may want to know
where his or her parent is at all times—even
following the parent from room to room.
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Anxiety Disorders 189
C U R R E N T C O N T R O V E R S Y
Separation Anxiety Disorder: Anxiety
Disorder or Developmental Difference?
DSM-5 has chapters of disorders that are loosely organized
based on when the disorders tend to emerge over the lifespan.
Separation anxiet y disorder, an extreme case of fear and
worry related to current or potential separation from oth-
ers, can occur across the lifespan but tends to emerge f irst
in childhood. However, it is grouped with anxiety disorders,
not with neurodevelopmental disorders (see Chapter 14).
Is separation anxiety disorder in the most appropriate place in
the DSM-5?
On the one hand, grouping the disorder with anxi-
ety disorders makes sense because it shares symptoms with
other anxiety disorders, including the pattern of fear out of
proportion to danger, worry about possible future events, and
physical symptoms triggered by anxiety. Treatment for this
disorder is similar to treatment for other anxiety disorders.
Separation anxiet y does not share the t ypes of symptoms
related to executive and intellectual functioning that are found
in neurodevelopmental disorders.
On the other hand, separation anxiety disorder, like the
neurodevelopmental disorders, typically starts in early child-
hood and can occur throughout the lifespan. Separation
anxiety itself is a normal developmental process; what makes
this a disorder is the range and severity of symptoms and the
appearance of symptoms at a later age than would be expected.
This could be seen as a divergence from the normal path of
development.
C RITI C AL TH I N KI N G When a disorder “f its” in more than
one category of disorders, as does separation anxiety disor-
der, would it be better if such disorders were cross-listed in
the relevant categories)? What would be the advantages and
disadvantages to doing this?
( James Foley, College of Wooster)
TABLE 6.15 • Separation Anxiety Disorder Facts at a Glance
Prevalence
• About 4% of adults had separation anxiety disorder in childhood (Shear et al., 2006).
• Separation anxiety disorder is the most prevalent anxiety disorder among children, particularly
those younger than 12 years old.
Onset
• The disorder can begin as early as the preschool years.
• Separation anxiety disorder may emerge after some type of stressful event, such as a move, the
death of a pet, or the illness of a relative.
Comorbidity
• Children with separation anxiety disorder are more likely to experience other anxiety disorders—
especially generalized anxiety disorder—than are children in the general population (Brückl et al.,
2006; Verduin & Kendall, 2003).
Course
• Symptoms often wax and wane.
• As the child gets older, symptoms tend to lessen; at some point before adulthood, most people no
longer meet the criteria for the disorder (Foley, Pickles et al., 2004; Shear et al., 2006).
Gender Differences
• In the general population, more females than males have this disorder; however, comparable num-
bers of males and females with this disorder are treated as outpatients.
Cultural Differences
• Different ethnic groups and cultures have different norms about what constitutes appropriate
responses to separation in children, which can affect parents’ inclination to perceive a separation
problem and create different thresholds for diagnosis across cultures.
Source: Unless otherwise noted, the source for information is American Psychiatric Association, 2013.
190 C H A P T E R 6
Understanding and Treating Separation Anxiety
Disorder
Separation anxiety disorder is more common among first-degree relatives (parents
and siblings) than in the general population, and the disorder is considered to
be moderately heritable (Roberson-Nay et al., 2012). However, the heritability
probably reflects a heritability of anxiety in general: Separation anxiety is more
common among children whose mothers have panic disorder than among chil-
dren whose mothers don’t have that disorder, as was true of JC in Case 6.6 (Cronk
et al., 2004).
But other factors create feedback loops: Overprotective family members may
reinforce behaviors associated with anxiet y about separation and may punish
behaviors associated with actual separation. If so, then children in such families
who have temperaments that are high in harm avoidance and reward dependence
(see Chapter 2) may be especially vulnerable because they will be relatively re-
sponsive to reward and punishment. Moreover, separation anxiet y disorder is
more common in children whose fathers are absent (Cronk et al., 2004), per-
haps because that absence leads the child to have a heightened fear of losing the
remaining parent.
As with other anxiety disorders, treatment of separation anxiety disorder may
involve CBT (with exposure and cognitive restructuring; Schneider et al., 2011).
Family therapy is included in treatment; the therapist identifies any family patterns
that maintain the disorder and helps parents change their interaction patterns to
encourage and reinforce their child to engage in appropriate separation behaviors
(Siqueland et al., 2005).
Thinking Like A Clinician
Nia is 12 years old and going through puberty. Lately she’s been coming home right after
school and staying home during the weekend, no longer hanging out with her friends. In fact,
Nia is unhappy when her mother (her parents are divorced) leaves her alone to go shopping or
to go out in the evening; sometimes she tearfully begs her mother not to leave but won’t—or
can’t—explain why she feels so upset. Based on what you have learned, how do you think
Nia—and her mother—should proceed? Should they wait and hope the symptoms pass or
try to find out more? Explain your answer in detail.
Follow-up on Earl Campbell
The most appropriate diagnoses for Campbell appears to be both panic disorder
and agoraphobia. Despite using medication, Campbell continues to have some
panic symptoms, but he makes good use of cognitive and behavioral methods and
of social support. He acknowledged his continuing efforts: “Even though crowds
and noise bother me, I’ll push myself to tolerate them for as long as I can. I know
I must keep trying to get past the fear. It takes far more discipline for me to get
through an average day with panic than it took for me to perform as a top run-
ning back in the NFL. The challenges of panic are greater” (Campbell & Ruane,
1999, p. 199).
Anxiety Disorders 191
Common Features of Anxiety
Disorders
• The key symptoms of anxiety disorders
are fear, extreme anxiety, intense arousal,
and attempts to avoid stimuli that lead to
fear and anxiety.
• The f ight-or-f light response (also called
the stress response) arises when people per-
ceive a threat; when the arousal feels out
of control—either because the person has
an overactive stress response or because he
or she misinterprets the arousal—the per-
son may experience panic. In response to
the panic, some people develop a phobia of
stimuli related to their panic and anxiety
symptoms.
• A n x iet y d i sorder s f requent ly co – oc-
cur with other psychological disorders,
such as depression or substance-use dis-
orders. Menta l hea lth cl in icians must
determine whether the anxiety symptoms
are the primary cause of the problem or
are the by-product of another t ype of
disorder.
• The high comorbidity of depression and
anxiety disorders suggests that the two
d isorders share some of the same fea-
tures, specifically high levels of negative
emotions and distress—which can lead
to concentration and sleep problems and
irritability.
Generalized Anxiety Disorder
• Generalized anxiety disorder is marked
by persistent and excessive worry about a
number of events or activities that are not
solely the focus of another disorder. Most
people with GA D also have comorbid
depression.
• Neurological factors associated with GAD
include:
° decreased arousal because the parasym-
pathetic ner vous system is extremely
responsive (this is unlike most other
anxiety disorders).
° abnor ma l activit y of serotonin, do-
pamine, and other neurotransmitters,
which in turn inf luences motivation,
response to reward, and attention.
° a genet ic pred isposit ion to become
a n x i o u s a n d /o r d e p r e s s e d . T h i s
predisposition, however, is not specific
to GAD.
• Psychological factors that contribute to
GAD include being hypervigilant for pos-
sible threats, a sense that the worr ying
is out of control, and the rein forcing
experience that worrying prevents panic.
• Social factors that contr ibute to GA D
include stressful life events, which can
trigger the disorder.
• Treatments for GAD include:
° medication (which targets neurological
factors), such as buspirone or an SNRI
or SSRI when depression is present as a
comorbid disorder.
° C BT (wh ich t a rg et s ps ycholog ic a l
factors), which may include breathing
retraining, muscle relaxation training,
worry exposure, cognitive restructur-
ing, self-monitoring, problem solving,
psychoeducation, and/or meditation.
Panic Disorder and Agoraphobia
• The hallmark of panic disorder is recur-
rent panic attacks—periods of fear and
discomfort along with physical arousal
symptoms or cognitive symptoms. Panic
attacks may be cued by particular stimuli
(usually internal sensations), or they may
arise without any clear cue. Panic disorder
also involves fear of further attacks and, in
some cases, restricted behavior in an effort
to prevent further attacks.
• People in dif ferent cultures may have
similar—but not identical—constellations
of panic symptoms, such as ataque de nervios
and wind-and-blood pressure.
• About half of people with panic disorder
also develop agoraphobia—avoiding situ-
ations that might trigger a panic attack
or from which escape would be difficult,
such as crowded locations or tunnels.
• Neurological factors that contribute to
panic disorder and agoraphobia include:
° A heightened sensitivity to breathing
changes, which in turn leads to hyper-
ventilation, panic, and a sense of need-
ing to escape.
° Too much norepinephrine (produced
by an over-reactive locus coeruleus),
wh ich i ncrea se s hea r t a nd re spi r a-
t ion r ates a nd ot her a spect s of t he
fight-or-flight response.
° A genetic pred isposition to an x iet y
d isorder s, wh ich m a kes some peo –
ple vulnerable to panic disorder and
agoraphobia.
• Psychological factors that contribute to
panic disorder and agoraphobia include:
° Conditioning of the initial bodily sen-
sations of panic (interoceptive cues) or
of external cues related to panic attacks,
which leads them to become learned
alarms and elicit panic symptoms. Some
people then develop a fear of fear and
avoid panic-related cues.
° Heightened anxiety sensitivity and mis-
interpretation of bodily symptoms of
arousal as symptoms of a more serious
problem, such as a heart attack, which
can, in tur n, lead to hyper vig ilance
for—and fear of—fur ther sensations
and cause increased arousal, creating a
vicious cycle.
• Social factors related to panic disorder and
agoraphobia include:
° g r e a t e r – t h a n – a v e r a g e n u m b e r o f
social stressors during childhood and
adolescence.
° cultural factors, which can inf luence
whether people develop panic disorder.
° the presence of a safe person, which
can decrease catastrophic thinking and
panic.
• The treatment that targets neurological
factors is medication, specif ically ben-
zodiazepines for shor t-ter m relief and
antidepressants for long-term use.
• CBT is the first-line treatment for panic
disorder and targets psychological fac-
tors. Behavioral methods focus on the
bodily signals of arousal, panic, and ago-
raphobic avoidance. Cognitive methods
(psychoeducation and cognitive restruc-
t u r i n g ) foc u s on t he m i s appr a i s a l of
bodily sensations and on mistaken infer-
ences about them.
• Treat ment s t h at t a rget soc ia l f actor s
include group therapy focused on panic
disorder, and couples or family therapy,
particularly when a family member is a
safe person.
Social Anxiety Disorder (Social Phobia)
• Social anxiety disorder is an intense fear
of or anxiety about being in any of three
t ypes of social situations: social inter-
actions (such as a conversation); being
observed (such as when eating or using
public restrooms); and performing (such
as g iving a speech). W hen such social
situations cannot be avoided, they trigger
panic or anxiety.
• The anxiety about performing poorly and
being evaluated by others can, in turn,
impair a person’s performance, creating
a vicious cycle. The symptoms of social
anxiet y disorder may lead people with
this disorder to be less successful than they
could other wise be because they avoid
job-related social interactions that are
required for advancement.
SUMMING UP
192 C H A P T E R 6
• Neurological factors that give rise to social
an x iet y d isorder include an amygda la
that is more easily activated in response
to social stimuli, too little dopamine and
serotonin, and a genetic predisposition
toward a shy temperament ( behavioral
inhibition).
• Psychological factors that give rise to so-
cial anxiet y disorder include cognitive
distor tions and hyper vig ilance for so-
cia l threats—par ticu larly about being
negatively eva luated. Classica l cond i-
tioning of a fear response in social situ-
ations may contribute to social anxiety
disorder; avoiding feared social situations
is then negatively reinforced (operant
conditioning).
• Social factors that give rise to social anxi-
ety disorder include parents’ encouraging
a child to avoid anxiety-inducing social
interactions. Moreover, people in differ-
ent cultures may express their social fears
somewhat differently (e.g., taijin kyofusho).
The rate of social anxiety disorder appears
to be increasing in more recent bir th
cohorts.
• Medication is the treatment that targets
neurological factors, specif ically beta-
blockers for periodic performance anxiety
and SSRIs or SNRIs for more general-
ized social anxiety disorder. CBT is the
treatment that targets psychological fac-
tors, specifically exposure and cognitive
restructuring. Group CBT and exposure
to feared social stimuli are the treatments
that target social factors.
Specific Phobia
• Specific phobia involves (a) marked anxi-
ety or fear related to a specif ic stimulus
that (b) is disproportional to the actual
danger posed, and (c) leads to attempts to
avoid that feared stimulus. DSM-5 speci-
fies five types of specific phobia: animal,
natural environment, blood-injection-
injury, situational, and other.
• Pe ople a r e biolog ic a l l y pr e pa r e d t o
develop specific phobia to certain stimuli
as well as to resist developing phobias to
certain other stimuli.
• Neurological factors, such as an overly
reactive amygdala, appear to contribute
to specif ic phobia. GA BA is one neu-
rotransmitter that is involved in specific
phobia. Research also suggests that some
genes are associated with specif ic pho-
bia general ly, whereas other genes are
associated with particular types of spe-
cific phobia.
• Psychological factors that give rise to spe-
cific phobia may include classical condi-
tioning (but rarely), operant conditioning
(negative reinforcement of avoiding the
feared stimu lus), and cog n itive biases
related to the stimulus (such as overes-
timating the probability that a negative
event will occur following contact with
the feared stimulus).
• Observational learning—a social factor—
can influence what particular stimulus a
person comes to fear.
• Treatment for specif ic phobia can in-
clude medication (targeting neurological
factors), specif ically a benzodiazepine.
However, medication is usually not nec-
essar y because CBT—the treatment of
choice for specific phobia—is extremely
effective (targeting psychological factors).
CBT—particularly when exposure is part
of the treatment—can be effective after
just one session.
Separation Anxiety Disorder
• Separation anxiety disorder is character-
ized by excessive anxiety about separation
from home or from someone to whom the
person is strongly attached.
• Separation anxiety disorder is most com-
mon in children but also can occur in
adults.
• Separation anxiety disorder is moderately
her itable; over protective family mem-
bers may inadvertently reinforce behav-
iors associated with separation anxiet y
and pun ish behav ior s associated w ith
appropriate separation.
• Separation an x iet y d isorder is treated
with methods used to treat other anxiety
disorders: CBT that includes exposure
and cognitive restructuring, along with
family therapy.
Anxiety (p. 156)
Anxiety disorder (p. 156)
Fight-or-flight response (p. 157)
Panic (p. 157)
Phobia (p. 157)
Generalized anxiety disorder (GAD) (p. 158)
Hypervigilance (p. 160)
Biofeedback (p. 162)
Habituation (p. 162)
Exposure (p. 162)
In vivo exposure (p. 163)
Psychoeducation (p. 163)
Panic attack (p. 165)
Panic disorder (p. 166)
Agoraphobia (p. 167)
Concordance rate (p. 169)
Interoceptive exposure (p. 173)
Social anxiety disorder (p. 176)
Specific phobia (p. 182)
Separation anxiety disorder (p. 188)
More Study Aids
For additional study aids related to this chapter, including
quizzes to make sure you’ve retained everything you’ve
learned and a Student Video Activity exploring how a
10-year-old boy struggles to overcome his phobia of dogs, go
to: www.worthpublishers.com/launchpad/rkabpsych2e.
Photodisc
More Study Aids
For additional study aids related to this chapter, including
quizzes to make sure you’ve retained everything you’ve
learned and a Student Video Activity exploring how a
10-year-old boy struggles to overcome his phobia of dogs, go
to: www.worthpublishers.com/launchpad/rkabpsych2e.
Photodisc
Key Terms
Anxiety Disorders 193
195
CHAPTER 7
Obsessive-Compulsive-
Related and Trauma-
Related Disorders
oward Hughes is famous for many things: He was an industrialist,
creating Hughes Aircraft Company and designing the planes his
company built; he was an aviator who broke flying records; he
was the owner of hotels and casinos; he was a reclusive billionaire who
directed an Academy Award–winning film. During his lifetime, people
around the world recognized his name and his accomplishments.
Hughes grew up in Texas, an only child in a wealthy family.
As a child and teenager, Hughes was shy and had only one friend;
he was “supersensitive”—he didn’t seem to take teasing in stride as
other children did—and he preferred to be alone or spend time with
his mother. When he was almost 17, his mother, a homemaker, died
unexpectedly of complications from a minor surgical procedure. Two
years later, his father died unexpectedly of a heart attack. Hughes was
independent and rich at the age of 19. Within the next 6 years, he’d
have triumphs and disasters: He’d win an Academy Award and survive
a horrific airplane crash that crushed his cheekbone. Four years later,
he would found Hughes Aircraft Company, and 3 years after that,
he’d set a world record for flight. As Hughes became more successful,
he also became reclusive, seeing fewer and fewer people. But it wasn’t
simply that he became a hermit. He went through periods of time
when he would do nothing but watch films, 24 hours a day, naked,
moving only from bed to chair and back, with occasional forays to
the bathroom. And Hughes was deathly afraid of being exposed to
germs—and so he developed elaborate precautions to avoid contact
with them (Barlett & Steele, 1979).
Obsessive-Compulsive Disorder and
Related Disorders
What Is Obsessive-Compulsive Disorder?
What Is Body Dysmorphic Disorder?
Understanding Obsessive-Compulsive Disorder
Treating Obsessive-Compulsive Disorder
Trauma-Related Disorders
What Are the Trauma-Related Disorders?
Understanding Trauma-Related Disorders: PTSD
Treating Posttraumatic Stress Disorder
Follow-up on Howard Hughes
Clearly, HugHes’s beHavior wasn’t normal. Hughes suffered
from symptoms of psychological disorders—to the point where he wasn’t
able to function adequately in any sphere of life. But what was the matter
with him? The symptoms from which Hughes suffered involve anxiety
(in fact, he appears to have suffered from social anxiety disorder). In
this chapter, we explore two categories of disorder that involve anxiety:
obsessive-compulsive-related disorders and trauma-related disorders.
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Howard Hughes in his youth was vibrant and
industrious; however, mental illness took a toll
on him as he aged. In the later years of his life,
he became a recluse. Few people saw him, and
there are almost no known photographs of
him from that period.
© breba/Bilderlounge/age fotostock. Photo for illustrative purposes only; any individual depicted is a model.
Obsessive-Compulsive Disorder
and Related Disorders
After his parents’ deaths, Hughes’s health concerns increased, and his profound fear
of germs—and the rituals and behaviors that he used to limit what he believed were
possible routes of contamination—came to restrict his life severely. But the protective
rituals and behaviors extended beyond himself (and beyond rational thinking); he
made his aides and associates undertake similar extreme precautions even though that
did not, in fact, decrease his risk:
He v iewed a nyone who ca me nea r a s a potent ia l ger m ca r r ier. Those whose
movements he could control—his aides, dr ivers, and message clerks—were re-
quired to wash their hands and slip on thin white cotton gloves . . . before handing
him documents or other objects. Aides who bought newspapers or magazines were
instr ucted to buy three copies—Hughes took the one in the m idd le. To escape
dust, he ordered unused windows and doors of houses and cars sealed with masking
tape.
(Barlett & Steele, 1979, p. 175)
And it wasn’t only exposure to germs that Hughes tried to control. Throughout
his life, he’d been overly preoccupied with details; at one time or another, he
concerned himself with ever y aspect of his companies—even demanding that
employees conduct a detailed study of the vending machines at the Hughes Aircraft
Company. Hughes’s preoccupations and ritualistic behaviors were symptoms of
obsessive-compulsive disorder.
What Is Obsessive-Compulsive Disorder?
Howard Hughes had obsessions and compulsions. Obsessions are in-
trusive and unwanted thoughts, urges, or images that persist or recur
and usually cause distress or anxiety; people try to ignore, suppress, or
neutralize these thoughts, urges, or images (American Psychiatric As-
sociation, 2013). For instance, Hughes had obsessions about germs; his
preoccupations about them were intrusive and persistent. Worries about
actual problems (such as, “How can I pay my bills this month?” or, “I
don’t think I can finish this project by the deadline”) are not considered
obsessions.
Whereas obsessions involve thoughts, urges, and images, compul-
sions involve behaviors. A compulsion is an excessive repetitive behav-
ior (such as avoiding stepping on sidewalk cracks) or mental act (such as
silently counting to 10) that a person feels driven to carry out; a compulsion usually
must be performed according to rigid “rules” or corresponds thematically to an ob-
session and serves to “ neutralize” the obsession and decrease anxiety or distress. For
instance, Howard Hughes was obsessed by the possibility that he might be exposed
to germs and was compelled to behave in ways that he believed would protect him
from such germs.
The key element of obsessive-compulsive disorder (OCD) is characterized
by having one or more obsessions or compulsions (See Table 7.1; American Psy-
chiatric Association, 2013). The obsession can cause great distress and anxiety, de-
spite a person’s attempts to ignore or drive out the intrusive thoughts. Most people
with OCD recognize that the beliefs that underlie their obsessions and compul-
sions are not valid in all situations. In a minority of cases, though, people may be-
lieve that their OCD-related beliefs are rational, and in DSM-5 such people might
be considered to have reduced insight into their condition (American Psychiatric
Association, 2013).
Obsessions
Intrusive and unwanted thoughts, urges, or
images that persist or recur and usually cause
distress or anxiety.
Compulsions
Repetitive behaviors or mental acts that a
person feels driven to carry out and that usually
must be performed according to rigid “rules” or
correspond thematically to an obsession.
Obsessive-compulsive disorder (OCD)
A disorder characterized by one or more
obsessions or compulsions.
People with OCD can spend hours dealing
with their compulsions, such as repeatedly
checking whether they turned off the stove in
response to doubts about whether they did it
properly the last time.
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196 C H A P T E R 7
Table 7.2 identifies common types of
obsessions and compulsions. Obsessions
(listed on the left side of Table 7.2) include
preoccupations with contamination, order, fear
of losing control, and doubts about whether the
patient performed an action. As noted earlier,
compulsive behaviors are usually related to
an obsession or anxiety associated with a
particular situation or stimulus (also listed
in Table 7.2) and include washing, ordering,
counting, and checking (Mataix-Cols et al.,
2005). Performing the behavior prevents
or relieves the anxiety, but only tempo-
rarily. However, compulsions that relieve
anxiety can take signif icant amounts of
time to complete—sometimes more than
an hour—and often create distress or im-
pa ir f unct ion ing. Hughes clearly had
compulsive symptoms of the contamina-
tion-washing type and had ordering types
of obsessions and compulsions.
Li ke t he ot her a n x iet y d i sorder s
we’ve discussed, OCD often involves an
unrealistic or disproportionate fear—in
this case, of adverse consequences if the
compulsive behavior is not completed. For
instance, people with an obsession about
contamination, like Hughes, fear that if all
germs aren’t washed off, they will die of
some disease. Additional facts about OCD
are provided in Table 7.3, and Case 7.1 de-
scribes one woman’s experience with OCD.
CASE 7.1 • FROM TH E INSIDE: Obsessive-Compulsive Disorder
For someone with OCD, just getting up in the morning and getting dressed can be fraught
with trials and tribulations:
Should I get up? It’s 6:15. No, I better wait till 6:16, it’s an even number. OK, 6:16, now I
better get up, before it turns to 6:17, then I’d have to wait till 6:22.
OK, I’ll get up, OK, I’m up, WAIT! I better do that again. One foot back in bed, one foot
on the floor, now the other foot in bed and the opposite on the floor. OK. Let’s take a
shower, WAIT! That shoe on the floor is pointing in the wrong direction, better fix it. Oops,
there’s a piece of lint there, I better not set the shoe on top of it. . . . OH, JUST TOUCH THE
SHOE TWICE AND GET OUTTA HERE!
All right, I got to the bedroom door without touching anything else, but I better step
through and out again, just to be sure nothing bad will happen. THERE, THAT WAS EASY!
Now to the bathroom. I better turn that light on, NO, off, NO, on, NO, off, NO, on, KNOCK
IT OFF! All right, I’m done using the toilet, better flush it. OK, now spin around, wait for
the toilet to finish a flush, now touch the handle, now touch the seat, remember you
have to look at every screw on the toilet seat before you turn around again. OK, now turn
around and touch the seat again, look at all the screws again. OK, now close the cover.
OK, let’s get some underwear. I want to wear the green ones because they fit the
best, but they’re lying on top of the T-shirt my grandmother gave me, and her husband
(my grandfather) died last year, so I better wash those again before I wear them. If I wear
them, something bad might happen.
(Steketee & White, 1990, pp. 4–5)
TABLE 7.1 • DSM-5 Diagnostic Criteria for Obsessive-Compulsive Disorder
A. Presence of obsessions, compulsions, or both:
Obsessions are defined by (1) and (2):
1. Recurrent and persistent thoughts, urges, or images that are experienced, at some time
during the disturbance, as intrusive and unwanted, and that in most individuals cause
marked anxiety or distress.
2. The individual attempts to ignore or suppress such thoughts, urges, or images, or to
neutralize them with some other thought or action (i.e., by performing a compulsion).
Compulsions are defined by (1) and (2):
1. Repetitive behaviors (e.g., hand washing, ordering, checking) or mental acts (e.g., praying,
counting, repeating words silently) that the individual feels driven to perform in response
to an obsession or according to rules that must be applied rigidly.
2. The behaviors or mental acts are aimed at preventing or reducing anxiety or distress, or
preventing some dreaded event or situation; however, these behaviors or mental acts are
not connected in a realistic way with what they are designed to neutralize or prevent, or
are clearly excessive.
Note: Young children may not be able to articulate the aims of these behaviors or mental acts.
B. The obsessions or compulsions are time-consuming (e.g., take more than 1 hour per day) or
cause clinically significant distress or impairment in social, occupational, or other important
areas of functioning.
C. The obsessive-compulsive symptoms are not attributable to the physiological effects of a
substance (e.g., a drug of abuse, a medication) or another medical condition.
D. The disturbance is not better explained by the symptoms of another mental disorder (e.g.,
excessive worries, as in generalized anxiety disorder; preoccupation with appearance,
as in body dysmorphic disorder; difficulty discarding or parting with possessions, as in
hoarding disorder; hair pulling, as in trichotillomania [hair-pulling disorder]; skin picking,
as in excoriation [skin-picking] disorder; sterotypies, as in stereotypic movement disorder;
ritualized eating behavior, as in eating disorders; preoccupation with substances or gambling,
as in substance-related and addictive disorders; preoccupation with having an illness, as in
illness anxiety disorder; sexual urges or fantasies, as in paraphillic disorders; impulses, as in
disruptive, impulse-control, and conduct disorders; guilty ruminations, as in major depressive
disorder; thought insertion or delusional preoccupations, as in schizophrenia spectrum and
other psychotic disorders; or repetitive patterns of behavior, as in autism spectrum disorder).
Reprinted with permission from the Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition, (Copyright ©2013).
American Psychiatric Association. All Rights Reserved.
Obsessive-Compulsive-Related and Trauma-Related Disorders 197
TABLE 7.3 • Obsessive-Compulsive Disorder Facts at a Glance
Prevalence
• Approximately 2–3% of Americans will develop OCD at some point in their lives (Burke &
Regier, 1994), with generally similar prevalence rates worldwide (Horwath & Weissman, 2000).
Comorbidity
• Over 90% of those with OCD have another disorder, with the most frequent categories of
comorbid disorders being mood disorders (63%) and anxiety disorders (76%).
Onset
• Among males with OCD, symptoms typically begin to emerge between the ages of 6 and 15.
• Among females, symptoms typically emerge between the ages of 20 and 29.
Course
• Symptoms typically build gradually until they reach a level that meets the diagnostic crite-
ria. Over the course of a lifetime, symptoms wax and wane, becoming particularly evident in
response to stress but typically are chronic.
Gender Differences
• Men and women have an equal risk of developing OCD.
Cultural Differences
• Although the prevalence rates of OCD and the types of symptoms are about the same
across cultures, the particular content of symptoms may reflect cultural or religious prohibi-
tions (Matsunaga et al., 2007; Millet et al., 2000).
Source: Unless otherwise noted, information in the table is from American Psychiatric Association, 2000, 2013.
OCD clearly involves fears and anxieties; it also often involves compulsive
behaviors over which patients feel they have no control. A number of other disorders,
such as hair-pulling disorder (also referred to as trichotillomania), skin-picking disorder
(also referred to as excoriation disorder), hoarding disorder, and body dysmorphic disorder
TABLE 7.2 • Common Types of Obsessions and Compulsions
Type of obsession
Examples of obsessions: People with OCD
may be preoccupied with anxiety-inducing
thoughts about . . . Type of compulsion
Examples of compulsions: In order to decrease
anxiety associated with an obsession, people may
repeatedly be driven to . . .
Contamination
germs, dirt
Washing
wash themselves or objects in order to minimize any
imagined contamination
Order
objects being disorganized, or a consuming
desire to have objects or situations conform
to a particular order or alignment
Ordering
order objects, such as canned goods in the cupboard,
so that everything in the environment is “just so”
(and often making family members and friends
maintain this order)
Losing control
the possibility of behaving impulsively or
aggressively, such as yelling during a funeral
Counting
count in response to an unwanted thought, which
leads to a sense that the unwanted thought is
neutralized (for instance, after each thought of blurting
out an obscenity, methodically counting to 50)
Doubt
whether an action, such as turning off the
stove, was performed Checking
check that they did, in fact, perform a behavior about
which they had doubts (such as repeatedly checking
that the stove is turned off)
198 C H A P T E R 7
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Two disorders that are part of the OCD
spectrum are hair-pulling disorder (left photo)
and hoarding (right photo). People with hair-
pulling disorder may feel so persistently
compelled to pull their hair that they develop
noticeable bald patches. Similarly, people
who hoard feel unable to throw away objects
even when the clutter is potentially life-
threatening. Some people who compulsively
hoard have died in fires in their homes
because the hoarded objects took up so much
space that it was difficult to leave once a fire
started, or firefighters had to spend too much
time trying to get into the house (Kaplan,
2007a). The woman in this photo found a cat
amongst the clutter.
Which of these people is more likely to have body dysmorphic disorder? Answer:
Statistically, neither. Body dysmorphic disorder affects both genders equally often,
but men and women tend to differ with regard to the specific body parts they view
as defective.
GETTING THE PICTURE
©
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Hoarding disorder
An obsessive-compulsive-related disorder
characterized by persistent difficulty throwing
away or otherwise parting with possessions—
to the point that the possessions impair
daily life, regardless of the value of those
possessions.
Body dysmorphic disorder
A disorder characterized by excessive
preoccupation with a perceived defect or
defects in appearance and repetitive behaviors
to hide the perceived defect.
share some of these features and are considered
to be related to obsessive-compulsive disorder:
• Hair-pulling disorder is characterized by the per-
sistent compulsion to pull one’s hair, leading to
hair loss and distress or impaired functioning.
• Skin-picking disorder is characterized by com-
pulsive skin picking to the point that lesions
emerge on the skin.
• Hoarding disorder is characterized by persistent
difficulty throwing away or otherwise parting
with possessions—to the point that the posses-
sions impair daily life, regardless of the value of
those possessions.
• Body dysmorphic disorder, discussed in detail
below, is characterized by preoccupations with
a perceived defect in appearance and repetitive behaviors to hide the perceived defect.
What these four disorders have in common with OCD is either or both of the
following: preoccupations that arise from beliefs that are out of proportion to actual
danger and/or compulsive behaviors that reduce tension or anxiety.
What Is Body Dysmorphic Disorder?
It’s a common experience to believe that a pimple on your forehead appears like a red
beacon for others to see; many people will try to cover up or hide a pimple. It’s also
common for people with a receding hairline to change their hairstyle to make the hair
loss less noticeable. What isn’t common—and, in fact, signals a psychological disorder—
is when a slight imperfection in appearance, even an imagined defect, causes significant
distress (Lambrou et al., 2011) or takes up so much time and energy that daily func-
tioning is impaired. These are the signs of body dysmorphic disorder. The specific
DSM-5 diagnostic criteria for this disorder (Table 7.4) indicate why body dysmorphic
disorder is considered to fall on the spectrum of OCD-related disorders: It involves
Obsessive-Compulsive-Related and Trauma-Related Disorders 199
preoccupations (some might say obsessions) about a perceived defect and, at some point,
repetitive mental acts or behaviors (that might be compulsive) related to these preoc-
cupations. The person might repeatedly compare his or her appearance to other people’s
(mental act) or repeatedly groom himself or herself or seek reassurance from others
about appearance (behavior). As with OCD, the behaviors can consume hours.
Common preoccupations for people with body dysmorphic disorder are thinning
or excessive hair, acne, wrinkles, scars, complexion (too pale, too dark, too red, and so
on), facial asymmetry, or the shape or size of some part of the face or body. Some peo-
ple are preoccupied with the belief that they aren’t muscular enough or that their body
build is too slight. The “defect” (or “defects”) may change over the course of the illness
(K. A. Phillips, 2001). People with body dysmorphic disorder may think that others are
staring at them or talking about a “defect.” Up to half of those with body dysmorphic
disorder are delusional—that is, they believe their perception of a “defect” is accurate
and not exaggerated (Phillips et al., 1994). Although Howard Hughes had beliefs about
his body (related to germs), they do not appear to have been beliefs about bodily defects.
People with body dysmorphic disorder may compulsively exercise, diet, shop for
beauty aids, pick at their skin, try to hide perceived defects, or spend hours looking
in the mirror (like Ms. A., described in Case 7.2, who believed that she had multiple
defects). A person with body dysmorphic disorder may seek reassurance (“How do
I look?”), but any positive effects of reassurance are transient; a half-hour later, the
person with body dysmorphic disorder may ask the same question—even of the same
person! These behaviors, which are intended to decrease anxiety about appearance,
actually end up increasing anxiety.
CASE 7.2 • FROM TH E OUTSIDE: Body Dysmorphic Disorder
Ms. A was an attractive 27-year-old single white female who presented with a chief com-
plaint of “I look deformed.” She had been convinced since she was a child that she was
ugly, and her mother reported that she had “constantly been in the mirror” since she was a
toddler. Ms. A was obsessed with many aspects of her appearance, including her “crooked”
ears, “ugly” eyes, “broken out” skin, “huge” nose, and “bushy” facial hair. She estimated
that she thought about her appearance for 16 hours a day and checked mirrors for 5 hours
a day. She compulsively compared herself with other people, repeatedly sought reassur-
ance about her appearance . . ., applied and reapplied makeup for hours a day, excessively
washed her face, covered her face with her hand, and tweezed and cut her facial hair. As
a result of her appearance concerns, she had dropped out of high school. . . . She avoided
friends and most social interactions. Ms. A felt chronically suicidal and had attempted sui-
cide twice because, as she stated, “I’m too ugly to go on living.”
(K. A. Phillips, 2001, pp. 75–76)
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Deceased pop star Michael Jackson’s face changed repeatedly over time, particularly his nose, chin, and cheeks, although he said that he only had
surgery on his nose to help his singing. Might Michael Jackson have suffered from body dysmorphic disorder?
TABLE 7.4 • DSM-5 Diagnostic Criteria
for Body Dysmorphic Disorder
A. Preoccupation with one or more
perceived defects or flaws in physical
appearance that are not observable or
appear slight to others.
B. At some point during the course
of the disorder, the individual has
performed repetitive behaviors (e.g.,
mirror checking, excessive grooming,
skin picking, reassurance seeking) or
mental acts (e.g., comparing his or
her appearance with that of others) in
response to the appearance concerns.
C. The preoccupation causes clinically
significant distress or impairment in
social, occupational, or other important
areas of functioning.
D. The appearance preoccupation is not
better explained by concerns with body
fat or weight in an individual whose
symptoms meet diagnostic criteria for
an eating disorder.
Reprinted with permission from the Diagnostic and
Statistical Manual of Mental Disorders, Fifth Edition,
(Copyright ©2013). American Psychiatric Association. All
Rights Reserved.
200 C H A P T E R 7
People who have body dysmorphic disorder may feel so self-conscious about a
perceived defect that they avoid social situations (American Psychiatric Association,
2013), which results in their having few (or no) friends and no romantic partner.
Some try to eliminate a “defect” through medical or surgical treatment such as plas-
tic surgery, dental work, or dermatological treatment. But surgery often does not
help; in fact, the symptoms of the disorder can actually be worse after surgery (Veale
et al., 2003). In extreme cases, when some people with body dysmorphic disorder
can’t find a doctor to perform the treatment they think they need, they may try to do
it themselves (so-called DIY, or do-it-yourself, surgery). Table 7.5 presents additional
facts about body dysmorphic disorder.
TABLE 7.5 • Body Dysmorphic Disorder Facts at a Glance
Prevalence
• Approximately 2.4% of the general population of the United States has body dysmorphic
disorder at any given time.
• Among people having plastic surgery or dermatological treatment, prevalence rates range
from 7% to 8% (American Psychiatric Association, 2013).
Comorbidity
• Up to 60% of people with body dysmorphic disorder are also depressed; body dysmorphic
disorder usually emerges first (Otto et al., 2001; K. A. Phillips, 2001).
• Thirty-eight percent of people with body dysmorphic disorder may also have social phobia
(Coles et al., 2006).
• Up to 30% of people with body dysmorphic disorder also have OCD (K. A. Phillips, 2001).
• In one survey, almost half of those with body dysmorphic disorder had (at the time or
previously) a substance-use disorder (Grant et al., 2005).
• Almost one third of those with body dysmorphic disorder will also develop an eating
disorder (Ruffolo et al., 2006).
Onset
• Body dysmorphic disorder usually begins in childhood or adolescence (Bjornsson et al.,
in press; Phillips, Menard, et al., 2005).
Course
• Body dysmorphic disorder is generally chronic if left untreated.
• Over 25% of adults with body dysmorphic disorder have been housebound for at least
1 week; 8% are unable to work and receive disability payments (Albertini & Phillips, 1999;
Phillips et al., 1994).
• Two surveys found that approximately 30% of people with body dysmorphic disorder had
attempted suicide (Phillips et al., 1994; Phillips, Coles, et al., 2005).
Gender Differences
• Body dysmorphic disorder affects both genders with approximately equal frequency, but
men and women tend to differ with regard to the specific body parts they view as defective
(Phillips, Menard, & Fay, 2006): Women are preoccupied with body weight, hips, breasts, and
legs and are more likely to pick their skin compulsively. In contrast, men are preoccupied
with body build, genitals, height, excessive body hair, and thinning scalp hair.
Cultural Differences
• Generally, symptoms of body dysmorphic disorder are similar across cultures, although
certain body attributes may be more likely to be the focus of concern, depending on what
physical attributes are valued in a given culture (Pope et al., 1997; Pope, Gruber, et al., 2000).
Obsessive-Compulsive-Related and Trauma-Related Disorders 201
Patients with body dysmorphic disorder exhibit a variety of cognitive biases.
Such patients tend to focus their attention on isolated body parts and are hyper-
vigilant for any possible bodily imperfections (Grocholewski et al., 2012). They also
engage in catastrophic thinking, believing that bodily imperfections will lead to dire
consequences; for example, the person might believe that having a pimple will lead
others to think he or she is deformed (Buhlmann et al., 2008; Lambrou et al., 2012).
In addition, people with body dysmorphic disorder often engage in behaviors that
temporarily reduce their anxiety. For example, they might try to avoid mirrors (and
possibly people) or develop new ways to hide a “defect”—with painstakingly applied
makeup or contrived use of clothing or hats (K. A. Phillips, 2001). If you think that
some of the descriptions of the symptoms of body dysmorphic disorder resemble those
of anxiety-related disorders, not just OCD, you’re right. Like phobia disorders (agora-
phobia, social anxiety disorder, and specific phobias), body dysmorphic disorder can
lead the person to avoid anxiety-causing stimuli. Like social anxiety disorder, it involves
an excessive fear of being evaluated negatively. And like OCD, it involves persistent
preoccupations and compulsive behaviors. Because body dysmorphic disorder is related
to OCD, in order to understand the former, we look to research on the latter.
Understanding Obsessive-Compulsive Disorder
Howard Hughes had neurological and psychological vulnerabilities for OCD that
may have been exacerbated by psychological and social factors. However, with OCD,
social factors have less influence than do neurological and psychological factors.
Neurological Factors
Researchers have made much progress in understanding the neurological underpin-
nings of OCD.
Brain Systems and Neural Communication
In general, when the frontal lobes trigger an action, there is feedback from the basal gan-
glia, in part via the thalamus (a brain structure involved in attention). Sometimes this
feedback sets up a loop of repetitive activity, as shown in Figure 7.1 (Breiter et al., 1996;
FI G U RE 7.1 • The Neural
Loop That May
Underlie Obsessive
Thoughts The basal
ganglia, the thalamus, and
the frontal lobes are part of
a neural loop of repeating
brain activity associated
with OCD.
Frontal lobe
Basal ganglia
Thalamus
Frontal lobe
Basal ganglia
Thalamus
202 C H A P T E R 7
Rapoport, 1991; Rauch et al., 1994, 2001). Many researchers now believe that
this neural loop plays a key role in obsessive thoughts, which intrude and cannot
be stopped easily. Performing a compulsion might temporarily stop the obses-
sive thoughts by reducing the repetitive neural activity (Insel, 1992; Jenike, 1984;
Modell et al., 1989). (But soon after the compulsive behavior stops, the obsessions
typically resume.)
Much research has focused on whether OCD arises from abnormalities in the
basal ganglia and frontal lobes in particular (Pigott et al., 1996; Saxena & Rauch,
2000). In fact, neuroimaging studies have revealed that both a part of the frontal
cortex and the basal ganglia function abnormally in OCD patients (Baxter, 1992;
Berthier et al., 2001; Saxena et al., 1998). This abnormal functioning could well
prevent the frontal lobe from cutting off the loop of repetitive neural activity, as it
appears to do in people who do not have this disorder.
OCD appears to arise in large part because brain circuits don’t operate normally,
but why don’t they do so? One reason may be that people with OCD have too
little of the neurotransmitter serotonin, which allows unusual brain activity to occur
(Mundo, Richter, et al., 2000). And, in fact, medications that increase the effects
of serotonin (such as Prozac), often by preventing reuptake of this neurotransmitter
at the synapse (see Chapter 5), can help to treat OCD symptoms (Micallef & Blin,
2001; Thomsen, et al., 2001).
Genetics
Twin studies have shown that if one monozygotic (identical) twin has OCD, the
other is ver y likely (65%) to have it. As expected if this high rate reflects com-
mon genes, the rate is lower (only 15%) for dizygotic twins (Pauls et al., 1991).
Moreover, as you would expect from the results of the twin studies, OCD is more
common among relatives of OCD patients (10 % of whom also have OCD) than
among relatives of control participants (of whom only 2% also have OCD) (Pauls
et al., 1995).
However, although such studies have documented a genetic contribution to
OCD, the link is neither simple nor straightforward: Members of the family of a
person with OCD are more likely than other people to have an anxiety disorder, not
OCD specifically (Black et al., 1992; Smoller et al., 2000).
W hen m a ny people f i r st lea r n about OCD, they recog n i ze tendencies
they’ve noticed in themselves. If you’ve had this reaction while reading this sec-
tion, you shouldn’t worr y: OCD may ref lect extreme functioning of brain sys-
tems that function the same way in each of us to produce milder forms of such
thinking.
Psychological Factors
Psychological factors that help to explain OCD focus primarily on the way
that operant conditioning affects compulsions and on the process by which
normal obsessional thoughts become pathological.
Behavioral Explanations: Operant Conditioning and
Compulsions
Compulsive behavior can provide short-term relief from anxiety that is
produced by an obsession. Operant conditioning occurs when the behavior
is negatively reinforced: Because the behavior (temporarily) relieves the
anxiety, the behavior is more likely to recur when the thoughts arise again.
All of Howard Hughes’s various eccentric behaviors—his washing, his
precautions against germs, his hoarding of newspapers and magazines—
temporarily relieved his anxiety.
Former soccer star David Beckham suffers from
OCD. His symptoms focus on ordering: “I have to
have everything in a straight line or everything
has to be in pairs. . . . I’ll go into a hotel room.
Before I can relax I have to move all the leaflets
and all the books and put them in a drawer.
Everything has to be perfect.” (Dolan, 2006).
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Obsessive-Compulsive-Related and Trauma-Related Disorders 203
Cognitive Explanations: Obsessional Thinking
If you’ve ever had a crush on someone or been in love, you may have spent a lot of time
thinking about the person—it may have even felt like an obsession. Such obsessions
are surprisingly frequent (Weissman et al., 1994), but they don’t usually develop into
a disorder. One theory about how a normal obsession becomes part of OCD is that
the person decides that his or her thoughts refer to something unacceptable, such as
killing someone or, as was the case with Howard Hughes, catching someone else’s
illness (Salkovskis, 1985). These obsessive thoughts, which the person believes imply
some kind of danger, lead to very uncomfortable feelings. Mental or behavioral ritu-
als arise in order to reduce these feelings.
Consistent with this view, researchers have found that some mental processes
function differently in people with OCD than in people without the disorder. In
particular, such patients are more likely to pay attention to and remember threat-
relevant stimuli, and they have impaired processing of complex visual stimuli (as,
for example, is necessary to decide whether an object has been touched by a dirty
or clean tissue among people with contamination fears; Muller & Roberts, 2005;
Radomsky et al., 2001). Such processing may make threatening stimuli easier to re-
member and harder to ignore, which keeps them in the patients’ awareness longer
than normal (Muller & Roberts, 2005) and makes the irrational fears seem more
plausible (Giele et al., 2011).
Social Factors
Two types of social factors can contribute to OCD: stress and culture.
Stress
The onset of OCD often follows a stressor, and the severity of the symptoms is often
proportional to the severity of the stressor (Turner & Beidel, 1988). However, such
findings are not always easy to interpret. For example, one study found that people
with more severe OCD tend to have more kinds of family stress and are more likely
to be rejected by their families (Calvocoressi et al., 1995). Note, however, that the
direction of causation is not clear: Although stress in the family may cause the greater
severity of symptoms, it is also possible that the more severe symptoms led the fami-
lies to reject the patients.
Stress greatly affected the course of Hughes’s symptoms. For much of his 20s,
30s, and early 40s, he was able to function relatively well, given the freedom his
wealth and position provided. However, during one particularly stressful period in
his late 30s, “Hughes began repeating himself at work and in casual conversations.
In a series of memoranda on the importance of letter writing, he dictated, over and
over again, ‘a good letter should be immediately understandable . . . a good letter
should be immediately understandable . . . a good letter should be immediately
understandable . . .” (Barlett & Steele, 1979, p. 132).
By the time Hughes was in his 50s, the stressors increased, and his functioning
diminished. There were periods when he was so preoccupied with his germ phobia
that he couldn’t pay attention to anything else.
Culture
Different countries have about the same prevalence rates of OCD, although culture
and religion can help determine the particular content of some obsessions or
compulsions (Weissman et al., 1994). For instance, religious obsessions and pray-
ing compulsions are more common among Turkish men than French men (Millet
et al., 2000) and more common among Brazilians than Americans or Europeans
(Fontenelle et al., 2004). And a devoutly religious patient’s symptoms can relate to
the specific tenets and practices of his or her religion (Shooka et al., 1998): Some-
one who is Catholic may have obsessional worries about having impure thoughts or
204 C H A P T E R 7
feel a compulsion to go to confession multiple times each day. In contrast, devout
Jews or Muslims may have symptoms that focus on extreme adherence to religious
dietary laws.
Feedback Loops in Understanding Obsessive-Compulsive
Disorder
One neurological factor that contributes to OCD appears to be a tendency toward
increased activity in the neural loop that connects the frontal lobes and the basal
ganglia (neurological factor). A person with such a neurological vulnerability might
learn early in life to regard certain thoughts as dangerous because they can lead to
obsessions. When these thoughts appear later in life at a time of stress, someone
who is vulnerable may become distressed and anxious about the thoughts and try to
suppress them. But a conscious attempt to suppress unwanted thoughts often has the
opposite effect: The unwanted thoughts become more likely to persist (Salkovkis &
Campbell, 1994; Wegner et al., 1987). Thus, the intrusive thoughts cause additional
distress, and so the person tries harder to suppress them, creating a vicious cycle
( psychological factor).
The content of a person’s unwanted thoughts determines the extent to which
those thoughts are unacceptable. When a person wants to suppress the unwanted
thoughts, he or she develops rituals and avoidance behaviors to increase a sense of
control and decrease anxiety; these behaviors temporarily reduce anxiety and are
thus reinforced. But the thoughts cannot be fully controlled and become obsessive;
the obsessions and compulsions impair functioning and can affect relationships. The
person with OCD may expect family members and friends to conform to compul-
sive guidelines; these people and others can become frustrated and dismayed at the
patient’s rituals and obsessions—which in turn can produce more stress for the patient
(social factors).
Treating Obsessive-Compulsive Disorder
The primar y targets of treatment for OCD are usually either neurological or
psychological factors.
Targeting Neurological Factors: Medication
An SSRI is usually the type of medication used first to treat OCD: paroxetine (Paxil),
sertraline (Zoloft), f luoxetine (Prozac), f luvoxamine (Luvox), or citalopram (Celexa)
(Soomro et al., 2008). OCD can also be treated effectively with the TCA clomip-
ramine (Anafranil), although a higher dose is required than that prescribed for depres-
sion or other anxiety disorders (Rosenbaum, Arana et al., 2005). People who develop
OCD in childhood are less likely to respond well to clomipramine or to other anti-
depressants (Rosario-Campos et al., 2001).
Hughes’s use of codeine and Valium did not appear to diminish his obsessions
and compulsions significantly; in fact, such medications are not routinely prescribed
for OCD. In any case, medication alone is not as effective as medication combined
with behavioral treatment, such as exposure with response prevention (discussed in
the following section). As with other anxiety disorders, when the medication is dis-
continued, OCD symptoms usually return (Foa et al., 2005).
Targeting Psychological Factors
Treatment that targets psychological factors focuses on decreasing the compulsive
behaviors and obsessional thoughts. Both behavioral and cognitive methods are
effective (Cottraux et al., 2001; Prazeres et al., 2013), and treatment may combine
both types of methods (Franklin et al., 2002).
O N L I N E
SP
N
Obsessive-Compulsive-Related and Trauma-Related Disorders 205
Behavioral Methods: Exposure With Response Prevention
Patients with OCD often undertake exposure with response prevention. For the
exposure part, the patient is exposed to the feared stimulus (such as touching dirt) or
the obsessive thought (such as the idea that the stove was left on) and, for the response
prevention part, the patient is prevented from engaging in the usual compulsion or
ritual. For instance, if someone were afraid of touching dirt, she would touch dirt
but would not then wash her hands for a while. Through exposure with response
prevention, patients learn that nothing bad happens if they don’t perform
their compulsive behavior; the fear and arousal subside without resorting
to the compulsion, and they experience mastery. They survive the anxi-
ety and in doing so exert control over the compulsion. When patients
successfully respond differently to a feared stimulus, this mastery over
the compulsion gives them hope and motivates them to continue to per-
form the new behaviors. Exposure with response prevention is also a
technique used to treat body dysmorphic disorder.
Cognitive Methods: Cognitive Restructuring
The goal of cognitive methods is to reduce the irrationality and fre-
quency of the patient’s intrusive thoughts and obsessions (Clark, 2005).
Cognitive restructuring focuses on assessing the accuracy of these
thoughts, making predictions based on them (“If I don’t go back to
check the locks, I will be robbed”), and testing whether these predic-
tions come to pass.
Although CBT for OCD hadn’t been sufficiently developed during Hughes’s life-
time, consider how it might have been used: There were periods when Hughes daily
and “painstakingly used Kleenex to wipe ‘dust and germs’ from his chair, ottoman,
side table, and telephone [for hours].” (Barlett & Steele, 1979, p. 233). During the
same period of time, he didn’t have his sheets changed for months at a time; to make
the sheets last longer, he laid paper towels over them and slept on those. Moreover,
he bathed only a few times a year. Clearly, such behavior was at odds with rational
attempts to protect against germs. CBT would have, in part, focused on his over-
estimation of the probability of contracting an illness and the irrationality of his
precautions.
Targeting Social Factors: Family Therapy
Although psychological and neurological factors are the primary targets of treat-
ment for OCD, in some cases, social factors may also be addressed—for example,
through family therapy or consultation with family members. This aspect of treat-
ment educates family members about the patient’s treatment and its goals and helps
the family function in a more normal way. Family members and friends may have
spent years conforming their behavior to the patient’s illness (e.g., using clean tissues
when handing an object to the patient), and they may be afraid to change their own
behavior as the patient gets better, for fear of causing a relapse.
Feedback Loops in Treating Obsessive-Compulsive Disorder
As we’ve seen, medication can be effective in treating the symptoms of OCD (at
least as long as the patient continues to take it). Medication works by changing
neurochemistry, which in turn affects thoughts, feelings, and behaviors. We’ve also
seen that CBT is effective. How does CBT have its effects? Could it be that therapy
changes brain functioning in the same way that medication does? Researchers set out
to answer this question.
In one study, researchers used PET scans to assess brain functioning in two
groups of OCD patients. One group received behavior therapy, and the other group
SP
N
O N L I N E
Patients with OCD often undertake exposure
with response prevention. For instance, if
someone were afraid of touching dirt, he
would touch dirt but would not then wash
his hands for a while. By not being able to
respond to the dirt, the patient learns that
nothing bad happens if compulsive behaviors
aren’t performed.
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re
a
s
S
ch
le
g
e
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tt
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ag
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s
Exposure with response prevention
A behavioral technique in which a patient is
carefully prevented from engaging in his or
her usual maladaptive response after being
exposed to a stimulus that usually elicits the
response.
206 C H A P T E R 7
received the SSRI fluoxetine (Prozac) to reduce OCD symptoms. Both behavior
therapy and Prozac decreased activity in a part of the basal ganglia that is involved
in automatic behaviors. Prozac also affected activity in two parts of the brain in-
volved in attention: the thalamus and the anterior cingulate (Baxter et al., 1992).
Later research replicated the effects of behavior therapy on the brain (Schwartz et al.,
1996). Although the altered brain areas overlapped, CBT changed fewer brain ar-
eas than did medication—which may reflect the fact that medication may have side
effects, whereas CBT does not.
In short, behavior therapy or CBT changes the brain (neurological factor). As
the patient improves, personal relationships change (social factor): The time and
energy that once went into the compulsions can be diverted to other areas of life,
including relationships. Moreover, the patient experiences mastery over the symp-
toms and develops hope and a new view of himself or herself (psychological factors).
In turn, this makes the patient more willing to continue therapy, which further
changes the brain, and so on, in a happy cycle of mutual feedback loops among neu-
rological, psychological, and social factors.
Thinking Like A Clinician
You visit a new friend. When you use her bathroom, you notice that all her toiletries
seem ver y organized. Her kitchen is also neatly ordered. The next day, you notice that
her classwork is unusually well organized—arranged neatly in color-coded folders and
notebook s. You don’t think t wice about it until she drops her open backpack and all
her stuff falls out, spilling all over the floor. She starts to cr y. Based on what you have
learned, do you think she has OCD? Why or why not? What el se would you want to
know before reaching a conclusion? If she has OCD, is it because she has inherited the
disorder? Explain your answer. If she does have OCD, what sor ts of treatments should
she consider?
Trauma-Related Disorders
Within a 15-year span, Howard Hughes suffered more than his share of brushes with
death—of his own and other people’s. He ran over and killed a pedestrian. He was
the pilot in three plane accidents: In the first one, his cheekbone was crushed; in the
second, two of his copilots died; in the third, he sustained such extensive injuries to
his chest that his heart was pushed to the other side of his chest
cavity, and he wasn’t expected to live through the night. Hughes
did survive, but he clearly had endured a highly traumatic event.
Some people who experience a traumatic or ver y stressful
event go on to develop a disorder in the DSM-5 category trauma-
and stressor-related disorders. According to DSM-5 (American Psy-
chiatric Association, 2013), a trauma-related disorder is marked
by four general types of persistent symptoms after exposure to the
traumatic event:
• Intrusive re-experiencing of the traumatic event. Intrusion may involve
flashbacks that can include illusions, hallucinations, or a sense of
reliving the experience, as well as intrusive and distressing mem-
ories, dreams, or nightmares of the event.
• Avoidance. The person avoids anything related to the trauma.
• Negative thoughts and mood, and dissociation. Symptoms include
persistent negative thoughts about oneself or others (“no one can
be trusted”), persistent negative mood (fear, for instance, and
©
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is
Howard Hughes survived several plane
crashes, including the one shown above, and
he ran over and killed a pedestrian (Fowler,
1986); any of these events would have been
traumatic for most people. Some people
who experience a traumatic event develop a
trauma-related disorder: acute stress disorder
or posttraumatic stress disorder.
Obsessive-Compulsive-Related and Trauma-Related Disorders 207
difficulty experiencing positive emotions), and dissociation (a sense of feeling dis-
connected or detached from experiences).
• Increased arousal and reactivity. Arousal and reactivity symptoms include difficulty
sleeping, hypervigilance, irritable behavior, angry outbursts, and a tendency to be
easily startled (referred to as a heightened startle response).
What Are the Trauma-Related Disorders?
Among the trauma-related disorders in DSM-5 are:
• acute stress disorder, which is the diagnosis when some of the above symptoms emerge
immediately after a traumatic event and last between 3 days and 1 month;
• posttraumatic stress disorder (PTSD), which requires a certain number of symptoms
from each of the four groups mentioned above, and the symptoms last more than
1 month.
Most people would agree that Hughes experienced a traumatic event when his air-
plane crashed and he was severely injured. But what constitutes a traumatic event?
The answer, according to DSM-5, is an event that involves:
• directly experiencing actual or threatened serious injury, sexual violation, or death;
• witnessing (in person) actual or threatened serious injury, sexual violation, or
death;
• learning of a violent or accidental death or threatened death of a close family mem-
ber or friend; or
• experiencing extreme exposure to aversive details about the traumatic event (as
might occur for first responders).
Traumatic events are more severe than the normal stress-
ful events we all regularly encounter. Examples of traumatic
events range f rom large-sca le catastrophes w ith mu lt iple
victims (such as disasters and wars) to unintended acts or
situations involving fewer people (such as motor vehicle ac-
cidents and life-threatening illnesses) to events that involve
intentional and personal violence, such as rape and assault
( Briere, 2004). Traumatic events are relatively common: Up
to 30 % of people wil l exper ience some t ype of disaster in
their lifetime, 25% have experienced a serious car accident
(Briere & Elliott, 2000), and 20 % of women report having
been raped during their lifetimes (most frequently by some-
one they know; Black et al., 2011). Note that according to the
DSM-5 definition, emotional abuse is not a traumatic event
because it does not involve actual or threatened physical in-
jury or death.
Several factors can affect whether a trauma-related disorder will develop
following a traumatic event:
• The kind of trauma. Trauma involving violence—particularly intended personal
violence—is more likely to lead to a stress disorder than are natural disasters (Breslau
et al., 1998; Briere & Elliott, 2000; Copeland et al., 2007; Dikel et al., 2005).
• The severity of the traumatic event, its duration, and its proximity. Depending on
the specifics of the traumatic event, those physically closer to it—nearer to the
primar y area struck by a tornado, for example—are more likely to develop a
stress disorder ( Blanchard et al., 2004; Middleton et al., 2002), as are those
who have experienced multiple traumatic events (Copeland et al., 2007). For
During times of political unrest, violence, or
terrorism, rates of trauma-related disorders
are likely to increase.
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208 C H A P T E R 7
Posttraumatic stress disorder (PTSD)
A traumatic stress disorder that involves
persistent (a) intrusive re-experiencing of
the traumatic event, (b) avoidance of stimuli
related to the event, (c) negative changes in
thoughts and mood, and (d) hyperarousal and
reactivity that persist for at least a month.
instance, Vietnam veterans were more likely to develop PTSD if they had been
wounded or if they had spent more time in combat (Gallers et al., 1988; King
et al., 1999). The same is true of veterans who returned from Iraq and Afghani-
stan: Soldiers who were involved in combat were up to three times more likely
to develop PTSD than soldiers who were not exposed to combat (Levin, 2007;
Smith et al., 2008).
Being exposed to a traumatic event is one component of a trauma-related disor-
der. The second component is the person’s response to the traumatic event. Although
certain types of traumatic events are more likely than others to lead to such disorders,
people differ in how they perceive the same traumatic event and how they respond
to it. These differences will be based, in part, on previous experience with related
events, appraisal of the stressors, and coping style.
What Is Posttraumatic Stress Disorder?
Posttraumatic stress disorder (PTSD) is diagnosed when people who have
exper ienced a trauma persistently (a) have intrusive re-exper iences the trau-
matic event, (b) avoid stimuli related to the event, (c) have negative changes in
thoughts and mood associated with the traumatic event, and (d) have symptoms of
reactivity and hyperarousal; all of these symptoms must persist for at least a month
( American Psychiatric Association, 2013). These four types of symptoms form the
posttrauma criteria for PTSD, as shown in Table 7.6, but symptoms may not emerge
until months or years after the traumatic event. (Note that Table 7.6 applies to
adults and children over the age of 6; DSM-5 contains separate criteria for chil-
dren 6 and younger.)
Some people with PTSD may be diagnosed with a subt ype that includes
symptoms of dissociation : an a ltered sense of rea l it y of sur round ing s or one-
self (such as feeling in daze, a sense of the environment’s or one’s body being
d istor ted or “not quite r ight,” or a sense of time slow ing down) (A mer ican
Psych iat r ic A ssociat ion, 2013 ; Stei n et a l., 2013 ). Table 7.7 present s add i-
tional infor mation about PTSD. Case 7.3 descr ibes the exper iences of a man
with PTSD.
CASE 7.3 • FROM TH E OUTSIDE: Posttraumatic Stress Disorder
A. C. was a 42-year-old single man, a recent immigrant who, one year before his appear-
ance at the clinic, had walked into his place of work while an armed robbery was taking
place. Two men armed with guns hit him over the head, threatened to kill him, tied him
up and locked him in a closet with four other employees. He was released from the closet
4 hours later when another employee came in to work. The police were notified and A. C.
was taken to the hospital where his head wound was sutured and he was released. For two
weeks after the robbery A. C. continued to function as he had before the robbery with no
increase in anxiety.
One day while waiting to meet someone on the street he was struck by the thought
that he might meet his assailants again. He began to shiver, felt his heart race, felt dizzy,
started to sweat and felt that he might pass out. He was brought to an emergency room,
examined and released with a referral to victims’ services. His anxiety increased so much
that he was unable to return to work because it reminded him of the robbery. He started
to have sleep difficulties, waking in the middle of the night to check the front door lock at
home. He quit his job and dropped out of school due to his anxiety. He would have flash-
backs of the guns that were used in the robbery and started to avoid people on the street
who reminded him of the robbers. He began to feel guilty that he had entered the office
while the robbery was in progress feeling that he somehow should have known what was
occurring. His avoidance extended to the subway, exercising and socializing with friends.
(New York Psychiatric Institute, 2006)
Obsessive-Compulsive-Related and Trauma-Related Disorders 209
TABLE 7.6 • DSM-5 Diagnostic Criteria for Posttraumatic Stress Disorder
Note: The following criteria apply to adults, adolescents, and children older than 6 years.
A. Exposure to actual or threatened death, serious injury, or sexual violence in one (or more) of the following ways:
1. Directly experiencing the traumatic event(s).
2. Witnessing, in person, the event(s) as it occurred to others.
3. Learning that the traumatic event(s) occurred to a close family member or close friend. In cases of actual or threatened death of a family
member or friend, the event(s) must have been violent or accidental.
4. Experiencing repeated or extreme exposure to aversive details of the traumatic event(s) (e.g., first responders collecting human remains; police
officers repeatedly exposed to details of child abuse).
Note: Criterion A4 does not apply to exposure through electronic media, television, movies, or pictures, unless this exposure is work related.
B. Presence of one (or more) of the following intrusion symptoms associated with the traumatic event(s), beginning after the traumatic event(s)
occurred:
1. Recurrent, involuntary, and intrusive distressing memories of the traumatic event(s).
Note: In children older than 6 years, repetitive play may occur in which themes or aspects of the traumatic event(s) are expressed.
2. Recurrent distressing dreams in which the content and/or affect of the dream are related to the traumatic event(s).
Note: In children, there may be frightening dreams without recognizable content.
3. Dissociative reactions (e.g., flashbacks) in which the individual feels or acts as if the traumatic event(s) were recurring. (Such reactions may
occur on a continuum, with the most extreme expression being a complete loss of awareness of present surroundings.)
Note: In children, trauma-specific reenactment may occur in play.
4. Intense or prolonged psychological distress at exposure to internal or external cues that symbolize or resemble an aspect of the traumatic event(s).
5. Marked physiological reactions to internal or external cues that symbolize or resemble an aspect of the traumatic event(s).
C. Persistent avoidance of stimuli associated with the traumatic event(s), beginning after the traumatic event(s) occurred, as evidenced by one or
both of the following:
1. Avoidance of or efforts to avoid distressing memories, thoughts, or feelings about or closely associated with the traumatic event(s).
2. Avoidance of or efforts to avoid external reminders (people, places, conversations, activities, objects, situations) that arouse distressing
memories, thoughts, or feelings about or closely associated with the traumatic event(s).
D. Negative alterations in cognitions and mood associated with the traumatic event(s), beginning or worsening after the traumatic event(s)
occurred, as evidenced by two (or more) of the following:
1. Inability to remember an important aspect of the traumatic event(s) (typically due to dissociative amnesia and not to other factors such as
head injury, alcohol, or drugs).
2. Persistent and exaggerated negative beliefs or expectations about oneself, others, or the world (e.g., “I am bad,” “No one can be trusted,” “The
world is completely dangerous,” “My whole nervous system is permanently ruined”).
3. Persistent, distorted cognitions about the cause or consequences of the traumatic event(s) that lead the individual to blame himself/herself or
others.
4. Persistent negative emotional state (e.g., fear, horror, anger, guilt, or shame).
5. Markedly diminished interest or participation in significant activities.
6. Feelings of detachment or estrangement from others.
7. Persistent inability to experience positive emotions (e.g., inability to experience happiness, satisfaction, or loving feelings).
E. Marked alterations in arousal and reactivity associated with the traumatic event(s), beginning or worsening after the traumatic event(s) occurred,
as evidenced by two (or more) of the following:
1. Irritable behavior and angry outbursts (with little or no provocation) typically expressed as verbal or physical aggression toward people or objects.
2. Reckless or self-destructive behavior.
3. Hypervigilance.
4. Exaggerated startle response.
5. Problems with concentration.
6. Sleep disturbance (e.g., difficulty falling or staying asleep or restless sleep).
F. Duration of the disturbance (Criteria B, C, D, and E) is more than 1 month.
G. The disturbance causes clinically significant distress or impairment in social, occupational or other important areas of functioning.
H. The disturbance is not attributable to the physiological effects of a substance (e.g., medication, alcohol) or another medical condition.
Reprinted with permission from the Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition, (Copyright ©2013). American Psychiatric Association. All Rights Reserved.
210 C H A P T E R 7
TABLE 7.7 • PTSD Facts at a Glance
Prevalence
• Among adults in the United States, approximately 8% develop PTSD, although this
number varies in part on large scale events. For instance, among members of the
U.S. military returning from Iraq and Afghanistan, rates of PTSD ranged from 5–20%
(Packnett et al., 2012).
Comorbidity
• About 80% of those with PTSD also have another psychological disorder, most commonly a
mood disorder, substance use disorder, or an anxiety disorder.
Onset
• Symptoms usually begin within 3 months of the traumatic event, although some people may
go months or years before symptoms appear.
• However, people who develop PTSD usually show symptoms in the immediate aftermath of
the trauma, although not necessarily all the symptoms required for the diagnosis.
• Approximately 80% of people with acute stress disorder go on to develop PTSD (Harvey &
Bryant, 2002).
Course
• Duration of the symptoms varies. About half of those with PTSD recover within 3 months,
whereas others continue to have persistent symptoms for more than a year after the
traumatic event. Still others have symptoms that wax and wane.
Gender Differences
• Women who have been exposed to trauma develop PTSD more often than do men, although
males are more likely be victims of trauma (Tolin & Foa, 2006).
Cultural Differences
• Across cultures, people with PTSD may differ in the particular symptoms they express
(e.g., more intrusive symptoms versus more arousal symptoms), depending on the coping
styles that are encouraged in a given culture.
Source: Unless otherwise noted, information in the table is from American Psychiatric Association, 2013.
What Is Acute Stress Disorder?
If A. C.’s symptoms had lasted for less than 1 month or if he had sought help from a
mental health clinician within a month of the event, A. C. might have been diagnosed
with acute stress disorder. Acute stress disorder involves at least 9 of 14 symptoms
that fall into five clusters: intrusively re-experiencing the traumatic event, avoiding
stimuli related to the event, hyperarousal, negative mood, and dissociation.
As noted in Table 7.8, the symptoms occur within 1 month of the trauma
(as A. C.’s did), must last at least 3 days but no more than 1 month, and must cause
significant distress or impair functioning. Approximately 80% of those with acute
stress disorder have symptoms that persist for more than a month, at which point for
most people the diagnosis then changes to PTSD (Harvey & Bryant, 2002). Unlike
A. C., though, most people who experience trauma do not develop PTSD (National
Collaborating Centre for Mental Health, 2005; Shalev et al., 1998).
PTSD and acute stress disorder clearly involve intrusive re-experiencing, avoid-
ance, negative mood, and hyperarousal. But unlike the other disorders we’ve reviewed
in this chapter, PTSD and acute stress disorder arise from a clear and consistent cause:
a traumatic event. A number of other disorders—one of which we will discuss in the
next chapter—appear to share this feature.
Acute stress disorder
A traumatic stress disorder that involves
(a) intrusive re-experiencing of the traumatic
event, (b) avoidance of stimuli related to the
event, (c) negative changes in thought and
mood, (d) dissociation, and (e) hyperarousal
and reactivity, with these symptoms lasting
for less than a month.
Obsessive-Compulsive-Related and Trauma-Related Disorders 211
Could Howard Hughes’s problems have been related to an undiagnosed post-
traumatic stress disorder? We don’t know whether Hughes intrusively re- experienced
any of his traumatic events or whether he had negative thoughts ormoods related to
the traumas, but he did not appear to have obvious avoidance symptoms related to the
traumatic experiences: He continued flying after each of his plane accidents. He did
have symptoms of increased arousal, such as irritability, hypervigilance, difficulty
concentrating, and sleep problems, but these symptoms are better explained by his
OCD and drug use. There is no clear evidence that Hughes suffered from PTSD.
TABLE 7.8 • DSM-5 Diagnostic Criteria for Acute Stress Disorder
A. Exposure to actual or threatened death, serious injury, or sexual violation in one (or more) of the following ways:
1. Directly experiencing the traumatic event(s).
2. Witnessing, in person, the event(s) as it occurred to others.
3. Learning that the event(s) occurred to a close family member or close friend. Note: In cases of actual or threatened death of a family member
or friend, the event(s) must have been violent or accidental.
4. Experiencing repeated or extreme exposure to aversive details of the traumatic event(s) (e.g., first responders collecting human remains, police
officers repeatedly exposed to details of child abuse).
Note: This does not apply to exposure through electronic media, television, movies, or pictures, unless this exposure is work related.
B. Presence of nine (or more) of the following symptoms from any of the five categories of intrusion, negative mood, dissociation, avoidance, and
arousal, beginning or worsening after the traumatic event(s) occurred:
Intrusion Symptoms
1. Recurrent, involuntary, and intrusive distressing memories of the traumatic event(s). Note: In children, repetitive play may occur in which
themes or aspects of the traumatic event(s) are expressed.
2. Recurrent distressing dreams in which the content and/or affect of the dream are related to the event(s). Note: In children, there may be
frightening dreams without recognizable content.
3. Dissociative reactions (e.g., flashbacks) in which the individual feels or acts as if the traumatic event(s) were recurring. (Such reactions may
occur on a continuum, with the most extreme expression being a complete loss of awareness of present surroundings.) Note: In children,
trauma-specific reenactment may occur in play.
4. Intense or prolonged psychological distress or marked physiological reactions in response to internal or external cues that symbolize or
resemble an aspect of the traumatic event(s).
Negative Mood
5. Persistent inability to experience positive emotions (e.g., inability to experience happiness, satisfaction, or loving feelings).
Dissociative Symptoms
6. An altered sense of the reality of one’s surroundings or oneself (e.g., seeing oneself from another’s perspective, being in a daze, time slowing).
7. Inability to remember an important aspect of the traumatic event(s) (typically due to dissociative amnesia and not to other factors such as
head injury, alcohol, or drugs).
Avoidance Symptoms
8. Efforts to avoid distressing memories, thoughts, or feelings about or closely associated with the traumatic event(s).
9. Efforts to avoid external reminders (people, places, conversations, activities, objects, situations) that arouse distressing memories, thoughts, or
feelings about or closely associated with the traumatic event(s).
Arousal Symptoms
10. Sleep disturbance (e.g., difficulty falling or staying asleep, restless sleep).
11. Irritable behavior and angry outbursts (with little or no provocation), typically expressed as verbal or physical aggression toward people or objects.
12. Hypervigilance.
13. Problems with concentration.
14. Exaggerated startle response.
C. Duration of the disturbance (symptoms in Criterion B) is 3 days to 1 month after trauma exposure.
Note: Symptoms typically begin immediately after the trauma, but persistence for at least 3 days and up to a month is needed to meet disorder criteria.
D. The disturbance causes clinically significant distress or impairment in social, occupational or other important areas of functioning.
E. The disturbance is not attributable to the physiological effects of a substance (e.g., medication or alcohol) or another medical condition (e.g., mild
traumatic brain injury) and is not better explained by brief psychotic disorder.
Reprinted with permission from the Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition, (Copyright ©2013). American Psychiatric Association. All Rights Reserved.
212 C H A P T E R 7
Understanding Trauma-Related Disorders: PTSD
We focus here on PTSD because more than three-quarters of people with acute stress
disorder go on to develop PTSD (see Table 7.7), the symptoms of PTSD—almost
by definition—last longer than those of acute stress disorder, and most research on
trauma-related disorders focuses on PTSD.
Neurological Factors
The neurological factors that contribute to PTSD include overly strong sympathetic
nervous system reactions and abnormal hippocampi. In addition, the neurotransmit-
ters norepinephrine and serotonin have been implicated in the disorder, and there is
evidence that genes contribute to (but by no means determine) the likelihood that
experiencing trauma will result in PTSD.
Brain Systems
Research has often shown that people who suffer from PTSD have sympathetic
nervous systems that react unusually strongly to cues associated with their trau-
matic exper ience. The cues can cause sweating or a racing hear t (Or r et al.,
1993, 2002; Prins et al., 1995). Furthermore, the changes in heart rate are dis-
tinct from the changes found in control participants who have been asked to
pretend to have PTSD (Orr & Pitman, 1993); thus, PTSD patients react more
strong ly to the relevant cues than would be expected if they d id not have a
disorder.
In addition, the hippocampus apparently must work harder than normal in
PTSD patients when they try to remember information, as shown by the fact that
this brain structure is more strongly activated in these patients during memory tasks
than in control participants (Shin et al., 2004). This is important because this brain
structure plays a crucial role in storing information in memory (Squire & Kandel,
2000), and thus an impaired hippocampus should impair memory. And, in fact, as
expected, PTSD patients have trouble recalling autobiographical memories ( McNally
et al., 1995).
Note that correlation does not imply causation; perhaps the brain abnormality
predisposes people to PTSD, or perhaps PTSD leads to the brain abnormality
(McEwen, 2001; Pitman et al., 2001). A twin study provides an important hint about
what causes what: In this study, researchers compared the sizes of the hippocampi
in veterans who had served in combat and had PTSD with the sizes of hippocampi
in their identical twins who had not served in combat and did not have PTSD.
The results were clear: In both twins, the hippocampi were smaller than normal
(Gilbertson et al., 2002). This finding implies that the trauma did not cause the
hippocampi to become smaller, but rather the smaller size is a risk factor (or is cor-
related with some other factor that produces the risk) that makes a person vulnerable
to the disorder.
Neural Communication and Genetics
The neurotransmitter norepinephrine appears to be involved in PTSD. For example,
Southwick and colleagues (1993) gave volunteers with and without PTSD a drug
that allows norepinephrine levels to surge. When norepinephrine levels became
very high, 70 % of the PTSD patients had a panic attack, and 40 % of them had a
flashback to the traumatic event that precipitated their disorder; the volunteers who
did not have PTSD exhibited minimal effects. Moreover, this drug resulted in more
extreme biochemical and cardiovascular effects for the PTSD patients than for the
controls.
Various types of evidence indicate that serotonin also plays a role in PTSD.
For one, SSRIs can help treat the disorder, and they apparently do so in part
by allowing serotonin to moderate the effects of stress (Corchs et al., 2009). In
Obsessive-Compulsive-Related and Trauma-Related Disorders 213
addition, people who have certain alleles of genes that produce serotonin are sus-
ceptible to developing the disorder following trauma (Adamec et al., 2008; Grabe
et al., 2009).
However, research has shown that the effects of such genes may depend on a
combination of factors, such as stressful environmental events in combination with
low social support—and the same factors that affect whether people develop PTSD
also affect whether they develop major depressive disorder (Kilpatrick et al., 2007;
Sartor et al., 2012). Moreover, genes appear either to play a smaller role than the
environment in predicting PTSD (McLeod et al., 2001) or are relevant only in
the context of complex interactions between genes and environment (Broekman
et al., 2007).
Psychological Factors: History of Trauma, Comorbidity, and
Conditioning
Psychological factors that exist before a traumatic event occurs affect whether
a person w il l develop PTSD. Such factors include the beliefs the person has
about himself or herself and the world. Two specif ic beliefs that can make a
person vulnerable to developing PTSD are considering yourself unable to con-
trol stressors (Heinrichs et al., 2005; Joseph et al., 1995) and the conviction that
the world is a dangerous place (Keane, Zimer ing, & Caddel l, 1985; Kushner
et al., 1992).
People can be vulnerable to developing
PTSD for a variety of other reasons. For example:
• by coping with a traumatic event by disso-
ciating (disrupting the normal processes of
perception, awareness, and memory; Shalev
et al., 1996);
• by having severe mental disorders such as bi-
polar disorder (see Chapter 5) or schizophre-
nia (Chapter 12);
• by having some t ype of an x iet y disorder
(Copeland et al., 2007), perhaps because
most anxiety disorders involve hyperarousal
and hypervigilance—which may lead peo-
ple to respond to traumatic events in ways
that promote a stress disorder; and
• by having exper ienced a pr ior traumatic
event (for example, having been assaulted and
then, years later, living through a hurricane).
A fter the traumatic event, classical conditioning and operant condition-
ing may help to explain how the person learns to avoid triggering PTSD attacks;
such explanations parallel those for such behavior in anxiety disorders (Mowrer,
1939; see Chapter 6). In terms of classical conditioning, the traumatic stress is the
unconditioned stimulus, and both internal sensations and external objects or situ-
ations can become conditioned stimuli, which in turn can come to induce power-
ful and aversive conditioned emotional responses (Keane, Zimmering, & Caddell,
1985). Thus, when a situation is similar to the traumatic one, it induces reactions
that are aversive, leading the person to avoid the situation. In terms of operant con-
ditioning, behaving in ways that avoid triggering PTSD symptoms is negatively
reinforced. In addition, drugs and alcohol can temporarily alleviate symptoms; such
substance use is also negatively reinforced, which explains why people with PTSD
have a higher incidence of substance use disorders than do people who experienced
Among people who experienced a common
type of traumatic event—a car accident—
those who coped during the accident by
dissociating were more likely to go on to
develop PTSD than those who did not (Shalev
et al., 1996). Other factors that increase the
likelihood of PTSD’s developing after a car
accident are ruminating about the accident
afterward, consciously trying to suppress
thoughts about it, and having intrusive,
unwanted thoughts and memories about it
(Ehlers, Mayou, & Bryant, 1998).
©
C
o
rb
is
/P
u
n
ch
st
o
ck
214 C H A P T E R 7
a trauma but did not go on to develop PTSD (Chilcoat & Breslau, 1998; Jacobsen
et al., 2001).
Social Factors: Socioeconomic Factors,
Social Support, and Culture
Social factors—both before a traumatic event and after ward—also help deter-
mine whether a person will develop PTSD after a trauma. As with other stress-
ors in life, socioeconomic factors can influence a person’s ability to cope. People
who face severe financial challenges—who aren’t sure whether they’ll be able
to feed, clothe, and house themselves or their families—have fewer emotional
resources available to cope with a traumatic event and so are more likely than
more financially fortunate people to develop PTSD after a trauma (Mezey &
Robbins, 2001).
In addition, socioeconomically disadvantaged people may be more likely to
experience trauma (Breslau et al., 1998; Himle et al., 2009). For instance, poorer
people are more likely to live in high-crime areas and are therefore more likely to
witness crimes or become crime victims (Norris et al., 2003).
On a more hopeful note, people who receive support from others after a trauma
have a lower risk of developing PTSD (Kaniasty & Norris, 1992; Kaniasty et al.,
1990). For example, military servicemen and women who have experienced trauma
during their service have a lower risk of developing PTSD if they have strong social
support upon returning home ( Jakupcak et al., 2006; King et al., 1999).
Final ly, even when a person does develop PTSD, his or her sur rounding
culture can help determine which PTSD symptoms are more prominent. Cul-
tural patterns might “teach” one coping style rather than another (Marsella et
al., 1996). For example, Hurricane Paulina in Mexico and Hurricane Andrew
in the United States were about equal in force, but the people who developed
PTSD afterward did so in different ways (after controlling for the severity of a
person’s trauma): Mexicans were more likely to have intrusive symptoms, such
as flashbacks about the hurricane and its devastation, whereas Americans were
more likely to have arousal symptoms, such as an exaggerated startle response or
hypervigilance (Norris et al., 2001). A similar finding was obtained from a study
comparing Hispanic Americans to European Americans after Hurricane Andrew
(Perilla et al., 2002).
Feedback Loops in Understanding Posttraumatic Stress Disorder
Neurological factors can make some people more vulnerable to developing PTSD
after a trauma (van Zuiden et al., 2011). For example, in a study of people who
were training to be firefighters, trainees who had a larger startle response to loud
bursts of noise (which indicates a ver y reactive sympathetic nervous system) at
the beginning of training were more likely to develop PTSD after a subsequent
fire-related trauma (Guthrie & Bryant, 2005). In another study, researchers found
that willingness to volunteer for combat and to accept riskier assignments is partly
heritable ( neurological factor; Lyons et al., 1993). This heritability may involve the
dimension of temperament called novelty seeking (see Chapter 2). Someone high
in novelty seeking pursues activities that are exciting and very stimulating, and a
person with this characteristic may be more likely to volunteer for risky assign-
ments ( psychological factor), increasing the chance of encountering certain kinds
of trauma. This means that neurological factors can influence both psychologi-
cal and social factors, which in turn can increase the risk of trauma. At the same
time, when a traumatic event is more severe (social factor), other types of factors
are less important in influencing the onset of PTSD (Keane & Barlow, 2002).
SP
N
Obsessive-Compulsive-Related and Trauma-Related Disorders 215
Furthermore, ways of viewing the world and other personality traits (psychologi-
cal factors) can influence the level of social support that is available to a person
after suffering trauma (social factor). Figure 7.2 illustrates these factors and their
feedback loops.
Treating Posttraumatic Stress Disorder
As usual, when a treatment is successful, changes in one factor affect the other
factors.
Brain Systems
Mental Processes and
Mental Contents
Family
Hippocampus
Genetics
Inherited tendency to seek
out situations that may have
a higher likelihood of trauma
Dissociation during
trauma
Beliefs that one is unable
to control stressors and
that the world is a
dangerous place
Behavior
Conditioned emotional
response to stimuli
associated with trauma
Negative reinforcement
of avoidance
Affect
Anxiety
Fear
Stressful Life Events
Socioeconomic stress
Lack of social support
Specific characteristics
of the traumatic event
No known major
contribution
Gender/Culture
Cultural influences on
symptom expression
NeuroPsychoSocial
NeuroPsychoSocial NeuroPsychoSocial
Neural Communication
Norepinephrine
Serotonin
FI G U RE 7.2 • Feedback Loops in Understanding PTSD
216 C H A P T E R 7
Targeting Neurological Factors: Medication
The SSRIs sertraline (Zoloft) and paroxetine (Paxil) are the first-line medications for
treating the symptoms of PTSD (Brady et al., 2000; Stein, Seedat, et al., 2000).
An advantage of SSRIs is that these medications can also help reduce comorbid
symptoms of depression (Hidalgo & Davidson, 2000)—which is important because
many people with PTSD also have depression. However, as with anxiety disorders,
when people discontinue the medication, the symptoms may return. This is why
medication is not usually the sole treatment for PTSD but rather is combined with
treatment that directly addresses psychological and social factors (Rosenbaum, Arana
et al., 2005).
Targeting Psychological Factors
Treatments that target psychological factors generally employ a combination of
behavioral methods and cognitive methods, which—separately or in combination—
are about equally effective (Keane & Barlow, 2002; Schnurr et al., 2007; Tarrier
et al., 1999).
Behavioral Methods: Exposure, Relaxation, and Breathing Retraining
Someone who has PTSD may go to unreasonable lengths to avoid stimuli associated
with the trauma. This is why treatment aims to increase a sense of control over PTSD
symptoms and to decrease avoidance. Just as exposure is used to decrease avoidance
associated with anxiety disorders, it is used to treat PTSD: Exposure aims to induce
habituation and to reduce the avoidance of internal and external cues associated with
the trauma (Bryant & Harvey, 2000; Keane & Barlow, 2002). In this case, the spe-
cific stimuli in an exposure hierarchy are those associated with the trauma. As the
person becomes less aroused and fearful of these stimuli and avoids them less, mastery
C U R R E N T C O N T R O V E R S Y
Eye Movement Desensitization and
Reprocessing (EMDR) Treatment for
Posttraumatic Stress Disorder
Eye movement desensitization and reprocessing (EMDR) is
a widely used but debated psychological treatment for post-
traumatic stress disorder (PTSD). The treatment rests on the
idea that the symptoms of PTSD arise from the inability to
process adequately the images and cognitions that arise when
a person experiences a traumatic event (Shapiro, 2001). The
treatment contains elements of both psychodynamic and cog-
nitive-behavior therapy, and it was originally designed to help
decrease negative emotions associated with traumatic memo-
ries (Shapiro & Maxfield, 2002). The phase of the treatment
most similar to exposure therapy has the client think about
the disturbing visual images or beliefs about the trauma while
“moving the eyes from side to side for 15 or more seconds” as
the therapist moves his or her fingers back and forth (Shapiro
& Maxfield, 2002, p. 937).
On the one hand, EM DR has received enough re-
search support to be considered one of a handful of treat-
ments for PTSD that research suggests is effective (Perkins
& Rouanzoin, 2002). However, what remains controversial
is whether EMDR imparts any benefit above and beyond
standard exposure therapy. Randomized trials comparing
EMDR to exposure therapies have found little to no dif-
ferences in outcomes for the t wo treatments (Ironson et
al., 2002 ; Lee et al., 2002 ; Power et al., 2002 ; Taylor et
al., 2003). From the perspective of a patient, the data sug-
gest that the treatment works. But thinking about it from
an ethical perspective, if EMDR does not lead to a better
outcome than CBT, is the expensive training and certifica-
tion required to practice the treatment warranted? In addi-
tion, some might argue that the eye movements increase the
public’s positive perception of the procedure as a medical
treatment, even though there is no good evidence that eye
movements enhance the benefit.
CRITICAL THINKING As a consumer, would you be concerned
about undergoing a treatment if no one completely under-
stood why all the components are helpful? What about taking
a medication when we know that the medication helps the
disorder but not exactly how it works?
(Randy Arnau, University of Southern Mississippi)
Obsessive-Compulsive-Related and Trauma-Related Disorders 217
and control increase. To help with anxiety and reduce arousal symptoms, relaxation
and breathing retraining are often included in treatment. Exposure can also be use-
ful in preventing PTSD for people who, in the days following a trauma, have some
symptoms of PTSD ( Shalev et al., 2012).
Howard Hughes apparently used exposure with himself, which helped him
resist developing PTSD. Before his near-fatal plane crash, he loved to fly. During his
convalescence after that plane crash, he grew concerned that he’d become afraid of
flying—perhaps because he was worried that stimuli associated with the crash (e.g.,
things related to planes) would lead to anxiety and flashbacks. Although Howard
Hughes was worried about developing a fear of flying, the anxiety about flying—
and an avoidance of it—didn’t materialize. Because of his passion for the activity, he
pushed himself to get back in the cockpit as soon as he was physically able (Barlett &
Steele, 1979), and then he flew repeatedly, successfully undergoing a self-imposed in
vivo exposure treatment.
Cognitive Methods: Psychoeducation and Cognitive Restructuring
To reduce the difficult emotions that occur with PTSD, educating patients about
the nature of their symptoms (psychoeducation) can be a first step. As patients learn
about PTSD, they realize that their symptoms don’t arise to-
tally out of the blue; their experiences become more under-
standable and less frightening.
In addition, cognitive methods can help patients under-
stand the meaning of their traumatic experiences and the
(mis)attributions they make about these experiences and the
aftermath (Duffy et al., 2007, Foa et al., 1991, 1999), such as “I
deserved this happening to me because I should have walked
down a different street.”
Studies have shown that CBT can signif icantly reduce
the number of people who, with time, would have had their
diagnosis change from acute stress disorder to PTSD (Bry-
ant et al., 2005, 2006, 2008) and can decrease the risk of
PTSD in people who, in the days after a traumatic event, ex-
hibit enough symptoms to meet the criteria for PTSD (Shalev
et al., 2012).
Targeting Social Factors: Safety, Support, and Family Education
Because a traumatic event is almost always a social stressor, the early focus of treatment
for PTSD is to ensure that the traumatized person is as safe as possible (Baranowsky et
al., 2005; Herman, 1992). For instance, in a case that involves a woman with PTSD
that arose from domestic abuse, the therapist and patient will spend time reviewing
whether the woman is safe from further abuse, and if not, how to make her as safe as
possible. For some types of traumatic events (such as combat-related trauma), group
therapy—of any theoretical orientation—can provide support and diminish the sense
of isolation, guilt, or shame about the trauma or the symptoms of PTSD (Schnurr et
al., 2003). Moreover, family or couples therapy can help to educate family members
and friends about PTSD and about ways in which they can support their loved one
(Goff & Smith, 2005; Sherman et al., 2005).
Feedback Loops in Treating Posttraumatic Stress Disorder
To appreciate the interactive aspects of the neuropsychosocial approach, consider a
study of people who developed PTSD after being in traffic accidents (as the driver,
passenger, or pedestrian; Taylor et al., 2001). Prior to beginning the treatment, 15 of
the 50 participants were taking an SSRI, a TCA, or a benzodiazepine. Treatment
SP
N
CBT conducted online helped people who
developed PTSD as a result of the September
11, 2001, terrorist attack on the Pentagon
(Litz et al., 2007).
U
.S
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218 C H A P T E R 7
Treatments Targeting
Neurological Factors
Medication: SSRIs
Changes neural
activity
Decreases isolation
and shame
Increases social
support
Improves
relationships
Treatments Targeting
Social Factors
Group therapy
Couples or family
therapy
Changes thoughts,
feelings, and
behaviors
Treatments Targeting
Psychological Factors
CBT: Breathing,
relaxation, exposure,
cognitive restructuring,
psychoeducation
EMDR
FI G U RE 7.3 • Feedback Loops in Treating PTSD
consisted of 12 weeks of group CBT that involved psychoeducation about traffic
accidents, their aftereffects, and PTSD; cognitive restructuring focused on faulty
thoughts (such as overrating the dangerousness of road travel); relaxation train-
ing; and imaginal and in vivo exposure. After treatment, participants reported that
they experienced less sympathetic nervous system reactivity, such as having fewer
“ hair-trigger” startle responses. In addition, they avoided the trauma-inducing stim-
uli less often and had fewer intrusive re-experiences of the trauma. These gains were
maintained at the 3-month follow-up. So, an intervention that targets both social
factors (group therapy with exposure to external trauma-related stimuli) and psycho-
logical factors (cognitive and behavioral interventions to change thinking and be-
havior) also apparently changed neurological functioning, as indicated by the reports
of decreased hyperarousal. This change in turn affected both the person’s thoughts
and social interactions. Successful treatments for PTSD that target one or two factors
ultimately affect all three. Figure 7.3 illustrates these feedback loops in treatment.
Thinking Like A Clinician
Two friends, Farah and Michelle, came back from winter break. Each had been devastated by
personal experiences that occurred during the break. Farah’s house burned down after the
boiler exploded; fortunately, everyone was safe. Michelle’s house had also been destroyed in
a fire, but the police believed it was set by an “enemy” of her father’s. Months pass, and by
the time they go home for summer vacation, one of the friends has developed PTSD. Based
on what you have read, which friend do you think developed PTSD, and why? What symp-
toms might she have and why? Based on what you have read, what do you think would be
appropriate treatment for her?
Obsessive-Compulsive-Related and Trauma-Related Disorders 219
Obsessive-Compulsive Disorder and
Related Disorders
• OCD is marked by persistent and intru-
sive obsessions or repetitive compulsions
that usually correspond to the obsessions.
People with OCD feel driven to engage in
the compulsive behaviors, which provide
only brief respite from the obsessions.
• Com mon obse s sion s i nclude a n x iet y
a b out c ont a m i n a t ion , o r d e r, lo s i n g
cont rol, a nd doubt s. Com mon com-
pu l sion s i nclude wa sh i n g, order i n g,
counting, and checking.
• Body dysmorphic disorder is character-
ized by an excessive preoccupation with
a perceived defect in appearance that is
either imag ined or sl ight, and menta l
acts or behaviors related to the preoccu-
pation. Body dysmorphic disorder shares
features with OCD: preoccupations that
arise from beliefs that are disproportional
to the situation and time-consuming cor-
responding compulsive behaviors.
• Neurological factors associated with OCD
include disruptions in the normal activity of
the frontal lobes, the thalamus, and the basal
ganglia; the frontal lobes do not turn off
activity in the neural loop among these three
brain areas, which may lead to the persistent
obsessions. Lower-than-normal levels of se-
rotonin also appear to play a role. And genes
appear to make some people more vulnera-
ble to anxiety-related disorders in general—
not necessarily to OCD specifically.
• Psycholog ical factors that may under-
lie OCD include negative reinforcement
of the compu lsive behav ior. In add i-
tion, normal preoccupying thoughts may
become obsessions when the thoughts are
deemed “unacceptable” and hence require
controlling. In turn, the thoughts lead
to anxiet y, which is then relieved by a
mental or behavioral ritual. People with
OCD have cognitive biases related to their
feared stimuli—in this case, regarding the
theme of their obsessions.
• Social factors related to OCD include so-
cially induced stress, which can influence
the onset and course of the disorder, and
culture, which can influence the particu-
lar content of obsessions and compulsions.
• Medication (such as an SSRI or clomip-
ra m i ne) d i rect ly t a rget s neu rolog ica l
factors that underlie OCD. The primary
treatment for OCD—exposure with re-
sponse prevention—directly targets psy-
chological factors. Family education or
therapy, targeting social factors, may be
used as an additional treatment.
Trauma-Related Disorders
• Trauma-related disorders are character-
ized by four types of persistent symptoms:
intrusive re-experiencing of the trauma,
avoidance of stimuli related to the event,
negative thoughts and mood and dissocia-
tion, and increased arousal and reactivity.
• DSM-5 includes two t ypes of trauma-
related disorders: acute stress disorder
and posttraumatic stress disorder (PTSD).
Acute stress disorder is diagnosed when
symptoms arise soon after the traumatic
event and have lasted for at least 3 days but
not more than 1 month; when symptoms
last more than 1 month, the diagnosis can
shift to PTSD. The diagnostic criteria for
acute stress disorder also include symp-
toms of dissociation.
• An event is considered traumatic if the
per son ex per ienced or w it ne s sed a n
actual or threatened death, serious injury,
or sexual violation. Types of traumatic
events are large-scale events with multiple
v ic t i m s , u n i n t e nd e d a c t s i nvol v i n g
smaller numbers of people, and interper-
sonal violence.
• An unusually small hippocampus is a risk
factor for PTSD. Patients with PTSD re-
spond to high levels of norepinephrine
Follow-up on Howard Hughes
Despite the traumatic events that Howard Hughes experienced, he does not ap-
pear to have developed PTSD. However, without a doubt, he suffered from OCD.
Although some of his symptoms apparently began in childhood, his OCD symp-
toms worsened significantly when he was in his 40s. There are several reasons for
his progressively impaired functioning at that time. First, he used increasingly larger
and more frequent doses of codeine and Valium, which probably led to diminished
cognitive functioning and control over his compulsions. Second, he had by then
suffered brain damage, which came about from two sources: (1) the 14 occurrences
of head trauma Hughes withstood from various plane and car accidents (Fowler,
1986) and (2) the effects of advanced syphilis (Brown & Broeske, 1996). Hughes
contracted syphilis when in his 30s, before antibiotics were available (Brown &
Broeske, 1996). To treat the disease, he underwent a painful and risky mercury
treatment, but the treatment was not a complete success, and the disease appears to
have progressed during his 40s. After Hughes’s death, his autopsy indicated that sig-
nificant brain cell death had occurred, which is a sign of advanced syphilis (a condi-
tion previously called general paresis; see Chapter 1). Symptoms can include gradual
personality changes and poor judgment, which may take up to 15 years to emerge.
SUMMING UP
220 C H A P T E R 7
by having panic attacks or f lashbacks;
they also have abnormal serotonin func-
t ion. A lthoug h genes—th roug h their
i n f luence on temper a ment—m ay a f-
fect a person’s tendency to enter r isky
situations, characteristics of a traumatic
event itself are more important in deter-
mining whether the person will develop
PTSD.
• Psychological factors that exist before a
traumatic event contribute to PTSD; these
factors include a history of depression or
other psychological disorders, a belief in
being unable to control stressors, and the
conviction that the world is a dangerous
place. After a traumatic event, classical
and operant conditioning contribute to
the avoidance symptoms.
• Social factors that contribute to PTSD
include the stress of low socioeconomic
status and a relative lack of social support
for the trauma victim. Culture can influ-
ence the ways that people cope with trau-
matic stress.
• Medication, specifically an SSRI, is the
treatment that directly targets neurologi-
cal factors. Treatments that target psycho-
logical factors include EMDR and CBT,
specif ically psychoeducation, exposure,
relaxation, breathing retraining, and cog-
nitive restructuring. Treatments that tar-
get social factors are designed to ensure
that the person is as safe as possible from
future trauma and to increase social sup-
por t through g roup therapy or fam ily
therapy.
Obsessions (p. 196)
Compulsions (p. 196)
Obsessive-compulsive disorder (OCD) (p. 196)
Hoarding disorder (p. 199)
Body dysmorphic disorder (p. 199)
Exposure with response prevention (p. 206)
Posttraumatic stress disorder (PTSD) (p. 209)
Acute stress disorder (p. 211)
Key Terms
More Study Aids
For additional study aids related to this chapter, including
quizzes to make sure you’ve retained everything you’ve
learned and a Student Video Activity exploring one woman’s
struggle with body dysmorphic disorder, go to: www.
worthpublishers.com/launchpad/rkabpsych2e.
Image Source
Obsessive-Compulsive-Related and Trauma-Related Disorders 221
223
CHAPTER 8
Dissociative and Somatic
Symptom Disorders
nna O., a well-to-do 21-year-old woman living in Austria in
the late 19th century, had been caring for her ill father for
weeks. Anna and her mother alternated shifts, Anna taking
the night shift, staying awake by his bedside. Her father was dying of
tuberculosis, and Anna also began to feel sick. Her symptoms included
severe vision problems, headaches, a persistent cough, paralysis (in her
neck, right arm, and both legs), lack of sensation in her elbows, and
daily periods of a state of consciousness similar to sleep-walking.
Anna was diagnosed with hysteria, an emotional condition marked
by extreme excitability and bodily symptoms for which there is no
medical explanation (hysteria is not a DSM-5 disorder).
For 2 years, Anna was treated by Dr. Joseph Breuer, a Viennese
neurologist. Breuer became a colleague of Sigmund Freud and told
Freud about Anna and her treatment, later described in Studies in
Hysteria (Breuer & Freud, 1895/1955). Prior to Breuer’s treatment of
Anna, hypnosis was often used to treat hysteria. The physician hyp-
notized the patient (usually a woman) and then gave her a sugges-
tion that the symptoms would go away. However, for some unknown
reason, Breuer did not give Anna any suggestions, although he did
hypnotize her. Instead, he asked her about her symptoms, and over
time she told him about them. Anna and Breuer often met daily for
treatment, sometimes twice a day. Anna’s treatment usually involved
Breuer’s hypnotizing her and then asking her to tell him what she
remembered about the origins of her symptoms. At other times, after
being hypnotized, she simply told him what was on her mind. Anna
referred to this process as the “talking cure.” Freud was fascinated
by Breuer’s account of Anna’s illness and her treatment; this “talking
cure” was a precursor to psychoanalysis, and Freud’s thoughts about
Breuer and Anna led to the beginnings of his psychoanalytic theory
(Freeman, 1980; see also Chapter 1).
Dissociative Disorders
Dissociative Disorders: An Overview
Dissociative Amnesia
Depersonalization-Derealization Disorder
Dissociative Identity Disorder
Treating Dissociative Disorders
Somatic Symptom Disorders
Somatic Symptom Disorders: An Overview
Somatic Symptom Disorder
Conversion Disorder
Illness Anxiety Disorder
Treating Somatic Symptom Disorders
Follow-up on Anna O.
Hysteria
An emotional condition marked by extreme
excitability and bodily symptoms for which
there is no medical explanation.
Shuji Kobayashi/The Image Bank/Getty Images. Photo for illustrative purposes only;
any individual depicted is a model.
A nn A wA s di Ag nos ed wi t h h y s t eri A — a com mon d iag nosis at the
time, particularly for women—but this term is a vague label for a condition that
includes a wide range of symptoms. In DSM-5, symptoms that were once con-
sidered signs of hysteria are now part of the diagnostic criteria for two categories
of disorders: dissociative disorders and somatic symptom disorders. The cen-
tral feature of dissociative disorders is dissociation, the separation of mental pro-
cesses—such as perception, memor y, and self-awareness—and behavior that are
normally integrated (Spiegel et al., 2011). Generally, each individual mental pro-
cess is not disturbed, but their normal integrated functioning is disturbed. (With
schizophrenia, in contrast, it is the mental processes themselves, such as the form
or pattern of thoughts, that are disturbed; see Chapter 12.) Somatic symptom and
related disorders (which we will refer to in this book simply as somatic symptom
disorders) are characterized by complaints about physical well-being along with
cognitive distortions about those bodily symptoms and their meaning; the focus
on these bodily symptoms causes significant distress or impaired functioning.
In this chapter we explore dissociative and somatic symptom disorders—their
diagnostic criteria, criticisms of those criteria, the causes of the disorders, and
treatments for them.
Dissociative Disorders
Breuer reported that Anna O. was an extremely bright young woman, prone to
“systematic day-dreaming, which she described as her ‘private theatre.’” Anna lived
“through fairy tales in her imagination; but she was always on the spot when spoken
to, so that no one was aware of it. She pursued this activity almost continuously
while she was engaged in her household duties” (Breuer & Freud, 1895/1955, p. 22).
These dissociative states, or “absences,” began in earnest when Anna became too
weak to care for her father, and they became more prominent after his death in
April 1881. In what follows we examine dissociative disorders in more detail and
then consider whether Anna’s symptoms would meet the criteria for any of these
disorders.
Dissociative Disorders: An Overview
Dissociation may arise suddenly or gradually, and it can be brief or chronic (Steinberg,
1994, 2001). Dissociative symptoms include:
• amnesia, or memory loss, which is usually temporary in dissociative disorders but,
in rare cases, may be permanent;
• identity problems, in which a person isn’t sure who he or she is or may assume a
new identity;
• derealization, in which the external world is perceived or experienced as
strange or unreal, and the person feels “detached from the environment” or as if
viewing the world through “invisible filters” or “a big pane of glass” (Simeon et al.,
2000); and
• depersonalization, in which the perception or experience of self—either one’s
body or one’s mental processes—is altered to the point where the person feels like
an observer, as though seeing oneself from the “outside.” People experiencing
depersonalization may describe it as feeling is if “under water” or “floating,” “like
a dead person,” “as if I’m here but not here,” “detached from my body,” or “like a
robot” (Simeon et al., 2000).
You may notice that some of these symptoms sound familiar. That’s because all
but identity problems are listed among the criteria for PTSD or acute stress disorder
Dissociation
The separation of mental processes—such as
perception, memory, and self-awareness—
that are normally integrated.
Amnesia
Memory loss, which in dissociative disorders
is usually temporary but, in rare cases, may be
permanent.
Identity problem
A dissociative symptom in which a person is
not sure who he or she is or may assume a
new identity.
Derealization
A dissociative symptom in which the external
world is perceived or experienced as strange
or unreal.
Depersonalization
A dissociative symptom in which the
perception or experience of self—either one’s
body or one’s mental processes—is altered
to the point that the person feels like an
observer, as though seeing oneself from the
“outside.”
Anna O. was diagnosed with hysteria, which
is a vague condition that is not in the DSM-5
classification system. Symptoms that were
seen as part of hysteria are now generally
considered to be symptoms of either
dissociative disorders or somatic symptom
disorders.
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224 C H A P T E R 8
(Chapter 7). In fact, as we’ll discuss later in the chapter, trauma is thought to play a
major role in dissociative disorders.
Anna O. appeared to experience derealization. After her father died, she
recounted “that the walls of the room seemed to be falling over” (Breuer & Freud,
1895/1955, p. 23). She also reported having trouble recognizing faces and needing
to make a deliberate effort to do so: “‘this person’s nose is such-and-such, his hair
is such-and-such, so he must be so-and-so.’ All the people she saw seemed like wax
figures without any connection with her” (Breuer & Freud, 1895/1955, p. 26).
Normal Versus Abnormal Dissociation
Experiencing symptoms of dissociation is not necessarily abnormal; occasional dis-
sociating is a part of everyday life (Seedat et al., 2003). For instance, you may find
yourself in a class but not remember walking to the classroom. Or, on hearing bad
news, you may feel detached from yourself, as if you’re watching yourself from the
outside.
In some cases, periods of dissociation are part of religious or cultural rituals
(Boddy, 1992). Consider the phenomenon of possession
trance observed in some societies: During a hypnotic trance,
a kind of spirit is believed to assume control of the person’s
body. Later, the person has amnesia for the experience, and
is otherwise normal. Moreover, people in different cul-
tures may express dissociative symptoms differently. For
example, latah, experienced by people—mostly women—
in Indonesia and Malaysia ( Bartholomew, 1994), involves
fleeting episodes in which the person uses profanity and
experiences amnesia and trancelike states. Unlike the typi-
cal course with psychosis, the “ possessed” person returns
to normal after the trance is over.
In some instances, dissociative experiences do indicate
a disorder, but not necessarily a dissociative disorder; other
psychiatric disorders can involve dissociative symptoms,
such as when depersonalization or derealization occurs
during a panic attack. DSM-5 reserves the categor y of
dissociative disorders for cases in which consciousness, memory, emotion, per-
ception, body representation, motor control, or identity are dissociated to the point
where the symptoms are pervasive, cause significant distress, and interfere with daily
functioning. Research findings suggest that pathological dissociation is qualitatively
different from everyday types of dissociation, such as “spacing out” (Rodewald et
al., 2011; Seedat et al., 2003). Only about 2% of the U.S. population reports having
experienced dissociation to the extent that would be considered abnormal (Seedat
et al., 2003).
Anna’s dissociative symptoms do appear to have been abnormal; she had disso-
ciations in perception, consciousness, memory, and identity:
Two entirely distinct states of consciousness were present which alternated very fre-
quently and without warning and which became more and more differentiated in the
course of the illness. In one of these states she recognized her surroundings; she was
melancholy and anxious, but relatively normal. In the other state she hallucinated
and was “naughty”—that is to say, she was abusive, used to throw the cushions at
people, . . . tore buttons off her bedclothes and linen with those of her fingers which
she could move, and so on. At this stage of her illness if something had been moved
in the room or someone had entered or left it [during her other state of consciousness]
she would complain of having “lost” some time and would remark upon the gap in her
train of conscious thoughts.
Dissociative disorders
A category of psychological disorders in which
consciousness, memory, emotion, perception,
body representation, motor control, or
identity are dissociated to the point where
the symptoms are pervasive, cause significant
distress, and interfere with daily functioning.
This woman is experiencing possession trance,
a culturally sanctioned form of dissociation.
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Dissociative and Somatic Symptom Disorders 225
These “absences” had already been observed before she took to her bed; she [would]
stop in the middle of a sentence, repeat her last words and after a short pause go on
talking. These interruptions gradually increased till they reached the dimensions
that have just been described. . . . At the moments when her mind was quite clear
she would complain of the profound darkness in her head, of not being able to
think, . . . of having two selves, a real one and an evil one which forced her to behave
badly, and so on.
(Breuer & Freud, 1895/1955, p. 24)
Anna’s dissociative experiences were clearly beyond normal: They were pervasive
and interfered with her daily functioning.
Types of Dissociative Disorders
DSM-5 def ines three types of specif ic dissociative disorders, described in the
following sections: dissociative amnesia, depersonalization-derealization disorder, and
dissociative identity disorder.
Dissociative Amnesia
Anna’s native language was German, but as her condition began to worsen while
she was nursing her father, she started to speak only English (a language in which
she was also f luent). She developed complete amnesia for speaking the German
language. Let’s examine why her amnesia for speaking in her native language might
be considered dissociative.
What Is Dissociative Amnesia?
Dissociative amnesia is a dissociative disorder in which the sufferer has signifi-
cantly impaired memory for autobiographical information—important experiences
or personal information—that is not consistent with ordinary forgetfulness (see
Table 8.1). The experiences or information typically involve traumatic or stressful
events, such as occasions when the patient has been violent or tried to hurt herself
or himself; the amnesia can come on suddenly. For example, soon after a bloody
and dangerous battlefield situation, a soldier may not be able to remember what
happened.
To qualify as dissociative amnesia, the memory problem cannot be explained
by a medical disorder, substance use, or other disorders that have dissociation as
a key symptom; as with all other dissociative disorders, it must also significantly
impair functioning or cause distress (American Psychiatric Association, 2013). In
Anna’s case, her amnesia for speaking German could not really be considered as
the loss of personal information but conceivably could be construed as the loss
of an important experience and couldn’t be explained by another disorder—and
her father’s illness and declining health had been extremely stressful for her.
The memory problems in dissociative amnesia can take any of several forms:
• Localized amnesia, in which the person has a memory gap for a specific pe-
riod of time, often a period of time just prior to the stressful event, as did
Mrs. Y in Case 8.1. This is the most common form of dissociative amnesia
(American Psychiatric Association, 2013).
• Selective amnesia, in which the person can remember only some of what
happened in an otherwise forgotten period of time. For instance, a soldier
may forget about a particularly traumatic battlefield skirmish but remember
what he and another person spoke about between phases of this skirmish.
• Generalized amnesia, in which the person can’t remember his or her entire
life. Although common in television shows and films, this type of amnesia
is, in fact, extremely rare (Spiegel et al., 2011).
Dissociative amnesia
A dissociative disorder in which the sufferer has
significantly impaired memory for important
experiences or personal information that
cannot be explained by ordinary forgetfulness.
Soldiers with dissociative amnesia may forget
combat experiences that were particularly
troubling or traumatic. Although we don’t
know anything about this soldier, many soldiers
encounter traumatic, and frequently mortal,
events on their tours of duty. This soldier is
attending a memorial service in Iraq for three of
his comrades who were killed in a convoy attack.
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TABLE 8.1 • DSM-5 Diagnostic Criteria for
Dissociative Amnesia
A. An inability to recall important autobiographical
information, usually of a traumatic or stressful
nature, that is inconsistent with ordinary forgetting.
B. The symptoms cause clinically significant distress
or impairment in social, occupational, or other
important areas of functioning.
C. The disturbance is not attributable to the physiological
effects of a substance (e.g., alcohol or other drug of
abuse, a medication) or a neurological or other medical
condition (e.g., partial complex seizures, transient global
amnesia, sequelae of a closed head injury/traumatic
brain injury, other neurological condition).
D. The disturbance is not better explained by
dissociative identity disorder, posttraumatic stress
disorder, acute stress disorder, somatic symptom
disorder, or major or mild neurocognitive disorder.
Reprinted with permission from the Diagnostic and Statistical Manual of
Mental Disorders, Fifth Edition, (Copyright ©2013). American Psychiatric
Association. All Rights Reserved.
226 C H A P T E R 8
CASE 8.1 • FROM TH E OUTSIDE: Dissociative Amnesia
Mrs. Y, a 51-year-old married woman . . . had a two-year history of severe depressive epi-
sodes with suicidal ideation, and reported total loss of memory for 12 years of her life . . .
from the age of 37 to 49. [The amnesia began at age 49 when] she had had a car acci-
dent from which she sustained a very minor injury, but no loss of consciousness [nor any]
posttraumatic stress symptoms. . . . She remembered what happened in the accident, and
immediately preceding it, but suddenly had total loss of memory for the previous 12 years.
Mrs. Y had no problems recalling events which had occurred since the accident. She
also had good autobiographical memory for her life events up to the age of 37.
Her parents and her grown-up children had told her that the . . . 12 years were pain-
ful for her. They would not tell her why, because they thought it would distress her even
more. She was not only amnesic for these reputedly painful events, [but was unable] to
recognize any of the friends she had made during that time. This included her present man
friend, who was the passenger in her car at the time of the accident. Her family had told
Mrs. Y that this gentleman (Mr. C) had been courting her for six years prior to the accident.
(Adapted from Degun-Mather, 2002, pp. 34–35)
In addition, some people with dissociative amnesia may have a subtype: dissociative
fugue, which involves sudden, unplanned travel and difficulty remembering the past—
which in turn can lead sufferers to be confused about who they are and sometimes to
take on a new identity. Such a fugue typically involves generalized amnesia. In some
cultures, people can develop a related set of symptoms referred to as a running syndrome.
Although this condition has some symptoms that are similar to those of a dissociative
fugue, it typically involves a sudden onset of a trancelike state and behavior such as
running or fleeing, which leads to exhaustion, sleep, and subsequent amnesia for the
experience. Running syndromes include (American Psychiatric Association, 2000):
• pibloktoq among native Arctic people,
• grisi siknis among the Miskito of Nicaragua and Honduras, and
• amok in Western Pacific cultures.
These syndromes have in com mon w ith dissociative fug ue the symptom of
unexpected travel, but amnesia occurs after the running episode is over, so the person
doesn’t remember that it happened. In contrast, with dissociative fugue, the memory
problem arises during the fugue state, and the person can’t remember his or her past.
In addition, other criteria for dissociative amnesia do not necessarily apply to running
syndromes. Additional facts about dissociative amnesia are listed in Table 8.2.
TABLE 8.2 • Dissociative Amnesia
Facts at a Glance
Prevalence
• Dissociative amnesia is rare, and its life-
time prevalence is unknown.
Comorbidity
• Depression, anxiety, and substance-related
disorders may be present along with
dissociative amnesia. (Note: If the amnesia
is a result of substance use, dissociative
amnesia will not be the diagnosis.)
Onset
• Children or adults can develop this disorder.
Course
• Patients may have one or multiple episodes
of amnesia.
• In some cases, the episode of amnesia
resolves quickly; in other cases it persists.
Gender Differences
• No gender differences in the prevalence of
dissociative amnesia have been reported.
Cultural Differences
• Dissociative amnesia may be a culture-
related diagnosis; there are no reported
cases of this disorder (due to a traumatic
event by itself, in the absence of brain
damage resulting from the trauma) prior
to 1800 (Pope et al., 2007).
Source: Unless otherwise noted, the source is American
Psychiatric Association, 2013. For more information see
the Permissions section.
Some cultures have syndromes that are similar
to dissociative fugue, such as grisi siknis, which
shares with dissociative fugue a sudden flight
from home and problems with memory. This
photo shows local healers of an indigenous
Miskito community in Nicaragua treating people
with grisi siknis.
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Dissociative and Somatic Symptom Disorders 227
People with dissociative amnesia typically are unaware—or only minimally
aware—of their memor y problems (American Psychiatric Association, 2013).
Some people may spontaneously remember forgotten experiences or information,
particularly if their amnesia developed in response to a traumatic event and they
leave the traumatic situation behind (such as occurs when a soldier with combat-
related localized amnesia leaves the battlefield). Anna O. recovered her ability to
speak German at the end of her treatment with Dr. Breuer, after she reenacted a
traumatic nightmare that she’d had at her father’s sickbed (and that marked the start
of her problems).
Understanding Dissociative Amnesia
The following sections apply the neuropsychosocial approach as a framework for
understanding the nature of dissociative amnesia. However, because the disorder is
so rare, not much is known about either the specific factors that give rise to it or how
those factors might influence each other.
Neurological Factors: Brain Trauma?
Neurological factors are clearly involved in cases of amnesia that arise following
brain injur y, such as that suffered in a car accident (Piper & Merskey, 2004a).
However, when amnesia follows brain injury, it is not considered to be dissociative
amnesia. Neurological factors that may contribute to dissociative amnesia are less
clear-cut.
Some researchers have suggested that dissociative amnesia may result in part
from damage to the hippocampus, which is critically involved in storing new
information about events in memor y. These researchers assume that periods of
prolonged stress affect the hippocampus so that it does not operate well when the
person is highly aroused ( Joseph, 1999). The arousal—which typically accompa-
nies a traumatic event—will impair the ability to store new information about that
event. Later, this process would lead to the symptoms of dissociative amnesia for
that event.
However, the idea that damage to the hippocampus underlies dissociative
amnesia cannot explain all cases of the disorder. Because such damage would
prevent information from being stored in the first place, the subsequent amnesia
would not be reversible: There would be no way to retrieve the memories later
because the memories would not exist (Allen et al., 1999). That is, the hippocam-
pus is a critical gate-keeper of memory; without it, new information about facts
cannot be stored. If damage to the hippocampus prevents new information from
being stored, then such information is not available for later retrieval (even if the
hippocampus itself recovers). Given that many cases of dissociative amnesia are
characterized by “recovered” memories, it is not clear which brain systems would
be involved.
Psychological Factors: Disconnected Mental Processes
The earliest theory of the origins of dissociative amnesia was dubbed the dissociation
theory ( Janet, 1907). Dissociation theory posits that very strong emotions (which may
occur in response to a traumatic stressor) narrow the focus of attention and also dis-
organize cognitive processes, which prevent them from being integrated normally.
According to this theory, the poorly integrated cognitive processes allow memory
to be dissociated from other aspects of cognitive functioning, leading to dissocia-
tive amnesia. At best, the theory provides only a broad explanation for dissociative
amnesia; it does not outline specific mechanisms to account for the dissociation and
possible later reintegration of memory.
In contrast, neodissociation theory (Hilgard, 1994; Woody & Bowers, 1994)
proposes that an “executive monitoring system” in the brain (specifically, the
228 C H A P T E R 8
f ront a l lobes ) nor m a l ly coord i n ates va r ious cog n it ive s ystem s, much l i ke
a chief executive of ficer coordinates the various departments of a large com-
pany. However, in some circumstances (such as while a person is experiencing
a traumatic event), the various cognitive systems can operate independently of
the executive monitoring system. When this occurs, the executive system no
longer has access to the information stored or processed by the separate cogni-
tive systems. Memor y thus operates as an independent cognitive system, and an
“amnestic barrier” arises between memor y and the executive system. This bar-
rier causes the information in memory to be cut off from conscious awareness—
that is, dissociated. Aspects of both dissociation and neodissociation theor ies
have received some support from research (Green & Lynn, 1995; Hilgard, 1994;
Kirsch & Lynn, 1998).
Social Factors: Indirect Effects
Many traumatic events result from social interactions, such as combat and abuse.
These kinds of social traumas are likely to contribute to dissociative disorders, partic-
ularly dissociative amnesia. In fact, people with a dissociative disorder report child-
hood physical or sexual abuse almost three times more often than do people without
a dissociative disorder (Foote et al., 2006). However, some researchers point out that
traumatic events can also induce anxiety, which can lead people to have dissociative
symptoms. Thus, traumatic events may not directly cause dissociative symptoms such
as amnesia; rather, such events may indirectly lead to such symptoms by triggering
anxiety (Cardeña & Spiegel, 1993; Kihlstrom, 2001).
As noted in Table 8.2, some researchers propose that dissociative amnesia is a
disorder of modern times because there are no written accounts of its occurring
before 1800 in any culture (Pope et al., 2007).
In sum, dissociative amnesia in the absence of physical trauma to the brain is
extremely rare, which makes research on etiology and treatment similarly rare.
Although researchers have proposed theories about why and how dissociative amnesia
arises, these theories address dissociation generally; dissociative amnesia as a disorder
is not well understood. These same deficiencies—a scarcity of research and vague
theories that do not adequately characterize the specific mechanisms—also limit our
understanding of the other dissociative disorders.
Depersonalization-Derealization Disorder
Li ke m a ny other people, you m ay have ex per ienced deper sona l iz at ion or
derealization. This does not mean that you have depersonalization-derealization dis-
order. A persistent feeling of being detached from one’s mental processes, body, or
surroundings is the key symptom of depersonalization-derealization disorder;
people who have this disorder may experience depersonalization only, derealization
only, or they may have both dissociative symptoms.
What Is Depersonalization-Derealization Disorder?
People afflicted with depersonalization-derealization disorder may feel “detached
from my body” or “like a robot,” or their surroundings may feel surreal, but
they do not believe that they are truly detached, that they are actually a robot, or
that their surroundings have actually become surreal. They still recognize real-
ity. (In contrast, people who have a psychotic disorder may feel and believe such
things; see Chapter 12.) In addition, people with depersonalization-derealization
disorder may not react emotionally to events; they may feel that they don’t control
their behavior and are just being swept along by what is happening around them.
These symptoms may lead sufferers to feel that they are “going crazy.” Table 8.3
presents the DSM-5 diagnostic criteria; symptoms meet the criteria for the disorder
Depersonalization-derealization disorder
A dissociative disorder, the primary symptom
of which is a persistent feeling of being
detached from one’s mental processes, body,
or surroundings.
TABLE 8.3 • DSM-5 Diagnostic Criteria
for Depersonalization-Derealization
Disorder
A. The presence of persistent or recurrent
experiences of depersonalization,
derealization, or both;
1. Depersonalization: Experiences of
unreality, detachment, or being an
outside observer with respect to one’s
thoughts, feelings, sensations, body,
or actions (e.g., perceptual alterations,
distorted sense of time, unreal or
absent self, emotional and/or physical
numbing).
2. Derealization: Experiences of
unreality or detachment with respect
to surroundings (e.g., individuals or
objects are experienced as unreal,
dreamlike, foggy, life-less, or visually
distorted).
B. During the depersonalization or
derealization experiences, reality testing
remains intact.
C. The symptoms cause clinically
significant distress or impairment in
social, occupational, or other important
areas of functioning.
D. The disturbance is not attributable to
the physiological effects of a substance
(e.g., a drug of abuse, medication)
or another medical condition (e.g.,
seizures).
E. The disturbance is not better explained
by another mental disorder, such as
schizophrenia, panic disorder, major
depressive disorder, acute stress
disorder, posttraumatic stress disorder,
or another dissociative disorder.
Reprinted with permission from the Diagnostic and
Statistical Manual of Mental Disorders, Fifth Edition,
(Copyright ©2013). American Psychiatric Association. All
Rights Reserved.
Dissociative and Somatic Symptom Disorders 229
TABLE 8.4 • Depersonalization-Derealization Disorder Facts at a Glance
Prevalence
• The prevalence of depersonalization-derealization disorder is unknown but thought to be from extremely low to 2.8% (Sar et al., 2007; Spiegel
et al., 2011).
Comorbidity
• People with depersonalization-derealization disorder may also have symptoms of anxiety (Bremner et al., 1998; Marshall et al., 2000; Segui et al.,
2000). In one sample of 204 people with depersonalization-derealization disorder, almost three quarters had an anxiety disorder at the time or
previously (Baker et al., 2003).
• Major depressive disorder is also a common comorbid disorder.
Onset
• The average age of onset of depersonalization-derealization disorder is 16 years old; it is very rare for it to develop after age 40.
• Episodes can be triggered by a wide range of events, including trauma, extreme stress, depression, panic, and the ingestion of a psychoactive drug
such as marijuana or alcohol (Raimo et al., 1999; Simeon, Knutelska, et al., 2003).
Course
• Episodes of depersonalization or derealization can last from hours to years.
• The course is often persistent, with a third of people with the disorder having discrete episodes, a third with continuous symptoms after onset,
and a third with symptoms initially episodic but eventually becoming continuous.
Gender Differences
• Equal numbers of males and females have this disorder.
Source: Unless otherwise noted, the source is American Psychiatric Association, 2013.
CASE 8.2 • FROM THE OUTSIDE: Depersonalization-Derealization Disorder
[Mr. E] was a 29-year-old, single man, employed as a journalist, who reported a 12-year his-
tory of [depersonalization-derealization] disorder. He described feeling detached from the
world as though he was living “inside a bubble” and found it difficult to concentrate since
he felt as though his brain had been “switched off.” His body no longer felt solid and he
could not feel himself walking on the ground. The world appeared two-dimensional and he
reported his sense of direction and spatial awareness to be impaired. He described himself as
having lost his “sense of himself” and felt that he was acting on “auto-pilot.” He also reported
symptoms of depression and some symptoms of OCD, which took the form of counting and
stepping on cracks in the pavement, although he did not report the latter as a problem.
Prior to the onset of his [depersonalization-derealization disorder], he experienced
transient [depersonalization] symptoms when intoxicated with cannabis. At the age of
17, he started at a new school and felt very anxious and experienced [depersonalization]
symptoms when not under the influence of cannabis. . . . He described the first time this
happened as “terrifying” since he felt he had “gone into another world.” He reported dif-
ficulty with breathing and believed he may have a brain tumor or that his “brain was
traumatized into a state of panic.” From the age of 17 to 19, the episodes of [deperson-
alization] became more frequent until they became constantly present. He reports the
symptoms as “enormously restricting” his life in that he felt frustrated since he has been
“unable to express or enjoy myself.”
(Hunter et al., 2003, Appendix A, pp. 1462–1463)
only when they occur independently of anxiety symptoms and when they impair
functioning or cause signif icant distress. Table 8.4 provides more facts about
depersonalization-derealization disorder, and Case 8.2 shares the story of Mr. E,
who has the disorder.
230 C H A P T E R 8
Understanding Depersonalization-Derealization Disorder
Researchers are beginning to chart the factors that contribute to depersonalization-
derealization disorder—but again, because the disorder is so rare, there are relatively
few studies of it.
Neurological Factors
Studies converge in providing evidence that depersonalization-derealization
disorder arises, at least in part, from disruptions of emotional processing ( Sierra
et al., 2002). For example, when patients with this disorder viewed faces with
high ly emotional expressions, activit y in the limbic system decreased rather
than increased, as it does for most people —and this occur red in response to
both ver y happy and ver y sad expressions (Lemche et al., 2007). This study
also showed that the patients had unusually high levels of activity in the fron-
tal lobes when viewing such facial expressions. This is important because the
frontal lobes can suppress emotional responses, which might produce the sense
of emotional detachment that such patients report. Such an effect might also
explain why brain areas involved in emotion are not activated when patients with
depersonalization-derealization disorder try to remember words that name emo-
tions, whereas these brain areas are activated when normal control participants
perform this task (Medford et al., 2006).
A PET study of patients with depersonalization-derealization disorder found
unusual levels of activation (either too high or too low) in parts of the brain spe-
cifically involved in various phases of perception—the temporal and parietal lobes
(Simeon et al., 2000). The researchers noted that these findings are consistent with
the idea that depersonalization-derealization disorder involves dissociations in
perception.
In addition, patients with depersonalization-derealization disorder do not
produce nor mal amounts of norepinephr ine. In fact, the more strongly they
exhibit symptoms of the disorder, the less norepinephrine they apparently pro-
duce (as measured in their urine; Simeon, Guralnick, et al., 2003). Norepineph-
rine is associated with activity of the autonomic ner vous system, and thus this
finding is consistent with the idea that these patients have blunted responses to
emotion.
Psychological Factors: Cognitive Deficits
Patients with depersonalization-derealization disorder have cognitive deficits that
range from problems with short-term memory to impaired spatial reasoning, but the
root cause of these difficulties appears to lie with attention: These patients cannot
easily focus and sustain their attention (Guralnik et al., 2000, 2007). This is consis-
tent with neuroimaging studies that reveal decreased activity in parts of the brain
involved in perception. However, it is not clear whether the attentional problems
are a cause or an effect of the disorder: On one hand, if a person were feeling dis-
connected from the world, he or she would not pay normal attention to objects and
events; on the other hand, if a person had such attentional problems, this could con-
tribute to feeling disconnected from the world. Moreover, given that many patients
with depersonalization-derealization disorder also have depression or an anxiety
disorder (Baker et al., 2003), it is not clear whether the problems with attention
are specifically related to depersonalization-derealization disorder or arise from the
comorbid disorder.
Social Factors: Childhood Emotional Abuse
We noted earl ier that st ressf u l event s (of ten a resu lt of socia l interact ions)
ca n t r ig ger deper sona l izat ion- derea l izat ion d isorder. Moreover, a speci f ic
Dissociative and Somatic Symptom Disorders 231
t ype of social stressor—severe and chronic emotional abuse experienced dur-
i ng ch i ld hood— seem s to pl ay a pa r t icu l a rly i mpor t a nt role i n t r ig ger i ng
depersonalization-derealization disorder (Simeon et al., 2001), although it is not
clear why such abuse might lead to depersonalization-derealization disorder only
in some cases. Once the disorder develops, the perception of threatening so-
cial interactions and new environments can exacerbate its symptoms (Simeon,
Knuteska, et al., 2003). For instance, if Mr. E in Case 8.2 had a fight with a
friend, his depersonalization symptoms would probably become worse during
the fight.
Feedback Loops in Understanding Depersonalization-Derealization
Disorder
One hypothesis for how depersonalization-derealization disorder ar ises is as
follows: First, a significant stressor (often a social factor) elicits neurological events
(partly in the frontal lobes) that suppress normal emotional responses (Hunter et
al., 2003; Sierra & Berrios, 1998; Simeon, Knutelska, et al., 2003). Following
this, the disconnection between the intensity of the perceived stress and the lack
of arousal may lead these patients to feel “unreal” or that their surroundings are
unreal, which they may then attribute (a psychological factor) to being mentally
ill (Baker, Earle, et al., 2007; Hunter et al., 2003). And, in turn, the incorrect
and catastrophic attributions that the patients make about their symptoms can lead
to further anxiety (as occurs with panic disorder). The attributions can also lead
to further depersonalization or derealization symptoms. Patients then become
extremely sensitive to and hypervigilant for possible symptoms of “unreality” and
come to fear that the symptoms indicate that they are “going crazy.” They may also
avoid situations likely to elicit the symptoms.
Dissociative Identity Disorder
Dissociative identity disorder, once known as multiple personality disorder, may be
the most controversial of all DSM-5 disorders. First we examine what dissociative
identity disorder is, then some criticisms of the DSM-5 diagnostic criteria, and then
factors that may contribute to the disorder. In the process of examining these factors,
we delve into the controversy about the disorder.
What Is Dissociative Identity Disorder?
The central feature of dissociative identity disorder (DID) is the presence of two
or more distinct “personality states” (sometimes referred to as alters) or an experience
of being “possessed,” which leads to a discontinuity in the person’s sense of self and
ability to control his or her functioning. Such a discontinuity can affect any aspect
of functioning, including mood, behavior, consciousness, memor y, perception,
thoughts, and sensory-motor functioning.
In some cases, these persona l it y states have separate character ist ics and
histor y, and they take turns controlling the person’s behavior. For example, a
person with this disorder might have an “adult” personalit y state that is ver y
responsible, thoughtful, and considerate and a “child” personalit y state that is
irresponsible, impulsive, and obnoxious. Each personality state can have its own
name, mannerisms, speaking style, and vocal pitch that distinguish it from oth-
ers. Some personality states report being unaware of the existence of others, and
thus they experience amnesia (because the memory gaps are longer than ordinary
forgetting).
Perhaps the most compelling characteristic of personality states is that, for some
patients, each personality state can have unique medical problems and histories: One
O N L I N E
SP
N
Dissociative identity disorder (DID)
A dissociative disorder characterized by the
presence of two or more distinct personality
states, or an experience of possession trance,
which gives rise to a discontinuity in the
person’s sense of self and agency.
232 C H A P T E R 8
might have allergies, medical conditions, or even EEG patterns that
the others do not have (American Psychiatric Association, 2000).
Stressful events can trigger a switch of personality states, whereby the
one that was dominant at one moment recedes and another becomes
the dominant. Although the number of personality states that have
been reported ranges from 2 to 100, most people diagnosed with
DID have 10 or fewer (American Psychiatric Association, 2000).
In other cases, the personality states may be less obvious and
other personality states only emerge for brief periods of time. Such
patients may report feeling detached from themselves (as if they were
observing themselves), hearing voices (such as children crying), or
having waves of strong emotion—out of the blue—over which they
have no control. Table 8.5 lists the DSM-5 diagnostic criteria for
DID, and Table 8.6 provides further information about the disorder.
People with DID may not be able to remember periods of time
in the past (such as getting married) or skills they learned (such as
how to drive a car or aspects of their job), or they may discover “ev-
idence” of actions they don’t remember performing, such as find-
ing new clothes in their closet or furniture moved. Moreover, they
may find themselves somewhere and not know how they got there
(American Psychiatric Association, 2013).
For some people, a personality state takes the form of “posses-
sion” by a spirit, ghost, or another person who has taken control. In
such cases, patients may act and speak as if they were the entity who
has “taken over,” such as the spirit of someone in the community
who died. (However, when possession is part of a spiritual practice,
these symptoms would be considered normal, and a diagnosis of DID
would not be made.) To qualify for a diagnosis of DID, the addi-
tional personality states must impair functioning or be significantly
distressing; in fact, 70% of people with this disorder attempt suicide
(American Psychiatric Association, 2013). Case 8.3 presents the per-
sonality states of someone with DID, which was previously called
multiple personality disorder (MPD).
TABLE 8.6 • Dissociative Identity Disorder Facts
at a Glance
Prevalence
• The prevalence rate for DID is difficult to determine, although
several surveys estimate it to be about 1% (Johnson, Cohen, et
al., 2006a; Loewenstein, 1994). However, some researchers view
this figure as a significant overestimate (Rifkin et al., 1998).
Comorbidity
• People with DID may also be diagnosed with a mood disor-
der, an anxiety disorder, a substance-related disorder, PTSD,
or a personality disorder (to be discussed in Chapter 13). DID
may be difficult to distinguish from schizophrenia or bipolar
disorder.
Onset
• It can take years to make the diagnosis of DID from the time
that symptoms first emerge. Because of this long lag time and
the rarity of the disorder, there is no accurate information
about the usual age of onset.
Course
• DID is usually chronic.
Gender Differences
• This disorder is equally prevalent in males and females.
Cultural Differences
• DID is observed only in some Western cultures and was extreme-
ly uncommon before the 1976 television movie Sybil, which was
about a “true case” of what was then called multiple personality
disorder (Kihlstrom, 2001; Lilienfeld et al., 1999).
Source: Unless otherwise noted, the source is American Psychiatric Association, 2013.
TABLE 8.5 • DSM-5 Diagnostic Criteria for Dissociative Identity Disorder
A. Disruption of identity characterized by two or more distinct personality states, which may be
described in some cultures as an experience of possession. The disruption in identity involves
marked discontinuity in sense of self and sense of agency, accompanied by related alterations
in affect, behavior, consciousness, memory, perception, cognition, and/or sensory-motor
functioning. These signs and symptoms may be observed by others or reported by the individual.
B. Recurrent gaps in the recall of everyday events, important personal information, and/or
traumatic events that are inconsistent with ordinary forgetting.
C. The symptoms cause clinically significant distress or impairment in social, occupational, or
other important areas of functioning.
D. The disturbance is not a normal part of a broadly accepted cultural or religious practice.
Note: In children, the symptoms are not better explained by imaginary playmates or other
fantasy play.
E. The symptoms are not attributable to the physiological effects of a substance (e.g.,
blackouts or chaotic behavior during alcohol intoxication) or another medical condition
(e.g., complex partial seizures).
Reprinted with permission from the Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition, (Copyright
©2013). American Psychiatric Association. All Rights Reserved.
Dissociative and Somatic Symptom Disorders 233
CASE 8.3 • FROM TH E INSIDE: Dissociative Identity Disorder
In Robert B. Oxnam’s memoir, A Fractured Mind, his various personality states (11 in all)
tell their stories. The following excerpts present recollections from 2 of the alters, beginning
with Robert:
This is Robert speaking. Today, I’m the only personality who is strongly visible inside and
outside. . . . Fifteen years ago, I rarely appeared on the outside, though I had considerable
influence on the inside; back then, I was what one might call a “recessive personality.”
Although [Bob, another alter] was the dominant MPD personality for thirty years, [he]
did not have a clue that he was afflicted by multiple personality disorder until 1990, the
very last year of his dominance. That was the fateful moment when Bob first heard that
he had an “angry boy named Tommy” inside of him.
(Oxnam, 2005, p. 11)
Another alter, Bob, recounts:
There were blank spots in my memory where I could not recall anything that happened
for blocks of time. Sometimes when a luncheon appointment was canceled, I would go
out at noon and come back at 3 P.M. with no knowledge of where I had been or what I had
done. I returned tired, a bit sweaty, but I quickly showered and got back to work. Once, on a
trip to Taiwan, a whole series of meetings was canceled because of a national holiday; I had
zero memory of what I did for almost three days, but I do recall that, after the blank spot
disappeared, I had a severe headache and what seemed to be cigarette burns on my arm.
(Oxnam, 2005, p. 31).
Criticisms of the DSM-5 Criteria
Significant problems plague the DSM-5 diagnostic criteria for DID, including the
following (Piper & Merskey, 2004b):
• DSM-5 does not define the separate “personality states”; accordingly, a normal
emotional state that emerges episodically—such as periodic angry outbursts—
could be considered a “personality state” that is different than the person’s “usual”
state. Thus, the criteria permit possibility that normal emotional fluctuations could
be considered pathological.
• DID—which is easy to role-play—can be difficult to distinguish from malingering
(Labott & Wallach, 2002; Stafford & Lynn, 2002). When people can easily fake symp-
toms of a disorder, the validity of the disorder as a diagnostic entity can be questioned.
• DID can be difficult to distinguish from rapid-cycling bipolar disorder because
both involve sudden changes in mood and demeanor. However, appropriate treat-
ments for bipolar disorder differ from those for DID, which is why accurate diag-
nosis is important (Piper & Merskey, 2004b).
Some of Anna O.’s dissociative experiences seem similar to those of patients with
DID, such as her “naughty” states (for which she had amnesia) and her feeling that
she had two selves, a real one and an evil one, which would “take control.”
Understanding Dissociative Identity Disorder
Research findings on various factors associated with DID can be at odds with each
other, which only fuels the controversy over the validity of the diagnosis itself. As we
shall see, much of the research on, and theorizing about, factors that may contribute
to DID hinge on the fact that many people with this disorder report having been
severely and chronically abused as children (Lewis et al., 1997; Ross et al., 1991).
Neurological Factors: Alters in the Brain?
One hallmark of DID is that memories acquired by one personality state are not
directly accessible to others. However, studies suggest that although alters may re-
port the subjective experience of amnesia, they do, in fact, have access to memories
of other alters (Huntjens et al., 2005, 2006, 2007; Kong et al., 2008). Consistent
with these findings, researchers have used changes in electrical activity on the scalp
Simply being sensitive to context or
responding differently when in different
emotional states does not mean that you have
“personality states.” For example, one study
found that people who are bilingual responded
differently to a personality test, depending
on which language was used for the test
(Ramírez-Esparza et al., 2006). Can you think
of reasons for this result that do not involve
personality states?
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234 C H A P T E R 8
to show that the brain responds as if the patient with DID recognizes previously
learned words, even when the learning took place when one alter was dominant
and the testing occurred when another alter was dominant (Allen & Movius, 2000).
Perhaps the key characteristic of DID is that each alter has a different “sense of
self.” To the person with DID, it feels as if different personalities “take over” in turn.
To explore the neural bases of this phenomenon, Reinders and colleagues (2003)
asked 11 DID patients to listen to stories about their personal traumatic history while
their brains were scanned using PET. Each patient was scanned once when an alter
who was aware of the past trauma was dominant and once when an alter who was not
aware of the past trauma was dominant. Two results are of particular interest: First,
and most basic, the brain responded differently for the two alters. This alone is evi-
dence that something was neurologically different when the person was in the two
states. Second, the traumatic history activated brain areas known to be activated by
autobiographical information—but only when the alter that was aware of that infor-
mation was dominant during the PET scanning.
However, it is difficult to interpret the results of many studies that investigate
neurological differences among alters because the studies do not include an appropri-
ate control group (Merckelbach et al., 2002). Researchers have found that hypnosis
can alter brain activity (Kosslyn et al., 2000), so it is possible that at least
some of the neurological differences between alters reflect a form of self-
hypnosis. That is, the person with DID—perhaps unconsciously—hypno-
tizes himself or herself, which produces different neurological states when
different alters come to the fore.
Researchers have also investigated what role genetics might play in
DID. Using a questionnaire, a team of researchers assessed the capacity for
dissociative experiences in monozygotic and dizygotic twins in the general
population ( Jang et al., 1998). This questionnaire did not address DID di-
rectly, but it did assess the capacity for both “normal” dissociations (such
as becoming very absorbed in a television show or a movie) and “abnor-
mal” dissociations (such as not recognizing your face in a mirror). These
researchers found that almost half the variation in abnormal dissociations
could be attributed to genes.
Psychological Factors
The primary psychological factor associated with DID is hypnotizabil-
ity: Patients with this diagnosis are highly hypnotizable and can easily
dissociate (Bliss, 1984; Frischholz et al., 1990, 1992). That is, they can
spontaneously enter a trance state and frequently experience symptoms of
dissociation, such as depersonalization or derealization. These abilities play
a critical role in a psychologically based theory of DID, described in the
upcoming section on feedback loops.
Social Factors: A Cultural Disorder?
Social factors have apparently affected the frequency of diagnosis of DID.
DID was rarely diagnosed until 1976 (Kihlstrom, 2001; Lilienfeld et
al., 1999; Spanos, 1994). What happened in 1976? The television movie Sybil was
aired and received widespread attention. This movie portrayed the “true story” of a
woman with DID. The movie apparently affected either patients (who became able
to express their distress in this popularized way) or therapists (who became more
willing to make the diagnosis) or both. However, years later, it was revealed that the
patient who was known as Sybil did not have alters but rather had been encouraged
by her therapist to “name” her different feelings as if they were alters; thus, what
Sybil’s therapist wrote about the alters was not based on Sybil’s actual experiences
(Borch-Jacobsen, 1997; Rieber, 1999).
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Some researchers attribute the increased
prevalence of DID since 1976 to the movie
Sybil, which claimed to portray the “true
story” of a woman with DID. In a scene near
the end of the movie, Sybil (played by Sally
Field, lying down) and her psychiatrist (Joanne
Woodward) work to “integrate” the different
alters. In fact, it was later revealed that the
real-life “Sybil” had been explicitly encouraged
to give names to different aspects of her
personality but did not actually dissociate, as
her psychiatrist had claimed she did.
Dissociative and Somatic Symptom Disorders 235
Consistent with the view that DID is a disorder induced by social factors present
in some cultures, many countries, such as India and China, have an extremely low or
zero prevalence rate of DID (Adityanjee et al., 1989; Draijer & Friedl, 1999; Xiao et
al., 2006). In other countries, such as Uganda, people with DID symptoms are con-
sidered to be experiencing the culturally sanctioned possession trance, not suffering
from DID (van Dujil et al., 2005).
Feedback Loops in Understanding Dissociative Identity Disorder:
Two Models for the Emergence of Alters
Two models of dissociative identit y disorder—the posttraumatic model and
the sociocognitive model—are based on the existence of feedback loops among
neurological, psychological, and social factors. However, the two models emphasize
the roles of different factors and have different accounts of how the factors influence
each other.
The Posttraumatic Model In addition to dissociating or entering hypnotic trances
easily, most DID patients have at least one alter that reports having suffered severe,
often recurring, physical abuse when young (which would imply a stress response;
neurological factor) (Lewis et al., 1997; Ross et al., 1991). This trauma, induced by
others (social factor), may increase the ease of dissociating (psychological factor).
In fact, children who experienced severe physical abuse later report that during the
traumatic events, their minds temporarily left their bodies (which presumably was
a way of coping); that is, they dissociated. Putting these observations together, the
posttraumatic model proposes that after frequent episodes of abuse with accompany-
ing dissociation, the child’s dissociated state can develop its own memories, iden-
tity, and way of interacting with the world, thereby becoming an “alter” (Bremner,
2010; Gleaves, 1996; Putnam, 1989).
Several studies support some aspects of the posttraumatic model. As would be
expected from this model, some people with DID do have documented histories of
severe physical abuse in childhood (Lewis et al., 1997; Putnam, 1989; Swica et al.,
1996) and also report having displayed signs of dissociation in childhood (Lewis
et al., 1997). Moreover, these patients report that they either don’t remember being
abused or remember very little of it (Lewis et al., 1997; Swica et al., 1996). In addi-
tion, girls who were easy to hypnotize and able to dissociate readily were found to be
the ones most likely to have been abused physically or sexually (Putnam et al., 1995).
In addition, research on sleep and dissociation may shed light on how DID
emerges (Lynn et al., 2012). Specifically, when healthy volunteers are deprived of
sleep, they are more likely to experience dissociative symptoms (Giesbrecht et al.,
2007). And when patients with dissociative symptoms receive treatment to help
improve their sleep, their dissociative symptoms diminish (van der Kloet, Giesbrecht,
et al., 2012). When someone’s sleep cycle is altered—perhaps because of a traumatic
experience—he or she may become more likely to dissociate or experience vivid
dreams when falling asleep or waking up (van der Kloet, Giesbrecht, et al., 2012; van
der Kloet, Merckelbach, et al., 2012). In turn, continued sleep deprivation leads to
cognitive deficits, such as difficulties with memory and attention, which are aspects
of symptoms of DID.
However, if the posttraumatic model is correct, there should be a significant
number of cases of childhood DID. In fact, very few such cases have been documented
(Giesbrecht et al., 2008, 2010; Boysen, 2011), and most studies of abused children
have found only a great ability to dissociate, not the presence of alters (Piper & Merskey,
2004a). Moreover, most studies of adults with DID who experienced childhood
abuse have not obtained independent corroborating evidence of abuse or trauma but
rather rely solely on the patient’s—or an alter’s—report of abuse during childhood
(Piper & Merskey, 2004a, 2004b).
O N L I N E
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236 C H A P T E R 8
The Sociocognitive Model In contrast to the posttraumatic
model of DID, the sociocognitive model proposes that social
interactions between therapist and patient (social factor) foster
DID by influencing the beliefs and expectations of the patient
(psychological factor). According to the sociocognitive model,
the therapist unintentionally causes the patient to act in ways
that are consistent with the symptoms of DID (Lilienfeld et al.,
1999; Lynn et al., 2012; Sarbin, 1995; Spanos, 1994). This
explanation is plausible in part because hypnosis was commonly
used to bring forth alters, and researchers have pointed out that
suggestible patients can unconsciously develop alters (and ensu-
ing neurological changes) in response to the therapist’s prompt-
ings (Spanos, 1994). For instance, a therapist may encourage
a patient to develop alters by asking leading questions (“Have
people come up to you who seem to know you, but they are
strangers to you?”) and then showing special interest when the patient answers “yes”
to any such question. One finding that supports the sociocognitive model is that
many people who have been diagnosed with DID had no notion of the existence of
any alters before they entered therapy (Lilienfeld et al., 1999). In fact, in reviewing
published studies on DID, no documented cases of DID occurring outside of therapy
could be found (Boysen & VanBergen, 2013). In addition, cultural cues regarding
DID (such as in portrayals in movies and memoirs or interviews of people with the
disorder) may influence a patient’s behavior.
The Debate About Dissociative Identity Disorder
The phenomenon of people presenting in treatment with different personality states
exists. The issue debated is how it arises and continues in a given patient. Propo-
nents of the sociocognitive model recognize that childhood trauma—at least in some
cases—can indirectly be associated with DID: Childhood trauma may lead people to
become more suggestible or more able to fantasize, which can magnify the effects on
their behavior of social interactions with a therapist (Lilienfeld et al., 1999; Lynn et
al., 2012). In other words, dissociation and DID symptoms may be indirect results of
childhood trauma rather than direct posttraumatic results.
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Dissociative identity disorder is described or
portrayed in various memoirs and films, such
as the popular 1999 film Fight Club. According
to the sociocognitive model of this disorder,
such media portrayals can help create
expectations in both patients and therapists
about how people with the disorder behave.
Therapists, in turn, unintentionally reinforce
patients for behaving in ways consistent with
such portrayals.
Which of these photos best captures the explanation for DID proposed by the sociocognitive model? Answer: The photo on the right,
in which the therapist’s actions (such as using hypnosis to bring forth alters) inadvertently lead the patient to behave in ways that are
consistent with DID.
GETTING THE PICTURE
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Dissociative and Somatic Symptom Disorders 237
Proponents of the sociocognitive model also point out that cultural influences,
such as the airing of the movie Sybil, may have led therapists to ask leading questions
regarding DID—and may have led highly suggestible patients to follow these leads
unconsciously; such influences would account for the great variability in the number
of cases over time. Proponents of the posttraumatic model counter that the increased
prevalence of DID after 1976 simply reflects improved procedures for assessment
and diagnosis.
In sum, we do know that severe trauma can lead to dissociative disorders and
can have other adverse effects (Putnam, 1989; Putnam et al., 1995). However, we
do not know whether all of the people who are diagnosed with DID have actually
experienced traumatic events, nor even how severe an event must be in order to be
considered “traumatic.” Similarly, experiencing a traumatic event does not specifically
cause DID (Kihlstrom, 2005); some people respond by developing depression or an
anxiety disorder. Further, as noted in Chapter 7, many people who experience a
traumatic event do not develop any psychological disorder.
Treating Dissociative Disorders
In general, dissociative amnesia improves spontaneously, without treatment.
However, clinicians who encounter people with other dissociative disorders have
used some of the treatments discussed below. Because dissociative disorders are
so rare, few systematic studies of treatments have been conducted—and none
have attempted to determine which treatments are most effective for a particu-
lar dissociative disorder. Thus, we consider treatments for dissociative disorders in
general.
Targeting Neurological Factors: Medication
In general, medication is not used to treat the symptoms of dissociative disorders
because research suggests that it is not helpful for dissociative symptoms (Sierra et al.,
2003; Simeon et al., 1998). However, people with dissociative disorders may receive
medication for a comorbid disorder or for anxiety or mood symptoms that arise in
response to the dissociative symptoms.
Targeting Psychological and Social Factors:
Coping and Integration
Treatments that target the psychological factors underlying dissociative disor-
ders focus on three elements: (1) reinterpreting the symptoms so that they don’t
create stress or lead the patient to avoid certain situations; (2) learning additional
coping strategies to manage stress (Hunter et al., 2005); and (3) for DID patients,
addressing the presence of alters and dissociated aspects of their memories or
identities. The first two foci are similar to aspects of treatment for PTSD (Kluft,
1999; see Chapter 7).
When addressing the presence of alters in patients with DID, the t ype of
treatment a clinician employs depends on which theory he or she accepts and thus
uses to guide treatment. Proponents of the posttraumatic model advise clinicians
to identify in detail (or to “map”) each alter’s personality, recover memories of
possible abuse, and then help the patient to integrate the different alters (Chu & In-
ternational Society for the Study of Dissociation, 2005). In contrast, proponents of
the sociocognitive model advise against mapping alters or trying to recover possible
memories of abuse (Gee et al., 2003). Instead, they recommend that the therapist
use learning principles to extinguish patients’ mention of alters: Alters are to be
ignored, and the therapist doesn’t discuss multiple identities. Alters are interpreted
238 C H A P T E R 8
as creations inspired by the patient’s desire for attention, and treatment
focuses on current problems rather than on past traumas (Fahy et al.,
1989; McHugh, 1993).
In addition, hypnosis has sometimes been used as part of treatment,
particularly by therapists who treat DID according to the posttrau-
matic model; in this case, hypnosis might be used to help the patient
learn about his or her different alters and integrate them into a single,
functional whole (Boyd, 1997; Kluft, 1999). Using hypnosis is, by its
ver y nature, a social event: The therapist helps the patient achieve a
hypnotic state through suggestions and bears witness to whatever the
patient shares about the dissociated experience. However, using hyp-
nosis to treat DID is controversial because the patient will be more
suggestible when in a hypnotic trance, and the therapist may inadver-
tently make statements that the patient interprets as suggestions to produce more
DID symptoms.
Treatment may also focus on reducing the traumatic stress that can induce
dissociative disorders. For instance, soldiers who experience dissociation dur-
ing combat may be removed from the battlef ield, which can then reduce the
dissociation.
Feedback Loops in Treating Dissociative Disorders
When Breuer was treating Anna O., he relied on the “talking cure”—having her
talk about relevant material, at first while in a hypnotic trance and later while not
in a trance. This use of hypnosis continues today and is often part of a treatment
program for people with dissociative disorders (Butler et al., 1996), including dis-
sociative amnesia and DID (Putnam & Loewenstein, 1993). Here we examine hyp-
notic treatment for DID as it has been used from the perspective of the posttraumatic
model, and we see how it leads to feedback loops among neurological, psychological,
and social factors.
Researchers have investigated the neurological changes that occur as a result
of hypnosis and established that hypnosis alters brain events (Crawford et al., 1993;
Kosslyn et al., 2000; Spiegel et al., 1985). The specific brain changes vary, however,
depending on the task being performed during the hypnotic trance. When hypno-
tized, patients may be able to retrieve information that was previously dissociated; in
turn, this may allow them to experience perceptions and memories in a more normal
way (psychological factor).
In addition, hypnosis can be induced only when patients are willing to be
hypnotized, and the beneficial effects of hypnosis occur when patients go along with
the therapist’s hypnotic suggestions (social factor). In turn, the hypnotic state brings
about changes in brain activity (neurological factor), which ultimately might play a
role in integrating the stored information that was previously dissociated.
The leading story of the evening news was that a 17-year-old young man murdered his
stepfather. The boy said that his stepfather brutally abused him as a child, and local medi-
cal and emergency room records indicate numerous “accidents” that were consistent with
such abuse. The young man also said that he has no memory of killing his stepfather; his
defense attorney and several psychiatrists claim that he has DID and that an alter killed the
stepfather. Based on what you have read in this chapter, how might this young man have
developed this disorder? (Mention neurological, psychological, and social factors and possible
feedback loops.) What would be appropriate treatments for him, and why? Do think it is fair
to punish a patient with DID for what an alter did? Why or why not?
Thinking Like A Clinician
SP
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When using hypnosis to treat dissociative
symptoms, the therapist may make suggestions
such as “You will feel yourself becoming
relaxed . . . you will notice yourself going into a
state of trance . . . you will find yourself about
to remember whatever was pushed aside.” One
goal is to help (re)integrate whatever has been
dissociated, such as specific memories.
Dissociative and Somatic Symptom Disorders 239
Somatic Symptom Disorders
Dur ing the course of her il lness, Anna O. developed medical symptoms that
her doctors could not explain. For instance, she saw an eye doctor for prob-
lems with her vision, but he was unable to identify the cause (Breuer & Freud,
1895/1955). Similarly, doctors were unable to find a medical explanation for her
chronic cough. How might persistent medically unexplained physical symptoms
such as these arise? How should they best be treated? Such bodily symptoms (also
called somatic symptoms) may fall under the category of somatic symptom disorders
in DSM-5.
Somatic Symptom Disorders: An Overview
The hallmark of somatic symptom disorders is complaints about physical well-
being along with cognitive distortions about bodily symptoms and their meaning; the
focus on these bodily symptoms causes significant distress or impaired functioning.
With these disorders, it is the person’s response to bodily symptoms that is notable
and excessive. Common bodily complaints of patients with somatic symptom disor-
ders are listed in Table 8.7.
Somatic symptom disorders are relatively rare in the general population but are
the most common type of psychological disorder in medical settings (Bass et al.,
2001). The medical costs of caring for patients with somatic symptom disorders are
substantial; according to one estimate, these costs come to over $250 billion each
year in the United States alone (Barsky et al., 2005).
Somatic symptom disorders are not new phenomena; they have a long history,
although different labels have been given to them over time. They were described by
the ancient Greek philosopher Hippocrates, who thought that somatic symptoms—
generally reported by women—were caused by a wandering uterus, from which the
term hysteria is derived (hystera is Greek for “uterus”; Phillips, 2001). Hysteria was
often used to refer to bodily symptoms that lack a medical explanation, as was true
of Anna O.; in addition, patients with hysteria typically describe their symptoms
dramatically.
One somatic symptom disorder that must be distinguished from the others is
factitious disorder, mentioned in Chapter 3, in which people intentionally induce
symptoms or falsely report symptoms that they do not in fact have in order to receive
attention from others. People who have any of the other somatic symptom disorders
neither pretend to have symptoms nor intentionally induce physical symptoms for
any type of gain. (However, in DSM-5, factitious disorder is considered a somatic
symptom disorder because bodily symptoms may be among those feigned.)
Putting aside factitious disorder, somatic symptom disorders share two common
features (Looper & Kirmayer, 2002):
1. bodily preoccupation, which is similar to the heightened awareness of panic-related
bodily sensations experienced by people with panic disorder (see Chapter 6),
except that with somatic symptom disorders, the patient can be preoccupied
with any aspect of bodily functioning; and
2. symptom amplification, or directing attention to bodily symptoms such as those in
Table 8.7, which in turn intensifies the symptoms (Kirmayer & Looper, 2006;
Looper & Kirmayer, 2002). A common example of symptom amplif ication
occurs when someone with a headache pays attention to the headache—and,
invariably, the pain worsens.
In the following sections, we focus on three of these disorders in turn—somatic
symptom disorder, conversion disorder, and illness anxiety disorder.
Symptoms of somatic symptom disorders have
existed for millennia and were written about in
the Papyrus Ebers, an ancient Egyptian medical
document dating to 1600 B.C.E. However, the
Egyptians believed that these symptoms had
an underlying medical cause.
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Somatic symptom disorders
A category of psychological disorders
characterized by symptoms about physical
well-being along with cognitive distortions
about bodily symptoms and their meaning;
the focus on these bodily symptoms causes
significant distress or impaired functioning.
TABLE 8.7 • Common Bodily
Complaints of Patients with Somatic
Symptom Disorders
• Muscle and joint pain
• Palpitations
• Lower back pain
• Irritable bowel
• Tension headache
• Dizziness
• Atypical facial pain
• Insomnia
• Chronic fatigue
• Non-ulcer dyspepsia (indigestion)
• Non-cardiac chest pain
Source: Mayou & Farmer, 2002. For more information see
the Permissions section.
240 C H A P T E R 8
Somatic Symptom Disorder
The hallmark of somatic symptom disorder (SSD) is at least one somatic symp-
tom that is distressing or disrupts daily life, about which the person has excessive
thoughts, feelings, or behaviors (American Psychiatric Association, 2013). For ex-
ample, Anna O.’s eye problems and her cough were both physical symptoms that dis-
rupted her daily life. Because the name of the disorder and this category of disorders
are so similar (the former is singular and the latter plural), we will abbreviate the
disorder as SSD.
What Is Somatic Symptom Disorder?
To be diagnosed with SSD according to DSM-5 criteria, the
person must have at least one distressing or impairing bodily
symptom and respond excessively to it. Examples of an ex-
cessive response are unrealistic thoughts about the seriousness
of the symptoms, significant anxiety about the symptoms or
health in general, or devoting excessive amount of time and
energy to it—such as seeing multiple doctors when such visits
aren’t necessary. For instance, a man who had a heart attack
might become preoccupied with his heart rate and be afraid to
go up and down stairs, lest he increase his heart rate and have
another heart attack— despite his doctor’s assuring him that
walking on stairs would be okay. Sometimes the single bodily
symptom is pain (American Psychiatric Association, 2013).
Table 8.8 lists the DSM-5 diagnostic criteria for SSD.
A clinician diagnoses SSD only if the person’s response to
the symptoms is more extreme than what would be expected
based on the medical assessment. SSD must be distinguished
from various other disorders, including anxiety disorders. Many laboratory tests and
visits to doctors may be required to rule out other medical and psychological diag-
noses, which is necessary before a diagnosis of SSD can be made (Hilty et al., 2001).
Table 8.9 lists additional facts about SSD.
People with SSD may avoid certain activities that they believe are associated with
their bodily symptoms, such as any type of exercise. In so doing, patients attempt to
minimize the physical sensations associated with the disorder. As a result, they may
become so out of shape that even normal daily activities, such as walking to a store
from the parking lot, may lead them to experience bodily symptoms—which creates
a vicious cycle of avoidance and increased bodily symptoms, impairing daily life.
For people with SSD, these symptoms impair daily life, which is what happened to
Edward in Case 8.4.
CASE 8.4 • FROM TH E OUTSIDE: Somatic Symptom Disorder
As an infant, Edward had scarlet fever and a mild form of epilepsy, from which he
recovered. By school age, he was complaining of stomachaches and joint pain and often
missed school. There were many doctors, but no dire diagnosis: Edward was healthy, but
many commented, a somewhat lonely and serious little boy.
Through high school and college Edward capitalized on those traits, achieving high
grades and going into the insurance business. At forty-five, he is plagued by mysterious
symptoms—heart palpitations, dizziness, indigestion, pain in his shoulders, back, and
neck, and fatigue—and lives with his parents. His physical disabilities have made it
impossible for Edward to hold a job, and his engagement was broken off. He remains on
disability and spends much of his time in and out of hospitals undergoing various tests
and procedures.
(Cantor, 1996, p. 54)
Somatic symptom disorder (SSD)
A somatic symptom disorder characterized
by at least one somatic symptom that is
distressing or disrupts daily life, about which
the person has excessive thoughts, feelings, or
behaviors.
TABLE 8.8 • DSM-5 Diagnostic Criteria for Somatic Symptom
Disorder
A. One or more somatic symptoms that are distressing or result in
significant disruption of daily life.
B. Excessive thoughts, feelings, or behaviors related to the somatic
symptoms or associated health concerns as manifested by at least
one of the following:
1. Disproportionate and persistent thoughts about the seriousness of
one’s symptoms.
2. Persistently high level of anxiety about health or symptoms.
3. Excessive time and energy devoted to these symptoms or health
concerns.
C. Although any one somatic symptom may not be continuously present, the
state of being symptomatic is persistent (typically more than 6 months).
Reprinted with permission from the Diagnostic and Statistical Manual of Mental Disorders, Fifth
Edition, (Copyright ©2013). American Psychiatric Association. All Rights Reserved.
Dissociative and Somatic Symptom Disorders 241
TABLE 8.9 • Somatic Symptom Disorder Facts at a Glance
Prevalence
• About 5–7% of the general population is estimated to have somatic symptom disorder (SSD).
• SSD is a serious problem in medical settings; patients with this disorder use at least three
times as many outpatient medical services and cost at least nine times more to treat than
people who do not have this disorder (Hollifield et al., 1999).
Comorbidity
• People with SSD often have other psychological disorders, most frequently an anxiety
disorder (particularly panic disorder) or depression.
• Patients with SSD who take benzodiazepines or narcotics for relief of bodily symptoms are at
increased risk for developing a substance-related disorder (Holder-Perkins & Wise, 2001).
Onset
• Initial symptoms of SSD can emerge any time between childhood and old age.
Course
• Symptoms may fluctuate in location or in intensity (so that the criteria for SSD are no longer
met), but symptoms usually never completely disappear.
• Patients with SSD often take many medications and receive numerous medical tests and diagnoses
(Holder-Perkins & Wise, 2001), and they can be extremely sensitive to medication side effects.
Gender Differences
• Women are more likely to have this disorder, or at least are more likely to report bodily
symptoms than are men.
Cultural Differences
• The specific symptoms of patients with SSD vary across cultures, and some ethnic groups
have a higher prevalence of this disorder than others.
Source: Unless otherwise noted, the source is American Psychiatric Association, 2013.
In an effort to minimize their bodily
symptoms, people with somatic symptom
disorder may restrict their activities. If this
model were suffering from somatic symptom
disorder, his inactivity could create additional
symptoms (such as back pain) or make
existing symptoms worse (such as increased
heart rate or difficulty breathing).
th
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to
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p
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m Understanding Somatic Symptom Disorder
SSD can be fully understood only by considering multiple
factors, including genetics, bodily preoccupation, symptom
amplification and catastrophic thinking, and other people’s
responses to illness.
Neurological Factors: Genetics
Most of the progress in understanding the neurological
factors that underlie SSD has been in the area of genetics.
For example, in a large-scale twin study, researchers found
that genetic effects may account for as much as half of the
variability in SSD (Kendler, Walters, et al., 1995). Note,
however, that this finding does not imply that the disor-
der itself is necessarily inherited; it could be that tempera-
ment or other characteristics that are influenced by genetics
predispose a person to develop the disorder in certain en-
vironments. (This same point can be made about most findings that link genes to
disorders.) Kendler and colleagues (1995) also reported that characteristics of families
have no consistent effect on whether members of the family develop this disorder.
This finding suggests that, in addition to genes, specific experiences of a particular
person—not shared experiences among members of a family—affect whether a per-
son develops the disorder.
242 C H A P T E R 8
Psychological Factors: Misinterpretation of Bodily Signals and Coping
Like all other somatic symptom disorders, SSD involves bodily preoccupation and
symptom amplification, as well as catastrophic thinking—in this case, about physical
sensations or fears of illness. These patients may believe, for example, that headaches
indicate a brain tumor. Their mental processes—particularly attention—focus on bodily
sensations, including the beating of their hearts (Barsky, Cleary, et al., 1993, 1994), lead-
ing to symptom amplification and catastrophic thinking. These effects also arise in part
from faulty beliefs about their bodies and bodily sensations. For example, people with
SSD may erroneously believe that health is the absence of any uncomfortable physical
sensations (Rief & Nanke, 1999). People who do not have a somatic symptom disorder
do not habitually develop catastrophic misinterpretations of such sensations.
Somatic symptoms can also serve as a coping strategy, leading the person to fo-
cus attention away from a stressor and onto a bodily sensation. This observation can
help to explain why somatic symptom disorders, including SSD, sometimes develop
after the death of a loved one (as happened to Anna O. after her father died) or after
another significant stressor (Hiller et al., 2002).
Social Factors: Observational Learning and Culture
Observational learning may also play a role in SSD. Such learning can explain the
finding that people with SSD are more likely than those without the disorder to have
had an ill parent (Bass & Murphy, 1995; Craig et al., 1993).
In these cases, an ill parent may have inadvertently mod-
eled illness behavior. Moreover, operant conditioning can
also be at work, when people reinforce a person’s illness
behavior: During the patient’s childhood, family members
may have unintentionally reinforced illness behavior by
paying extra attention to the child or buying special treats
for the child when he or she was ill (Craig et al., 2004;
Holder-Perkins & Wise, 2001). Similarly, adults with SSD
may be reinforced for their symptoms by the attention of
medical personnel, family, friends, or coworkers (Maldo-
nado & Spiegel, 2001).
In addition, in many cultures—including in the United
States— somatic symptoms may be regarded as an accept-
able way to express helplessness, such as by those who ex-
perienced abuse during childhood (Walling et al., 1994).
The use of somatic symptoms to express helplessness may
explain the bodily symptoms of Anna O. and other upper-middle-class women of
the Victorian era, whose lives were severely restricted by societal conventions. How-
ever, although symptoms of SSD occur around the globe, the nature of the symptoms
differs across cultures. For instance, symptoms of burning hands or feet are more
common in Africa and South Asia than in Europe or North America (American Psy-
chiatric Association, 2000).
Feedback Loops in Understanding Somatic Symptom Disorder
It is common for people with SSD to have had a disease, an illness, an accident, or
another form of trauma prior to developing the disorder. In fact, people with this
disorder are more likely to report a history of childhood abuse than are other medical
patients (Brown et al., 2005). People who are genetically predisposed to SSD (neu-
rological factor), interpret the bodily sensations caused by an illness or accident as
signaling a catastrophic illness (psychological factor). In turn, this misinterpretation
may cause the person to change his or her behavior in a way that ultimately becomes
dysfunctional, restricting activities and straining relationships.
Such misinterpretations may initially grow out of modeling. For example, children
whose parents have chronic pain are more likely to report abdominal pain themselves
SP
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Children whose parents have chronic pain may
be more likely to report pain themselves.
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Dissociative and Somatic Symptom Disorders 243
NeuroPsychoSocialNeuroPsychoSocial
Affect
Anxiety
Distress
Mental Processes and
Mental Contents
Bodily preoccupation
Symptom amplification
Catastrophic thinking
about illness
Behavior
Avoidance of
behaviors that
increase bodily
sensations
associated
with symptoms
NeuroPsychoSocial
Genetics
Genetic vulnerability
Brain Systems
No known major
contribution
Neural Communication
No known major
contribution
Family
Gender/Culture
Stressful Life Events
History of significant
social stressor Modeling and
reinforcement
of illness
behavior
Symptoms can be a
cultural expression of
helplessness;
members of some
ethnic and SES groups
are more likely to
develop this disorder
FI G U RE 8.1 • Feedback Loops
in Understanding Somatic
Symptom Disorder
Conversion disorder
A somatic symptom disorder that involves
sensory or motor symptoms that are
incompatible with known neurological and
medical conditions.
and to use more pain relievers than a comparison group of children ( Jamison &
Walker, 1992). These children’s experiences with their ill parent (social factor) may in-
fluence their body via their brains (perhaps they have more stomach acid because they
are more anxious and stressed; neurological factor), their attention to and attributions
for bodily sensations (psychological factors), and their reporting of pain (social factor).
Moreover, a patient’s symptoms may have been unintentionally reinforced by
friends and family members (social factor). And, as with panic disorder (see Chap-
ter 6), the arousal that occurs in response to stress can increase troubling bodily
sensations that then become the focus of preoccupations (see Figure 8.1).
Conversion Disorder
Conversion disorder involves sensory or motor symptoms that are incompatible or
inconsistent with known neurological or medical conditions.
244 C H A P T E R 8
What Is Conversion Disorder?
Patients who have conversion disorder do not consciously produce the symptoms
they experience (as in factitious disorder or malingering), and these patients are sig-
nificantly distressed or their functioning is impaired by the symptoms (see Table
8.10). Conversion disorder is similar to SSD in that both involve physical symptoms;
however, conversion disorder is limited to sensory and motor symptoms that appear
to be neurological (that is, related to the nervous system) but, on closer examination,
are inconsistent with the effects of known neurological or medical disorders (see Fig-
ure 8.2). A diagnosis of conversion disorder can be made only after physicians rule
out all possible medical causes—and this process can take years. Conversion disorder
is sometimes referred to as functional neurological symptom disorder because the neuro-
logical symptom relates to the functioning of some aspect of the nervous system but not
to an underlying medical cause of the symptom.
Conversion disorder is characterized by one or more of three types of symptoms
(American Psychiatric Association, 2000; Maldonado & Speigel, 2001):
• Motor symptoms. Examples include tremors that become worse when the person pays
attention to them, tics or jerks, muscle spasms, swallowing problems, staggering,
and paralysis (sometimes referred to as pseudoparalysis, which may also involve
significant muscle weakness).
• Sensory symptoms. Examples include blindness, double vision, deafness, auditory
hallucinations, and lack of feeling on the skin that doesn’t correspond to what is
produced by malfunctioning of an actual nerve path.
• Seizures. Examples include not only the motor symptoms of twitching or jerking
of some part of the body but also loss of consciousness with uncontrollable spasms
of the large muscles in the body, causing the person to writhe on the floor. These
seizures are often referred to as nonepileptic seizures because they do not have a
neurological origin and are not usually affected by medication for seizures. The
nonepileptic seizures are likely to occur when other people are present.
Anna O. had both motor conversion symptoms (paralysis of her neck, arm, and legs)
and sensory conversion symptoms (problems with vision, a lack of sensation in her
elbows). Breuer did not report any seizure-like symptoms.
In conversion disorder, symptoms do not correspond to what would be produced
by the relevant nerve pathways, but rather they arise from the patients’ (perhaps
unconscious) ideas about what would happen if certain nerve pathways were dis-
rupted. Thus, a patient may not be able to write but can scratch an itch, which
would be impossible with true paralysis of the hand muscles. Similarly, when the
sensory symptom of blindness occurs in conversion disorder, medical tests reveal that
all parts of the visual system function normally, as was true for Mary, described in
Case 8.5.
CASE 8.5 • FROM TH E INSIDE: Conversion Disorder
On graduating from high school, Mary decided to enter a convent, and by the age of 21 had
taken her vows of poverty, chastity, and obedience. This came as a shock to her family, who,
although they were practicing Catholics, had been far from religious. “I had a great need to
help people and do something spiritual and good,” Mary recalls. . . .
For the first decade she enjoyed the sense of community and the studious aspect of convent
life. . . . But as time went on she became disenchanted with the church, which she felt was
“out of touch with real people. . . . The church required blind obedience and no disagreement.”
Mary began feeling nervous and anxious. She was rarely sick, but one day [when she
was 36 years old] developed soreness in the back of her eye. Every time she moved it,
she’d feel pins and needles. . . . By the fourth day she couldn’t see out of one eye. A neurol-
ogist said it was optic neuritis, a diagnosis of nerve inflammation of unknown origin. She
was hospitalized and given cortisone, but her sight didn’t improve.
(a) (b)
FI G U RE 8.2 • Conversion Disorder:
Glove Anesthesia Patients who suffer
from conversion disorder have sensory or
motor symptoms that at first may appear to
be neurological but on further investigation do
not correspond to true neurological damage.
One example is glove anesthesia, in which the
person reports that his or her hand—and only
the hand—has no sensation, as shown in (a).
However, the neural pathways that would
create such an anesthesia in the hand would
also create a lack of sensation in the arm (b);
the color-coded regions show the areas
served by different nerves. Thus, conversion
disorder may be the appropriate diagnosis
when a patient reports glove anesthesia in the
absence of anesthesia of the arm.
TABLE 8.10 • DSM-5 Diagnostic
Criteria for Conversion Disorder
(Functional Neurological Symptom
Disorder)
A. One or more symptoms of altered
voluntary motor or sensory function.
B. Clinical findings provide evidence of
incompatibility between the symptom
and recognized neurological or medical
conditions.
C. The symptom or deficit is not better
explained by another medical or mental
disorder.
D. The symptom or deficit causes clinically
significant distress or impairment in social,
occupational, or other important areas of
functioning or warrants medical evaluation.
Reprinted with permission from the Diagnostic and
Statistical Manual of Mental Disorders, Fifth Edition,
(Copyright ©2013). American Psychiatric Association. All
Rights Reserved.
Dissociative and Somatic Symptom Disorders 245
. . . Mary took a leave of absence and spent the good part of a year at a less stressful
convent in the countryside. She began meeting regularly with a psychologist. . . . “I dis-
covered I was a perfectionist, overworking to avoid my growing doubts.”. . . Her eyesight
gradually came back, and shortly after that she left the church.
. . . “During that period in my life I was undergoing deep psychological trauma. I was so
unhappy, and I literally didn’t want to see,” she says. “I believed then, as I do today, that
the body was telling me something, and I had to listen to it.”
(Cantor, 1996, pp. 57–58)
People with conversion disorder may react in radically different ways to their
symptoms and to what they might imply: Some seem indifferent whereas others
respond dramatically. Anna O.’s response was “a slight exaggeration, alike of cheer-
fulness and gloom; hence she was sometimes subject to moods” (Breuer & Freud,
1895/1955, p. 21). Table 8.11 provides more facts about conversion disorder.
TABLE 8.11 • Conversion Disorder Facts at a Glance
Prevalence
• Persistent conversion disorder is very rare, with prevalence estimates from 0.001% to
0.005% in the general population and up to 5% of those who are referred to neurologists.
Comorbidity
• Studies have found that up to 85% of people with conversion disorder also have major depres-
sive disorder (Roy, 1980; Ziegler et al., 1960); comorbid anxiety disorders are also common.
• Patients with conversion disorder may also have a neurological disorder, such as multiple
sclerosis or a condition that produces seizures (Maldonado & Spiegel, 2001).
• A history of sexual or physical abuse is common among patients with conversion disorder
(Bowman, 1993).
Onset
• This disorder can arise throughout life.
• Symptoms typically emerge suddenly after a significant stressor, such as the loss of a loved
one, or a physical injury (Stone et al., 2009).
• For men, the disorder is most likely to develop in the context of the military or industrial
accidents (American Psychiatric Association, 2000; Maldonado & Spiegel, 2001).
Course
• Symptoms typically last only a brief period of time.
• Between 25% and 67% of those with the disorder have a recurrence up to 4 years later
(Maldonado & Spiegel, 2001).
Gender Differences
• Conversion disorder is two to three times more common among women than men.
Cultural Differences
• Conversion disorder is more common in rural populations, among those from lower SES back-
grounds, and among those less knowledgeable about psychological and medical concepts.
• It is also more common in developing countries than in industrialized countries, and as a
country becomes industrialized, the prevalence of conversion disorder decreases.
• Small “epidemics” of conversion disorder have been reported in countries undergoing
cultural change or significant stress (Piñeros et al., 1998; Cassady et al., 2005).
Source: Unless otherwise noted, the source is American Psychiatric Association, 2000, 2013.
246 C H A P T E R 8
Criticisms of the DSM-5 Criteria
Both the diagnosis of conversion disorder and its placement among the somatic
symptom disorders are controversial (Brown & Lewis-Fernández, 2011). Some
researchers have suggested that conversion disorder is not a distinct disorder but
rather a variant of SSD; these researchers point out that both disorders may involve
the bodily expression of psychological distress (Bourgeois et al., 2002). Other re-
searchers believe that conversion symptoms in general, and nonepileptic seizures in
particular, are more like dissociative symptoms than like symptoms of other somatic
symptom disorders (Kihlstrom, 2001; Mayou et al., 2005). As they note, dissociation
can not only affect memory and the sense of self but also can disrupt the integration
of sensory or motor functioning.
Understanding Conversion Disorder
Research on neurological factors in conversion disorder focuses on how brain systems
operate differently in people with the disorder than in other people.
Neurological Factors: Not Faking It
When considering making a diagnosis of conversion disorder, clinicians must rule
out simple malingering, or faking of symptoms, which is difficult to do (Stone et al.,
2010). Could all cases of conversion disorder just be faking? Neuroimaging findings
suggest that muscle weakness arising from conversion disorder is not the same as
consciously simulated muscle weakness. For example, Stone and colleagues (2007)
scanned the brains of patients with conversion disorder and of healthy control par-
ticipants while their ankles were flexed. The patients with conversion disorder all
reported weakness in the manipulated ankle prior to the study; during the study,
participants in the control group were asked to pretend that their ankles were weak.
The results were clear: Some brain areas were more activated in the patients than in
the controls (such as the insula, which is involved in registering bodily sensations),
and some brain areas (including areas in the frontal lobes) were less activated in the
patients than in the controls. These findings are good evidence that the patients in
this study were not simply faking their disorder.
In addition, some patients with chronic pain develop sensory deficits, a kind of
“psychological” anesthesia. In one study, researchers scanned the brains of four such pa-
tients, using fMRI, while sharp plastic fibers were pressed into the skin (Mailis-Gagnon
et al., 2003). These patients had apparent sensory deficits in only one limb, and thus
the researchers could directly compare stimulation of the normal and affected limbs.
When the researchers stimulated the normal limb, the sharp plastic fibers activated
a brain network that registers pain, as is normal. In contrast, this network was not
activated when the researchers stimulated the affected limb, as is shown in Figure 8.3.
These findings indicate that the “psychological” anesthesia actually affected the brain
and inhibited activation in the brain areas that register sensation and pain.
Other studies have shown that conversion disorder is not a direct consequence
of abnormal functioning of brain areas that register peripheral sensations but rather
reflects abnormal functioning of brain areas that interpret sensations and manage other
brain areas (that is, areas that are involved in “executive functions”) (Hoechstetter
et al., 2002; Lorenz et al., 1998). At least in some cases, abnormal processing in
brain areas responsible for executive functions might inhibit brain areas that process
sensation and pain or that produce movements, which in turn causes them to fail to
function properly.
Psychological Factors: Self-Hypnosis?
There is no generally accepted explanation for how psychological factors might pro-
duce the selective bodily symptoms in conversion disorder (Halligan, Athwal, et al.,
2000). But self-hypnosis offers one possible explanation—that the disorder is the
Dissociative and Somatic Symptom Disorders 247
result of unintended self-hypnotic suggestion. According to this
theory, patients have, consciously or unconsciously, “suggested”
to themselves that they have symptoms (Kozlowska, 2005); that is,
particular sensations have become dissociated. This theory receives
support from the fact that people with conversion disorder are un-
usually hypnotizable (Roelofs, Hoogduin, et al., 2002) and from
the finding that areas of the brain activated by hypnotically induced
paralysis are similar to those activated by paralysis in patients with
conversion disorder (Halligan, Bass, & Wade, 2000; Oakley, 1999).
Social Factors: Stress Response
Life stressors, such as combat, can trigger conversion disorder. More-
over, the greater the severity or number of stressors, the more severe
the conversion symptoms ( Roelofs et al., 2005). As we saw with SSD,
somatic symptoms can be a culturally accepted way to express feelings of helplessness (Cel-
ani, 1976), which may explain why some soldiers develop conversion disorder in combat.
Conversion disorder can also be a way to obtain the attention associated with being sick.
This was certainly true for Anna O., as well as for many other women of the Victorian era.
Illness Anxiety Disorder
People who are diagnosed with illness anxiety disorder have either no or minor
medical symptoms but nonetheless are preoccupied with a fear or belief that they
have a serious disease; they engage in excessive behaviors related to this belief, such
as repeatedly checking their bodies for sign of an illness or avoiding medical care.
Despite the fact that physicians cannot identify a medical problem, patients with ill-
ness anxiety disorder persist in clinging strongly to their conviction that they have
a serious disease. This diagnosis is in some ways similar to the DSM-IV diagnosis
of hypochondriasis. However, in DSM-IV the disorder hypochondriasis included two
groups of people—those without any significant medical symptoms (now classified as
illness anxiety disorder) and those with at least one medical symptom but whose psy-
chological response to the symptom is excessive (now classified as somatic symptom
disorder). Although people with SSD and those with illness anxiety disorder share a
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Symptoms of conversion disorder may be
more common after significant psychological
stressors, such as military combat. This soldier
is displaying muscular spasms as part of his
conversion disorder. Such symptoms among
soldiers are thought to resolve a conflict
between their loyalty to comrades and their
fear of battle: Soldiers with such symptoms
are unable to fight (Spiegel, 1974).
FI G U RE 8.3 • Brain Activation in Conversion
Disorder: Healthy Limb Versus Affected
Limb Brain areas activated when the skin of the
healthy, nonaffected limb was stimulated (top row)
compared to those activated when the skin of the
affected limb was stimulated (bottom row); arrows
show the key areas of activation (Mailis-Gagnon et al.,
2003). It’s clear that the scans in the bottom row show
much less activation.
Source: A. Mailis-Gagnon, M.D., et al., Neurology 2003;60:1501–1507.
© 2003 American Academy of Neurology.
Illness anxiety disorder
A somatic symptom disorder marked by a
preoccupation with a fear or belief of having
a serious disease in the face of either no
or minor medical symptoms and excessive
behaviors related to this belief.
248 C H A P T E R 8
focus on bodily symptoms, only people with illness anxiety disorder believe that they
have a serious illness, despite reassurance from doctors and minimal physical symp-
toms, if any.
What Is Illness Anxiety Disorder?
Patients with illness anxiety disorder may or may not realize that their
worries are excessive for the situation; when they do not, they are
said to have poor insight into their condition. Consider a man who sees
floating “spots” and does not believe his eye doctor when told that
such floaters are normal and nothing to worry about. The man prob-
ably doesn’t think that the doctor is lying about the spots, but he may
believe that the doctor didn’t do a thorough enough eye examination;
he may think that the floaters indicate that he is going blind or that he
has a tumor. His worries about this problem are distressing and preoc-
cupying to the point that he functions less well at work—not because
of the floaters but because of his frequent thoughts about the floaters.
People with this disorder may spend hours on the Internet, search-
ing for illness-related information to reassure themselves, only to be-
come more anxious or worried (Starcevic & Berle, 2013). To be
diagnosed with this disorder, this kind of preoccupation with a per-
ceived health problem must cause significant distress or impair the per-
son’s functioning and must have continued for at least 6 months (see
Table 8.12). Because illness anxiety disorder is a newly defined disor-
der and most people (75%) previously diagnosed with hypochondriasis
would now be diagnosed with somatic symptom disorder, additional
facts about illness anxiety disorder, such as prevalence and course, are
not known at this time. However, two thirds of people with this disor-
der are estimated to have at least one other psychological disorder, com-
monly anxiety or depressive disorders, and the disorder typically begins
in early to middle adulthood (American Psychiatric Association, 2013).
C U R R E N T C O N T R O V E R S Y
Omission of Hypochondriasis from
DSM-5: Appropriate or Overreaction?
The previous edition of the DSM, DSM-IV, included the
diagnosis of hypochondriasis, which pertained to people who
worr y excessively about their physical symptoms or about
potential illnesses. This term was not included in DSM-5,
partly because the DSM-5 team felt it had become pejorative
(e.g., “acting like a hypochondriac”) (American Psychiatric
Association, 2013). As noted in this chapter, people previously
diagnosed with hypochondriasis are now diagnosed either
with somatic symptom disorder (in which the response to physical
symptoms is greater than would be expected) or illness anxiety
disorder (in which patients worry persistently about potentially
having or developing a medical condition). Is this change
warranted?
On one hand, it is not clear that the new categories make
sense. If illness anxiety is so different from worries about
actual symptoms, then why isn’t it grouped with anxiety
disorders (Frances, 2013)? If the difference is about the pres-
ence of actual bodily symptoms, maybe instead of two sep-
arate categories, we might have two traits that each fall on
a spectrum of intensity of physical symptoms and levels of
anxiety.
On the other hand, the new, separate diagnoses are useful
because they may lead more people to appropriate treatment;
both disorders apply to people who are more likely to go, at
least initially, to a medical doctor’s office rather than a mental
health clinician’s office. And physicians may be more likely to
use the new labels because they feel the new labels are less pe-
jorative—at least for now.
C R I T I C A L T H I N K I N G W h ich of these th ree d iag noses—
hypochondriasis, SSD, or illness anxiety disorder—do you
think is most pejorative, and which do you think is least
stigmatizing? Why? How would you explain each of these
diagnoses to patients?
( James Foley, College of Wooster)
TABLE 8.12 • DSM-5 Diagnostic Criteria for Illness
Anxiety Disorder
A. Preoccupation with having or acquiring a serious illness.
B. Somatic symptoms are not present or, if present, are only
mild in intensity. If another medical condition is present or
there is a high risk for developing a medical condition (e.g.,
strong family history is present), the preoccupation is clearly
excessive or disproportionate.
C. There is a high level of anxiety about health, and the individual
is easily alarmed about personal health status.
D. The individual performs excessive health-related behaviors
(e.g., repeatedly checks his or her body for signs of illness)
or exhibits maladaptive avoidance (e.g., avoids doctor
appointments and hospitals).
E. Illness preoccupation has been present for at least 6 months,
but the specific illness that is feared may change over that
period of time.
F. The illness-related preoccupation is not better explained by
another mental disorder, such as somatic symptom disorder,
panic disorder, generalized anxiety disorder, body dysmorphic
disorder, obsessive compulsive disorder, or delusional disorder,
somatic type.
Reprinted with permission from the Diagnostic and Statistical Manual of Mental
Disorders, Fifth Edition, (Copyright ©2013). American Psychiatric Association. All
Rights Reserved.
Dissociative and Somatic Symptom Disorders 249
Like people with SSD, those with illness anxiety disorder don’t understand that
even healthy people sometimes have aches and pains and other bodily discomforts.
Instead, like the woman in Case 8.6, they unrealistically believe that having “good
health” implies not having any unpleasant bodily symptoms (Barsky, Coeytaux,
et al., 1993).
CASE 8.6 • FROM TH E INSIDE: Illness Anxiety Disorder
I attended graduate school, held jobs, was married, had children. But my existence was
peppered with episodes of illness. When the going got tough, I’d get sick. Or just the
opposite: when things seemed to be going well, I’d come down with a symptom, or at
least what I interpreted as one. It might be stomach pain, dizziness, black and blue marks,
swollen glands, an achy heel. Anything. Whatever the symptoms, I always interpreted it as
a precursor of some crippling illness: leukemia, Lou Gehrig’s disease, scleroderma. I knew
just enough about most diseases to cause trouble. Eventually I’d get past each episode,
but it always took time—the cure a mysterious concoction of enough negative tests, a
lessening of symptoms, some positive change in my life. And when the event was over, the
realization that I was healthy and wasn’t going to die, at least not immediately, was like a
high, a reprieve, a new lease on life. That is, until the next time.
(Cantor, 1996, pp. 9–10)
Illness Anxiety Disorder, Anxiety Disorders, and OCD:
Shared Features
Illness anxiety disorder has many features in common with anxiety disorders. In
fact, certain forms of illness anxiety disorder and anxiety disorders are so similar that
some researchers have advocated moving illness anxiety disorder from the category
of somatic symptom disorders to the category of anxiety disorders (Mayou et al.,
2005). Illness anxiety disorder, phobias, and panic disorder are all characterized by
high levels of fear and anxiety, as well as a faulty belief of harm or danger. However,
with illness anxiety disorder and panic disorder, the perceived danger is from an in-
ternal event that is thought to be producing a bodily sensation, whereas with phobias,
it is from an external object (such as a snake) or a situation (such as giving a speech;
Fava, Mangelli, & Ruini, 2001). People with panic disorder, phobias, and illness
anxiety disorder all may try to avoid certain stimuli or situations; with panic disorder
and illness anxiety disorder, what is avoided may be an elevated heart rate (Hiller et
al., 2002).
In addition, both patients with illness anxiety disorder and those with obsessive-
compulsive disorder (OCD) have obsessions and compulsions (Abramowitz & Braddock,
2006). In particular, patients with illness anxiety disorder obsess about possible illnesses
or diseases they believe they might have. They may compulsively ask doctors, friends,
or family members for reassurance or compulsively “check” their body for particular
sensations. People with some forms of illness anxiety disorder spend hours compulsively
consulting medical websites. It’s important to keep in mind that some medically related
Internet chat rooms or websites can spread false or misleading information.
Understanding Illness Anxiety Disorder
Because illness anxiety disorder is a diagnosis new to DSM-5, most research related
to this disorder studied people diagnosed with hypochondriasis. Hence we use the
term hypochondriasis when discussing studies of people with that diagnosis, and the
term illness anxiety disorder when discussing experiences and symptoms that clearly
apply to the new disorder. Most research has examined psychological factors, and not
enough is known about neurological and social factors to understand the feedback
loops among the types of factors.
250 C H A P T E R 8
Neurological Factors
Some researchers have suggested that the neurotransmitter serotonin does not func-
tion properly in at least some cases (King, 1990). As we’ll see in the section on treat-
ment, there is some indirect support for this hypothesis, based on the observation that
SSRIs (which selectively affect serotonin reuptake) appear to improve the disorder.
That is, the mere fact that SSRIs can improve the symptoms is evidence that the
symptoms arise, at least in part, from disruption of the activity of serotonin. In addi-
tion, results from one twin study suggest that genetic differences contribute to hypo-
chondriasis (Gillespie et al., 2000).
Psychological Factors: Catastrophic Thinking About the Body
People with hypochondriasis have specific biases in their reasoning: Not surprisingly,
given their disorder, they both tend to seek evidence of health threats and also may
fail to consider evidence that such threats are minimal or nonexistent (Salkovskis,
1996; Smeets et al., 2000). For instance, a man with illness anxiety disorder who
notices a bruise on his leg might interpret it as evidence that he
has leukemia rather than try to remember whether he recently
bumped into something that could cause a black-and-blue mark.
In addition, people afflicted with illness anxiety disorder focus
attention closely on unpleasant sensations. They commonly focus on
the functioning of body parts (such as the stomach or the heart), mi-
nor physical problems (such as a sore throat), and ambiguous physi-
cal sensations (such as “aching veins”). Moreover, they interpret
bodily sensations as abnormal, pathological, and symptomatic of
disease (Barsky, 1992; Barsky et al., 2000). In fact, like patients with
SSD, patients with hypochondriasis (and likely with illness anxiety
disorder) may engage in catastrophic thinking about their physical sen-
sations or fears of illness, just as the woman in Case 8.6 did when she
interpreted physical sensations as signs of “crippling illness.”
As is the case with many anxiety disorders, people with illness
anxiety disorder may engage in behaviors that temporarily reduce
their anxiety. For example, they may repeatedly take their blood pressure, perform urine
dipstick tests, feel body parts for cancerous lumps, or call their doctor about new symp-
toms. Such behaviors maintain their faulty beliefs and can, through negative reinforce-
ment, sustain their anxiety in the long term.
Social Factors: Stress Response
As with other somatic symptom disorders, research has shown that stressful events
can precipitate hypochondriasis (Fallon & Feinstein, 2001). In addition, such people
are more likely than people without the disorder to report having experienced
traumatic sexual contact, physical violence, or major familial upheaval (such as their
parents’ divorce) (Barsky, Wool, et al., 1994). Moreover, through their attention and
concern, relatives and friends may unintentionally reinforce patients’ symptoms.
Treating Somatic Symptom Disorders
When treating any of the three somatic symptom disorders (SSD, conversion
disorder, or illness anxiety disorder), clinicians target neurological, psychological,
and social factors—individually or in combination. As we discuss below, cognitive-
behavior therapy is generally the treatment of choice for somatic symptom disorders.
Targeting Neurological Factors
There has not been much rigorous research on neurologically-based treatments for
somatic symptom disorders in general; the studies that have been reported have rarely
included appropriate control groups, such as a placebo group or a wait-list control
Concern for one’s health is normal. How do we
begin to assess when the concern is excessive?
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Dissociative and Somatic Symptom Disorders 251
group to determine whether the disorder spontaneously improves with time. Some
treatments target specific symptoms. For instance, medications, such as an SSRI, or
St. John’s wort may be used to treat some anxiety-related symptoms of somatic symp-
tom disorders. As with anxiety disorders, however, when the medication is stopped,
the anxiety- related symptoms usually return. Other types of treatments, such as bio-
feedback, target muscle tension.
Were Anna O. to be treated by a mental health clinician today, she might receive
medication. Anxiety or depression may have contributed to her symptoms, and if
medication for these disorders did not alleviate her hallucinations, the clinician might
recommend an antipsychotic medication (Martorano, 1984). Note that Anna O. was
given medications frequently used at that time: morphine (typically given for pain
relief ) and chloral hydrate (a narcotic used to induce sleep). She became addicted to
both of these substances, and after her “talking cure” with Breuer ended, she needed
inpatient treatment to end her addiction.
Targeting Psychological Factors: Cognitive-Behavior Therapy
Research indicates that the treatment of choice for most somatic symptom disorders is
cognitive-behavior therapy (CBT). As shown in Table 8.13, the cognitive and behavioral
methods used to treat each of the disorders vary because each disorder has
different symptoms. Cognitive methods focus on identifying and then
modifying irrational thoughts and shifting attention away from the body
and bodily symptoms (Gropalis et al., 2013). Behavioral methods focus
on decreasing compulsive behaviors and avoidance.
Targeting Social Factors: Support and Family Education
Patients with any of the somatic symptom disorders can be helped, in
part, merely by feeling that someone understands the pain and distress
they feel (Looper & Kirmayer, 2002). For SSD and conversion disor-
der, the therapist strives to understand the context of the symptoms
and of their emergence and the way the symptoms affect the patient’s
TABLE 8.13 • Cognitive-Behavior Therapy for Somatic Symptom Disorders
Disorder Cognitive focus Behavioral focus Comment
Somatic
symptom
disorder
(SSD)
Psychoeducation; cognitive restructuring
to modify faulty or irrational beliefs
about bodily sensations; teach patients
not to amplify the sensations
Identify and then decrease avoidant behaviors,
sensations, and activities that lead to physical
or psychological discomfort or restriction of
activitiesa; assertiveness training; relaxation to
decrease physical tension
CBT is generally the most effective
treatment for somatic symptom
disorder.b
Conversion
disorder
Psychoeducation; identify stressors or
conflicts associated with the emergence
of symptoms; develop alternative ways
to resolve the conflict or cope with
stressors (problem solving)c
Assertiveness training; to decrease symptoms,
use paradoxical intention (suggest that the
patient continue to have the symptom), as
appropriated
Insight-oriented treatment is
sometimes used to help patients with
conversion disorder understand the
meaning of the symptoms. Once the
meaning is understood, the symptoms
may improve spontaneously.e
Illness
anxiety
disorder
Identify and modify faulty or irrational
beliefs about health worries and bodily
sensations (cognitive restructuring); teach
patients not to amplify these sensations;
decrease catastrophic attributions about
sensations and illness worries
Identify sensations and activities that lead to
discomfort; identify avoidant behaviors and
decrease avoidance; use exposure with response
prevention for compulsive behaviors such as
checking the body, seeking reassurance, or
visiting doctors frequently
CBT is the most effective treatment
for illness anxiety disorder.f Pilot
studies have adapted interpersonal
therapy to treat illness anxiety
disorder, and initial results are
promising.g
aMayou & Farmer, 2002; O’Malley et al., 1999; bAllen et al., 2006; Bass et al., 2001; cMaldonado & Spiegel, 2001; dAtaoglu et al., 2003; eMaldonado & Spiegel, 2001; fBarsky & Ahern, 2004;
Taylor et al., 2005; Wattar et al., 2005; gStuart & Noyes, 2005; Stuart et al., 2008.
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Perhaps the most effective treatment for leg
paralysis due to conversion disorder may be
the simplest: Educate the patient about the
nature of the symptoms. At least for three
patients in one study, simply showing them
their normal test results and contradictions
from their physical exam did the trick. These
patients walked out of the hospital unaided
immediately after these results were given to
them (Letonoff et al., 2002).
252 C H A P T E R 8
interactions with others (Holder-Perkins & Wise, 2001); with these two disorders,
treatment may focus on helping the patient communicate more assertively—which
can help to relieve the social stressors that contribute to the disorders.
Treatment may also focus on the family— educating family members about the
disorder and the ways they may have inadvertently contributed to or reinforced the
patient’s symptoms. The therapist may teach family members how to reinforce positive
change and to extinguish behavior related to the symptoms (Looper & Kirmayer,
2002; Maldonado & Spiegel, 2001). For instance, if the patient has SSD, family mem-
bers may be asked not to inquire about the patient’s bodily symptoms. In addition, sup-
port groups may help patients feel less alone and isolated (Looper & Kirmayer, 2002).
Feedback Loops in Treating Somatic Symptom Disorders
CBT can provide new skills and new ways to interpret the sensations and modify the
preoccupying thoughts, which in turn can decrease the bodily symptoms (neurological
factor) and the attention paid to them (psychological factor). Similarly, although bio-
feedback and medication primarily target neurological factors, these techniques can in
turn affect the type and quality of attention paid to bodily sensations and can change
the meaning made of bodily sensations (psychological factors). In addition, the relation-
ship with a therapist (social factor) can provide reassurance and support; as family mem-
bers change how they respond to the patient’s symptoms (social factor), positive change
can be enhanced. Figure 8.4 shows how successful treatment of somatic symptom dis-
orders affects the different types of factors directly and through their feedback loops.
SP
N
Treatments Targeting
Neurological Factors
Medication: Medication
for anxiety symptoms
(e.g., SSRIs)
Relaxation/biofeedback
Decreases bodily
tension
Changes neural activity
Treatments Targeting
Social Factors
Group therapy/support
group
Family therapy
Decreases isolation
Increases social support
Changes social
interactions
Changes family response
to patient’s behavior
Treatments Targeting
Psychological Factors
CBT: Breathing,
relaxation, cognitive
restructuring,
psychoeducation,
exposure and
exposure with
response prevention
Changes thoughts,
feelings, and behaviors
FI G U RE 8.4 • Feedback
Loops in Treating Somatic
Symptom Disorders
Dissociative and Somatic Symptom Disorders 253
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Despite Breuer’s poor prognosis for Anna’s
future, she went on to live a full life, becoming
an accomplished advocate for and benefactor of
poor women and children. In Anna’s time, having
a psychological disorder was neither a personal
disaster nor a signal that life had to become
constrained and unrewarding. This is still the case.
Follow-up on Anna O.
Anna O.’s symptoms do not fit neatly into any single one of the disorders discussed in
this chapter. She had hallucinations, dissociative symptoms, and bodily symptoms—
but they probably wouldn’t meet the diagnostic criteria for SSD. Today, she would
probably be diagnosed with more than one disorder.
Anna’s symptoms cleared up near the end of her treatment with Breuer.
However, after their final session, she had a major relapse, and Breuer refused to
continue to treat her. He found the therapy sessions with Anna too time- and
energ y-consum ing, and, g iven her relapse, he was not optim istic about her
prognosis.
Anna’s history for the 6 years after her treatment with Breuer remains largely
unknown, although we do know that she was hospitalized several times for her
addiction to morphine and chloral hydrate, which Breuer had prescribed for her.
Despite Breuer’s negative prognosis, Anna O. went on to accomplish great things.
Her real name was Bertha Pappenheim, and she became a social worker, the di-
rector of an orphanage, and the founder of a home for unwed mothers that was
dedicated to teaching the women skills to support themselves and their children.
For the rest of her life, she strove to improve the lives of poor women and children
(Freeman, 1990).
Thinking Like A Clinician
Now 57 years old, Mr. Andre left his native Haiti 5 years ago and moved to the United
States. Unemployment rates in the United States were high at the time of his arrival, and
Mr. Andre had a hard time finding a job; he felt that he was being discriminated against.
His wife supported the family for 2 years by cleaning houses. After 2 years of looking, Mr.
Andre did get a job. However, within 4 months of starting this job, he had a bout of the flu,
and he continued to feel tired even after he recovered from it. He began to worry that he
might be developing cancer. (His father had died of cancer.) He went to see his doctor and
had a variety of tests that were all negative. Nonetheless, Mr. Andre thinks that the doctors
may have “missed something” or not given him the right test. He worries about this, and
frequent visits to the doctor mean that he must rearrange his work schedule or miss work.
What factors should (and shouldn’t) clinicians take into account when evaluating Mr. Andre
for some type of somatic symptom disorder? If they do think he has such a disorder, which
one do you think it might be, and why? What treatment(s) should be recommended to Mr.
Andre if you are correct? On what basis could some of the somatic symptom disorders be
ruled out?
Dissociative Disorders
• Dissociation involves a separation of men-
tal processes that are normally integrated—
such as consciousness, memory, emotion,
or identity. To qualify as a dissociative
disorder, this separation must cause sig-
nif icant distress or impair functioning.
Specif ic symptoms of dissociative disor-
ders include amnesia, identity problems,
derealization, and depersonalization.
• Dissociative amnesia is characterized by
significantly impaired memory for impor-
tant experiences or for personal informa-
tion that cannot be explained as ordinary
forgetfulness or accounted for by another
psychological disorder, substance use, or a
medical condition.
• A subtype of dissociation amnesia, disso-
ciative fugue, is characterized by sudden,
unplanned travel and diff iculty remem-
bering the past, which in turn leads to
identity confusion.
• Depersonalization-derealization disorder
is characterized by the persistent feeling
of being detached from oneself or one’s
surroundings.
• Di s sociat ive ident it y d i sorder ( DI D )
hinges on the presence of two or more
SUMMING UP
254 C H A P T E R 8
distinct personality states, which gives rise
to a discontinuity in the person’s sense of
self and agency.
• A lthough neuroimaging studies of pa-
tients with DID f ind that their brains
function differently when different alters
are dominant, such studies generally have
not used appropriate control groups. Peo-
ple with this disorder are more hypnotiz-
able and dissociate more readily than do
people who do not have this disorder.
• Two models have been formulated to ex-
plain DID. The posttraumatic model pro-
poses that DID is caused by severe, chronic
physical abuse during childhood, which
leads to dissociation during the abuse; the
dissociated states come to constitute alters,
with their own memories and personality
traits. The sociocognitive model proposes
that DID arises as the result of interactions
between a therapist and a suggestible pa-
tient, during which the therapist inadver-
tently encourages the patient to behave in
ways consistent with the diagnosis. Both
interpretations are consistent with the
finding that severe childhood trauma is as-
sociated with the disorder.
• The goal of treatment for dissociative dis-
orders is to reduce the symptoms them-
selves and lower the stress they induce.
Somatic Symptom Disorders
• Somatic symptom disorders center on
complaints about physical well-being along
with cognitive distortions about those
bodily symptoms and their meaning; the
focus on these symptoms causes significant
distress or impairs functioning. All somatic
symptom disorders involve bodily preoc-
cupation and symptom amplification.
• Somatic symptom disorder (SSD) is char-
acterized by at least one somatic symp-
tom about which the person has excessive
thoughts, feelings, or behaviors, and that
is distressing or disrupts daily life.
• Factors that contribute to SSD include
genes, catastrophic thinking about illness,
symptom amplif ication, bodily preoc-
cupation, other people’s responses to ill-
ness, and the way symptoms function as a
means of expressing helplessness.
• Conversion disorder centers on sensor y
systems, motor symptoms, and seizures
that may initia l ly appear to have neu-
rolog ica l causes but in fact are incon-
sistent w ith a neurolog ica l or med ica l
condition.
• Illness anxiety disorder is characterized
by misinterpretation of or worr y about
bodily sensations and symptoms, which
leads to a belief that the person has a se-
r iou s i l l ne s s — de spite t he absence of
evidence of a medical problem and reas-
surance from health care personnel.
• CBT is generally the treatment of choice
for somatic symptom disorders; medi-
c at ion s , when u sed , t a r g et a n x iet y-
related sy mptom s. Group a nd f a m i ly
therapy are generally used as supplemen-
tary treatments.
Hysteria (p. 223)
Dissociation (p. 224)
Amnesia (p. 224)
Identity problem (p. 224)
Derealization (p. 224)
Depersonalization (p. 224)
Dissociative disorders (p. 225)
Dissociative amnesia (p. 226)
Depersonalization-derealization
disorder (p. 229)
Dissociative identity disorder (DID) (p. 232)
Somatic symptom disorders (p. 240)
Somatic symptom disorder (SSD) (p. 241)
Conversion disorder (p. 244)
Illness anxiety disorder (p. 248)
Key Terms
More Study Aids
For additional study aids related to this chapter, including
quizzes to make sure you’ve retained everything you’ve
learned and a Student Video Activity exploring methods for
treating and coping with pain, go to: www.worthpublishers.
com/launchpad/rkabpsych2e.
Image Source
Dissociative and Somatic Symptom Disorders 255
257
CHAPTER 9
Mads Perch/Stone/Getty Images. Photo for illustrative purposes only; any individual depicted is a model.
Substance Use Disorders
he musical group the Beatles were so famous that the four
members—John Lennon, Paul McCartney, George Harrison,
and Ringo Starr—found that they were essentially prisoners in
their hotel rooms when on tour. Frenzied fans would try to steal into
the rooms, going so far as to lower themselves down from the ho-
tel roof ! Sick of it all, the Beatles stopped touring and just recorded
music in the studio. Many of their songs broke all the conventions of
rock-and-roll music, and the Beatles developed the first themed rock
album, with Sgt. Pepper’s Lonely Hearts Club Band. The album practi-
cally reeked of drug use, and the band members became famous both
for their music and for their lifestyles—setting a model for a genera-
tion that experimented with mind-altering drugs. Beneath the musi-
cal history of the Beatles is a story of substance use and use disorders
that illustrates the focus of this chapter.
Substance Use: When Use
Becomes a Disorder
The Beatles used some drugs because that was what their peers did.
For instance, almost all boys—and some girls—their age in Liver-
pool, England, smoked cigarettes. It was simply what was done. Sim-
ilarly, the young band members drank alcohol; again, doing so was
the norm. Sometimes they used a drug specifically for the effect it
brought, such as when they took “uppers” (stimulants) to stay awake
when performing late at night. When they toured in the early 1960s,
they took drugs to relieve the monotony of life on the road; they
would swallow a pill, “ just to see what would happen” (Norman,
1997, p. 244). A few years later, they took “acid” (LSD) to help them
understand the meaning of life and attain enlightenment and peace.
All four members of the Beatles tried various psychoactive substances.
Psychoactive substances, commonly called drugs, are chemicals
that alter mental ability, mood, or behavior. Frequent use of a psy-
choactive substance can develop into a substance use disorder.
Substance Use: When Use Becomes
a Disorder
Substance Use Versus Intoxication
Substance Use Disorders
Culture and Context
Stimulants
What Are Stimulants?
Understanding Stimulants
Depressants
What Are Depressants?
Understanding Depressants
Other Abused Substances
What Are Other Abused Substances?
Understanding Other Abused Substances
Feedback Loops in Understanding Substance
Use Disorders
Treating Substance Use Disorders
Goals of Treatment
Targeting Neurological Factors
Targeting Psychological Factors
Targeting Social Factors
Feedback Loops in Treating Substance
Use Disorders
Psychoactive substance
A chemical that alters mental ability, mood, or
behavior.
According to DSM-5, substance use disorders are
characterized by a loss of control over urges to use a psy-
choactive substance, even though such use may impair func-
tioning or cause distress. With substance use disorders, the
psychoactive substance is taken repeatedly either because of its
effect on mood, behavior, or cognition or because it prevents
uncomfortable symptoms if the person stops taking the drug
(American Psychiatric Association, 2013). The DSM-5 set of
substance use disorders includes specific disorders for each sub-
stance. We first discuss substance use disorders in general and
then focus on specific substances.
Substance Use Versus Intoxication
The Beatles, individually and collectively, experimented with
numerous drugs. Paul McCartney is generally described as
having been the most cautious about drugs, whereas John
Lennon used them regularly, sometimes continually. At one
time or another, each Beatle could have been diagnosed with
substance intoxication: reversible dysfunctional effects on
thoughts, feelings, and behavior that arise from the use of a
psychoactive substance (see Table 9.1). The specific effects of
substance intoxication depend on the substance and whether a
person uses it only occasionally (e.g., getting drunk on Saturday night) or chronically
(e.g., drinking to excess every night).
In contrast to substance intoxication, substance use is a general term that indicates
simply that a person has used a substance—via smoking, swallowing, snorting,
injecting, or otherwise absorbing it. This term does not indicate the extent or effect
of the exposure to the substance.
Substance Use Disorders
The Beatles used stimulants nightly when perform-
i ng i n Ger m a ny, but doe s t h at mea n t hey were
abusing the drugs or had a substance use disorder?
Were they addicted? Some mental health clinicians
and researchers have avoided using the term addic-
tion, partly because of its negative moral connota-
tions. However, other clinicians and researchers are
in favor of using the term addiction (O’Brien et al.,
2006). Those clinicians and researchers define addic-
tion as the compulsion to seek and then use a psycho-
active substance either for its pleasurable effects or,
with continued use, for relief from negative emo-
tions such as anxiety or sadness. These compulsive
behaviors persist, despite negative consequences (American Society of Addiction
Medicine, 2011).
Like this definition of addiction, the DSM-5 definition of substance use disor-
ders focuses on the behaviors related to obtain ing and using a drug, as well as the
consequences of that use. Whereas intoxication refers to the direct results of using a
substance, the criteria of a substance use disorder focus both on the indirect effects of re-
peated use, such as unmet obligations or risky behavior while using the substance (for
instance, driving while under the influence), and the cravings and biological changes
Substance use disorders
Psychological disorders that are characterized
by loss of control over urges to use a
psychoactive substance, even though such use
may impair functioning or cause distress.
Substance intoxication
The reversible dysfunctional effects on
thoughts, feelings, and behavior that arise
from the use of a psychoactive substance.
TABLE 9.1 • DSM-5 Diagnostic Criteria for Substance Intoxication
• The development of a reversible substance-specific syndrome attributable to
recent ingestion of (or exposure to) a substance that is not listed elsewhere or
is unknown.
• Clinically significant problematic behavioral or psychological changes that are
attributable to the effect of the substance on the central nervous system (e.g.,
impaired motor coordination, psychomotor agitation or retardation, euphoria,
anxiety, belligerence, mood lability, cognitive impairment, impaired judgment,
social withdrawal) and develop during, or shortly after, use of the substance.
• The signs or symptoms are not attributable to another medical condition and
are not better explained by another mental disorder, including substance intoxi-
cation with another substance.
Reprinted with permission from the Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition,
(Copyright ©2013). American Psychiatric Association. All Rights Reserved.
258 C H A P T E R 9
Sgt. Pepper’s Lonely Hearts Club Band was
the Beatles’ first album that incorporated
many references to drug use. The album’s
drug theme also reflects the band members
increasing use of mind-altering substances in
their personal lives.
M
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that can occur with repeated use or stopping use. DSM-5 defines craving as a strong
desire or urge to use the substance. Table 9.2 lists the DSM-5 diagnostic criteria.
Two neurologically based symptoms of substance use disorders can contribute
to the diagnosis: tolerance and withdrawal (American Psychiatric Association, 2013).
Tolerance occurs when, with repeated use, more of the substance is required to
obtain the same effect. For instance, someone who drinks alcohol regularly is likely
to develop tolerance to alcohol and find that it takes more drinks to obtain a “buzz”
and even more drinks to get drunk. With regular use of alcohol and some drugs,
the body adapts and tries to compensate for the repeated influx of the substance (see
Figure 9.1). People who have been given certain medications for medical problems,
such as some pain relievers, may develop tolerance even when taking the medications
as prescribed; in such cases, tolerance would not be considered a symptom of a sub-
stance use disorder.
Withdrawal refers to the set of symptoms that arises when a regular substance
user decreases intake of the substance. As shown in Figure 9.1, withdrawal arises
because the body has compensated for the repeated influx of a drug, and the neuro-
logical compensatory mechanisms are still in place when the person stops taking the
drug, but the drug is no longer there to compensate for them. Withdrawal symptoms
“T
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DSM-5 uses the term use disorder rather than
addiction, in part because the word addiction
has been overused. However, use disorder may
come to be similarly overused.
Tolerance
The biological response that arises from
repeated use of a substance such that more of
it is required to obtain the same effect.
Withdrawal
The set of symptoms that arises when a
regular substance user decreases or stops
intake of an abused substance.
TABLE 9.2 • DSM-5 Diagnostic Criteria for Substance Use Disorders
A. A problematic pattern of use of an intoxicating substance leading to clinically significant
impairment or distress, as manifested by at least two of the following, occurring within a
12-month period:
1. The substance is often taken in larger amounts or over a longer period than was intended.
2. There is a persistent desire or unsuccessful efforts to cut down or control use of the
substance.
3. A great deal of time is spent in activities necessary to obtain the substance, use the
substance, or recover from its effects.
4. Craving, or a strong desire or urge to use the substance.
5. Recurrent use of the substance resulting in a failure to fulfill major role obligations at
work, school, or home.
6. Continued use of the substance despite having persistent or recurrent social or
interpersonal problems caused or exacerbated by the effects of its use.
7. Important social, occupational, or recreational activities are given up or reduced
because of use of the substance.
8. Recurrent use of the substance in situations in which it is physically hazardous.
9. Use of the substance is continued despite knowledge of having a persistent or recurrent
physical or psychological problem that is likely to have been caused or exacerbated by
the substance.
10. Tolerance, as defined by either of the following:
a. A need for markedly increased amounts of the substance to achieve intoxication or
desired effect.
b. A markedly diminished effect with continued use of the same amount of the
substance.
11. Withdrawal, as manifested by either of the following:
a. The characteristic withdrawal syndrome for other (or unknown) substance.
b. The substance (or a closely related substance) is taken to relieve or avoid withdrawal
symptoms.
Reprinted with permission from the Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition, (Copyright
©2013). American Psychiatric Association. All Rights Reserved.
Substance Use Disorders 259
can make it difficult for habitual users of some substances
to cut back or stop their use: As they cut back, they
may experience uncomfortable or even life-threatening
symptoms that are temporarily alleviated by resuming
use of the substance. In most cases, substances that can
lead to tolerance with regular use are also likely to pro-
duce withdrawal symptoms if stopped or taken at lower
doses. As with tolerance, people taking certain medica-
tions for a medical problem may experience withdrawal
symptoms if the medication is stopped or the dosage
lowered. In such cases, withdrawal would not be consid-
ered a symptom of a substance use disorder.
Substance Use Disorder as a Category or on
a Continuum?
According to DSM-5, a habitual drug user either is or is not
diagnosed with a substance use disorder; this is a categorical
decision. However, research suggests that a more meaning-
ful way to conceptualize harmful substance use, at least of
alcohol, is on a continuum of severity (Heath et al., 2003; Langenbucher et al., 2004;
Sher et al., 2005). According to this view, a substance use disorder anchors one end of a
continuum, and unproblematic substance use anchors the other end. This continuum can
be defined by the frequency, quantity, and duration of use, as well as the effects of use
on daily functioning. The more frequent the use, the larger the quantity, or the longer
the use has been going on, the more likely the use is to become a substance use disorder.
According to the continuum approach, we would determine whether any of the
Beatles had a stimulant use disorder based on how much, how often, and for how
long each of them took the stimulant, and the extent to which such use impaired
their daily functioning.
FI G U RE 9.1 • Tolerance and Withdrawal Using a see-saw as a
metaphor for the body’s response to repeated drug use, this figure illustrates the
progression to tolerance and withdrawal: (a) no drug use; (b) an imbalance arises
from drug use; (c) the brain and body adapt to the drug, and tolerance begins;
(d) more of the drug is taken to overcome tolerance; (e) the brain and body adapt
to this higher level of drug use; (f) because of the adaptation, when drug use is
discontinued (or reduced) that adaptation creates withdrawal symptoms.
©
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is
(a) Normal (b) Drug effect (c) Adaptation (tolerance)
(d) Drug effect overcomes
tolerance
(e)
Drug
Drug
Drug
Drug BCR
Note: BCR stands for “body’s compensatory response.” Source: Adapted from Goldstein, 1994.
Drug BCR
BCR
BCR
BCR
Drug
BCR
(f ) WithdrawalTolerance; condition
apparently normal,
dependence masked
260 C H A P T E R 9
Can you match each of these photos to each corresponding pathway by which substance use can become a use disorder? The three pathways
are: (1) the psychoactive component is a side effect of a medication taken to treat a medical problem; (2) through environmental exposure;
(3) setting out to use a substance for its psychoactive effects. Answer: Matching the photos to the pathway, from left to right: A-2, B-1, C-3.
GETTING THE PICTURE
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Use Becomes a Problem
People can develop substance use disorders in three general ways. First, substance
use disorders can arise unintentionally, as can occur through environmental expo-
sure. Second, substance use disorders can develop when the psychoactive element
is a side effect, and the substance is taken for medicinal reasons unrelated to the
psychoactive effect. Third, substance use disorders can develop as a result of the
intentional use of a substance for its psychoactive effect. In this third path toward
substance use disorders, someone may know the risks of using the substance but
nonetheless underestimate his or her own level of risk (Weinstein, 1984, 1993). It
is this third path toward developing substance use disorders that has been the target
of most research, and two main models have been proposed to explain this type of
slide from use to disorder.
Common Liabilities Model
The common liabilities model (also called problem behavior theory; Donovan &
Jessor, 1985) explains how neurological, psychological, and social factors make a per-
son vulnerable to developing a variety of problematic behaviors. It was developed in
response to the results from a study that followed students from grades 7–9 into adult-
hood; the researchers found that adolescents who exhibited “problem behaviors,”
such as drug and alcohol use, early sexual intercourse, and delinquent behaviors (e.g.,
stealing and gambling), were likely later in life to develop a substance use disorder.
The researchers proposed that these various problem behaviors at different ages may
stem from the same underlying factors, called common liabilities. Subsequent studies
have supported this explanation (Agrawal et al., 2004; Ellickson et al., 2004; Windle
& Windle, 2012). One particularly important common liability is a problem with
impulsivity—especially with difficulty restraining urges to engage in potentially
harmful behaviors—which also underlies a variety of other disorders that involve
compulsive behaviors, such as gambling.
Gateway Hypothesis
Another model that researchers have used to a explain the progression from use to a
substance use disorder is the gateway hypothesis and the related stage theory (Kandel,
2002; Kandel & Logan, 1984). According to the gateway hypothesis, “entry”
drugs such as cigarettes and alcohol serve as a gate-
way to (or the first stage in a progression to) use of
“harder” drugs, such as cocaine, or illegal use of
prescription medication. Researchers have found
that some, but not all, adolescent users of entry
drugs did go on to use marijuana (White et al.,
2007), and some of these marijuana users moved
on to harder drugs and hard liquor (Kandel, 2002;
Kandel & Logan, 1984). Teens are unlikely to
experiment with marijuana unless they first exper-
imented with legal—but restricted—substances such as alcohol. Similarly, adolescents
and young adults don’t generally try other illegal substances without having used
marijuana (see Figure 9.2).
This general pattern of progression has been found in various countries and
among different ethnic groups (Kandel & Yamaguchi, 1985). Moreover, people
who develop a substance use disorder often passed through a particular progression
of stages of drug use: initiation, experimentation, casual use, regular use, and then
substance use disorder (Clayton, 1992; Werch & Anzalone, 1995). Of course, not
everybody progresses to the end of this sequence. In fact, the gateway hypothesis is
not a blueprint for all users; rather, it is a way to understand how people who use sub-
stances can end up having a substance use disorder.
Beer/wine
Nonuse
Marijuana
Stage 1 Stage 2 Stage 3 Stage 4
Marijuana Harder drugs
Marijuana
Cigarettes
CigarettesHa
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or
Har
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quo
r
FI G U RE 9.2 • Stages of Drug Use
Common liabilities model
The model that explains how neurological,
psychological, and social factors make a
person vulnerable to a variety of problematic
behaviors, including substance use disorders;
also called problem behavior theory.
Gateway hypothesis
The proposal that use can become a use
disorder when “entry” drugs serve as a
gateway to (or the first stage in a progression
to) use of “harder” drugs.
Source: Kandel & Yamaguchi, 1999
Substance Use Disorders 261
Comorbidity
As we’ve noted in earlier chapters, many people with psychological disorders
abuse substances—that is, they develop one or more symptoms of a substance use
disorder— particularly alcohol, marijuana, cocaine, and opiates (Lingford-Hughes &
Nutt, 2000). Studies have found that almost half of people with alcohol use disor-
der (the name for the substance use disorder when the substance is alcohol) also had
another psychological disorder—and almost three-quarters of those with a different
type of substance use disorder had another psychological disorder (Conway et al.,
2006; Regier et al., 1993). Common comorbid disorders include mood disorders
(most frequently depression), posttraumatic stress disorder (PTSD), schizophrenia,
and attention-deficit/hyperactivity disorder (ADHD, discussed in Chapter 13), a disor-
der marked by problems sustaining attention or by physical hyperactivity (Brady &
Sinha, 2005). People who have a non-substance-related psychological disorder have
a greater risk of substance use turning into a use disorder (Lev-Ran et al., 2013).
When substance use disorder develops after another psychological disorder has devel-
oped, clinicians may infer that the person is using substances in an attempt to allevi-
ate symptoms of the other disorder—to self-medicate.
Polysubstance Abuse
As was true of the Beatles, some people abuse more than one substance, a behavior
pattern that is called polysubstance abuse. One study found that among alcoholics,
64% also had an additional type of substance use disorder (Staines et al., 2001). Poly-
substance abuse is dangerous because of the ways that drugs can interact: One lethal
combination occurs when someone takes a drug that slows down breathing, such as
barbiturates (which are often used as sleeping pills), along with alcohol. A form of
polysubstance abuse that is seldom recognized is the combination of alcohol and ciga-
rettes (nicotine): Cigarettes are the biggest killer of all drugs, and this is particularly
true among alcoholics. Most alcoholics are more likely to die from nicotine-related
medical consequences, such as cardiovascular disease, than from alcohol-related ones
(Hurt et al., 1996).
Prevalence and Costs
The various types of substance use disorders are among the most common psy-
chological disorders. In 2009, an estimated 9% of Americans aged 12 and older, or
22.5 million people, had a substance use disorder (Substance Abuse and Mental
Health Services Administration [SAMHSA], 2010). Generally, men are more likely
than women to be diagnosed with a substance use disorder, although women are
more likely to be diagnosed with a substance use disorder related to legally obtained
prescription medications (Simoni-Wastila et al., 2004).
The prevalence of drug use and substance use disorders varies across ethnic and
racial groups in the United States. However, significant variations occur within each
broad ethnic or racial category. For example, among Americans of Hispanic descent,
the 1-month prevalence rate of heavy drinking (five or more drinks in a sitting) for
Cuban Americans is 1.7%, whereas it is 7.4% for Mexican Americans (NIDA, 2003).
Therefore, prevalence rates of racial and ethnic groups provide only a general over-
view, and they do so only at a particular moment in time.
A substance use disorder affects not only the user but also family members
and friends, coworkers, and colleagues. Substance use disorders are associated with
violence toward family members and neglect of children (Easton et al., 2000; Stuart
et al., 2003). Parents who abuse substances may feel guilty and ashamed about their
substance abuse, which ironically may lead them to increase their substance use to
cope with these feelings (Gruber & Taylor, 2006). Children may find themselves
Using or abusing more than one substance
can increase the risk of accidental overdose;
actor Heath Ledger died in 2008 from taking
a combination of drugs, reportedly for
his chronic insomnia. The autopsy results
indicated that he’d taken pain killers, several
benzodiazepines (used to decrease anxiety),
and an over-the-counter antihistamine
that can induce drowsiness. He may have
developed tolerance to standard doses of
these medications; in combination, they
caused his heart or breathing to slow down so
much that he died (Falco, 2008).
K
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Polysubstance abuse
A behavior pattern of abusing more than one
substance.
262 C H A P T E R 9
shouldering adult tasks and responsibilities (Haber, 2000). Children of parents who
abuse substances are at increased risk of developing emotional and behavioral prob-
lems (Grant, 2000; Kelley & Fals-Stewart, 2002).
Culture and Context
The line between use and abuse shifts over time and across cul-
tures and ethnic groups. For example, cocaine was used legally as
a remedy for many ills in the second half of the 19th century, but
it has now been illegal for decades. And, during the Prohibition
era (1920–1933) in the United States, alcohol use was illegal.
Various cultures use psychoactive substances for different
purposes. Some Native American tribes, for example, use pey-
ote or psilocybin mushrooms (which, when eaten, produce vivid
hallucinations) as part of sacred rituals. Such cultural use of
psychoactive substances is strongly regulated, and there are pen-
alties for abusing those substances, including being put to death
(Trimble, 1994).
In the remaining sections of this chapter we discuss specific
substances that can develop into use disorders. We first describe what they are and
consider the ways in which they have their effects. Because treatments for various
types of substance use disorders are similar, we consider treatment for all types of
substance use disorders in the final section of the chapter.
Jorge and his friend Rick worked hard and played hard in high school. On weekend evenings,
usually their only free time, they’d binge drink, along with others in their group. They went
to different colleges. Jorge kept up his “study hard, party hard” lifestyle; Rick didn’t do much
binge drinking in college, but he started smoking marijuana in the evenings when he was
done studying and he’d go dancing on Saturday nights and sometimes take stimulants. What
information would you want to know in order to determine whether Jorge or Rick had a sub-
stance use disorder?
Thinking Like A Clinician
Stimulants
Stimulants are named for their effect on the central nervous system: They stimulate it,
causing increased activity and arousal. Stimulants include nicotine and amphetamines
(including Ritalin), which are restricted, as well as cocaine, crack, and MDMA
( Ecstasy, or “e”), which are illegal. At low doses, a stimulant can make the user feel
alert, less hungry, and more energetic, mentally and physically.
In 1960, when the Beatles first started playing in Germany, they got through
their performances by taking a legal stimulant, Preludin. A bouncer at the club simply
handed pills to the boys and suggested that they take them. The pills had their effect:
The musicians played for hours and then stayed up for hours afterward, going to
other clubs (Spitz, 2005). And Preludin wasn’t the only stimulant that they took; they
also drank coffee and tea and smoked cigarettes, all of which are legal stimulants.
What Are Stimulants?
In this section we first consider the illegal drugs cocaine and crack, and then we
consider drugs that have both legal and illegal uses—amphetamines, methamphet-
amines, Ritalin, and MDMA.
Cultures may promote substance use
in some contexts and not others. These
Brazilian women are followers of Santo
Daime, a spiritual practice that involves
drinking hoasca, a tea made of plant-based
hallucinogens. Hoasca is legal in Brazil and
the United States when it is used as part of a
religious practice.
Ja
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R
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s
Although all the Beatles smoked cigarettes
during their teenage years, some of them
continued to smoke. George Harrison (at right)
smoked heavily for almost all of his adult life,
up to the point where he was diagnosed with
throat cancer, in 1998. He also developed lung
cancer, which led to his death in 2001.
D
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Substance Use Disorders 263
Cocaine and Crack
Derived from the coca leaf, cocaine was a popular medicine for various ailments in
18th-century Europe and North America. Its use was declared illegal at the beginning
of the 20th century, after it became clear that the drug was being abused and leading
to tolerance and withdrawal (Rebec, 2000). Cocaine that is obtained in the form of
a powder is typically inhaled, or “snorted”; as crack, a crystalline form, it is smoked.
Cocaine acts as a local anesthetic. Thus, when snorted, it leaves the user’s nose
feeling numb; repeated snorting can lead to diminished sense of smell and difficulty
swallowing (NIDA, 2007b). Although the first few experiences of cocaine use may
provide a heightened sense of well-being that can last for up to an hour, this positive
state becomes increasingly harder to attain as tolerance develops (NIDA, 2007b).
Higher doses of cocaine bring many negative effects: paranoia, to the
point of delusions; hallucinations, such as feeling insects crawling on the body
when there are none; compulsive, repetitive behaviors such as teeth grind-
ing; and increased heart rate and blood pressure, with the accompanying risk
of heart attack and sudden death. (The hallucinations occur because cocaine
causes sensory neurons to fire spontaneously.) Users also lose their appetite,
so people who have cocaine use disorder may develop malnutrition. Table 9.3
lists these and additional effects of regular cocaine use. People with cocaine
use disorder often also have alcohol use disorder (Brady et al., 1995; Carroll
et al., 1993; Regier et al., 1990); when these two substances are used at the
same time, the risk of sudden death increases (NIDA, 2007b).
Smoked crack acts more quickly than snorted cocaine and has more intense
effects. Like snorting cocaine, smoking crack leads to a sense of well-being, en-
ergy, and mental clarity. However, this “high” usually lasts only minutes (NIDA,
2007b). As with other stimulants, when the high from crack is over, it leaves in its
wake a sense of depression and craving for more of the drug, as related by Mr. R.
in Case 9.1. These aftereffects may lead the user to take more of the drug and may
lead to tolerance or withdrawal. Moreover, whereas tolerance of or withdrawal
from cocaine may take months or even years of use to develop, such symptoms can develop
extremely rapidly when people take crack—within weeks (NIDA, 2004; Rebec, 2000).
CASE 9.1 • FROM TH E INSIDE: Cocaine Use Disorder—Crack
Mr. R, a 28-year-old man, describes his abuse of crack:
I first started using cocaine about 4 years ago. I don’t remember the first time I smoked the
crack cocaine. It puts you in another world. I can’t explain this euphoric feeling that it gives you,
but it’s a feeling I had never experienced before. I just want to sit there and enjoy the feeling and
not think about anything or do anything. I have to keep doing it constantly to keep up the high.
I actually started staying out all night. I was smoking about five times a week and lost
my apartment, lost everything. Everything was falling apart with my relationship, and I was
starting to miss work a lot. But I just couldn’t control it. You know, it overtook me. That’s all
I thought about and all I wanted to do was to keep smoking. Everything else was secondary.
An intense craving for me is when my heart starts beating fast—actually, I get a lit-
tle sweaty—and all I think about doing is just going to smoke. That’s it. Nothing else—
everything that’s on my mind just kind of disappears.
(Hyman, 2001, pp. 25–87)
As often happens when people develop a substance use disorder, Mr. R.’s life became focused on
obtaining and using crack, and his intense cravings made it difficult for him to stop using the drug.
Amphetamines
Amphetamines typically produce the same effects as does cocaine, although these
effects last longer. Common amphetamines include Benzedrine, Dexedrine, and Adderall.
Amphetamines are usually available as pills, which typically are swallowed, although
TABLE 9.3 • Effects of Cocaine Abuse
Long-term effects
of cocaine
Medical consequences of
cocaine abuse
• Addiction
• Irritability and
mood disturbances
• Restlessness
• Paranoia
• Hallucinations
Cardiovascular effects:
• disturbances in heart rhythm
• heart attacks
Respiratory effects:
• chest pain
• respiratory failure
Neurological effects:
• strokes
• seizures and headaches
Gastrointestinal complications:
• abdominal pain
• nausea
Source: NIDA, 2004, p. 5.
264 C H A P T E R 9
the contents of the pills may be snorted or diluted and injected. Amphetamines are
legally used to treat some disorders, particularly ADHD and the sleep disorder narco-
lepsy, in which the sufferer spontaneously falls asleep for brief periods of time.
With repeated use of amphetamines, people may become hostile toward others,
develop a sense of grandiosity, or exhibit disorganized thinking or behavior (Krystal
et al., 2005). Because tolerance develops, repeat users may take high doses, which can
cause amphetamine psychosis, a condition characterized by paranoid delusions and hal-
lucinations (symptoms similar to those of paranoid schizophrenia; see Chapter 12).
An amphetamine use disorder can have irreversible effects—including problems with
memory and physical coordination—that arise from enduring changes in neurons
(Volkow et al., 2001a), as well as reversible effects of irritability and violent behavior
(Leccese, 1991; Wright & Klee, 2001). Withdrawal symptoms may include depres-
sion, fatigue, anxiety, and irritability.
Methamphetamine
Methamphetamine (“meth” or “speed”) is chemically similar to amphetamines but has
a greater and longer-lasting effect on the central nervous system. It can be inhaled,
swallowed, smoked, or injected, in all cases leading to an intense “rush” of pleasure.
Use rapidly becomes use disorder.
In addition to causing irritability, heart problems, hallucinations and paranoia at
high doses (McKetin et al., 2013; NIDA, 2007e), methamphetamine use can adversely
affect the functioning of the neurotransmitters dopamine and serotonin, which leads
to motor problems, impaired memory, and emotional dysregulation. Moreover, the in-
creased blood pressure that results from taking the drug can cause strokes (NIDA, 2007e;
Thompson et al., 2004). Table 9.4 summarizes the effects of long-term methamphet-
amine abuse. Some—but not all—of the brain damage inflicted by methamphetamine
abuse is reversible with long-term abstinence (Salo et al., 2011; Volkow et al., 2001a).
Ritalin
Ritalin (methylphenidate hydrochloride) is frequently prescribed for ADHD. Its
neurological effect is similar to, but slower than, that of cocaine. People who abuse
Ritalin take the stimulant in any of three ways:
• swallowing pills, which does not usually lead to use disorder;
• inhaling or snorting crushed pills, which leads to a quicker “high” and causes lung
problems; or
• injecting the drug in liquid form, which produces an effect similar to that of cocaine.
Both inhaling and injecting Ritalin can lead to use disorder. People who do not have
ADHD may occasionally swallow Ritalin pills for the stimulant effects—heightened
alertness, increased attention, and decreased appetite. Although such casual use does
not meet the criteria for a use disorder, it still carries the risk of adverse medical side
effects, including heart problems and stroke.
MDMA (Ecstasy)
Methylenedioxymethamphetamine (MDMA), commonly called Ecstasy or simply “e,” is
usually taken in tablet form. It is chemically similar both to methamphetamine and to
the hallucinogen mescaline, and it has the effects of both types of drugs: the stimulant
effect of increased energy and the hallucinogenic effect of distorted perceptions. When
first using it, people report heightened feelings of well-being, empathy, and warmth
toward others, and a greater sensitivity to touch. This experience is less pervasive
with subsequent use. Other effects are reduced anxiety and distorted time perception
(NIDA, 2007e). Abuse can result in poor mood and difficulty regulating emotions, as
well as anxiety and aggression, sleep problems, and decreased appetite (NIDA, 2008b).
TABLE 9.4 • Long-Term Effects of
Methamphetamine Abuse
• Dependence
• Psychosis, including:
° Paranoia
° Hallucinations
• Repetitive motor activity
• Changes in brain structure and function
• Memory loss
• Aggressive or violent behavior
• Mood disturbances
• Severe dental problems
• Weight loss
• Increased blood pressure and possible
stroke
Source: Adapted from NIDA, 2008c.
Substance Use Disorders 265
In addition, M DM A users can develop impaired cognitive functioning,
especially problems with memory, after the drug wears off. These cognitive defi-
cits become more severe when the drug is abused (Verkes et al., 2001). One sur-
vey of MDMA users found that almost 60 % reported withdrawal symptoms that
included poor concentration, depression, decreased appetite, and fatigue; moreover,
almost half of these users developed MDMA use disorder (NIDA, 2007e; Stone et al.,
2006). Frequent users of MDMA may experience tolerance and withdrawal symp-
toms (Leung & Cottler, 2008). Lynn Smith, in Case 9.2, recounts her experience of
MDMA use disorder.
The psychoactive substance known as
“bath salts” is not used for soaking in
the tub. Rather it is a type of stimulant. Users
typically report intense craving for more.
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CASE 9. 2 FROM TH E INSIDE: MDMA Use Disorder
Sometimes I stopped eating and sleeping. I worked only two days a week to support my habit.
The rest of the time was spent getting high, almost always on Ecstasy. The utter bliss of my
first Ecstasy experience was a distant memory. Of course, I never could recapture that first
high, no matter how much Ecstasy I took.
In five months, I went from living somewhat responsibly while pursuing my dream to a per-
son who didn’t care about a thing—and the higher I got, the deeper I sank into a dark, lonely
place. When I did sleep, I had nightmares and the shakes. I had pasty skin, a throbbing head and
the beginnings of feeling paranoid.(Partnership for a Drug-Free America, 2007)
MDMA’s side effects are similar to those of other stimulants, including increased
blood pressure and heart rate. Excessive sweating, another side effect, can cause acute
dehydration and hyperthermia (abnormally high body temperature). The effects of
MDMA may be difficult to predict in part because the tablets often contain other
drugs, such as ketamine, cocaine, or other stimulants (Green, 2004).
“Bath Salts”
Another type of stimulant is commonly known as bath salts. These drugs are not to
be confused with traditional bath salts, such as Epsom salts, which are used to en-
hance the experience of soaking in a bathtub; those bath salts are not psychoactive
substances. Stimulant bath salts are a family of drugs that contains a chemical related
to cathinone, which is found in the khat plant; it is chemically similar to amphet-
amines and Ecstasy. However, the exact composition of each packet of bath salts
varies, and packets typically contain at least one other type of drug, such as MDMA.
Bath salts may lead some users to feel more outgoing and happy, but other users
become agitated and paranoid and even hallucinate or become violent (Penders
et al., 2012). Users—even those who have had an unpleasant experience—re-
port intense cravings for more of the substance (Slomski, 2012). Bath salts
are typically sold as a powder, which is swallowed, inhaled, or injected;
adverse effects occur most often when bath salts are snorted or injected
(NIDA, 2012).
Bath salts increase the activation of dopamine and may kill neu-
rons (Slomski, 2012). Users of bath salts may need to go to a hospital
emergency room because of medical symptoms such as chest pains or
racing heart or because of psychological symptoms such as hallucinations,
paranoia, or panic attacks. Some people have died as a result of the side effects of
using bath salts.
Understanding Stimulants
For the most part, use disorders of the different stimulants arise for similar reasons;
thus, in what follows we will consider the roles of the three kinds of factors in lead-
ing to use disorders of all stimulants.
266 C H A P T E R 9
Nucleus
accumbens
Ventral
tegmental
area
FI G U RE 9.3 • The Dopamine Reward
System Key brain areas of the dopamine
reward system.
Brain Systems and Neural Communication:
Dopamine and Abuse
Dopamine plays a key role in both the pleasurable experience of taking
stimulants and the abuse of stimulants (Kalivas & Volkow, 2005). To see
how, we need to consider the neural circuits that rely on dopamine. To
begin, let’s consider one classic study. Researchers placed tiny electrodes
in parts of rats’ brains; when the rats pressed a lever, they got a small
jolt of electricity, which activated neurons near the electrodes (Olds &
Milner, 1954). The researchers discovered that the animals worked
hard to receive electrical stimulation to certain parts of the brain.
In fact, they sometimes seemed to prefer such stimulation to food
or drink! (This cannot help but remind us of some forms of drug
abuse, in which users sacrifice food and drink for the drug.) This sort
of finding eventually led researchers to define a “reward system” in the
brain. This reward system includes the ventral tegmental area, which in
turn activates the nucleus accumbens (see Figure 9.3). The neurons in this
system rely on the neurotransmitter dopamine. In fact, if animals are given
a drug that blocks the effects of dopamine, they will not work as hard to receive
electrical stimulation in these areas (Fibiger & Phillips, 1988). For this reason, the
reward system is usually referred to as the dopamine reward system. A wide
range of pleasurable activities, such as eating and having sex, activate the dopamine
reward system.
All stimulant drugs affect the dopamine reward system directly (Tomkins &
Sellers, 2001). Many other substances (e.g., alcohol) also activate the dopamine
system directly, and still other types of substances activate it indirectly by al-
tering other brain areas or neurotransmitters that, in turn, affect dopamine
(Leone et al., 1991). Researchers have thus proposed the dopaminergic hypothesis
of substance abuse: The rewarding effects of a drug arise from the dopamine
reward system (Koob & Le Moal, 2008; Robbins & Everitt, 1999a, 1999b;
Tomkins & Sellers, 2001).
Because of the neural changes that occur with continued abuse, af-
ter a while, the person needs the substance to feel “ normal” and expe-
riences cravings when not using the drug. Moreover, larger doses of the
drug are necessar y to experience pleasure. For example, consider how
cocaine affects neurons in the dopamine reward system: Cocaine binds to
dopamine transporters—the molecules that take excess dopamine from the
synapse and bring it back to dopamine- containing sacs within the termi-
nal buttons of the transmitting neuron (see Figure 9.4). When cocaine binds
to these transporter molecules, the transporters don’t operate as effectively to
remove dopamine from the synapses—and thus more dopamine lingers there,
which causes the receptors on the receiving neuron to become less sensitive. Thus,
larger doses of the drug are needed to produce more dopamine before it produces
pleasurable sensations.
A similar mechanism is at work when someone takes methamphetamine.
Again, the drug binds to the molecules that transport excess dopamine back to the
terminal buttons and prevents reuptake from operating effectively—thereby leaving
more dopamine in the synapse, which in turn leads the dopamine receptors eventu-
ally to become desensitized. Moreover, as shown in Figure 9.5, not all of the dam-
age inflicted on the brain by long-term methamphetamine use is reversible. The
images in the figure show the distribution of dopamine transporters in the brain of
a person who abused methamphetamine. As is evident, even 2 years after the person
stopped using methamphetamine, the neurological effects of chronic abuse are not
totally reversed.
Dopamine reward system
The system of neurons, primarily in the nucleus
accumbens and ventral tegmental area, that relies
on dopamine and gives rise to pleasant feelings.
FI G U RE 9.4 • Cocaine Use and
Dopamine This schematic illustrates how
cocaine binds to dopamine transporters, which
prevents normal reuptake of dopamine back
into the transmitting neuron and increases the
amount of dopamine in the synapse—which
thereby desensitizes the receptors and requires
more dopamine to have an effect.
Dopamine
receptors
Receiving
neuron
Dopamine
packaged
in sacs
Transmitting
neuron
Cocaine
Dopamine
transporter
blocked by
cocaine
Dopamine
transporter
functioning
normally
Substance Use Disorders 267
As researchers have come to understand the dopamine reward system in more
detail, they have begun to gain insight into an age-old puzzle: Are some people
more susceptible to developing a use disorder because they have less “charac-
ter” or a weak “moral compass”? No. In fact, at least part of the answer is that
the dopamine reward system is more sensitive and responsive in some people.
For example, in one study, participants were given an injection of the stimulant
Ritalin; participants who rated the experience as pleasant had fewer dopamine
receptors in their brains than those who found it unpleasant (Volkow et al., 1999).
Such findings support the hypothesis that people with fewer dopamine receptors
may be more vulnerable to drug use (and use disorders); the smaller quantity of
receptors means they have reduced activation in the reward system, which is boosted
by substance use (Swanson & Volkow, 2002).
However, we want to end this section with an observation: As we’ve noted
previously, brain areas work together in systems and often more than one sys-
tem is involved in producing a particular behavior. This is true of use disorders
of stimulants in particular and substance use disorders in general. Although the
dopamine reward system plays a crucial role in leading people to abuse drugs,
many other neurotransmitters and their related brain systems have been implicated
in drug abuse, particularly gamma-aminobutyric acid (GA BA), glutamate, and
serotonin. Table 9.5 lists the neurological factors that contribute to use disorders
of stimulants.
Psychological Factors: From Learning to Coping
Various psychological factors contribute to use disorders of stimulants and to sub-
stance use disorders in general. In what follows we examine these psychological
factors in more detail.
Operant Conditioning
Operant conditioning influences stimulant use and whether a person will develop
a substance use disorder in several ways. First, if stimulant use is followed by pleas-
ant consequences, those consequences act as positive reinforcement (which leads
to recurrent use). Research on the dopamine reward system shows that aspects
of this type of learning have neurological underpinnings. In fact, the dopamine
reward system begins to be activated with the expectation of a drug’s positive ef-
fects (that is, the expectation of reinforcement), which leads to a specific type of
craving, reward craving—the desire for the gratifying effects of using a substance
(Verheul et al., 1999).
Second, using stimulants can independently lead to negative reinforcement—
alleviating a negative state, thereby producing a desirable experience. (Remember
that negative reinforcement is not the same as punishment.) In fact, such negatively
reinforcing effects contribute to substance use disorders among people trying to
manage the psychological aftereffects of physical or emotional abuse (Bean, 1992;
Catanzaro & Laurent, 2004; Ireland & Widom, 1994); in particular, using drugs may
(temporarily) distract them from painful memories or their present circumstances
and hence be reinforcing.
The temporary emotional relief provided by substance use can create cravings
for the drug when a person experiences negative emotions; this type of craving is
sometimes referred to as relief craving (Verheul et al., 1999). Both reward crav-
ing and relief craving can cause people to use drugs compulsively, even when they
would like to quit. Thus, cravings of both types are thought to play a primary role in
maintaining substance use disorders, and having such cravings is one of the criteria
for this category of disorders (American Psychiatric Association, 2013; Torrens &
Martín-Santos, 2000).
TABLE 9.5 • Neurological Factors That
Contribute to Stimulant Use
Disorders
• Stimulants bind to dopamine transporters,
leading to increased dopamine in the
synapse.
• Substance activates the dopamine reward
system, specifically the nucleus accum-
bens and ventral tegmental area.*
• Associations between drug-related stimuli
and drug use can activate the limbic sys-
tem (and the dopamine reward system).*
*This factor is not unique to stimulant use disorders.
Reward craving
The desire for the gratifying effects of using a
substance.
Relief craving
The desire for the temporary emotional relief
that can arise from using a substance.
FI G U RE 9.5 • Long-Term
Methamphetamine Use : Reversible
and Irreversible Brain Damage
(a) This scan shows the distribution of
dopamine transporters in a normal brain.
(b) This scan shows the brain of a person who
had used methamphetamine over a period of
years; as is evident, even 1 month after this
person stopped using the drug, the dopamine
transporters are still in short supply. (c) This
scan shows the brain of the same abuser
more than a year after stopping the use of
methamphetamine; although there is some
recovery of function, the effects of chronic
abuse are not completely reversed.
(a) (b) (c)No history of
methamphet-
amine use
1 month after
abuse stops
1 year after
abuse stops
Source: Nora D. Volkow et al., The Journal of Neuroscience,
December 1, 2001, 21(23):9414–9418.
268 C H A P T E R 9
A third way that operant conditioning contributes to substance use disorders also
involves negative reinforcement, but in this case it occurs because using the substance
can eliminate withdrawal symptoms, which can range from mildly unpleasant to
extremely unpleasant and potentially lethal. Substance use eliminates the unpleasant
withdrawal state, which increases the likelihood of subsequent use.
Classical Conditioning
Stimuli associated with drug use (such as drug paraphernalia or the music and crowds
at a club) are referred to as drug cues, and they come to elicit conditioned re-
sponses through their repeated pairings with drug use. Connections among different
brain areas, such as the amygdala and hippocampus, store such associations between
drug use and the stimuli related to drug use. The drug cues are then associated with
the reinforcing (positive or negative) effects of the drug; once such associations are
established, these drug-related stimuli themselves can trigger the dopamine reward
system (Tomkins & Sellers, 2001). That is, classical and operant conditioning in-
teract: When the consequences (effects) of drug use are rewarding, the person is
likely to use drugs again and again. Repeated drug use, in turn, can produce classical
conditioning, whereby stimuli associated with drug use, such as the vial containing
crack, elicit a craving for the drug (Epstein et al., 2009). Such factors affect each other
and can become feedback loops that create a spiral of a substance use disorder. For
example, people often handle money when buying cocaine and then use the cocaine
shortly afterward; handling money can then become a conditioned stimulus. Thus,
a person addicted to cocaine can come to crave it after handling money (Hamilton
et al., 1998).
Moreover, simply imagining drug cues can activate structures in the limbic sys-
tem (Dackis & O’Brien, 2001), which is tightly tied to the dopamine reward system,
and lead to drug cravings (Hyman, 2005; Stewart et al., 1984). Even after successful
treatment for substance use disorders, being exposed to drug cues can lead a former
abuser to experience powerful cravings and can increase the risk of relapse (Hyman,
2005; Torrens & Martín-Santos, 2000). Cravings do not last indefinitely, however.
When a person craves a substance but does not use it, the craving normally disap-
pears within an hour (Wertz & Sayette, 2001). Researchers have found that a person
is more likely to feel the craving when he or she expects to be able to take the drug.
Table 9.6 summarizes the psychological factors that contribute to use disorders
of stimulants.
Social Factors
Various social factors can promote substance use disorders, such as patterns of family
interactions and perceived social norms. Moreover, sociocultural factors increase the
vulnerability of some people for developing use disorders of stimulants and substance
use disorders in general.
Family Relations and Peers
Research grounded in the stage theory (introduced earlier in this chapter) found
that teenagers whose drug use progressed from marijuana to other illegal substances
did not have close relationships with their parents (Andrews et al., 1991). However,
this finding is only a correlation; it could be that the factors that led to a use disor-
der also soured relationships between teenager and parents or that bad relationships
contributed to drug abuse—or that some third factor, such as a particular tem-
perament, contributed to both factors. In addition, many studies have found that
adolescents who have dysfunctional family interactions (for example, have expe-
rienced child abuse, violence in the household, or parental substance abuse) are
more likely to use and abuse substances (Becoña et al., 2012; Hawkins et al., 1992;
Kilpatrick et al., 2000).
Drug cues
The stimuli associated with drug use that
come to elicit conditioned responses through
their repeated pairings with use of the drug.
TABLE 9.6 • Psychological Factors
That Contribute to Stimulant Use
Disorders
• Observational learning: People observe
models using substances as a coping
strategy and develop expectations about
drug use.*
• Operant conditioning:
° Positive reinforcement leads to subse-
quent expectations of reward, which in
turn lead to reward craving.*
° Substance use alleviates a negative state,
which provides negative reinforcement
and leads to relief craving; substance use
can become a chronic coping strategy.*
• Classical conditioning: Drug cues elicit a
craving*
*This factor is not unique to stimulant use disorders.
Substance Use Disorders 269
A person’s family members can affect whether he or she comes to use or abuse
substances. For instance, when older siblings use drugs, their closer-in-age younger
siblings are more likely to do the same than are their further-apart-in-age younger
siblings. And within the first year of when a spouse registers with a drug problem, his
or her partner is at increased risk of abusing drugs (Kendler, Ohlsson, et al., 2013).
Another social factor involves peers. Friends do things together; they often have
common views or activities they enjoy. It’s not surprising, then, that peers’ substance
use can influence a friend’s use and abuse of psychotropic substances (Brewer et al.,
1998; Keyes et al., 2012). Studies have found that if a person’s peers use or abuse
substances, that person is likely to do the same (Dishion & Medici Skaggs, 2000;
Fergusson et al., 2002). The influence of peers can also help explain findings that
support the gateway hypothesis about increasing drug use. Once a (susceptible) per-
son repeatedly uses an illicit entry drug, such as marijuana, he or she is then more
likely to spend time with peers who also use this drug and become socialized into a
subculture favorable to drug use.
Norms and Perceived Norms
Societies specify norms of behavior, which include the degree to which psychoactive
substances can be taken without being considered a use disorder. The Beatles changed
the social norms, at least for a while, of some portions of the population through
their public association with drugs: Their arrests for possession of illegal drugs, Paul
McCartney’s admission that he used LSD, and song lyrics referring to drug use (such
as, “I get high with a little help from my friends”). Many fans perceived that drug use
was “in” and that they would not be “cool” unless they used drugs, too.
This observation highlights an important fact about social norms: It’s a person’s
perception of the norms, not the actual social norms, that is the key. That is, when
people think that “everyone” in their school, neighborhood, social class, or clique uses
drugs, they are more likely to use drugs themselves. In contrast, people who think
that only a minority of their classmates, neighbors, or friends use drugs will be less
likely to use drugs. In fact, just watching movies can be enough to shift perceptions
of social norms. For example, teenagers who watch movies in which the characters
drink are more likely to binge drink themselves (Hanewinkel et al., 2012). The extent
of the group’s actual drug use is less important than what the person perceives it to be.
Which photo shows a group of people more likely to have a social norm of frequent drug use? Answer: You may have guessed the photo on the
left. However, from the perspective of perceived social norms, it doesn’t matter which group actually does more drugs. People behave according
to the perceived social norms of the social group with which they identify.
GETTING THE PICTURE
Je
n
ke
d
co
/S
h
u
tt
e
rs
to
ck
Te
rr
y
H
a
rr
is
/A
la
m
y
270 C H A P T E R 9
Sociocultural Factors
In addition to family and friends, other social forces can nudge individuals closer to
or further away from a stimulant use disorder as well as substance use disorders in
general. People who are experiencing economic hardship and are unemployed are
at increased risk of developing substance use disorders (Reid et al., 2001; SAMHSA,
2000). Consider that children who grow up in economically disadvantaged neighbor-
hoods are more likely to be exposed to ads for legal psychoactive substances (alcohol
and cigarettes) and to have easier access to these legal psychoactive substances as well
as to illegal ones. Children who live in such neighborhoods may also observe more
abuse of substances among family members, peers, or adults; as noted earlier, such
modeling can have an adverse effect. Moreover, these children are also more likely to
experience or witness traumatic events and develop PTSD (see Chapter 7), which is
associated with substance use disorders ( Johnson, 2008; Stewart, 1996).
Society at large also influences substance use by establishing legal
consequences (Torrens & Martín-Santos, 2000). Society’s influence
is also seen in how access to drug treatment centers is regulated and
in the national policies that direct resources toward effective preven-
tion and treatment programs. Table 9.7 summarizes the social factors
associated with stimulant use disorder.
As noted by the asterisks in Tables 9.5, 9.6, and 9.7, most of the
factors that contribute to use disorders of stimulants also contribute
to use disorders of other substances; the one exception is the specific
neurological effects of stimulant drugs. Because most of the factors
contribute to substance use disorders generally, we do not examine
the feedback loops among the factors until after we review all types
of substance use disorders.
Thinking Like A Clinician
One night before a major class project was due, Sierra had hours of work left to do, and she’d
had all the coffee she could stand. She took one of her roommate’s Ritalin pills and stayed
up all night, completing the project by morning. Sierra gradually got in the habit of using
amphetamines to help her stay up late and do course work. After college, Sierra took a job
with lots of deadlines and lots of late hours. She continued to use stimulants to help her
work, sometimes taking cocaine when she could get it.
At what point would Sierra’s use of stimulants become a use disorder? What would be
some specific symptoms that would indicate that she had cocaine use disorder? What symp-
toms would you expect to see if Sierra were taking a high dose of stimulants? According
to the neuropsychosocial approach, what factors might have led Sierra to abuse stimulants,
if she were abusing them?
Depressants
Two members of the Beatles, Ringo Starr and John Lennon, both had long periods
when they had alcohol use disorder. Starr reported that he “wasted” some years on
alcohol, initially feeling that drinking gave him confidence but realizing later that it
really didn’t (Graff, 1989). And Lennon was frequently drunk during his 18-month
separation from his wife, Yoko Ono.
What Are Depressants?
Alcohol is a depressant. Other depressants are opiates, barbiturates, and benzodiaz-
epines such as diazepam (Valium). In contrast to stimulants, depressants tend to slow
a person down, decreasing behavioral activity and level of awareness. Regular use
TABLE 9.7 • Social Factors That Contribute to Stimulant
Use Disorders
• Dysfunctional family interactions are correlated with the
presence of substance use disorders.*
• An individual’s substance use is related to that of his or her
peers.*
• Norms and perceived norms influence substance use.*
• Substance use disorders are correlated with economic hardship
and unemployment.*
*This factor is not unique to stimulant use disorders.
Substance Use Disorders 271
of depressants tends to lead to tolerance, and discontinuing the use of depressants or
cutting back on the dosage or frequency can produce withdrawal symptoms. In this
section, we will discuss the effects of use and use disorders of three types of depres-
sants: alcohol, barbiturates, and benzodiazepines.
Alcohol
Approximately 6% of Americans aged 12 or older (15 million people) are considered
to have alcohol use disorder. Those who start to drink alcohol earlier in life are more
likely to develop the disorder (SAMHSA, 2010).
Blood Alcohol Concentration
The crucial variable that determines intoxication is blood alcohol concentration,
which is affected by the number of drinks consumed, the period of time over which
they were consumed, the time since the person has last eaten, the person’s body
weight, and the person’s gender. Different concentrations of alcohol in the blood are
associated with different neurological and psychological states (see Figure 9.6). In the
United States, Canada, and Mexico, 0.08% is the legal limit of blood alcohol concen-
tration for driving.
The same amount of alcohol will have a slightly greater effect on a woman
than a man of the same size and weight because men and women metabolize the
drug differently (Frezza et al., 1990). This sex difference arises in part because
women have, on average, less total water content in their bodies than do men,
which means that ingested alcohol is less diluted (Greenfield, 2002; Van Thiel
et al., 1988).
FI G U RE 9.6 • Blood Alcohol Concentration and Its Effects
Different blood alcohol concentrations are, on average, associated with different effects. People may be motivated to drink alcohol
because of the way it can affect thoughts, feelings, and behavior, but the same effects can impair functioning and, with repeated
use, lead to alcohol use disorder. As shown in the graph on the right, alcohol’s effects—both desirable and undesirable—may be
experienced within a few minutes and last a number of hours. The more someone has had to drink, the more impaired he or she will be
for a longer period of time.
Source: Figure from BSCS. (2003). Understanding Alcohol: Investigations into Biology & Behavior. NIH publication No. 04-4991. Copyright © 2003 by BSCS. All rights
reserved. Used with permission.
Changes in thoughts,
feelings, and behavior
Impaired functions
and activities
(continuum)
Blood alcohol
concentration
(percentage)
Relaxation
Sense of well-being
Loss of inhibition
Pleasure
Numbing of feelings
Nausea
Sleepiness
Emotional arousal
Mood swings
Anger
Sadness
Mania
Aggression
Reduced sensations
Depression
Stupor
Unconsciousness
Death possible
Coma
Death
0.01 – 0.05
0.06 – 0.10
0.11 – 0.20
0.21 – 0.30
0.31 – 0.40
0.41 and greater
B
lo
o
d
a
lc
o
h
o
l
co
n
ce
n
tr
at
io
n
(
p
er
ce
n
ta
g
e)
0
1 2 3 4 5 6
0.02
0.01
0.03
0.04
0.05
0.06
0.07
0.08
0.09
0.10
Time (hours)
Alertness
Visual tracking
Judgment
Coordination
(especially fine motor
skills)
Reasoning and
depth perception
Social behavior
(e.g., obnoxiousness)
Speech (slurred)
Balance
Temperature
regulation
Bladder control
Breathing
Heart rate (slowed)
272 C H A P T E R 9
Not only do the effects of a given amount of alcohol differ by gender, but there
are also individual differences. Some people have a more intense response to alcohol
than do others. This variability appears to be mediated in part by genes (Webb et al.,
2011), but it is also related to the level of tolerance a person has acquired.
Binge Drinking
Binge drinking, or heavy episodic drinking, occurs when a person drinks until his or her
blood alcohol concentration reaches at least 0.08% in a 2-hour period (which gener-
ally translates into four or more drinks for women, five or more for men; one drink is
equivalent to 12 ounces of beer, 5 ounces of wine, or 1.5 ounces of 80-proof liquor)
(National Institute on Alcohol Abuse and Alcoholism National Advisory Coun-
cil, 2004). Binge drinking is likely to occur when a person sets out to get drunk
(Schulenberg et al., 1996). Repetitive binge drinking can lead to alcohol use disorder.
Alcohol Use Disorder
Chronic drinking leads to tolerance and withdrawal, thus fulfilling the minimum
two criteria for alcohol use disorder (sometimes referred to as alcoholism). According
to the National Institute on Alcohol Abuse and Alcoholism (2012), alcoholism is
marked by four symptoms:
• craving, which is a strong need, or urge, to drink;
• loss of control, which consists of an episode of drinking during which the person
finds it difficult to stop compulsively drinking;
• physical dependence, which brings withdrawal symptoms, such as nausea, sweating,
shakiness, and anxiety after stopping drinking; and
• tolerance, which causes a person to need to drink greater amounts of alcohol to
get “high.”
Which of these two people is likely to experience greater effects of alcohol? Answer: The female. Men
and women metabolize alcohol differently, in part, because women have, on average, less total water
content in their bodies than do men, and hence the alcohol is less diluted in women’s blood.
GETTING THE PICTURE
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CASE 9.3 • FROM TH E INSIDE: Alcohol Use Disorder
Caroline Knapp describes her alcohol use disorder in her memoir Drinking: A Love Story (1997):
By that point I don’t even think the alcohol worked anymore. Certainly drinking was no
longer fun. It had long ago ceased to be fun. A few glasses of wine with a friend after work
could still feel reassuring and familiar, but drinking was so need driven by the end, so vis-
ceral and compulsive, that the pleasure was almost accidental. Pleasure just wasn’t the
point. At the end I didn’t even feel like myself until I had a drink or two, and I remember
that scared me a little: alcohol had become something I felt I needed in order to return to
a sense of normalcy, in order to think straight. After one or two drinks I’d feel like I’d come
back into my own skin—more clearheaded, more relaxed—but the feeling would last for
only half an hour or so. Another few drinks and I’d be gone again, headed toward oblivion.
(p. 231)
In Case 9.3, Knapp describes the four elements of alcoholism: craving (“need
driven”), loss of control (she would continue to drink until she was “headed toward
oblivion”), physical dependence (“something I felt I needed in order to return to nor-
malcy”), and tolerance (the alcohol didn’t have as strong an effect as it had initially).
Alcohol use disorder is also associated with memory problems, in particular,
blackouts, periods of time during which the drinker cannot later remember what trans-
pired while he or she was intoxicated. Knapp (1997) described her blackouts: “Some-
times I’d wake up at Sam’s [a friend’s] house, in his bed, wearing one of his T-shirts.
I don’t think we ever had sex but I can’t say for sure” (p. 154).
Sedative-Hypnotic Drugs
Sedative-hypnotic drugs reduce pain and anxiety, relax muscles, lower blood pressure, slow
breathing and heart rate, and induce sedation and sleep. In general, drugs in this class cause
disinhibiting and depressant effects similar to those of alcohol (impaired physical coordi-
nation and mental judgment and increased aggressive or sexual behavior). Although these
psychoactive substances can lower inhibitions and bring a sense of well-being, they also
can cause memory problems, confusion, poor concentration, fatigue, and even respiratory
arrest (NIDA, 2008e). When sedative-hypnotic drugs are mixed with another depres-
sant, such as alcohol, the combined effect can be lethal: The person’s breathing and heart
rate can slow to the point where the person dies. Chronic use of these drugs can lead to
tolerance. Two general types of drugs are in this class: barbiturates and benzodiazepines.
Barbiturates
Barbiturates, which include amobarbital (Amytal), pentobarbital (Nembutal), and
secobarbital (Seconal), are usually prescribed to treat sleep problems. Although use of
a barbiturate is legal with a prescription, this type of medication is commonly abused
by both those with a prescription and those who obtain the drug illegally. As with
other depressants, repeated barbiturate use leads to tolerance, so the person takes ever
larger doses to get to sleep or reduce anxiety. Repeated barbiturate use can also lead
to withdrawal symptoms, including agitation and restlessness, hallucinations, confu-
sion, and, in some cases, seizures (NIDA, 2005c). People with barbiturate use disor-
der who want to discontinue or decrease their intake of the drug should do so with
care; they should first consult a knowledgeable physician to determine an appropriate
schedule for tapering off without inducing dangerous withdrawal symptoms. If they
discontinue the drug abruptly, they risk having convulsions and could even die.
Benzodiazepines
Benzodiazepines are usually prescribed to alleviate muscle pain, to aid sleep, or as a short-
term treatment for anxiety (see Chapter 6); however, long-term use leads to tolerance
and withdrawal. Examples of benzodiazepines include lorazepam (Ativan), triazolam
(Halcion), clonazepam (Klonopin), diazapam (Valium), and alprazolam (Xanax). As with
barbiturate use disorder, a person with benzodiazepine use disorder should gradually
taper off of the drug, in consultation with a physician; abruptly stopping use can lead
274 C H A P T E R 9
FI G U RE 9.7 • Alcohol Use Disorder:
Effects on the Brain One of the effects of
long-term alcohol use disorder—alcoholism—is
enlarged ventricles (the cavities in the brain
filled with cerebrospinal fluid). (a) The ventricles
in this MRI scan are normal size; (b) the enlarged
ventricles in this MRI scan are those of a man
with alcohol use disorder. The enlargement
of the ventricles reflects the reduced size of
a number of brain areas. These neurological
changes may explain some of the memory
problems associated with alcohol use disorder.
Source: Rosenbloom et al. (2003). Alcohol Research &
Health 27(2):146–152 .
(b)(a)
to seizures and psychosis. A benzodiazepine-like class of sedative drugs, referred to as
nonbenzodiazepines, can also be abused and have similar effects, side effects, and risks.
Examples include zolpidem (Ambien), eszopiclone (Lunesta), and zaleplon (Sonata).
Understanding Depressants
In what follows, we will first discuss how brain systems and neural communication are
affected by depressants in general and then turn to the effects of alcohol in particular.
Neurological Factors
In this section, we consider a set of closely related topics: the effects of depressants on
the brain systems and neural communication, biological by-products of alcohol use
disorder, and the genetics of alcoholism.
Brain Systems and Neural Communication
Benzodiazepines (such as Xanax), barbiturates, and alcohol directly affect the
GA BAnergic system, which is widespread in the brain and primarily activates
inhibitory neurons. The resulting inhibition affects neurons in brain structures that
are involved in anxiety, such as the amygdala. As we’ve noted before, the amygdala
plays a key role in fear, and hence inhibiting it dulls the sense of fear and the related
feeling of anxiety. Thus, it is not surprising that people who experience anxiety, for
whatever reasons, find the use of depressants particularly reinforcing.
Although alcohol consumption induces the production of dopamine, which is re-
warding, chronic use of alcohol stimulates the production of a type of neurotransmitter
called endogenous opioids, sometimes referred to as “pleasure chemicals.” (There is a class
of drugs referred to as opioids or opiates, which we’ll discuss later in the chapter. The
word endogenous—which means arises from an inside source—is used to distinguish the
neurotransmitter opioids from the drugs of the same name.) Endogenous opioids are
responsible for “runner’s high,” the feeling that occurs when someone has pushed her-
self or himself to a physical limit and experiences a sense of deep pleasure. In chronic
drinkers, the activity of endogenous opioids occurs only in response to alcohol; when
they stop drinking, their bodies no longer produce endogenous opioids. Thus, when a
chronic drinker isn’t consuming alcohol, he or she may experience symptoms related
to opioid withdrawal, which are unpleasant. This experience in turn may induce the
person to consume more alcohol to produce more opioids (Gianoulakis, 2001). In
addition, a single drink releases more opioids in heavy drinkers than in light drinkers
(Mitchell et al., 2012). This is only a correlation, but one possible explanation for it
is that some people may become heavy drinkers, in part, because their brains release
more opioids in response to alcohol, thus activating the dopamine reward system.
Biological By-products of Alcohol Use Disorder
People who frequently drink a lot of alcohol may become malnourished when the
calories in alcohol substitute for calories from food (Mehta et al., 2006). Such mal-
nourishment can include a deficiency in vitamin B1, which even-
tually causes several key parts of the brain to atrophy—including
brain structures important for storing new information in mem-
ory. Thus, drinking a lot of alcohol can indirectly lead to chronic
memory problems (which produces a condition called Korsakoff’s
syndrome). Figure 9.7 shows a result of such brain atrophy: the in-
creased size of the fluid-filled hollow areas, the ventricles, in the
center of the brain.
For people with alcohol use disorder, a hangover indicates
that their bodies are going through alcohol withdrawal as the al-
cohol leaves the system (Cicero, 1978); drinking more alcohol can
temporarily diminish the discomfort of the withdrawal symptoms.
Substance Use Disorders 275
For a heavy drinker, withdrawal symptoms include headaches, weakness, tremors,
anxiety, higher blood pressure, seizures, and increased heart and breathing rates. An
extremely heavy drinker can also experience fever, agitation, and irritability, as well
as more severe symptoms such as uncontrollable shaking, confusion, convulsions, and
visual hallucinations. All these alcohol withdrawal symptoms are collectively referred
to as delirium tremens (also simply called “the DTs”). Such withdrawal symptoms
normally begin within 4 days after the person last drank alcohol (Romach & Sellers,
1991). Delirium tremens can be potentially lethal; when people with alcohol use dis-
order are ready to stop drinking, they should have a physician supervise the process.
Genetics of Alcoholism
The tendency to abuse drugs is affected by genes (Palmer et al., 2012). One sign of this is
the fact that substance use disorders tend to run in families. However, only the genetics
of alcoholism has been studied in depth. Researchers have found that
biological offspring of alcoholics are about twice as likely to become
alcoholics as people without such a family history (Nurnberger et al.,
2004; Russell, 1990). Twin studies have also provided evidence for
a genetic contribution to alcoholism (Carmelli et al., 1993). In ad-
dition, sometimes the offspring of alcoholics are adopted by parents
who are not alcoholics, and researchers have studied some of these
children after they’ve become adults. One striking finding is that even
when they were raised by nonalcoholic parents, children whose bio-
logical parents were alcoholics are much more likely to abuse alcohol
as adults than are those whose biological parents were not alcoholics
(Kendler, Sundquist, et al., 2013). Table 9.8 summarizes the neuro-
logical factors that contribute to use disorders of depressants.
Psychological Factors
Many of the psychological factors that contribute to use disorders of stimulants also con-
tribute to use disorders of depressants (see the starred items in Table 9.6); in particular:
• observational learning of depressant use, which promotes expectations about
experiences from such use and promotes such use as a coping strategy;
• operant conditioning, in which
positive reinforcement leads to positive expectations of depressant use and to
reward craving;
negative reinforcement can lead to relief craving and to depressant use becoming
a chronic coping strategy; and
• classical conditioning, whereby drug cues elicit cravings.
Let’s examine in a bit more detail the role of coping strategies and expectations in
alcohol use. Some people use alcohol as a way to cope with their problems. Consider
Charles’s experience in Case 9.4.
CASE 9.4 • FROM TH E OUTSIDE: Alcohol Use Disorder as a Coping
Strategy
Charles, a high-school teacher with a long-standing problem of alcohol [use disorder],
identified boredom and anger as key high-risk relapse factors. His problem with anger
involved a pattern of avoiding interpersonal conflicts and letting his anger build up. Over
time, Charles would reach a point of total frustration and use his angry thoughts and feel-
ings to justify drinking binges. [He had perceived his anger to be a] “bad feeling that could
only be expressed through drinking” . . . he often became upset and angry because of cer-
tain beliefs he held about how others “should” treat him.
(Daley & Salloum, 1999, p. 258)
TABLE 9.8 • Neurological Factors That Contribute to
Depressant Use Disorders
• Increased activity of the GABAnergic system leads to increased
inhibition of anxiety-related brain structures.
• Depressants indirectly activate the dopamine reward system.
• Depressants generally cause the nervous system to be less
responsive.
• Some substances directly activate the dopamine reward system,
including the nucleus accumbens and the ventral tegmental area.*
• Associations between drug-related stimuli and drug use can activate
the limbic system (and the dopamine reward system).*
*This factor is not unique to depressant use disorder.
Delirium tremens (DTs)
The symptoms of alcohol withdrawal that
include uncontrollable shaking, confusion,
convulsions, visual hallucinations, and fever.
276 C H A P T E R 9
Like Charles, other people use alcohol to try to cope with particular emotions. In
Charles’s case, it was anger; for other people, the emotions might be sadness, anxiety,
fear, shame, or any of a range of other emotions (Gaher et al., 2006). Particular
factors lead some people to have a higher risk of using alcohol to cope. One such
factor relates to the trait of anxiety sensitivity (see Chapter 6): People who are high
in this trait find alcohol to be very calming, which explains why an anxiety disorder
frequently precedes an alcohol use disorder in people who have both kinds of disor-
ders (Robinson et al., 2011; Stewart et al., 2001).
Finally, even when they are not related to a coping strategy, expectations of what
will happen as a result of drinking can also affect behavior after drinking (Kirsch &
Lynn, 1999): People who drink to get “wasted” are in fact more likely to feel and act
more drunk than are people who drink while having dinner with friends in a restaurant,
even when people in both situations end up with the same blood alcohol concentration.
Social Factors
A variety of social factors can contribute to substance use disorders (see the starred
items in Table 9.7). For depressants, including alcohol, such factors include:
• dysfunctional family interactions (such as child abuse or neglect);
• peers’ use of depressants;
• norms or perceived norms about depressant use (as in a subculture where drinking
is the norm or is perceived to be so); and
• economic hardship and unemployment.
Another social factor is culture: Culture affects both the
degree of alcohol abuse and the ways in which alcohol is used
(Abbott & Chase, 2008). For example, the rate of alcohol use
disorder among American women has increased over time.
Historically, women in the United States had much lower rates
of alcoholism than did men, but as social mores and roles for
women changed, the incidence of alcoholism among women
has come to approach that of men (Greenfield, 2002).
Cultures also create social norms for appropriate and inap-
propriate use of alcohol, such as allowing “fiesta” drunkenness
on certain occasions (Finch, 2001; Room & Makela, 2000).
Moreover, the media influence norms and perceived norms.
One correlational study found that adolescents and young adults
who saw more ads for alcohol drank more alcohol ( Snyder et al.,
2006), possibly because seeing more ads for alcohol led them to
perceive the norm for alcohol use to be greater than it was.
Thinking Like A Clinician
When you see your neighbor in the hallway in the evenings, she sometimes can’t seem to
walk in a straight line, her speech is slurred, and she reeks of alcohol. She frequently misses
when she tries to put her key in the lock and begins giggling. Once you saw her vomit after
such an incident. On a few occasions, she hasn’t been so obviously “wasted” and has turned
to you and roughly said, “What are you staring at?” One time, when you smirked as she tried
to put her key in the lock, she came over to you and threatened to “kick your butt.” Even dur-
ing the daytime, though, she’s not very nice or friendly.
Do you think this neighbor has a problem with alcohol, and if so, does it reach the level
to be considered alcohol use disorder? Why or why not? What supports or refutes the con-
clusion that she has an alcohol problem? What information would you want to know before
making a confident decision? According to the neuropsychosocial approach, what factors
might underlie this neighbor’s use of alcohol?
The rate of alcohol use disorder among
American women has increased over
time—so, too, has the number of images of
women drinking in TV shows, movies, and
advertisements.
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Other Abused Substances
This chapter has focused so far on stimulants and depressants because they are the
most commonly abused substances. However, they are not the only substances that
people abuse. In this section we briefly review three classes of other substances that
are often abused: opioids (such as codeine and heroin), hallucinogens (such as mari-
juana), and dissociative anesthetics (such as ketamine).
What Are Other Abused Substances?
By 1969, the Beatles had not performed for 3 years. In that year, they agreed to
perform and have their rehearsals filmed. They spent a month in a recording studio,
composing and arranging songs, learning their parts, and rehearsing the songs.
Rather than a true concert, however, the project culminated in a live, rooftop per-
formance that was filmed. Some of this arduous process and the final concert were
captured in the film Let It Be, which shows glimpses of the effects of John Lennon’s
heroin use. Lennon had difficulty remembering song lyrics from hour to hour and
day to day, had trouble getting up each morning and arriving at the sessions on time,
and had difficulty concentrating on writing and finishing songs (Spitz, 2005; Sulpy
& Schweighardt, 1994). Such problems are typical of heroin use in particular and of
the use of opioids more generally.
Opioids: Narcotic Analgesics
Opioids—also called opiates or narcotic analgesics—are derived from the opium poppy
plant or chemically related substances. These substances are perhaps best character-
ized as exogenous opioids (exogenous means “arising from an outside source”). Exog-
enous opioids include methadone and heroin (to be discussed in more detail shortly),
as well as codeine, morphine, and synthetic derivatives found in prescription pain
relief medications such as oxycodone (OxyContin), hydrocodone (Vicodin), and others.
Legal but restricted narcotic analgesics are generally prescribed for persistent cough-
ing, severe diarrhea, and severe pain. These drugs can be injected, snorted, or taken
by mouth.
All analgesics relieve pain, and people who take analgesics for recreational pur-
poses may temporarily experience pleasant, relaxing effects. However, this category
of drugs is highly addictive: Their use rapidly leads to tolerance and withdrawal and
compulsive behavior related to procuring and taking the drug. Although users may
experience euphoria after taking such a drug, that mood fades to apathy, unhap-
piness, impaired judgment, and psychomotor agitation (the “fidgets”) or psychomo-
tor retardation (sluggishness). Users may also experience confusion—as happened
to John Lennon—as well as slurred speech, sedation, or unconsciousness. Narcotics
depress the central nervous system and can cause drowsiness and slower breathing,
which can lead to death if an opioid is taken with a depressant.
Withdrawal from an opioid typically begins within 8 hours after the drug was
last used and peaks within several days. Physical symptoms of withdrawal include
nausea and vomiting, muscle aches, dilated pupils, sweating, fever, and diarrhea;
many of the symptoms are similar to those of a bad case of the flu. Depressed mood,
irritability, and a sense of restlessness are also common during withdrawal.
Heroin is one of the stronger opioids and is ver y addictive. The contrast
between the euphoria that the drug induces and the letdown that comes when its
effects wear off can drive some people to crave the euphoria, and so they take the
drug, again and again—which in turn leads to tolerance. Tolerance makes the same
dose of heroin fall short: Instead of causing euphoria, it often causes irritability
(NIDA, 2007c).
Although some narcotic analgesics are
derived from the opium poppy plant, others
are synthetic derivatives. Repeated use of
any type of narcotic analgesic rapidly leads
to tolerance and withdrawal—signs of a use
disorder.
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Surveys of people who have used heroin find that the typical user starts out snort-
ing heroin (as Lennon did), progresses to injecting heroin under the skin but not into
blood vessels (termed skin popping), and then ends up injecting into blood vessels
(termed mainlining). Injecting heroin causes a more intense experience—a “rush,” a
feeling of immediate intensity. Most users proceed from occasional use to daily use,
and their primary motivation in life becomes obtaining enough money to procure
the next dose, or “fix.” Because users become tolerant to the drug, they must increase
the amount they use in order to get an effect.
Heroin use disorder is associated with a variety of medical problems, such as
pneumonia and liver disease. In addition, heroin users who inject the drug are at risk
of contracting HIV and hepatitis as well as collapsed veins—and an overdose can be
fatal (NIDA, 2007c).
Hallucinogens
Hallucinogens are substances that induce sensor y or perceptua l distor tions—
hallucinations in any of the senses. That is, users think they see, hear, taste, or feel
something that is not actually present or not present in the way it is perceived. Some
hallucinogens also can induce mood swings. Hallucinogens frequently taken for rec-
reational purposes include the following:
• LSD (a synthetic hallucinogen, also called acid),
• mescaline (a psychoactive substance produced by certain kinds of cacti),
• psilocybin (a psychoactive substance present in psilocybin mushrooms, commonly
referred to as “magic mushrooms”), and
• marijuana (the dried leaves and flowers of the hemp plant, cannabis sativa).
The first three of these drugs are chemically similar to the neurotransmitter sero-
tonin. A single moderate dose of any of these drugs (or a very high dose of mari-
juana) is enough to induce visual hallucinations. In what follows we examine the use
disorders that can arise when people take LSD or marijuana.
LSD
All of the Beatles used LSD at one point or another, but John Lennon reported that
he took LSD thousands of times—which surely would constitute abusing the drug.
LSD is a hallucinogen because it alters the user’s visual or auditory sensations and
perceptions; it also induces shifting emotions. LSD normally has an effect within 30
to 90 minutes of being ingested, and the effects last up to 12 hours (NIDA, 2001).
The effects of LSD can be unpredictable. A “bad trip” (that is, an adverse reaction
to LSD) can include intense anxiety, fear, and dread; a user may feel as if he or she is
totally losing control, going crazy, or dying. People who are alone when experiencing
a bad trip may get hurt or kill themselves as they respond to the hallucinations.
Two aftereffects can occur from LSD use, even after the pharmacological effects of
the drug have worn off: psychosis (hallucinations and visual disturbances) and “flash-
backs” (involuntary and vivid memories of sensory distortions that occurred while
under the influence of the drug). Such aftereffects are rare, although LSD abuse can
induce enduring psychotic symptoms in a small number of people (NIDA, 2007d).
Marijuana
The Beatles also smoked marijuana. The resin from the hemp plant’s flowering tops
is made into another, more potent drug, hashish. The active ingredient of marijuana
and hashish is tetrahydrocannabinol (THC). Both marijuana and hashish can be either
smoked or ingested.
Marijuana’s effects are subtler than those of other hallucinogens, creating minor
perceptual distortions that lead a person to experience more vivid sensations and
to feel that time has slowed down (NIDA, 2005b). The user’s cognitive and motor
Substance Use Disorders 279
abilities are also slowed or temporarily impaired, which produces poor driving skills
(Ramaekers et al., 2006). THC ultimately activates the dopamine reward system
(NIDA, 2000). Not everyone who uses marijuana develops a use disorder, but some
people do develop such a disorder. If a person develops cannabis use disorder (as is it is
called in DSM-5), he or she will experience withdrawal symptoms after he or she
stops using marijuana; such symptoms include irritability, anxiety, depression, de-
creased appetite, and disturbed sleep (Allsop et al., 2012; Kouri & Pope, 2000). Stud-
ies have found that chronic marijuana use adversely affects learning, memory, and
motivation—even when the user has not taken the drug recently and is not under its
direct influence (Lane et al., 2005; Pope et al., 2001; Pope & Yurgelin-Todd, 1996).
These effects are particularly likely to occur if the person started to use marijuana
heavily during adolescence (Meier et al., 2012).
Dissociative Anesthetics
A dissociative anesthetic produces a sense of detachment from the user’s surroundings—
a dissociation. The word anesthetic in the name reflects the fact that many of these drugs
were originally developed as anesthetics to be used during surgery. Dissociative
anesthetics act like depressants and also affect glutamate activity (Kapur & Seeman,
2002). These drugs can distort visual and auditory perception. Drugs of this type are
included in the term “club drugs” because they tend to be taken before or during an
evening of dancing at a nightclub. The most commonly abused members of this class
of drugs are phencyclidine and ketamine, which we discuss in the following sections.
Phencyclidine (PCP)
Phencyclidine (PCP, also known as “angel dust” and “rocket fuel”) became a street
drug in the 1960s. It can be snorted, ingested, or smoked, and users can quickly
begin to take it compulsively. PCP abusers may report feeling powerful and invul-
nerable while the drug is in their system, but they may become violent or suicidal
(NIDA, 2007f ).
PCP has deleterious effects even when taken at low to moderate doses. Medical
effects include increased blood pressure, heart rate, and sweating, coordination prob-
lems, and numbness in the hands and feet. At higher doses, PCP users may experi-
ence hallucinations, delusions, paranoia, disordered thinking, and memory problems
as well as speech and cognitive problems (as did the man in Case 9.5)—even up to a
year after last use (NIDA, 2007f ).
CASE 9.5 • FROM TH E OUTSIDE: Phencyclidine Use Disorder
The patient is a 20-year-old man who was brought to the hospital, trussed in ropes, by his
four brothers. This is his seventh hospitalization in the last 2 years, each for similar behavior.
One of his brothers reports that he “came home crazy,” threw a chair through a window, tore
a gas heater off the wall, and ran into the street. The family called the police, who appre-
hended him shortly thereafter as he stood, naked, directing traffic at a busy intersection. He
assaulted the arresting officers, escaped from them, and ran home screaming threats at his
family. There his brothers were able to subdue him.
On admission, the patient was observed to be agitated, with his mood fluctuating between
anger and fear. He had slurred speech and staggered when he walked. He remained extremely
violent and disorganized for the first several days of his hospitalization, then began having
longer and longer lucid intervals, still interspersed with sudden, unpredictable periods in which
he displayed great suspiciousness, a fierce expression, slurred speech, and clenched fists.
After calming down, the patient denied ever having been violent or acting in an unusual
way (“I’m a peaceable man”) and said he could not remember how he got to the hospital. He
admitted using alcohol and marijuana socially, but denied phencyclidine (PCP) use except for
once, experimentally, 3 years previously. Nevertheless, blood and urine tests were positive for
phencyclidine, and his brother believes “he gets dusted every day.”
(Spitzer et al., 2002, pp. 121–122)
280 C H A P T E R 9
Ketamine
Ketamine (“Special K” or “vitamin K”) induces anesthesia and hallucinations and can
be injected or snorted. Ketamine is chemically similar to PCP but is shorter acting
and has less intense effects. With high doses, some users experience a sense of disso-
ciation so severe that they feel as if they are dying (NIDA, 2001). Ketamine use and
abuse are associated with temporary memory loss, impaired thinking, a loss of con-
tact with reality, violent behavior, and breathing and heart problems that are poten-
tially lethal (Krystal et al., 2005; White & Ryan, 1996). Regular users of ketamine
may develop tolerance and cravings ( Jansen & Darracot- Cankovic, 2001).
Understanding Other Abused Substances
In what follows, we first consider neurological factors for each class of substances and
then turn to psychological and social factors.
Neurological Factors
Depending on the abused substance, different brain systems and neural communica-
tion processes are critical.
Opioids
Among the narcotic analgesics, researchers have focused most of their attention on
heroin—in large part because it poses the greatest problem. Like other opioids, her-
oin slows down activity in the central nervous system. It directly affects the part of
the brain involved in breathing and coughing—the brainstem—and thus historically
was used to suppress persistent coughs. In addition, heroin binds to opioid recep-
tors in the brain, which has the effect of decreasing pain, and indirectly activates the
dopamine reward system (NIDA, 2000). Continued heroin use also decreases the
production of endorphins, a class of neurotransmitters that act as natural painkillers.
Thus, over time heroin abuse reduces the body’s natural pain-relieving ability. In
fact, someone with heroin use disorder has his or her endorphin production reduced
to the point that, when withdrawal symptoms arise, endorphins that would have
kicked in to reduce pain are not able to do so, making the symptoms feel even worse
than they otherwise would be.
Hallucinogens
THC, the active ingredient in marijuana, is chemically similar to the type of neu-
rotransmitters known as cannabinoids, and it activates the dopamine reward system.
People who began abusing marijuana at an early age have atrophy of brain areas that
contain many receptors for cannabinoids (De Bellis et al., 2000; Ernst & Chefer,
2001; Wilson et al., 2000), especially the hippocampus and the cerebellum. Atrophy
of the hippocampus can explain why chronic marijuana users develop memory prob-
lems, and atrophy of the cerebellum can explain why they develop balance and co-
ordination problems. Cannabinoids also modulate other neurotransmitters and affect
pain and appetite (Wilson & Nicoll, 2001).
The genetic bases of abuse of most types of substances have not been studied
in depth. However, one twin study of cannabis use disorder (Lynskey et al., 2002)
estimated that genes account for 45% of the variance in vulnerability to cannabis use
disorder, shared environmental factors account for 20%, and nonshared environmen-
tal factors account for the remaining 35%.
Dissociative Anesthetics
PCP and ketamine increase the level of glutamate, a fast-acting excitatory neuro-
transmitter. Glutamate can be toxic; it actually kills neurons if too much is pre-
sent. Thus, by increasing levels of glutamate, dissociative anesthetics may, eventually,
Substance Use Disorders 281
lead to cell death in brain areas that have receptors for this neurotransmitter—which
would explain the memory and other cognitive deficits observed in people who
abuse these drugs.
Psychological Factors
Abuse of these other types of substances is affected by most of the same psychologi-
cal factors that influence abuse of stimulants and depressants (see the starred items in
Table 9.6): observational learning, operant conditioning, and classical conditioning
all contribute to substance use disorders as a maladaptive coping strategy. We exam-
ine here the unique aspects of classical conditioning that are associated with heroin
use disorder.
Classical conditioning can help explain how some accidental heroin “over-
doses” occur (Siegel, 1988; Siegel et al., 2000). The quotation marks around the
word overdoses are meant to convey that, in fact, the user often has not taken more
than usual. Rather, he or she has taken a usual dose in the presence of novel stim-
uli (Siegel & Ramos, 2002). If a user normally takes heroin in a particular place,
such as the basement of the house, he or she develops a conditioned response to
being in that place: The brain triggers biological changes to get ready for the
influx of heroin, activating compensator y mechanisms to dampen the effect of
the about-to-be-taken drug (see Figure 9.1). This response creates a tolerance for
the drug, but—and here’s the most important point—only in that situation. The
stimuli in a “neutral” setting (not associated with use of the drug), such as a bed-
room, have not yet become paired with taking heroin—and hence the brain does
not trigger these compensator y mechanisms before the person takes the drug.
If the conditioned stimulus (e.g., the basement) is not present to elicit the com-
pensatory response, the same dose of heroin can have a greater effect—causing an
“overdose.”
Social Factors
The social factors that are commonly associated with use disorders of stimulants and
depressants also apply to opioids, hallucinogens, and dissociative anesthetics (see the
starred items in Table 9.7). These include dysfunctional family interactions and a
higher proportion of substance-abusing peers, which in turn affects the perceived
norms of substance use and abuse (Kuntsche et al., 2009). Moreover, economic hard-
ship and unemployment are associated with substance use disorders, perhaps because
of chronic stress that arises from economic adversity as well as increased exposure to
substance abuse.
Feedback Loops in Understanding Substance Use
Disorders
The neurological, psychological, and social factors that contribute to substance use
disorders in general do not act in isolation but affect each other through various feed-
back loops (see Figure 9.8).
Clearly, neurological factors play a key role, but can do so in different ways.
Some neurological factors tend to have a direct relationship with substance use
disorders: The effects that a given substance produces in the brain can be directly
influenced by specific genes and a person’s prior exposure to the drug—either in the
mother’s womb or after birth. Neurological factors, such as genes and their influ-
ence on temperament, can also have indirect effects: For example, some people have
SP
N
282 C H A P T E R 9
a temperament that leads them to be more responsive to reward (and to a drug’s
rewarding effects) than others are.
Psychological factors and social factors also play a role in the development of
substance use disorders. Experiencing child abuse, neglect, or another significant
social stressor increases the risk for substance use disorders ( Compton et al., 2005).
Brain Systems
Neural Communication
Mental Processes and
Mental Contents
Family and Peers
Gender/Culture
Nucleus accumbens
Ventral tegmental
area
Hippocampus
Amygdala
Dopamine and, depending
on the substance abused,
GABA, glutamate, serotonin,
cannabinoids
Genetics
Inherited risk for
alcoholism and other
substance use disorders
Expectancies about
substance’s effects and
substance use as (failed)
coping strategy
Behavior
Observational learning
of expectancies about
substance use and how
to cope by using
substances
Positive reinforcement
and negative
reinforcement
Classical conditioning of
drug cues
Affect
Anxiety or depression lessened
by substance, but abuse and
dependence create anxiety
and poor mood
Different social conventions
of substance use for men
and women over time
Legal consequences
Stressful Life Events
Economic hardship
and unemployment
Dysfunctional family
interactions
Distant relationship
with parents
Level of peers’ substance
use associated with an
individual’s substance use
Norms and perceived norms
NeuroPsychoSocial
NeuroPsychoSocial NeuroPsychoSocial
FI G U RE 9.8 • Feedback Loops in Understanding Substance Use Disorders
Substance Use Disorders 283
Moreover, as we saw for alcohol use, peer and family interactions and culture
(social factors) help deter m ine perceived social nor ms, which in tur n alter a
person’s expectations about the effects of taking a substance and his or her will-
ingness to try the substance or continue to use it (psychological factor) (Kendler,
Sundquist, et al., 2013). And once a person has tried a drug, its specific neuro-
logical effects and other consequences of its use—such as whether the experience
of taking the drug is reinforced and how friends respond to the drug use (psy-
chological and social factors) —will affect how likely the person is to continue
using it.
Thinking Like A Clinician
Nat didn’t care much for drinking; his drugs of choice were ketamine and LSD. His friends
worried about him, though, because every weekend he’d either be clubbing (and taking ket-
amine) or tripping on LSD. What might be some of the sensations and perceptions that each
drug induced in Nat, and why might his friends be concerned about him? Suppose he stopped
using LSD but started smoking marijuana daily. What symptoms might he experience, and
why might his friends become concerned? If he switched from taking ketamine to snorting
heroin before clubbing, what difference might it make in the long term?
How would you determine whether Nat’s substance use should be considered a use
disorder? What other information might you want to know before making such a judg-
ment? Do you think he might develop withdrawal symptoms? Why or why not? If so, which
ones? According to the neuropsychosocial approach, what factors might underlie Nat’s use
of drugs?
Treating Substance Use Disorders
Three of the four Beatles were known to have at least one type of substance use dis-
order: George Harrison, on nicotine (cigarettes), Ringo Starr on alcohol (for which
he received treatment), and John Lennon on alcohol and heroin. It is not known
whether any of the Beatles (other than Starr) received professional treatment for their
use disorder.
We begin by considering the goals of treatment and what the best outcomes can
be. Then we examine the treatments that target each of the three types of factors, and,
when appropriate, note the use of specific treatments for particular types of substance
use disorders. However, as we shall see, many treatments that target psychological
and social factors can effectively treat more than one type of substance use disorder.
Goals of Treatment
Treatments for substance use disorders can have two competing ultimate goals.
One goal is abstinence—leading the person to stop taking the substance entirely.
When this is the goal of treatment, relapse rates tend to be high (up to 60 % , by
some estimates), particularly among patients with comorbid disorders (Brown &
D’Amico, 2001; Curran et al., 2000; NIDA, 1999, 2008f ). To help patients achieve
abstinence, pharmaceutical companies have focused their efforts on developing two
types of medications: (1) those that minimize withdrawal symptoms and (2) those
that block the “high” if the substance is used, thereby leading to extinction of the
conditioned responses arising from substance use disorders.
Given that abstinence-focused treatments have not been as successful as hoped,
an alternative goal of treatment has emerged, which focuses on harm reduction— trying
to reduce the harm to the individual and society that may come from substance use
disorders. For example, needle exchange programs give users a clean needle for each
Two competing, alternate goals guide
treatments for substance use disorders: One
is abstinence (completely stopping the use
of the substance), and the other is harm
reduction (reducing the harmful effects
related to the substance use, such as lowering
the incidence of HIV/AIDS among heroin users
by discouraging needle sharing).
Ja
ck
M
e
rr
it
t/
A
la
m
y
284 C H A P T E R 9
heroin injection, which decreases the transmission of HIV/AIDS because users don’t
need to share needles that may be contaminated. In some cases, harm reduction pro-
grams may also seek to find a middle ground between use disorders and abstinence:
controlled drinking or drug use. In the United States, most treatment programs have
the goal of abstinence.
Targeting Neurological Factors
Many treatments of substance use disorders are directed toward neurological factors.
Detoxification
Detoxification (also referred to as detox) is medically supervised discontinuation
of substance use. Detoxification may involve a gradual decrease in dosage over
a period of time to prevent potentially lethal withdrawal symptoms, such as sei-
zures. People with use disorders of alcohol, benzodiazepine, barbiturate, or opioids
should be medically supervised when they stop taking the substance, particularly
if they were using high doses. Use of other drugs, such as nicotine, cocaine, mari-
juana, and other hallucinogens, can be stopped abruptly without fear of medical
problems, although the withdrawal symptoms may be unpleasant. John Lennon
was not medically supervised when he stopped using heroin, and he described his
disturbing withdrawal experience in his song “Cold Turkey”: “Thirty-six hours/
Rol ling in pain/Praying to someone/Free me again.” Because substance use
C U R R E N T C O N T R O V E R S Y
Once an Alcoholic, Always an
Alcoholic?
Most substance abuse treatment programs, especially those
based on the Twelve-Step approach, insist that clients abstain
from alcohol for the rest of their lives. With this approach, the
assumption is that someone who has developed an alcohol use
disorder will never again be able to drink without relapsing.
This position is often summarized as, “Once an alcoholic, al-
ways an alcoholic.” But is this true?
Many who advocate for an abstinence-only position do
so based on both personal anecdotes of problem drinkers who
tried to moderate their drinking and on treatment outcome
studies in which relatively small proportions of former patients
were able to moderate their drinking. (Unfortunately, only
small proportions manage to abstain consistently.) The absti-
nence-only position is also grounded in the assumption that it
is safer to counsel those with a drinking problem to quit com-
pletely because it’s not possible to predict who will be able to
moderate their drinking.
However, for the past 50 years, there has been growing
support for the alternative position that at least some prob-
lem drinkers are able to moderate or control their drinking
(Sobell & Sobell, 2006). Successful controlled drinking is
typically defined as a reduction in the amount or frequency
of consumption and the experience of fewer if any negative
substance-related consequences associated with that consump-
tion (e.g., Rosenberg, 2002). Research reviews suggest that
problem drinkers are more likely to moderate their drinking
if they have not adopted an “alcoholic identity,” have selected
controlled drinking as their outcome goal, are more psycho-
logically and socially stable, and have a supportive posttreat-
ment environment (Rosenberg, 1993). One advantage of
offering controlled drinking is that it could attract and retain
in treatment those problem drinkers who are ambivalent about
abstaining for the rest of their lives (Ambrogne, 2002). Fur-
thermore, behavioral techniques such as exposure to drink-
ing cues have helped some problem drinkers moderate their
consumption (Saladin & Santa Ana, 2004). Nonetheless,
most treatment services in the United States and Canada do
not offer controlled drinking training, even though accep-
tance of controlled drinking as an outcome goal is widespread
in Australia and many Western Europe countries (Davis &
Rosenberg, in press).
CRITICAL THINKING Based on what you have read, if a friend
or family member who had a drinking problem wanted to
control or moderate their drinking, on what basis would you
support or resist their outcome goal? Why?
(Harold Rosenberg, Bowling Green State University)
Detoxification
Medically supervised discontinuation of
substances for those with substance use
disorders; also referred to as detox.
Substance Use Disorders 285
disorders can cause permanent brain changes (which are evident even years after
withdrawal symptoms have ceased; Hyman, 2005), O’Brien (2005) proposed that
treatment for substance use disorders should not end with detox but rather should
be a long-term venture, similar to long-term treatment for chronic diseases such
as diabetes and hypertension.
Medications
Medications that treat substance use disorders operate in any of several ways: (1) They
interfere with the pleasant effects of drug use; (2) they reduce the unpleasant effects
of withdrawal; or (3) they help maintain abstinence. Because of the high relapse
rate among those with substance use disorders, however, medications should be
supplemented with the sorts of relapse prevention strategies we describe later, in the
sections on treatments targeting psychological and social factors (O’Brien, 2005). We
now turn to consider medications that are used to treat substance-related disorders of
various specific types of drugs.
Stimulants
Of all drugs, stimulants have the most direct effects on the dopamine reward system,
but medications that modify the action of dopamine receptors in this system have
not yet been developed. However, some medications do affect the functioning of
dopamine. For example, a medication that helps people stop smoking is bupropion
(marketed as Zyban), which alters the functioning of several neurotransmitters—
including dopamine. Bupropion can help to decrease cravings for methamphetamines
(Killen et al., 2006; Newton et al., 2006).
Depressants
Medication for use disorders of depressants (such as alcohol use disorder) minimizes
withdrawal symptoms by substituting a less harmful drug in the same category for
the more harmful one. For example, longer-acting benzodiazepines, such as Valium,
may be substituted for alcohol or other depressants.
Disulfiram (Antabuse), a medication for treating alcohol use disorder, relies on
a different approach. Antabuse causes violent nausea and vomiting when it is mixed
with alcohol. When an alcoholic takes Antabuse and then drinks alcohol, the result-
ing nausea and vomiting should condition the person to have negative associations
with drinking alcohol. When Antabuse is taken consistently, it leads people with
alcohol use disorder to drink less frequently (Fuller et al., 1986; Sereny et al., 1986).
However, many patients choose to stop taking Antabuse instead of giving up drink-
ing alcohol (Suh et al., 2006).
Naltrexone (reVia and Vivitrol) is another medication used to treat alcohol use
disorder; after detox, it can help maintain abstinence. Naltrexone indirectly reduces
activity in the dopamine reward system, making drinking alcohol less rewarding; it is
the most widely used medication to treat alcoholism in the United States, and it has
minimal side effects.
Finally, people with alcohol use disorder who are undergoing detox may develop
seizures; to prevent seizures and decrease symptoms of DTs, patients may be given
benzodiazepines, along with the beta-blocker atenolol. However, a patient with DTs
should be hospitalized (Arana & Rosenbaum, 2000).
Opioids
Medications that are used to treat opioid use disorder are generally chemically simi-
lar to the drugs but reduce or eliminate the “high”; treatments with these medica-
tions seek harm reduction because the medications are a safer substitute. For instance,
heroin users may be given methadone, a synthetic opiate that binds to the same recep-
tors as heroin. For about 24 hours after a current or former heroin user has taken
Antabuse
A medication for treating alcohol use disorder
that induces violent nausea and vomiting
when it is mixed with alcohol.
286 C H A P T E R 9
methadone, taking heroin will not lead to a high because methadone prevents the
heroin molecules from binding to the receptors. Methadone also prevents heroin
withdrawal symptoms and cravings (NIDA, 2007c). Treatment of opioid use disorder
with substitution medications, such as methadone, is generally more successful than
promoting abstinence (D’Ippoliti et al., 1998; Strain et al., 1999; United Nations
International Drug Control Programme, 1997).
Because methadone can produce a mild high and is effective for only 24 hours,
patients on methadone maintenance treatment generally must go to a clinic to
receive a daily oral dose, a procedure that minimizes the sale of methadone on
the black market. Methadone blocks only the effects of heroin, so those taking it
might still use cocaine or other drugs to experience a high (El-Bassel et al., 1993).
Another medication, LAAM (levo-alpha-acetyl-methadol), blocks the effects of opioids
for up to 72 hours and does not produce a high. However, LAAM can cause heart
problems and so is prescribed only for patients with opioid use disorder when other
treatments have proven inadequate.
Methadone and LAAM are generally available only in drug treatment clinics.
However, people seeking medication to treat opioid use disorder can receive a
prescription for buprenorphine (Subutex) in a doctor’s off ice. Buprenorphine is
also available in combination with naloxone (Suboxone). In either preparation,
buprenorphine has less potential for being abused than methadone because it does not
produce a high.
Naltrexone is also used to treat alcohol use disorder and, in combination with
buprenorphine, to treat opioid use disorder (Amass et al., 2004). Naltrexone is
generally most effective for those who are highly motivated and willing to take
medication that blocks the reinforcing effects of alcohol or opioids (Tomkins &
Sellers, 2001).
Finally, the beta-blocker clonidine (Catapres) may help with withdrawal symptoms
(Arana & Rosenbaum, 2000). A summary of medications used to treat substance use
disorders is found in Table 9.9.
TABLE 9.9 • Medications Used to Treat Withdrawal and Promote Maintenance
in People with Substance Use Disorders
Class of drugs To treat withdrawal To promote maintenance
Depressants
Longer-acting depressants
(such as Valium) that block
withdrawal symptoms
Antabuse, naltrexone
Narcotic analgesics
Methadone,
buprenorphine, clonidine
Methadone, buprenorphine, LAAM,
naltrexone
Hallucinogens
People who abuse LSD and want to quit can generally do so without withdrawal
symptoms or signif icant cravings. Thus, marijuana is the only substance in this
category that has been the focus of research on treatment, which generally targets
psychological factors and social factors, not neurological ones (McRae et al., 2003).
Targeting Psychological Factors
Treatments that target psychological factors focus on four elements: (1) increasing a
user’s motivation to cease or decrease substance use, (2) changing the user’s expecta-
tions of the drug experience, (3) increasing the user’s involvement in treatment, and
Substance Use Disorders 287
(4) decreasing the (classically and operantly) conditioned behaviors associated with
use of the drug. We first consider motivation, and then see how CBT and Twelve-
Step Facilitation address other aspects of treatment.
Motivation
For people with substance use disorders, stopping or decreasing use is at best
unpleasant and at worst is ver y painful and extremely aversive. Therefore, the
user’s motivation to stop or decrease strongly affects the ultimate success of any
treatment.
Stages of Change
Extensive research has led to a theory of treatment that posits different stages of
readiness for changing problematic behaviors. Research on this theory of stages of
change has also led to methods that promote readiness for the next stage (Prochaska
et al., 2007). Whereas most other treatments rely on a dichotomous view of sub-
stance use—users are either abstinent or not—this approach rests on the idea of
intermediate states between these two extremes; the five stages of readiness to change
are as follows:
1. Precontemplation. The user does not admit that there is a problem and doesn’t
intend to change. A temporary decrease in use in response to pressure from
others will be followed by a relapse when the pressure is lifted.
2. Contemplation. The user admits that there is a problem and may contemplate tak-
ing action. However, no actual behavioral change occurs at this stage; behavior
change is considered for the future.
3. Preparation. The user is prepared to change. He or she has a specific commit-
ment to change, a plan for change, and the ability to adjust the plan of action
and intends to start changing the substance use within a month. The user is
very aware of the abuse, how it reached its current level, and available solutions.
Although users in this stage are prepared to change, some are more ambivalent
than others and may revert to the contemplation stage.
4. Action. The user actually changes his or her substance use behavior and environ-
ment. At this stage, others most clearly perceive the user’s intentions to stop or
decrease substance use; it is during this stage that family members and friends
generally offer the most help and support.
5. Maintenance. The user builds on gains already made in stopping or decreas-
ing substance use and tries to prevent relapses. Former substance users who do
not devote significant amounts of energy and attention to relapse prevention
are likely to relapse al l the way back to the contemplation—or even the
precontemplation—stage. Friends and family members often mistakenly think
that because the substance abuse has stopped or diminished, the former user is
finished taking action. In fact, the former user must actively prevent relapses,
and help and support from friends and family members is very important in
this stage.
This description of the five steps suggests a lock-step process: Each stage has
discrete tasks that lead to the next stage in a linear progression. Research, however,
suggests that the stages are not mutually exclusive (Littell & Girvin, 2002). For
example, most people in the stage of action have occasional relapses and engage in the
unwanted behavior, but they do not totally relapse into the old patterns. Also, unin-
terrupted forward progress is not the most typical path. People often regress before
moving forward again. For example, only 5% of smokers who think about quitting
Stages of change
A series of five stages that characterizes
how ready a person is to change problematic
behaviors: precontemplation, contemplation,
preparation, action, and maintenance.
288 C H A P T E R 9
go through all the stages of change within 2 years without a relapse (Prochaska,
Velicer, et al., 1994).
Motivational Enhancement Therapy
Motivational enhancement therapy (also referred to as motivational interviewing) is
specifically designed to boost patients’ motivation to decrease or stop substance use
(Bagøien et al., 2013; Hettema et al., 2005; Miller & Rollnick 1992). In this therapy,
the patient sets his or her own goals regarding substance use, and the therapist points
out discrepancies between the user’s stated personal goals and his or her current
behavior. The therapist then draws on the user’s desire to meet the goals, helping him
or her to override the rewarding effects of drug use. Therapists using motivational
enhancement therapy do not dispense advice or seek to increase any specific skills;
rather, they focus on increasing the motivation to change drug use, discussing both
positive and negative aspects of drug use, reasons to quit, and how change might
begin (Miller, 2001).
Studies have shown that this treatment is more successful when patients have
a positive relationship with their therapist and are at the outset strongly moti-
vated to obtain treatment (Etheridge et al., 1999; Joe et al., 1999). The beneficial
effects of motivational enhancement therapy tend to fade over the course of a year
(Hettema et al., 2005).
Cognitive-Behavior Therapy
Cognitive-behavior therapy (CBT) for substance use disorders has three general foci:
1. understanding and changing thoughts, feelings, and behaviors that lead to
substance use;
2. understanding and changing the consequences of the substance use; and
3. developing alternative behaviors to substitute for substance use (Carroll, 1998;
Marlatt & Gordon, 1985).
CBT treatment may focus in particular on decreasing the positive consequences
of drug use and on increasing the positive consequences of abstaining from drug
use (referred to as abstinence reinforcement). As patients are able to change these con-
sequences, they should be less motivated to abuse the substance. CBT may be used
more generally for contingency management, in which reinforcement is contingent on
the desired behavior’s occurring, or the undesired behavior’s not occurring (Stitzer &
Petry, 2006).
CBT has been used to treat a variety of types of substances, including heroin
and cocaine (Higgins et al., 1993; Higgins & Silverman, 1999; Petry et al., 2011).
The desired behavior (such as attendance at treatment sessions or abstinence from
using cocaine, as assessed by urine tests) is reinforced with one or more of these
consequences:
• monetar y vouchers, the value of which increases with continued abstinence
( Jones et al., 2004; Silverman et al., 1999, 2001, 2004);
• decreasing the frequency of mandatory counseling sessions if treatment has been
court ordered;
• more convenient appointment times; or
• being allowed to take home a small supply of methadone (requiring fewer trips to
the clinic) for people being treated for heroin use disorder.
Positive incentives (obtaining reinforcement for a desired behavior) are more
ef fective than negative consequences (i.e., punishment, such as tak ing away
Motivational enhancement therapy
A form of treatment specifically designed
to boost a patient’s motivation to decrease
or stop substance use by highlighting
discrepancies between stated personal goals
related to substance use and current behavior;
also referred to as motivational inter viewing.
Substance Use Disorders 289
privileges) in helping patients to stay in treatment and to decrease substance use
(Carroll & Onken, 2005). The cost of providing such rewards can be high, and
relapse often increases once rewards are discontinued, which limits the practicality
and effectiveness of abstinence reinforcement as a long-term treatment (Carroll &
Onken, 2005).
Once the patient has stopped abusing the substance, CBT may focus on
preventing relapse by extinguishing the conditioned response (including cravings) to
drug- related cues. Treatment may also focus on decreasing the frequency or intensity
of emotional distress, which can contribute to relapse (Vuchinich & Tucker, 1996).
One way treatment can help patients regulate emotional distress is by helping them
to develop healthier coping skills, which will then increase self-control. Thus, many
of the CBT methods used to treat depression and anxiety also can be effective here;
such methods include self-monitoring, cognitive restructuring, problem solving, and
various relaxation techniques.
Twelve-Step Facilitation (TSF)
Twelve-Step Facilitation (TSF) is based on the 12 steps or principles that form the basis
of Alcoholics Anonymous (AA) (see Table 9.10). AA views alcohol abuse as a disease
that can never be cured, although alcohol-related behaviors can be modified by the
alcoholic’s recognizing that he or she has lost control and is powerless over alco-
hol, turning to a higher power for help, and seeking abstinence. Research suggests
that the AA approach can help people who are trying to stop their substance abuse
(Laffaye et al., 2008).
TABLE 9.10 • Twelve Steps of Alcoholics Anonymous
(1) We admitted we were powerless over alcohol—that our lives had become
unmanageable.
(2) Came to believe that a Power greater than ourselves could restore us to sanity.
(3) Made a decision to turn our will and our lives over to the care of God as we understood Him.
(4) Made a searching and fearless moral inventory of ourselves.
(5) Admitted to God, to ourselves and to another human being the exact nature of our
wrongs.
(6) Were entirely ready to have God remove all these defects of character.
(7) Humbly asked Him to remove our shortcomings.
(8) Made a list of all persons we had harmed, and became willing to make amends to them all.
(9) Made direct amends to such people wherever possible, except when to do so would
injure them or others.
(10) Continued to take personal inventory and when we were wrong promptly admitted it.
(11) Sought through prayer and meditation to improve our conscious contact with God as
we understood Him, praying only for knowledge of His will for us and the power to carry
that out.
(12) Having had a spiritual awakening as the result of these steps, we tried to carry this
message to alcoholics, and to practice these principles in all our affairs.
Source: www.aa.org/en_pdfs/smf-121_en .
The Twelve Steps are reprinted with permission of Alcoholics Anonymous World Services, Inc. (“AAWS”)
Permission to reprint the Twelve Steps does not mean that AAWS has reviewed or approved the contents
of this publication, or that AAWS necessarily agrees with the views expressed herein. A.A. is a program of
recovery from alcoholism only- use of the Twelve Steps in connection with programs and activities which
are patterned after A.A., but which address other problems, or in any other non-A.A. context, does not
imply otherwise.
290 C H A P T E R 9
AA’s groups are leaderless, whereas TSF’s groups are led by mental health profes-
sionals, whose goal is to help group members become ready to follow the 12 steps of
AA. The Twelve-Step model has been used by people who abuse narcotics (Narcotics
Anonymous [NA]) and in numerous inpatient and outpatient treatment programs run
by mental health professionals (Ries et al., 2008). TSF targets motivation to adhere to
the steps. In essence, its goals are like those of motivational enhancement therapy, but
the enhanced motivation focuses on sticking with a specific type of treatment.
Targeting Social Factors
Treatments that target social factors aim to change interpersonal and community
antecedents (i.e., the events that lead up to) and consequences of substance abstinence and
use. Antecedents might be addressed by decreasing family tensions, increasing sum-
mer employment among teens, and decreasing community violence. Consequences
might be addressed by increasing community support for abstinence and providing
improved housing or employment opportunities for reduced use or for abstinence.
Residential Treatment
Some people who seek treatment for substance use disorders may need more inten-
sive help, such as the assistance that can be found in residential treatment (also called
inpatient treatment or psychiatric hospitalization), which provides a round-the-clock
therapeutic environment (such as the Betty Ford Center in California). Because it
is so intensive, residential treatment can help a person more rapidly change how
he or she thinks, feels, and behaves. Some residential treatment programs have a
spiritual component. Depending on the philosophy of the program, various combi-
nations of methods—targeting neurological, psychological, and social factors—may
be available.
Group-Based Treatment
Treatments that target social factors are usually provided in groups. One approach fo-
cuses on providing group therapy, which typically takes place in residential treatment
programs, methadone clinics, drug counseling centers, and day- treatment programs (to
which patients come during the day to attend groups and receive individual therapy
but do not stay overnight—also called partial hospitalization or intensive outpatient
treatment). In addition, there are a number of self-help groups for people with sub-
stance use disorders.
Group Therapy
CBT may be used in a group format to help people with substance use disorders.
The group provides peer pressure and support for abstinence (Crits-Christoph et al.,
1999). Moreover, members may use role-playing to try out
new skills, such as saying “no” to friends who offer drugs.
Other types of groups include social-skills training groups,
where members learn ways to communicate their feelings and
desires more effectively, and general support groups to decrease
shame and isolation as members change their substance abuse
patterns.
Self-Help Groups
Self-help groups (sometimes called support groups), such as those
that adopt the Twelve-Step programs of Alcoholics Anony-
mous and Narcotics Anonymous, hold regular meetings.
Attending such a group might supplement other treatment or
might be the only treatment a person pursues. As noted earlier,
such groups often view belief in a “higher power” as crucial to
Various types of treatment for substance use
disorders can be offered in the community,
including day-treatment programs, methadone
clinics (such as the one shown here), group
therapy, and self-help groups.
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Substance Use Disorders 291
recovery, and even people who are not religious can improve through such meetings
(Humphreys & Moos, 2007; Moos & Timko, 2008). AA also provides social support,
both from other group members and from a sponsor—a person with years of sobriety
who serves as a mentor and can be called up when the newer member experiences
cravings or temptations to drink again. A variety of other self-help groups and orga-
nizations address recovery from substance use disorders without a Twelve-Step reli-
gious or spiritual component.
A meta-analysis showed that attending a self-help group at least once a week is
associated with drug or alcohol abstinence (Fiorentine, 1999). Other research con-
firms that longer participation in AA is associated with better outcomes (Moos &
Moos, 2004). Just like group therapy, a self-help group can be invaluable in decreasing
feelings of isolation and shame. In general, self-help groups can be valuable sources
of information and support, not only for the person with a substance use disorder but
also for his or her relatives.
Family Therapy
Family therapy is a treatment that involves an entire family or some portion of a
family. Family therapy can be performed using any theoretical approach; the main
focus is on the family rather than the individual. The goals of this type of therapy
are tailored to the specific problems and needs of each family, but such therapy typi-
cally addresses issues related to communication, power, and control (Hogue et al.,
2006). To the extent that family interactions lead to or help sustain abuse of a sub-
stance, changing the patterns of interaction in a family can modify these factors
(Saatcioglu et al., 2006; Stanton & Shadish, 1997). Among adolescents treated for
substance use disorders, outpatient family therapy can help them to abstain (Smith et
al., 2006; Szapocznik et al., 2003), which suggests that changes in how parents and
adolescents interact can promote and maintain abstinence. In fact, family therapy is
usually a standard component of treatment for adolescents with substance use disor-
ders (Austin et al., 2005).
Feedback Loops in Treating Substance Use Disorders
The following considerations help determine whether an intervention was successful.
Did the person:
• complete the treatment, or is he or she still using or abusing the substance? (Is he or
she abstinent—yes or no?)
• experience fewer harmful effects from the substance? (Is he or she using clean
needles or no longer drinking to the point of passing out?)
• decrease use of the substance? (How much is the person using after treatment?)
• come to behave more responsibly? (Does he or she attend regular AA meetings or
get to work on time?)
• feel better? (Is the person less depressed, anxious, “strung out,” or are drug cravings
less intense?)
• come to conform to societal norms? (Has he or she stayed out of jail?)
The treatments we’ve discussed can lead to improvement according to these
considerations, but different types of treatments provide different paths toward
improvement. Moreover, many people with substance use disorders may quit
multiple times. In addition, like studies of treatments for other types of disor-
ders, studies of treatments for substance use disorders have found a dose-response
relationship: Longer treatment produces better outcomes than shorter treatment
SP
N
Family therapy
A treatment that involves an entire family or
some portion of a family.
292 C H A P T E R 9
Treatments Targeting
Psychological Factors
Motivational
enhancement therapy
Twelve-Step Facilitation
CBT: Cognitive
restructuring, self-
monitoring, problem
solving, relaxation
Treatments Targeting
Social Factors
Family therapy
Group therapy and
self-help groups
Community-based and
residential treatment
Treatments Targeting
Neurological Factors
Detoxification
Medication: For with-
drawal symptoms
and/or to block the
effects of the drug
Changes neural activity
Changes thoughts,
feelings, and
behaviors
Changes social
interactions
Decreases family conflict
Increases social support
FI G U RE 9.9 • Feedback Loops in Treating Substance Use Disorders
( Hubbard et al., 1989; Simpson et al., 2002). And for those people who abuse more
than one type of substance, treatment is most effective when it addresses the entire
set of substances.
Ultimately, all successful treatments address all three types of factors that are
identified in the neuropsychosocial approach. When people with a substance use
disorder first stop abusing the substance, they will experience changes that are,
at minimum, uncomfortable (neurological and psychological factors). Moreover,
how they think and feel about themselves will change (psychological factor) —
from “abuser” or “addict” to “ex-abuser” or “in recover y.” Their interactions
with others will change (social factors): Perhaps they will make new friends who
don’t use drugs, avoid friends who abuse drugs, behave differently with family
members (who in turn may behave differently toward them), perform better at
work, or have fewer run-ins with the law. Other people’s responses to them will
also affect their motivation to continue to avoid using the substance and endure
the uncomfortable withdrawal effects and ignore their cravings. Thus, as usual,
treatment ultimately relies on feedback loops among the three types of factors (see
Figure 9.9).
Substance Use Disorders 293
Substance Use: When Use Becomes a
Disorder
• The hallmark of substance use disorders
is loss of control over urges to use a psy-
choactive substance, even though such use
might lead to significant problems.
• The term addiction focuses on the com-
pulsive behaviors related to regular drug
taking but is not used in DSM-5.
• Tolerance and withdrawal are symptoms
of substance use disorders.
• The common liabilities model focuses on
underlying factors that may contribute to
a variety of problem behaviors, includ-
ing substance use disorders. The gateway
hypothesis focuses on factors that lead
individuals to progress from using entry
drugs to using harder drugs.
• S u b s t a n c e u s e d i s o r d e r s f r e q u e n t l y
co-occur with mood disorders (particularly
depression), PTSD, schizophrenia, and
ADHD. Many people with substance use
disorders engage in polysubstance abuse.
• Cultures can promote or regulate sub-
stance use through the use of rituals and
penalties.
Stimulants
• Stimulants, which increase arousal and
brain activity, are the psychoactive sub-
stances in which use is most l ikely to
lead to a use disorder. Unlike many other
types of drugs, they act directly—rather
than indirectly—on the dopam ine re-
ward system by bind ing to dopam ine
transporters in the synapse.
• Stimulants include cocaine and crack,
a m p h e t a m i n e s , m e t h a m p h e t a m i n e ,
Ritalin, MDMA, and nicotine. In high
do se s , mo st of t he se st i mu l a nt s c a n
cause paranoia and hallucinations. With
continued use, stimulants lead to tolerance
and withdrawal.
• A neurological factor that contributes to
substance use disorders is activation of the
dopamine reward system.
• Psychological factors related to substance
use disorders include operant reinforce-
ment of the effects of the drug, classical
conditioning of stimuli related to drug
use, and observational learning of expec-
tancies about the effects of drugs and their
use of them.
• Social factors related to substance use
d isorder s i nclude the speci f ic n at u re
of a person’s relationships with fam ily
members, socioeconomic factors, and cul-
tural and perceived norms about appropri-
ate and inappropriate uses of substances.
Depressants
• Depressants decrease arousal, awareness,
a nd ner vous system act iv it y. Depres-
sants include alcohol, barbiturates, and
benzodiazepines.
• Continued use of depressants leads to tol-
erance and withdrawal. Some withdrawal
symptoms are potentially lethal; people
with a depressant use disorder should be
medically supervised while tapering off
the use of the drug.
• The effects of alcohol depend on its con-
centration in the blood. Repeated binge
drinking can lead to alcohol use disorder.
Long-term alcohol use disorder is associ-
ated with a variety of cognitive problems,
as well as atrophy of certain brain areas and
enlarged ventricles. Withdrawal symptoms
include delirium tremens.
• Depressants directly affect the GABAnergic
neurotransmitter system, which in turn
dampens activity in key brain areas that
give rise to anxiety. Depressants also indi-
rectly activate the dopamine reward system.
• Psychological factors related to depres-
sant use disorders include observational
learning to expect specif ic effects from
depressant use and to use depressants as
a coping strateg y, positive and negative
reinforcement of the effects of the drug,
and classical conditioning of drug cues
that leads to cravings.
• Social factors related to depressant use
disorders include the nature of a person’s
r el a t ion s h ip s w it h f a m i l y me m b er s ,
peers’ use of depressants, and norms and
perceived norms about appropriate and
inappropriate use of depressants.
Other Abused Substances
• Exogenous opioids can du l l pain and
decrease awareness. Continued opioid use
quickly leads to tolerance and withdrawal, as
well as compulsive drug-related behaviors.
Heroin is an opioid. Opioids activate the
dopamine reward system. They also depress
the central nervous system and decrease
endorphin production, thereby reducing the
body’s inherent ability to relieve pain.
• Hallucinogens include LSD, mescaline,
psilocybin, and marijuana. Hallucinogens
have unpredictable effects, which depend
in part on the user’s expectations and the
context in which the drug is taken. LSD
affects serotonin functioning.
• Cannabis use disorder affects motivation,
learning, and memory. The active ingre-
dient in marijuana, THC, activates the
dopamine reward system. Chronic mari-
juana users may develop withdrawal.
• D i s s oc i a t ive a ne s t het ic s ( s omet i me s
referred to as “club drugs”) are so named
because they induce a sense of dissocia-
tion and cause anesthesia. Dissociative
anesthetics include PCP and ketamine.
Use and abuse of this type of drug impairs
cognitive functioning and can lead to
violent behavior.
• Genes may predispose some people to
develop a substance use disorder.
SUMMING UP
Thinking Like A Clinician
Karl has been binge drinking and smoking marijuana every weekend for the past couple of
years. He’s been able to maintain his job, but Monday mornings he’s in rough shape, and
sometimes he’s had blackouts when he drinks. He’s decided that he wants to quit drinking
and smoking marijuana, but he feels that he needs some help to do so. Based on what you’ve
read in this chapter, what would you advise for Karl, and why? What wouldn’t you suggest to
him as an appropriate treatment, and why? How would your answer change if he’d been using
cocaine frequently?
294 C H A P T E R 9
Psychoactive substance (p. 257)
Substance use disorders (p. 258)
Substance intoxication (p. 258)
Tolerance (p. 259)
Withdrawal (p. 259)
Common liabilities model (p. 261)
Gateway hypothesis (p. 261)
Polysubstance abuse (p. 262)
Dopamine reward system (p. 267)
Reward craving (p. 268)
Relief craving (p. 268)
Drug cues (p. 269)
Delirium tremens (DTs) (p. 276)
Detoxification (p. 285)
Antabuse (p. 286)
Stages of change (p. 288)
Motivational enhancement therapy (p. 289)
Family therapy (p. 292)
Key Terms
More Study Aids
For additional study aids related to this chapter, including
quizzes to make sure you’ve retained everything you’ve learned
and a Student Video Activity exploring how hallucinogens
affect brain activity, go to: www.worthpublishers.com/
launchpad/rkabpsych2e.
Don Farrall/Digital Vision/Getty Images
• Psycholog ica l factor s related to other
substance use disorders include observa-
tional learning of what to expect from
taking the drugs and of using the drugs
as a coping strategy. Classical condition-
ing of stimuli related to drug use can lead
to cravings and can play a role in building
tolerance. In addition, the disorders may
arise in part from operant conditioning.
• Social factors related to other substance
use disorders include the person’s relation-
ships with family members, peers’ use of
substances, cultural norms and perceived
norms about appropriate and inappropri-
ate use of substances, and socioeconomic
factors.
Treating Substance Use Disorders
• A treatment that focuses on neurological
factors is detox to help reduce symptoms
of withdrawal that come from substance
use disorders. Medications may reduce
u nple a s a nt w it hd r awa l s y mptom s or
block the pleasant ef fects of using the
sub st a nce, wh ich c a n help m a i nt a i n
abstinence.
• Treat ment s t h at t a rget ps ycholog ica l
factors, such as motivational enhance-
ment therapy, are designed to motivate
people to decrease substance use. CBT
addresses antecedents, consequences, and
specific behaviors related to substance use.
Twelve-Step Facilitation provides struc-
ture and support to help patients abstain.
• Social factors are targeted by residential
treatment and other types of community-
based treatment (group therapy and self-help
groups), as well as family therapy to address
issues of communication, power, and control.
Substance Use Disorders 295
297
CHAPTER 10
Eating Disorders
y the time she was 9 years old, Mar ya Hor nbacher had
developed bulimia nervosa, which is an eating disorder
characterized by binge eating along with vomiting or other
behaviors to compensate for the large number of calories ingested.
This was an unusually young age to develop an eating disorder. By the
time she reached 15, she had anorexia nervosa, an eating disorder
characterized by significantly low body weight along with an intense
fear of gaining weight or using various methods to prevent weight
gain. For the next 5 years, she careened from one eating disorder to
another. By Hornbacher’s own account, she had “been hospitalized
six times, institutionalized once, had endless hours of therapy, been
tested and observed and diagnosed . . . and fed and weighed for so
long that I have begun to feel like a laboratory rat” (Hornbacher,
1998, p. 3). At the age of 23, Hornbacher wrote Wasted: A Memoir of
Anorexia and Bulimia about her experiences with eating disorders, in
which she observes that an eating disorder:
. . . is an attempt to find an identity, but ultimately it strips you of any
sense of yourself, save the sorry identity of “sick.” It is a grotesque
mockery of cultural standards of beauty that winds up mocking no
one more than you. It is a protest against cultural stereotypes of
women that in the end makes you seem the weakest, the most needy
and neurotic of all women. It is the thing you believe is keeping you
safe, alive, contained—and in the end, of course, you find it’s doing
quite the opposite. (1998, p. 6)
An eating disorder is characterized by abnormal eating and a
preoccupation with body image. Approximately 90% of the people
diagnosed with eating disorders are females, and so in this chapter,
we will refer to a person with an eating disorder as “she” or “her”;
however, the number of males with eating disorders has been slowly
increasing (Hudson et al., 2007).
Anorexia Nervosa
What Is Anorexia Nervosa?
Medical, Psychological, and Social Effects of
Anorexia Nervosa
Bulimia Nervosa
What Is Bulimia Nervosa?
Medical Effects of Bulimia Nervosa
Is Bulimia Distinct From Anorexia?
Binge Eating Disorder and “Other” Eating
Disorders
What Is Binge Eating Disorder?
Disordered Eating: “Other” Eating Disorders
Understanding Eating Disorders
Neurological Factors: Setting the Stage
Psychological Factors: Thoughts of and Feelings
About Food
Social Factors: The Body in Context
Feedback Loops in Understanding
Eating Disorders
Treating Eating Disorders
Targeting Neurological and Biological Factors:
Nourishing the Body
Targeting Psychological Factors: Cognitive-
Behavior Therapy
Targeting Social Factors
Feedback Loops in Treating Eating Disorders
Follow-up on Marya Hornbacher
Bulimia nervosa
An eating disorder characterized by binge
eating along with vomiting or other behaviors
to compensate for the large number of
calories ingested.
Anorexia nervosa
An eating disorder characterized by
significantly low body weight along with an
intense fear of gaining weight or using various
methods to prevent weight gain.
Eating disorder
A category of psychological disorders
characterized by abnormal eating and a
preoccupation with body image.
In thIs chapter, we discuss three disorders from the DSM-5
category of feeding and eating disorders: anorexia nervosa, bulimia nervosa,
and binge eating disorder. We examine the criteria for and the medical
effects of these disorders and discuss research f indings that can
illuminate why eating disorders develop and the various methods
used to treat them.
ImageSource/age fotostock. Photo for illustrative purposes only; any individual depicted is a model.
Anorexia Nervosa
After years of struggling with bulimia, Marya Hornbacher began “ inching”
toward anorexia; she gradually became signif icantly under weight by
severely restricting her food intake, refusing to eat enough to obtain a
healthy weight:
Anorexia started slowly. It took time to work myself into the frenzy that the dis-
ease demands. There were an incredible number of painfully thin girls at [school],
dancers mostly. The obsession with weight seemed nearly universal. Whispers and
longing stares followed the ones who were visibly anorexic. We sat at our cafeteria
tables, passionately discussing the calories of lettuce, celery, a dinner roll, rice.
(Hornbacher, 1998, p. 102)
Hornbacher wanted to be thin, to be in control of her eating, and to feel
more in control of herself generally. She began to eat less and less, to the
point where she began to pass out at school.
What Is Anorexia Nervosa?
Key features of anorexia nervosa (often referred to simply as anorexia) are that the
person will not maintain at least a low normal weight and employs various methods
to prevent weight gain (American Psychiatric Association, 2013). Despite medical
and psychological consequences of a low weight, people who have anorexia nervosa
continue to pursue extreme thinness. Anorexia has a high risk of death: About
10–15% of people hospitalized with anorexia eventually die as a direct or indirect
consequence of the disorder (Zipfel et al., 2000).
Anorexia Nervosa According to DSM-5
To be diagnosed with anorexia nervosa according to DSM-5, symptoms must meet
three criteria (American Psychiatric Association, 2013):
1. A significantly low body weight for the person’s age and sex, which results from
not ingesting enough calories relative to the calories burned. Being slightly
underweight is not enough.
2. An intense fear of becoming fat or gaining weight, or behaving in ways that interfere with
weight gain, despite being significantly underweight. This fear is often the primary
reason that the person refuses to attain a healthy weight. A person who has anorexia
is obsessed with her body and food, and her thoughts and beliefs about these topics
are usually illogical or irrational, such as imagining that wearing a certain cloth-
ing size is “worse than death.” Moreover, her feelings about herself rise and fall
with her caloric intake, weight, or how her clothes seem to fit. If someone with
anorexia eats 50 more calories (for comparison, a single pat of butter provides about
35 calories) than she had allotted for her daily intake, she may experience intense
feelings of worthlessness. People who suffer from anorexia often deny that they
have a problem and do not see their low weight as a source of concern.
3. Distortions of body image (the person’s view of her body). People with anorexia often feel that
their bodies are bigger and “fatter” than they actually are and overly value their body’s
weight or shape (see Figure 10.1). Note that people who have anorexia and people
who have body dysmorphic disorder both have a distorted body image (Chapter 7);
however, people with anorexia focus on overall body shape and weight, whereas
people with body dysmorphic disorder typically focus on the face or a single body
part. Moreover, the former typically have an actual physical problem with their body
(that is—they are in fact significantly underweight) that they typically do not want to
improve, whereas the latter have no or only a minimal “defect” but perceive it to be
significant and want to hide it or minimize it in other ways (Hrabosky et al., 2009).
Marya Hornbacher
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People who have anorexia nervosa have
a very low weight and, despite medical
consequences, refuse to maintain a healthy
weight. This young woman had been on her
college swim team when she suffered a heart
attack; her anorexia persisted, and she was
considered to be a danger to herself and
banned from campus.
298 C H A P T E R 1 0
Research suggests that people with anorexia also have distorted perceptions of the
size of their meal portions, overestimating how much food is in a portion (Milos et
al., 2013). Table 10.1 lists the DSM-5 diagnostic criteria for anorexia; additional facts
about anorexia are provided in Table 10.2, and Caroline Knapp, Case 10.1, provides
a glimpse of life with anorexia.
FI G U RE 10.1 • Body Image Distortion With respect
to body image, women with anorexia may simply represent
an extreme end of “normal” distortions; many other women
do not assess their bodies accurately (Thompson, 1990). Here
IDEAL is the average figure that women rated as ideal. ATT MEN
(“attractive to men”) shows the average figure that women rated
as most attractive to men, whereas OTHER illustrates the average
figure that men selected as most attractive. THINK depicts the
average figure that women thought of as best matching their
own, and FEEL depicts the average figure that women felt best
matches their own.
Source: Larry Pasman, J. Kevin Thompson, International Journal of Eating Disorders
Copyright © 1988 Wiley Periodicals, Inc., A Wiley Company.
TABLE 10.2 • Anorexia Nervosa Facts at a Glance
Prevalence
• In the course of a lifetime, about 1% of females and up to 0.3% of males will develop
anorexia (Hoek & van Hoeken, 2003; Hudson et al., 2007).
Comorbidity
• Most studies find that at least half—but as high as 90%—of patients with anorexia have at
least one comorbid psychological disorder. The most common types of comorbid disorders
are depression, anxiety disorders, personality disorders, and body dysmorphic disorder
(Cassin & van Ranson, 2005; Dingemans et al., 2012; Godart et al., 2003; Lucka, 2006;
Sansone & Sansone, 2011).
Onset
• Anorexia typically emerges during adolescence or young adulthood, although the disorder
can make its first appearance at an earlier or a later age (American Psychiatric Association,
2013).
Course
• Anorexia has the highest mortality rate of any psychological disorder—up to 15%
(Zipfel et al., 2000). Half of the deaths are from suicide, and the others are from medical
complications of the disorder. People with anorexia who also abuse substances have an
even higher risk of death (Keel et al., 2003).
• According to some studies, fewer than 50% of people who survive fully recover (Keel et al.,
2005; Von Holle et al., 2008), about 33% improve but do not recover, and 20% develop
chronic anorexia (Fichter et al., 2006; Steinhausen, 2002); other studies have found higher
rates of full recovery (Johnson et al., 2003; Keski-Rahkonen et al., 2007).
Gender Differences
• Approximately 75–90% of people with anorexia nervosa are female (Hoek & van Hoeken,
2003; Hudson et al., 2007).
Cultural Differences
• In the United States, females of Black, Hispanic, or Asian background are less likely to be
diagnosed with anorexia nervosa than are White females (Alegría et al., 2007; Nicdao et al.,
2007; Taylor et al., 2007).
TABLE 10.1 • DSM-5 Diagnostic
Criteria for Anorexia Nervosa
A. Restriction of energy intake relative to
requirements, leading to a significantly
low body weight in the context of age,
sex, developmental trajectory, and
physical health. Significantly low weight
is defined as a weight that is less than
minimally normal or, for children and
adolescents, less than that minimally
expected.
B. Intense fear of gaining weight or of
becoming fat, or persistent behavior that
interferes with weight gain, even though
at a significantly low weight.
C. Disturbance in the way in which one’s
body weight or shape is experienced,
undue influence of body weight or shape
on self-evaluation, or persistent lack of
recognition of the seriousness of the
current low body weight.
Reprinted with permission from the Diagnostic and
Statistical Manual of Mental Disorders, Fifth Edition,
(Copyright ©2013). American Psychiatric Association. All
Rights Reserved.
Eating Disorders 299
CASE 10.1 • FROM TH E INSIDE: Anorexia Nervosa
Caroline Knapp suffered from both anorexia and alcohol use disorder (see the excerpt from
her book, Drinking: A Love Stor y, in Chapter 9, Case 9.3). In describing her relationship with
food, she noted that people with anorexia nervosa develop bizarre eating habits and a kind of
tunnel vision—focusing on food, on eating, and on not eating:
When you’re starving . . . it’s hard to think about anything else [except eating or not eating.
It’s] very hard to see the larger picture of options that is your life, very hard to consider
what else you might need or want or fear were you not so intently focused on one crushing
passion. I sat in my room every night, with rare exceptions, for three-and-a-half years. In
secret, and with painstaking deliberation, I carved an apple and one-inch square of cheddar
cheese into tiny bits, sixteen individual slivers, each one so translucently thin you could
see the light shine through it if you held it up to a lamp. Then I lined up the apple slices
on a tiny china saucer and placed a square of cheese on each. And then I ate them one by
one, nibbled at them like a rabbit, edge by tiny edge, so slowly and with such concentrated
precision the meal took two hours to consume. I planned for this ritual all day, yearned for
it, carried it out with the utmost focus and care.
(Knapp, 2003, pp. 48–49)
If, as you read Knapp’s description of her eating ritual, you were reminded of
symptoms of obsessive-compulsive disorder (OCD, see Chapter 7), you’re on to
something. Some symptoms of anorexia overlap with symptoms of OCD and related
disorders: obsessions about symmetry, compulsions to order objects precisely, and
hoarding. However, other symptoms of OCD—such as obsessions about contamina-
tion and checking and cleaning compulsions—do not overlap with those of anorexia
(Halmi et al., 2003).
Two Types of Anorexia Nervosa: Restricting and
Binge Eating/Purging
People with anorexia become extremely thin and maintain their very low weight
by using one of two methods: restricting what they eat or binge eating and then
purging. DSM-5 categorizes two types of anorexia, based on which method is used:
• Restricting type. Low weight is achieved and maintained through severe undereating
or excessive exercise. (Mental health clinicians consider exercise to be excessive
if the person feels high levels of guilt when she postpones or misses a workout;
Mond et al., 2006.) There is no binge eating or purging. This is the classic type
of anorexia, and Knapp’s description in Case 10.1 illustrates the pattern of eating
that is common among people with the restricting type.
• Binge eating/purging type. Some people with anorexia may engage in binge
eating—eating much more food at one time than most people would eat in the
same period of time or context. People often feel out of control while binge eat-
ing. For example, a “snack” might consist of a pint or two of ice cream with a
whole jar of hot fudge sauce, and the person feels unable to stop at just one scoop.
Among people with anorexia, binge eating is followed by purging, which is an
attempt to reduce the ingested calories by vomiting or by using diuretics, laxatives,
or enemas.
Medical, Psychological, and Social Effects of
Anorexia Nervosa
Anorexia has serious negative effects on many aspects of bodily functioning.
Because of the daily deficit between calories needed for normal functioning and
calories taken in, the body tries to make do with less. However, this process comes
at a high cost.
Binge eating
Eating much more food at one time than most
people would eat in the same period of time
or context.
Purging
Attempting to reduce calories that have
already been consumed by vomiting or using
diuretics, laxatives, or enemas.
300 C H A P T E R 1 0
Medical Effects of Anorexia
One possible effect of anorexia is that the heart muscle becomes thinner as the
body, using available energy sources to meet its caloric demands, cannibalizes mus-
cle generally and the heart muscle in particular. Muscle wasting is the term used
when the body breaks down muscle in order to obtain needed calories. When
people with anorexia exercise, they are not building muscle but losing it, espe-
cially heart muscle—which can be fatal. Excessive exercise is actively discouraged
in people with anorexia, and even modest exercise may be discouraged, depending
on the person’s weight and medical status.
A physical examination and lab tests are likely to reveal
other medical effects of anorexia, as the body adjusts to con-
serve energy. These include low heart rate and blood pres-
sure, abdominal bloating or discomfort, constipation, loss
of bone density (leading to osteoporosis and easily fractured
bones), and a slower metabolism (which leads to lower body
temperature, diff icult y tolerating cold temperatures, and
downy hairs forming on the body to provide insulation)
(Mascolo et al., 2012). More visible effects include dry and
yellow-orange skin, br ittle nails, and loss of hair on the
scalp. Symptoms that may not be as obvious to others include
irritability, fatigue, and headaches (Mehler, 2003; Pomeroy,
2004). People with anorexia may also appear hyperactive or
restless, which is probably a by-product of starvation, given
that such behavior also occurs in starved animals (Klein &
Walsh, 2005).
People with anorexia who purge may believe that they
are getting rid of all the calories they’ve eaten, but they’re
wrong. In a starved state, the body so desperately needs cal-
ories that once food is in the mouth, the digestive process begins more rapidly
than normal, and calories may begin to be absorbed before the food reaches the
stomach; even if vomiting occurs, some calories are still absorbed, although water
the body needs is lost. Diuretics (i.e., substances that force the body to excrete
water) decrease only water in the body, not body fat or muscle, and laxatives and
enemas simply get rid of water and the body’s waste before it would otherwise be
eliminated.
All four methods of purging—vomiting, diuretics, laxatives, and enemas—can
result in dehydration because they all deprive the body of needed fluids. In turn,
dehydration can create an imbalance in the body’s electrolytes—salts that are critical
for neural transmission and muscle contractions, including those of the heart muscle.
When dehydration remains untreated, it can lead to death. In addition, recent studies
of the long-term consequences of starvation during puberty indicate an increased risk
of heart disease (Sparén et al., 2004).
Psychological and Social Effects of Starvation
Researchers in the 1940s documented a number of unexpected psychological and
social effects of extreme caloric restriction, which were first discovered in what is
sometimes called the starvation study (Keys et al., 1950). When healthy young men
were given half their usual caloric intake for 6 months, they lost 25% of their origi-
nal weight and suffered other changes: They became more sensitive to the sensations
of light, cold, and noise; they slept less; they lost their sex drive; and their mood
worsened. The men lost their sense of humor, argued with one another, and showed
symptoms of depression and anxiety. They also became obsessed with food—talking
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Like this woman, underweight people may
develop lanugo hair—fine downy hair similar
to that of newborns—on the abdomen, back,
and face. Lanugo hair disappears when normal
weight is attained.
Eating Disorders 301
and dreaming about food and collecting and sharing recipes. They began to hoard
food and random items such as old books and knick-knacks. These striking effects
persisted for months after the men returned to their normal diets, and abnormal
eating and ruminations about food continued even 50 years later (Crow & Eckert,
2000). Such findings have since been substantiated by other researchers (Favaro et al.,
2000; Polivy, 1996). It is sobering that, even on this diet, the participants in the star-
vation study still ate more each day than do many people with anorexia.
The participants in the starvation study were psychologically healthy adult
men, and they developed the noticeable symptoms after less than 6 months on what
would now be considered a relatively strict diet. Most people (females) with anorexia
develop the disorder when they are younger than were the men in the study and
maintain unhealthy eating patterns for a longer time than the 6 months of the study;
the consequences of restricting eating at a young age may be more severe than those
noted in the starvation study.
Moreover, some people with anorexia may have such distorted thinking about
their weight and body that they may come to believe that there’s really nothing
wrong with their weight or restricted food intake (Csipke & Horne, 2007; Gavin et
al., 2008). A minority may come to view anorexia as a lifestyle choice rather than
a disorder. Unfortunately, anorexia has serious physical and mental health conse-
quences, which are swept under the rug by such positive views of the condition.
Since the age of 12, Chris has been very thin, in part because of hours of soccer practice
weekly. Now, at the age of 17, Chris eats very little (particularly staying away from foods
high in fat), continues exercising, and gets angry when people comment about weight. What
would you need to know to determine whether Chris has anorexia nervosa? If Chris does have
anorexia, what would be some possible medical problems that might arise? What if Chris
were male—would it change what you’d need to know to make the diagnosis? Explain your
answer.
Thinking Like A Clinician
Bulimia Nervosa
Marya Hornbacher describes her descent into bulimia nervosa:
I woke up one morning with a body that seemed to fill the room. Long since having
decided I was fat, it was a complete crisis when my body, like all girls’ bodies, acquired
a significantly greater number of actual fat cells than it had ever possessed. At puberty,
what had been a nagging, underlying discomfort with my body became a full-blown,
constant obsession. . . . When I returned [from the bathroom after throwing up],
everything was different. Everything was calm, and I felt very clean. Everything was in
order. Everything was as it should be.
(1998, pp. 40–44)
For Hornbacher, as for many other people with bulimia, the maladaptive
eating behaviors started as an attempt to cope with negative feelings about weight,
appearance, or eating “too much.” In this section we examine the criteria for bulimia
nervosa and the medical effects of the disorder.
What Is Bulimia Nervosa?
A key feature of bulimia nervosa (often simply referred to as bulimia) is repeated
episodes of binge eating followed by inappropriate efforts to prevent weight gain.
Such inappropriate efforts to prevent weight gain can include vomiting or using
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In the starvation study (Keys et al., 1950), men
ate half their usual daily calories for 6 months.
In this short amount of time, participants
became preoccupied with food, as frequently
occurs among people with anorexia. They
also developed symptoms of depression
and anxiety, which are often comorbid with
anorexia. This photo shows a researcher
obtaining information about a participant’s
body before the participant began to restrict
his caloric intake.
302 C H A P T E R 1 0
TABLE 10.4 • Bulimia Nervosa Facts at a Glance
Prevalence
• Over the course of a lifetime, 1–2% of women and 0.1–0.5% of men develop the disorder (Hoek & van Hoeken, 2003; Hudson et al., 2007).
Comorbidity
• Up to 75% of people with bulimia have at least one other disorder, often an anxiety disorder or depression (Godart et al., 2003).
Onset
• Bulimia usually begins in late adolescence or early adulthood.
• People in more recent birth cohorts (that is, those born more recently) have a higher risk for developing bulimia (Hudson et al., 2007).
Course
• At a 15-month follow-up, almost one third of people diagnosed with bulimia still met the criteria for the diagnosis; at a 5-year follow-up, that
proportion dropped to 15% (Fairburn et al., 2000); other studies find similar results (Zeeck et al., 2011). However, people who no longer meet the
DSM-5 criteria for the disorder may nevertheless continue to have persistent symptoms of bulimia, although not the number, frequency, or intensity
specified by the criteria (Ben-Tovim, 2003; Keel et al., 1999).
• People who have less intense negative attitudes about their bodies and who function better in daily life are more likely to have a healthier outcome
(Ben-Tovim, 2003; Keel et al., 1999).
Gender Differences
• Approximately 75–90% of people who have bulimia nervosa are female (Hoek & van Hoeken, 2003; Hudson et al., 2007).
Cultural Differences
• Some studies find significant differences in prevalence, frequency, and symptoms of eating disorders across ethnic groups within the United States.
Specifically, Black and Hispanic American women are less likely to be diagnosed with bulimia than are Asian American or White American women
(Alegría et al., 2007; Nicdao et al., 2007; Taylor et al., 2007).
Source: Unless otherwise noted, the source for information is American Psychiatric Association, 2013.
diuretics, laxatives, enemas, or engaging in other behaviors to prevent
weight gain, such as fasting or excessive exercise.
As noted earlier, some people with anorexia may purge or fast.
In those cases, according to DSM-5, the symptom that distinguishes
the two disorders is that people with anorexia have significantly low
weight whereas those with bulimia do not. Bulimia is two to three
times more prevalent than anorexia and, like anorexia, is much more
prevalent among females than among males (American Psychiatric
Association, 2013). Like people with anorexia, people with bulimia
typically overvalue their appearance and body image (Crowther &
Williams, 2011; Delinsky et al., 2011). The DSM-5 criteria for buli-
mia nervosa are presented in Table 10.3, and additional facts about the
disorder are listed in Table 10.4.
Often, people with bulimia don’t simply eat normally at meals
and then binge between meals (Walsh, 1993). Rather, they tr y to
control what they eat, restricting their caloric intake at meals (try-
ing to be “good” and eat less), but later they become ravenous, and
their hunger feels out of control. They then binge eat, which in
tur n makes them feel physical ly and emotional ly “ bad ” because
they “lost control” of themselves. As a result of such feelings, they
TABLE 10.3 • DSM-5 Diagnostic Criteria for
Bulimia Nervosa
A. Recurrent episodes of binge eating. An episode of binge
eating is characterized by both of the following:
1. Eating, in a discrete period of time (e.g., within any
2-hour period), an amount of food that is definitely larger
than what most individuals would eat in a similar period
of time under similar circumstances.
2. A sense of lack of control over eating during the episode
(e.g., a feeling that one cannot stop eating or control
what or how much one is eating).
B. Recurrent inappropriate compensatory behaviors in order
to prevent weight gain, such as self-induced vomiting;
misuse of laxatives, diuretics, or other medications; fasting;
or excessive exercise.
C. The binge eating and inappropriate compensatory behaviors
both occur, on average, at least once a week for 3 months.
D. Self-evaluation is unduly influenced by body shape and weight.
E. The disturbance does not occur exclusively during episodes of
anorexia nervosa.
Reprinted with permission from the Diagnostic and Statistical Manual of Mental
Disorders, Fifth Edition, (Copyright ©2013). American Psychiatric Association. All
Rights Reserved.
Eating Disorders 303
may purge and subsequently strive to eat less, restricting their caloric intake at
meals and creating a vicious cycle of restricting, bingeing, and usually purging
(Fitzgibbon & Stolley, 2000). In Case 10.2, Gabriella presents a similar story.
CASE 10.2 • FROM TH E OUTSIDE: Bulimia Nervosa
[Gabriella is] a young Mexican woman whose parents moved to the U.S. when she was just
a child. While her mother and father continue to speak Spanish at home and place a high
value on maintaining their Mexican traditions, Gabriella wants nothing more than to fit in
with her friends at school. She chooses to speak only English, looks to mainstream fashion
magazines to guide her clothing and make-up choices, and wants desperately to have a
fashion-model figure. In an attempt to lose weight, Gabriella has made a vow to herself
to eat only one meal a day—dinner—but on her return home from school, she is rarely
able to endure her hunger until dinnertime. She often loses control and ends up “eating
whatever I can get my hands on.” Frantic to keep her problem hidden from her family, she
races to the store to replace all the food she has eaten.
(Fitzgibbon & Stolley, 2000)
Medical Effects of Bulimia Nervosa
Like anorex ia, bulim ia can lead to sig nif icant physica l changes and medica l
problems. For instance, chronic vom iting, a purg ing method used by Mar ya
Hornbacher, can cause the parotid and salivar y glands (in the jaw area) to swell
(creating a kind of “chipmunk” look) and can erode dental enamel, making teeth
more vulnerable to cavities and other problems. People who use syrup of ipecac
to induce vom it ing may develop hear t and muscle problems
(Pomeroy, 2004; Silber, 2004).
Furthermore, many people with bulimia use laxatives reg-
ularly, which can lead to a per manent loss of intestinal func-
tioning as the body comes to depend on the chemical laxatives
to digest food and eliminate waste. In such cases, the malfunc-
tioning intestinal section must be surgically removed (Pomeroy,
2004). Bulimia can also produce constipation, abdominal bloat-
ing and discomfort, fatigue, and irregular menstruation ( Mascolo
et al., 2012 ; Pomeroy, 2004). As noted earlier, in the section
on anorexia, all forms of purging can cause dehydration and an
imbalance of the body’s electrolytes, which disrupt normal neural
transmission and heart contractions. The medical effects of buli-
mia can create significant—and enduring— problems, as they did
for the woman in Case 10.3.
CASE 10.3 • FROM TH E INSIDE: Bulimia Nervosa
A 32-year-old woman describes how bulimia nervosa has affected her:
My life revolves around food and exercise. Because of my abuse of diet pills and purging,
I had a stroke when I was 23. I now have headaches. I am at risk of having another stroke,
and this time I have a high chance of not coming out of it. Emotionally, it’s a daily battle.
I’m depressed because I want to eat, and I’m depressed because I know if I do eat, I’ll get
fat and gain all the weight back that I have lost.
Everyone around me is terrified that I may die from this, and it has put a lot of stress
on my marriage. I have no bedroom life anymore because I refuse to let my husband touch
me or even look at my body. My kids are affected greatly by it because I usually have no
energy to do anything with them, and when I do have energy, I am staying busy to burn
the calories I have put in my body.
(Anonymous, 2003, p. 382)
Frequent vomiting can permanently erode
dental enamel, shown here, and lead to
cavities and related problems.
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304 C H A P T E R 1 0
Is Bulimia Distinct From Anorexia?
About half of people with anorexia go on to develop bulimia (Bulik et al., 1997; Tozzi
et al., 2005), which may indicate that anorexia and bulimia are not distinct but rather
represent phases of the same eating disorder, with the symptoms shifting over time.
Some researchers have argued that a person’s diagnosis may better reflect where she is
in the course of the eating disorder at the time she is diagnosed ( Fairburn & Cooper,
2011). In fact, the characteristics of the binge eating/ purging type of anorexia have
more in common with bulimia than with the restricting type of anorexia (Gleaves,
Lowe, Snow, et al., 2000; Peterson et al., 2011). All that distinguishes the binge
eating/purging type of anorexia from bulimia is the low weight.
Binge Eating Disorder and
“Other” Eating Disorders
Like most other people, you’ve probably had occasions when you’ve eaten too much—
when you felt stuffed and uncomfortable. You may even have felt as if you “binged.”
Odds are, though, that you don’t have binge eating disorder, which is characterized
by a pattern of binge eating without subsequent purging (American Psychiatric
Association, 2013). Or perhaps you—or people you know—have a pattern of eating
that is disordered but doesn’t quite meet the criteria for anorexia, bulimia, or binge
eating disorder. In what follows, we discuss binge eating disorder and disordered eating.
What Is Binge Eating Disorder?
As noted in Table 10.5, binge eating disorder is marked by a
specif ic pattern of out-of-control binge eating in which the
person must have at least three of the following symptoms: eat
faster than normal, eat until uncomfortably full, eat a lot even
when not hungry, eat alone because of being embarrassed by
the quantity eaten, or have significant negative feelings about
himself or herself about the amount eaten. People with this
disorder do not typically fantasize about food or enjoy eating
( either when bingeing or when not bingeing), and the bingeing
causes distress. Note that binge eating disorder involves out-of-
control binge eating and not weight per se; being overweight is
not a psychological disorder.
Binge eating disorder is different from bulimia in two
main ways:
• People with binge eating disorder do not persistently try to
compensate for the binges; for instance, they don’t purge or
compulsively exercise.
• Most people with binge eating disorder are obese; people
with bulimia generally range in weight from somewhat un-
derweight to overweight but are not generally obese (Grucza
et al., 2007; Hudson et al., 2007).
People with binge eating disorder are also more likely to de-
velop medical problems as a result of their nutritional intake,
such as diabetes, high blood pressure, high cholesterol, and
heart disease. (Binges are typically high in fats, sugars, and/or
salt, as was the case for the woman in Case 10.4.) Research sug-
gests that the gender difference typical of other eating disorders
Binge eating disorder
An eating disorder characterized by binge
eating without subsequent purging.
TABLE 10.5 • DSM-5 Diagnostic Criteria for Binge Eating
Disorder
A. Recurrent episodes of binge eating. An episode of binge eating is
characterized by both of the following:
1. Eating, in a discrete period of time (e.g., within any 2-hour period),
an amount of food that is definitely larger than what most people
would eat in a similar period of time under similar circumstances.
2. A sense of lack of control over eating during the episode (e.g., a
feeling that one cannot stop eating or control what or how much
one is eating).
B. The binge-eating episodes are associated with three (or more) of the
following:
1. Eating much more rapidly than normal.
2. Eating until feeling uncomfortably full.
3. Eating large amounts of food when not feeling physically hungry.
4. Eating alone because of feeling embarrassed by how much one is
eating.
5. Feeling disgusted with oneself, depressed, or very guilty afterward.
C. Marked distress regarding binge eating is present.
D. The binge eating occurs, on average, at least once a week for 3 months.
E. The binge eating is not associated with the recurrent use of
inappropriate compensatory behavior as in bulimia nervosa and
does not occur exclusively during the course of bulimia nervosa or
anorexia nervosa.
Reprinted with permission from the Diagnostic and Statistical Manual of Mental Disorders,
Fifth Edition, (Copyright ©2013). American Psychiatric Association. All Rights Reserved.
Eating Disorders 305
is less pronounced with binge eating disorder. This disorder is more common than
anorexia nervosa and bulimia nervosa combined (Grucza et al., 2007; Hudson et al.,
2007). Table 10.6 contains additional facts about binge eating disorder.
CASE 10.4 • FROM TH E OUTSIDE: Binge Eating Disorder
The 48-year-old African-American woman described below sought treatment for her binge
eating disorder.
The patient reported an onset of “eating binges” at approximately age 16. The binge eat-
ing began soon after she began babysitting for neighborhood children. [. . .] During those
times she would “load up on junk food” that the family had provided. She recalled that she
would eat chips, cookies, and brownies “non-stop,” and that these eating episodes often
lasted throughout the evening. She recalled feeling a loss of control during these episodes
and stated that she would continue to eat despite not feeling physically hungry and that she
would not stop until feeling physically ill. She reported that she was very embarrassed and
secretive about these eating behaviors. [. . .] She denied any history of extreme inappropri-
ate weight control or purging behaviors such as self-inducing vomiting or misusing laxatives.
Around 6 months ago her binge eating increased in frequency to three to four times per
week during her mother’s illness, and increased to six to seven times per week following
her mother’s death [. . .] The patient described her typical binge episode as starting with an
evening meal and extending for several hours [. . . when] she would then eat the “leftovers”
while cleaning up after the meal, such that overall she would have consumed the equiva-
lent of two full meals. She would then eat various foods throughout the rest of the evening
until bedtime. During these episodes, she would alternate between salty and sweet snacks.
(White et al., 2010, p. 12)
TABLE 10.6 • Binge Eating Facts at a Glance
Prevalence
• During their lifetime, 4–5% of Americans will develop binge eating disorder; it is more
prevalent than anorexia and bulimia combined.
• Up to 30% of people seeking weight loss treatments have binge eating disorder
( Hudson et al., 2007).
Comorbidity
• Almost 80% of people with binge eating disorder also have another psychological disorder
(Hudson et al., 2007).
Onset
• Binge eating disorder typically begins when people are in their 20s (Kessler et al., 2013).
• The onset of binge eating is often followed by strenuous dieting.
Course
• Left untreated, people with binge eating disorder may cycle through periods of dieting
followed by bingeing and weight gain.
Gender Differences
• Almost twice as many women as men will be diagnosed with binge eating disorder.
Cultural Differences
• In the United States, binge eating disorder is more common among Latinos and African-
Americans than Whites (Marques et al., 2011).
Source: Unless otherwise noted, the source for information is American Psychiatric Association, 2013.
306 C H A P T E R 1 0
C U R R E N T C O N T R O V E R S Y
Is Binge Eating Disorder Diagnosis
a Good Idea?
When using DSM-IV, clinicians and researchers ended up
evaluating a significant number of people who had disordered
eating but whose symptoms did not fully meet the necessary
cr iter ia for bu l i m ia or a norex ia—the on ly t wo eat i ng
disorders in that edition. But because the symptoms none-
theless caused significant distress or impaired functioning,
such patients received the diagnosis eating disorder not otherwise
specified, which was the nonspecif ic “other” diagnosis for
the eating disorders category. In fact, more people received
this “other” diagnosis than were diagnosed with anorexia or
bulimia combined.
To address this problem, DSM-5 added the disorder
binge eating disorder, which fit a subset of people with the “not
otherwise specified” diagnosis. As noted in Table 10.5, the
criteria for binge eating disorder involve more than simply
overeating occasional ly. But adding what is, in essence,
out-of-control eating without “inappropriate” attempts to
compensate for the calories is controversial.
On the one hand, some (Frances, 2013) criticize including
this set of symptoms as a disorder. Although this type of over-
eating may feel bad—both physically and psychologically—
it shouldn’t be its own disorder. If such behavior constitutes
a disorder, then any other form of self-control problem that
makes the person feel bad should be considered a psychological
disorder.
On the other hand, if the binge eating were accom-
panied by purging, it would be considered to be bulimia.
So purging—or the absence of it—should not be the key
determinant of whether disordered eating is considered an
eating disorder. Moreover, making binge eating disorder
a “disorder” allows treatment to be eligible for payment by
insurance companies.
C R I T I C A L T H I N K I N G Even if the patter n of symptoms in
binge eating disorder sounds disordered, is it really enough
to be considered a valid diagnosis? Should we call something
a disorder just because being out of control in some way is
distressing?
( James Foley, College of Wooster)
Partial cases
Cases in which patients have symptoms that
meet only some of the necessary criteria
but not enough symptoms to meet all the
necessary criteria for the diagnosis of a disorder.
Subthreshold cases
Cases in which patients have symptoms that
fit all the necessary criteria, but at levels
lower than required for the diagnosis of a
disorder.
Disordered Eating: “Other” Eating Disorders
Many adolescents and adults with significantly disturbed eating don’t meet all
the criteria for anorexia, bulimia, or binge eating disorder; those people may be
diagnosed with a nonspecific “other” eating disorder. In one study, one quar-
ter of patients with an eating disorder had this t ype of diagnosis (Fairburn &
Cooper, 2011).
Because this “other” t ype does not specif y particular criteria, people who
are given this diagnosis have a wide range in number, frequency, and duration of
symptoms. Nevertheless, people with this “other” diagnosis often fall into one
of two groups. One group consists of people with partial cases, meaning that
their symptoms meet some of the diagnostic criteria for a specific disorder but
not enough to justify the diagnosis of that disorder. An example of a partial case
of binge eating disorder would be someone whose symptoms meet all the other
criteria for the disorder but who does not eat quick ly, eat alone, or eat when
not hungr y; she would thus be diagnosed with the nonspecific “other” eating
disorder.
Another group consists of people with subthreshold cases; they have symp-
toms that fit all the diagnostic criteria for a specific disorder but at levels lower
than required for the diagnosis of that disorder. For instance, such people may
have had anorexia or bulimia but then improved to the point where their symp-
toms no longer meet the criteria for either disorder. Nevertheless, these people still
have clinically significant symptoms of an eating disorder. This was true of Marya
Hornbacher: As the symptoms of her eating disorder abated, she no longer met
the criteria for either anorexia or bulimia, and her diagnosis would be changed to
“other” eating disorder.
Eating Disorders 307
Tanya had been dieting, but after a month or so, she began to pig out toward bedtime. After
the first few of these gorging sessions, she felt both physically uncomfortable and ashamed of
herself, and she would make herself vomit. After about a week, though, she stopped throwing
up; instead, she began exercising for about an hour each day. This pattern of daily exercising
and pigging out in the evening has persisted for about 6 months. Does Tanya have bulimia
nervosa, binge eating disorder, the nonspecific “other” eating disorder, or just disordered
eating but no DSM-5 diagnosis? What were the key factors that determined your answer?
Thinking Like A Clinician
Understanding Eating Disorders
In the sections that follow, we focus on the two eating disorders that are best
understood and for which treatments have been researched most extensively: anorexia
and bulimia. Moreover, given that up to half of the people who have anorexia or
bulimia have had or will have another of these disorders, it makes sense to examine
the etiology of these disorders collectively rather than individually.
Why do these eating disorders arise? Marya Hornbacher asked this question and
ventured the following response:
While depression may play a role in eating disorders, either as cause or effect, it cannot
always be pinpointed directly, and therefore you never know quite what you’re dealing
with. Are you trying to treat depression as a cause, as the thing that has screwed up
your life and altered your behaviors, or as an effect? Or simply depressing? Will drug
therapy help, or is that a Band-Aid cure? How big a role do your upbringing and family
play? Does the culture have anything to do with it? Is your personality just problematic
Imagine that you know that both of these women are afraid of getting fat and believe themselves to
be overweight. If you had to guess based on their appearance, which of these models would you think
didn’t meet all the criteria for anorexia nervosa and instead had a partial case? The woman on the
right is more likely to have a partial case because, based on these photos, she does not appear to be
significantly underweight.
GETTING THE PICTURE
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308 C H A P T E R 1 0
by nature, or is there, in fact, a faulty chemical pathway in your brain? If so, was it
there before you started starving yourself, or did the starving put it there? . . . All of
the above?
(1998, pp. 195–196)
In this passage, Hornbacher is trying to understand how, or why, some people—but
not others—develop an eating disorder. Note that she mentions explanations that in-
volve all three of the types of factors in the neuropsychosocial approach, although she
does not consider ways in which such factors might interact.
Once an eating disorder has developed, it is difficult to disentangle the causes of
the eating disorder from the widespread effects of an eating disorder on neurological
(and, more generally, biological), psychological, and social functioning. This diffi-
culty in untangling cause and effect means that researchers do not know which of
the neuropsychosocial factors that are associated with eating disorders actually pro-
duce the disorders. All that can be said at this time is that a number of factors are
associated with the emergence and maintenance of eating disorders (Dolan-Sewall &
Insel, 2005; Jacobi et al., 2004; Striegel-Moore & Cachelin, 2001).
An additional challenge to researchers is the high rate of comorbidity of other
psychological and medical disorders with eating disorders, which makes it diffi-
cult to determine the degree to which risk factors uniquely lead to eating disor-
ders rather than being associated more generally with the comorbid disorders ( Jacobi
et al., 2004).
Neurological Factors: Setting the Stage
We’ve already noted that the excessive caloric restriction in anorexia leads to specific
medical effects, notably changes in metabolism, and body functioning. The eating
changes and purging involved in bulimia (and anorexia, if purging occurs) bring
their own medical effects and biological changes.
Brain Systems
Neuroimaging studies have revealed many differences between the brains of people
with eating disorders and those of control participants (Frank et al., 2004; Kaye,
Frank et al., 2005). Most notably, people who have anorexia have unusually low
activity in two key areas of the brain: (1) the frontal lobes, which
are involved in inhibiting responses and in regulating behavior
more generally (a def icit in such processing may contribute to
eating too much or eating too little), and (2) the portions of the
temporal lobes that include the amygdala, which is involved in fear
and other strong emotions (fear helps prevent people from putting
themselves in danger, and dampening this emotion may contribute
to eating disorders).
Neuroimaging studies not only have documented abnormal-
ities in the functioning of different parts of the brain in people
who have eating disorders but also have shown that the structure
of the brain itself changes with these disorders. In fact, anorexia
is associated with loss of both gray matter (cell bodies of neu-
rons) and white matter (myelinated axons of the neurons) in
the brain ( Addolorato et al., 1997; Frank et al., 2004; Herholz,
1996). The gray matter carries out various sorts of cognitive and
emotion-related processes, such as those involved in learning and
in fear responses. Deficits in white matter may imply that different
parts of the brain are not communicating appropriately, which could contribute to
the problems patients with anorexia have when they try to convert an intellectual
This student is trying to learn. Anorexia
affects the brain’s structure and function,
including the ability to learn (and engage in
various other cognitive processes).
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Eating Disorders 309
understanding of their disorder into changes in their behavior. Many of these
structural deficits improve when the patient recovers, although they do not necessary
disappear completely (Frank et al., 2004; Herholz, 1996). Thus, an eating disorder
may have long-term consequences for a person’s neural functioning, which in turn
affects cognitive abilities and emotional responses.
Neural Communication: Serotonin
Losing large amounts of weight (as occurs in anorexia) and the associated malnutri-
tion clearly change the amounts of serotonin and other neurotransmitters. We will
focus here on serotonin because it is involved in regulating a wide variety of behaviors
and characteristics that are associated with eating disorders, including binge eating
and irritability (Hollander & Rosen, 2000; McElroy et al., 2000).
Neuroimaging research has shown that serotonin receptors function abnormally
in patients with anorexia and bulimia (Kaye, Bailer et al., 2005; Kaye, Frank et al.,
2005). However, evidence seems to imply that the serotonin receptors are abnor-
mal before patients develop anorexia. As discussed in Chapters 5 and 6, serotonin
is related to mood and anxiety. Prior to developing anorexia, patients tend to be
anxious and obsessional, and these traits persist even after recovery, which suggests a
biologically based anxious temperament; this temperament may be related to
serotonin levels or functioning (Kaye et al., 2003).
Consistent with this view, researchers have found that people with
anorexia (Kaye, Bailer et al., 2005) and bulimia (Kaye et al., 2000; Smith
et al., 1999) are less responsive to serotonin than normal. In fact, the worse
the symptoms of bulimia, the less responsive to serotonin the patient gener-
ally is ( Jimerson et al., 1992).
Genetics
When Marya Hornbacher told her parents that she had been making herself
throw up, her mother admitted, “I used to do that.” Did Hornbacher’s genes pre-
dispose her to developing bulimia? As is true for people with mood disorders and
anxiety disorders, people with an eating disorder are more likely than average
to have family members with an eating disorder—but not necessarily the same
disorder that they themselves have (Lilenfeld & Kaye, 1998; Strober et al., 2000).
Like genetic studies of other types of disorders, such studies of eating
disorders compare identical twins to fraternal twins. The research findings
indicate that anorexia has a substantial heritability, but estimates range from as
low as 33% to as high as 88% (Bulik, 2005; Jacobi et al., 2004). Twin studies
of bulimia also indicate that the disorder is influenced by genes and also yield
a wide range of estimates of heritability, from 28% to 83% (Bulik 2005; Jacobi
et al., 2004). Given that many people with bulimia previously had anorexia, it
isn’t surprising that both disorders have the same wide range of heritabilities;
there is significant overlap in the two populations. The large variation in heri-
tabilities may simply indicate, once again, that genes aren’t destiny; the way the
environment interacts with the genes is also important.
Psychological Factors: Thoughts of and Feelings
About Food
Eating and breathing are both essential to life, but eating can also evoke powerful feel-
ings, memories, and thoughts. Hornbacher recalls her associations to eating:
My memories of childhood are almost all related to food. . . . I was my father’s darling,
and the way he showed love was through food. I would give away my lunch at school,
then hop in my father’s car, and we’d drive to a fast-food place and, essentially, binge.
These identical twins both suffered from
anorexia. Eating disorders may have a genetic
component, but genes are only one of a
variety of factors associated with developing
an eating disorder.
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My mother was another story altogether. She ate, some. She would pick at cottage
cheese, nibble at cucumbers, scarf down See’s Candies. But she, like my father, and like
me, associated food with love, and love with need.
(1998, p. 27)
Many psychological risk factors are not uniquely associated with eating disor-
ders. Factors such as negative self-evaluation, sexual abuse and other adverse expe-
riences, the presence of comorbid disorders (e.g., depression and anxiety disorders;
Jacobi et al., 2004), and using avoidant strategies to cope with problems (Pallister
& Waller, 2008; Spoor et al., 2007) are also associated with psychological disorders
more generally. Thus, many researchers have focused on factors that are specifically
related to symptoms of eating disorders—factors associated with food, weight, ap-
pearance, and eating. In the following sections we examine research findings about
these factors.
Thinking About Weight, Appearance, and Food
People with eating disorders have automatic, irrational, and illogical thoughts about
weight, appearance, and food (Garfinkel et al., 1992; Striegel-Moore, 1993). We
consider two kinds of such thoughts in the following sections.
Excessive Concern With Weight and Appearance
Some people with eating disorders have excessive concern with—and tend to over-
value—their weight, body shape, and eating (Fairburn, 1997; Fairburn & Cooper,
2011). For instance, they may weigh themselves multiple times a day and feel bad about
themselves when the scale indicates that they’ve gained half a pound. Some people are
so concerned with weight and appearance that their food intake,
weight, and body shape come to define their self-worth.
The two characteristics that are the most consistent pre-
dictors of the onset of an eating disorder are dieting and being
dissatisf ied with one’s body (Neumark-Sztainer et al., 2011;
Thompson & Smolak, 2001). Such concerns help maintain
bulimia because people with these characteristics believe that
their compensatory behaviors reduce their overall caloric intake
(Fairburn et al., 2003).
Abstinence Violation Effect
Many people who have an eating disorder engage in automatic,
illogical, black-or-white thinking about food: Vegetables are
“good,” whereas desserts are “bad.” They may come to view
themselves in the same way: They are “good” when acting to lose
weight and “bad” when eating a “bad” food or when they feel
that their eating is out of control. The abstinence violation ef-
fect (Polivy & Herman, 1993) occurs when the violation of a self-
imposed rule about food restriction leads to feeling out of control with food, which then
leads to overeating. For instance, having taken a taste of a friend’s ice cream, a person
thinks, “I shouldn’t have had any ice cream; I’ve blown it for the day, so I might was well
have my own ice cream—in fact, I’ll get a pint and eat the whole thing.” Then, after she
eats the ice cream, she tries to negate the calories ingested during the binge by purging or
using some other compensatory behavior. Thus, the abstinence violation effect explains
bingeing that occurs after the person has “transgressed.”
Operant Conditioning: Reinforcing Disordered Eating
As with many disorders, operant conditioning plays a role in the development and
maintenance of symptoms—in this case, as we explain below, symptoms of disor-
dered eating.
People with eating disorders often
(mistakenly) categorize each type of food as
“good” or “bad.” According to the abstinence
violation effect, if someone with bulimia eats
even a small amount of a “bad” food, she feels
she has transgressed, gives up trying to “be
good,” and binges on the tempting food.
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Abstinence violation effect
The result of violating a self-imposed rule
about food restriction, which leads to feeling
out of control with food, which then leads to
overeating.
Eating Disorders 311
First, the symptoms of most eating disorders—anorexia, bulimia, or binge
eating disorder—may inadvertently be reinforced through operant conditioning.
For instance, preoccupations with food and weight or bingeing and purging can
provide distractions from work pressures, family conflicts, or social problems.
The never-ending preoccupations with food, weight, and body are negatively
reinforced because they provide relief from what the person might other wise
be preoccupied about. (Remember that negative reinforcement is still reinforce-
ment, but it occurs when something aversive is removed, which is not the same
as punishment.)
Second, operant conditioning occurs when restricting behaviors are positively
reinforced by the person’s sense of power and mastery over her appetite, although
such feelings of mastery are often short-lived as the disease takes over (Garner, 1997).
Hornbacher noted: “The anorexic body seems to say: I do not need. It says: Power
over the self ” (1998, p. 85).
A third way in which operant conditioning affects eating disorders occurs when
people are positively reinforced for “losing control” of their appetite and bingeing.
How can losing control be positively reinforcing? Easy: They’ve set up the rules so
that they get to eat certain foods they enjoy (positive reinforcement) only when they
let themselves lose control of their food intake. That is, during a binge, people eat
foods that they normally don’t eat at all or eat only in small quantities—typically fats,
sweets, or carbohydrates. This means that the only way some people can eat foods
they may enjoy—such as ice cream, cake, candy, or fried foods—is by being “out of
control.”
Fourth, bingeing can also induce an endorphin rush, which creates a pleasant
feeling much like a “runner’s high,” which is positively reinforcing. And, fifth, oper-
ant conditioning may occur because purging can be negatively reinforcing by reliev-
ing the anxiety and fullness that are created by overeating.
Personality Traits as Risk Factors
Particular personality traits are associated with—and are considered risk factors
for—eating disorders: perfectionism and low self-esteem. Perfectionism is a per-
sistent striving to attain perfection and excessive self-criticism about mistakes
( Antony & Swinson, 1998; Franco-Paredes et al., 2005). Numerous studies find
that people with eating disorders have higher levels of perfectionism than do peo-
ple who do not have these disorders (Forbush et al., 2007). High perfectionism
may lead to an intense drive to attain a desired weight or body shape and thus
may contribute to the thoughts and behaviors that underlie an eating disorder. As
illustrated in Figure 10.2, perfectionists are painfully aware of their imperfections,
which is aversive for them. This heightened awareness of personal flaws—real or
imagined—is called aversive self-awareness and leads to significant emotional dis-
tress, which may temporarily be dulled by focusing on immediate aspects of the
environment, such as occurs with bingeing. Thus, bingeing may provide an escape
FI G U RE 10.2 • Bingeing as Escape For perfectionists, bingeing can be an escape from aversive
feelings. Being aware of imperfections (referred to as aversive self-awareness) causes emotional distress.
People high in perfectionism try to decrease this emotional distress by focusing on immediate aspects of
the environment (referred to as cognitive narrowing), which they attain through bingeing (Blackburn et al.,
2006; Heatherton & Baumeister, 1991).
Perfectionism
Aversive self-
awareness
Emotional
distress
Cognitive
narrowing
Binge eating
312 C H A P T E R 1 0
from the emotional distress associated with perfectionism (Blackburn et al., 2006;
Heatherton & Baumeister, 1991).
In addition, people who have low self-esteem may try to raise their self-esteem
by controlling their food intake, weight, and shape, believing that such changes
will increase their self-worth (Geller et al., 2000). For instance, they may think,
“If I restrict my calories, that’ll prove that I’m in control of myself and worthy of
respect.” However, efforts to increase self-worth in this way end up having a para-
doxical effect: To the extent that the person fails to control food intake, weight,
and shape, her self-esteem falls even lower—she feels that she’s failed, yet again, to
achieve something she wanted.
Dieting, Restrained Eating, and Disinhibited Eating
Frequently restricting specific foods—such as “fattening” foods—or overall caloric
intake (as occurs when dieting or tr ying to maintain one’s current weight) is
referred to as restrained eating. If you’ve ever been on some type of diet, you
know that continuing to adhere to such restrictions can be challenging. And at
times the diet may feel so constraining that you get discouraged and frustrated
and simply give up—which can lead to a bout of disinhibited eating, bingeing on
a restricted type of food or simply eating more of a nonrestricted type of food
(Polivy & Herman, 1985). In fact, dieters and people with eating disorders often
alternate restrictive eating with disinhibited eating (Fairburn et al., 2005; Polivy &
Herman, 1993, 2002).
Restrained eaters can become insensitive to internal cues of hunger
and fullness. In order to maintain restricted eating, they may stop eat-
ing before they get a normal feeling of fullness and so end up tr ying
to tune out sensations of hunger. If they binge, they may eat past the
point of normal fullness. They therefore need to rely on external guides,
such as portion size or elapsed time since their last meal, to control their
food intake (Polivy & Herman, 1993). However, using external guides
to direct food intake requires cognitive effort—to monitor the clock or
to calculate how much food was last eaten and how much food should be
eaten next. When a person is thinking about other tasks (such as a job or
homework assignment), she may temporarily stop using external guides
and simply eat, which in turn may lead to disinhibited or binge eating
(Baumeister et al., 1998; Kahan et al., 2003).
Other Psychological Disorders as Risk Factors
Another factor associated with the subsequent development of an eating
disorder is the presence of a psychological disorder in early adolescence
(see Figure 10.3), particularly depression. A longitudinal study of 726 ado-
lescents found that having a depressive disorder during early adolescence
was associated with an increased risk for later dietary restriction, purging, recurrent
weight fluctuations, and the emergence of an eating disorder. This was the case even
when researchers statistically controlled for other disorders or eating problems before
adulthood ( Johnson, Cohen, Kotler, et al., 2002).
Social Factors: The Body in Context
Various social factors contribute to eating disorders. One social factor is the influ-
ence of family and friends, and another social factor is culture, which can contribute
to eating disorders by promoting an ideal body shape. In this section we discuss
these social factors as well as explanations of why so many more females than males
develop eating disorders.
Restrained eating can lead people to rely on
external cues, such as eating only at very
specific times of day, rather than on the
body’s internal hunger cues.
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FIGURE 10.3 • Psychological Disorders
and the Risk of Developing an
Eating Disorder The more psychological
disorders an adolescent—particularly a female
adolescent—has, the more likely he or she is
to develop an eating disorder (Johnson, Cohen,
Kasen, & Brook, 2002).
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Number of psychological disorders
during early adolescence
No disorder 1 disorder 2 disorders 3+ disorders
Females
Males
Restrained eating
Restricting intake of specific foods or overall
number of calories.
Eating Disorders 313
The Role of Family and Peers
Researchers have had trouble disentangling the influences of genes on eating disor-
ders from the influences of the family for two main reasons:
1. Family members provide a model for eating, body image, and appearance
concerns through their own behaviors (Stein, Wooley, Cooper, et al., 2006). For
example, parents who spend a lot of time on their appearance before leaving the
house model that behavior for their children.
2. Family members affect a child’s concerns through their responses to the child’s
body shape, weight, and food intake (Stein, Wooley, Senior, et al., 2006; Tan-
tleff-Dunn et al., 2004; Thompson et al., 1999). For example, if a parent inquires
daily about how much food his or her child ate at lunch (or weighs the child
daily), the child learns to pay close attention to caloric intake and daily fluctua-
tions in weight.
Children whose parents are overly concerned about these matters are more likely to
develop an eating disorder (Strober, 1995). But this finding could also reflect shared
genes.
Peers can shape a person’s relationship to eating, food, and body, especially if
they tease or criticize a person concerning her weight, appearance, or food intake;
such comments can have a lasting influence on her (dis)satisfaction with her body,
her willingness to diet, and her self-esteem. Such influences can make a person more
vulnerable to developing an eating disorder (Cash, 1995; Keery et al., 2005).
Unfortunately, many girls and women feel that symptoms of eating disorders—
particularly preoccupations with food and weight—are “normal” and that talking
about these topics is a way to bond with others. Hornbacher was aware
of this social facet of eating disorders and its underlying drawback:
Women use their obsession with weight and food as a point of connection
with one another, a commonality even between strangers. Instead of talking
about why we use food and weight control as a means of handling emotional
stress, we talk ad nauseum about the fact that we don’t like our bodies.
(1998, p. 283)
The Role of Culture
Some researchers believe that eating disorders have become more com-
mon and pervasive in recent decades. However, a meta-analysis of the
incidence of eating disorders across cultures over the 20th century found
only a small increase in the number of cases of anorexia. In contrast, the
incidence of bulimia substantially increased from 1970 to 1990 (Keel &
Klump, 2003)—which suggests a cultural influence—because bulimia arises only in
the context of concerns about weight (Striegel-Moore & Cachelin, 2001).
Three elements come together to create the engine driving the culturally
induced increase in eating disorders (Becker et al., 2002):
1. a cultural ideal of thinness,
2. repeated media exposure to this thinness ideal, and
3. a person’s assimilation of the thinness ideal.
In order to examine the cultural ideal of thinness, David Garner and colleagues
(1980) conducted an innovative study: They tracked the measurements of Miss America
contestants and Playboy centerfold playmates over time and found that their waists and
hips gradually became smaller. Other studies have found similar results (Andersen &
DiDomenico, 1992; Field et al., 1999; Nemeroff et al., 1994). In fact, while the size of
playmates’ bodies has decreased over time (as assessed by the body mass index, or BMI,
A girl whose mother is overly concerned
about appearance and weight is more likely to
develop an eating disorder.
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For a teenage girl, her friends’ comments
can have a lasting influence on how she feels
about her body, her willingness to diet, and
her self-esteem.
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314 C H A P T E R 1 0
an adjusted ratio of weight to height), the average BMI of women age
20–29 has increased (see Figure 10.4; Ogden et al., 2004, Gammon,
2009). During the same period studied by Garner and colleagues,
the prevalence of eating disorders increased in the United States. It
is not clear whether the contestants and playmates were creating or
f ollowing a cultural trend in ideal body shape. What is clear is that
society’s pressure to be thin increases women’s—and girls’—dissat-
isfaction with their bodies, which is a risk factor for eating disorders
(Grabe & Hyde, 2006; Lynch et al., 2008).
The cultural influence on weight and appearance isn’t limited to
women: Men who regularly engage in activities such as modeling
and wrestling, which draw attention to their appearance and weight,
are increasingly likely to develop eating disorders (Garner et al.,
1998; Sundgot-Borgen, 1999). Similarly, men who have a heightened
awareness of appearance (Ousley et al., 2008), such as some in the gay community, are
also more likely to develop eating disorders (Russell & Keel, 2002).
Eating Disorders Across Cultures
Eating disorders occur throughout the world but are found mainly in industrialized
Wester n or Wester n ized countr ies ( Lee et a l., 1992 ; Pike & Wa lsh, 1996).
Immigration to a Western country and internalization of Western norms increase
the risk of developing symptoms of an eating disorder, as occurs among people who
immigrate from China and Egypt to Western countries (Lee & Lee, 1996; Perez
et al., 2002). Westernization (or modernization) of a culture similarly increases diet-
ing (Gunewardene et al., 2001), which is a risk factor for eating disorders. In addition,
as girls and women move into a higher socioeconomic bracket, they are increasingly
likely to develop an eating disorder (Polivy & Herman, 2002).
Within the United States, prevalence rates of eating disorders vary across ethnic groups,
based on different ideals of beauty and femininity: Native Americans have a higher risk for
eating disorders than do other ethnic groups (Crago et al., 1996), and Black Americans
have had the lowest risk (Striegel-Moore et al., 2003). However, prevalence rates are
increasing among Black and Latina women (Franko et al., 2007; Gentile et al., 2007; Shaw
et al., 2004; Taylor et al., 2007), perhaps because of the growing number of ethnic models
in mainstream ads who are as thin as their White counterparts (Brodey, 2005).
The Power of the Media
The power of the media to inf luence cultural ideals of beauty and femininity is
illustrated by the results of an innovative study in Fiji (a group of islands in the South
Pacific) by Anne Becker and colleagues (2002). Prior to 1995, there was no television
in Fiji. Traditional Fijian culture promoted robust body shapes and appetites, and
there were no cultural pressures for thinness or dieting. Researchers collected data
from adolescent girls shortly after the introduction of television in 1995 and again
3 years later. At the beginning of the study, when a large body size was the cultural
ideal, they found almost no one who felt they were “too big or fat.” After 3 years
of watching television (primarily shows from Western countries), however, 75%
reported that they felt “too big or fat” at least some of the time. In addition, feeling
too big was associated with dieting to lose weight, which had become very prevalent:
62% of the girls had dieted within the prior 4 weeks.
A similar process might be occurring in industrialized societies, where ideals of thin-
ness saturate the environment through television, movies, magazines, advertisements,
books, and even cartoons. Numerous studies have documented associations between
media exposure and disordered eating (Bissell & Zhou, 2004; Kim & Lennon, 2007);
for instance, the more time adolescent girls spent watching television, the more likely
28
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1954 1960 1966 1972 1978
Year
1984 1990 1996 2002 2008
U.S. average BMI trend
of young women
Playmate BMI trend
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FI G U RE 10.4 • Women’s Body Size
Over Time: Playmates and Average
Young Women Over the past five
decades, the size (specifically, the body mass
index [BMI]) of the average young woman’s
body has become larger (orange line). Over
the same period of time, the body size of
Playboy playmates has become smaller
(purple line), presenting an increasingly
unattainable ideal.
When females move from a non-Western
country to a Western country, their risk of
developing an eating disorder increases.
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Eating Disorders 315
they were to report disordered eating a year later (Harrison & Hefner, 2006). However,
not all girls and women who view these media images end up with an eating disorder.
Some people are more affected than others, perhaps because of a combination of neu-
rological, psychological, and social risk factors. For them, chronic exposure to these
types of images may tip the scales and set them on a course toward an eating disorder
( Ferguson et al., 2011; Levine & Harrison, 2004).
Objectification Theory: Explaining the Gender Difference
Objectification theory posits that girls learn to consider their bodies as objects and
commodities, which explains how the cultural ideal of thinness makes women vulner-
able to eating disorders (Fredrickson & Roberts, 1997). Western culture promotes the
view of male bodies as agents—instruments that perform tasks—and of female bodies
as objects mainly to be looked at and evaluated in terms of appearance (see Figure 10.5).
Marya Hornbacher recounted her sense of being objectified:
I remember the body from the outside in. . . . There will be copious research on the
habit of women with eating disorders perceiving themselves through other eyes, as if
there were some Great Observer looking over their shoulder. Looking, in particular, at
their bodies and finding, more and more often as they get older, countless flaws.
(1998, p. 14)
Implicit in Hornbacher’s musings about her perceptions of her body is the sense of her
body as an object—to be looked at and evaluated and, all too frequently, found defective.
According to the theory, objectification encourages eating disorders because female
bodies are evaluated according to the cultural ideal, and girls and women strive to have
their bodies conform so that they will be positively evaluated. As they internalize the
ideal of thinness, they increase their risk for eating disorders (Calogero et al., 2005;
Thompson & Stice, 2001)—especially in combination with learning to see their bodies
as objects from the outside: If they hold an ideal of thinness and see their bodies as
objects, they become more likely to pay attention to their flaws and to feel ashamed
of their bodies, and these feelings motivate restrained eating (Fredrickson & Roberts,
1997; Moradi et al., 2005). Even preschool children attribute more negative qualities to
fat women than to fat men (Turnbull et al., 2000).
Another possible explanation for the gender difference in prevalence rates of
eating disorders focuses on the politics of a cultural ideal of thinness for women.
Some researchers note that as women’s economic and political power has increased,
female models have become thinner and less curvaceous, creating a physical ideal of
womanhood that is harder—if not impossible—to meet. Women then spend significant
FI G U RE 10.5 • Objectification and Eating Problems Objectification theory helps to explain
the large gender difference in the prevalence of eating disorders. This theory proposes that whereas boys are
encouraged to view their bodies as instruments that can perform tasks (agents), girls are encouraged to consider
their bodies as objects and commodities to be evaluated (objects)—which makes girls more vulnerable to
developing an eating disorder.
Source: Adapted from Smolak & Murmen, 2004.
Objectification theory
The theory that girls learn to consider their
bodies as objects and commodities.
Female body = Object
Male body = Agent
Messages from:
Media
Peer teasing
Sexual harassment
Role models
Parents
Sexual violence
Internalization of
ideal of thinness
Internalization of
ideal of strength
and action
Eating and body
image problems
Issues reflecting
power/aggression
Internalization of
gaze of others–body
as object (girls)
Internalization of
role as
observers/evaluators
(boys)
316 C H A P T E R 1 0
time, energy, and money trying to emulate this thinner ideal through
exercise, diet, medications, and even surgery, which in turn dissipates
their economic and political power (Barber, 1998; Bordo, 1993).
Although today males are much less likely to develop any type
of eating disorder than are women, this large gender discrepancy
may not last. Data suggest that male physical ideals are increasingly
unrealistic: Male film stars and Mr. Universe winners are increas-
ingly muscular (Pope, Phillips, & Olivardia, 2000), paralleling
the changes in women’s bodies in the media. Just as females covet
bodies similar to those promoted in the media, so do males (Ric-
ciardelli et al., 2006): Two thirds of men want their bodies to be
more similar to cultural ideals of the male body (McCabe & Ric-
ciardelli, 2001a, 2001b; Ricciardelli & McCabe, 2001). However,
rather than suffer from the specific sets of symptoms for anorexia
or bulimia, males are more likely to develop a form of ”other” eat-
ing disorder, with symptoms that focus on muscle building, either
through excessive exercise or steroid use ( Weltzin et al., 2005).
Sam, in Case 10.5, is preoccupied with losing muscle mass.
CASE 10.5 • FROM TH E INSIDE: An “Other” Eating Disorder
Forty-year-old Sam recounts his preoccupations with his muscles:
I would get up in the morning and already wonder whether I lost muscle overnight while
sleeping. I would rather be thinking about the day and who I was going to see, et cetera.
But instead, the thoughts always centered on my body. Throughout the day, I would think
about everything I ate, every physical movement I did, and whether it contributed to
muscle loss in any way. I would go to bed and pray that I would wake up and think about
something else the next day. It’s a treadmill I can’t get off of.
(Olivardia, 2007, pp. 125–126)
Feedback Loops in Understanding Eating Disorders
As we have seen, many neurological, psychological, and social factors are associated
with the development and maintenance of eating disorders. In what follows we look
at some theories about how these factors interact through feedback loops.
Most females in Western societies are exposed to images of thin women as ideals
in the media, but only some women develop an eating disorder. Why? Neurological
factors (such as a genetic vulnerability) may make some people more susceptible to the
psychological and social factors related to eating disorders (Bulik, 2005). For instance,
researchers hypothesize that young women who are prone to anxiety ( neuroticism)—
which is both a psychological factor and a neurological factor—are more susceptible to
the effects of a familial focus on appearance, a social factor ( Davis et al., 2004). Indeed,
after statistically controlling for body size, researchers found that young women who
were preoccupied with weight were more prone to anxiety and were more likely to
have families that focused on appearance. This preoccupation both could result from
anxiety and familial focus on appearance and could cause these effects. A preoccupa-
tion with weight can also lead to dieting, which can create its own neurochemical
changes (neurological factor) that may lead to eating disorders (Walsh et al., 1995).
In addition, the stringent rules that people may set for a diet can lead them to feel
out of control with eating if they “violate” those rules ( psychological factor). Fur-
ther, people with higher levels of perfectionism and body dissatisfaction (psycho-
logical factors) may elicit comments about their appearance (social factor) or pay
more attention to appearance-related comments (psychological factor) (Halmi et al.,
2000). Figure 10.6 illustrates the feedback loops for eating disorders.
SP
N
Many female dolls have unattainable physical
proportions; this is increasingly also becoming
true of male dolls. As seen in this comparison
of a 1970 G. I. Joe action figure (left) with one
from 2010 (right), male action figures have
become more muscular over this 40-year span
(Baghurst et al., 2006).
©
A
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ag
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©
A
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a
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Eating Disorders 317
Suppose scientists discover genes that are associated with eating disorders. What could—and
couldn’t—you infer about the role of genetics in eating disorders? How could genes contribute
to eating disorders if bulimia is a relatively recent phenomenon? In what ways does the environ-
ment influence the development of eating disorders? Why do only some people who are exposed
to familial and cultural emphases on weight, food, and appearance develop an eating disorder?
Thinking Like A Clinician
Treating Eating Disorders
One important goal when treating a patient with anorexia is to help her attain a medi-
cally safe weight by helping her to eat more and/or purge less often; if that safe weight
cannot be reached with outpatient treatment (treatment that does not involve an over-
night stay in a hospital), then inpatient treatment becomes imperative. Inpatient treat-
ment occurs in a psychiatric hospital or psychiatric unit of a general hospital; inpatient
treatment for eating disorders may also take place at special stand-alone facilities.
FI G U RE 10.6 • Feedback Loops in
Understanding Eating Disorders NeuroPsychoSocial
Stressful Life Events
Family
Gender/Culture
NeuroPsychoSocial
Teasing or other negative
comments about body or
eating Familial focus
on food,
weight, and
appearance
Brain Systems
GeneticsNeural Communication
Serotonin Inherited vulnerability
for an eating disorder
Sex difference in
prevalence attributed
to objectification
Western cultural ideal
of thinness,
propagated through
media exposure
Frontal lobes
Temporal lobes
Amygdala
With anorexia,
loss of gray and
white matter
Behavior
Affect
NeuroPsychoSocial
Anxiety
Depression
Mental Processes and
Mental Contents
Positive and
negative
reinforcement
of restricting,
bingeing, and
purging
Restrained
eating
Irrational thoughts
and excessive
concerns about
food, weight, and
appearance
Personality traits
of perfectionism,
and low self-esteem
318 C H A P T E R 1 0
When someone with an eating disorder isn’t underweight enough to require
inpatient treatment, many different factors can be the initial targets of treatment. In
this section we examine specific treatments that target neurological (and biological,
more broadly), psychological, and social factors and the role of hospitalization.
As with treatment for other disorders, the intensity of treatment for eating
disorders can range from hospitalization, to day or evening programs, to residential
treatment (staffed facilities in which patients sleep, take breakfast and dinner, and
perhaps participate in evening groups), to weekly visits with a therapist. In all these
forms of treatment, cognitive-behavior therapy (CBT) is generally considered the
method of choice. Regardless of the severity of the eating disorder, frequent visits
with an internist or a family doctor are an important additional component of treat-
ment. The physician determines whether a patient should be medically hospitalized
and, if not, whether she is medically stable enough to partake in daily activities. In
what follows, we examine treatment options from the neuropsychosocial perspective.
Targeting Neurological and Biological Factors:
Nourishing the Body
Neurologically and biologically focused treatments are designed to create a pattern
of normal healthy eating and to stabilize medical problems that arise from the eating
disorder. Treatments that focus specifically on these goals include nutritional coun-
seling to improve eating, medical hospitalization to address significant medical prob-
lems, and medication to diminish some symptoms of the eating disorder as well as
symptoms of comorbid anxiety and depression.
A Focus on Nutrition
For people with any type of eating disorder, increasing the nutrition and variety of
foods eaten—and not purged—is critical. A nutritionist will help develop meal plans for
increasing caloric intake at a reasonable pace. In the process of nutritional counseling,
the nutritionist may identify a patient’s mistaken beliefs about food and weight; the
nutritionist then seeks to educate the patient and thus help her correct such beliefs. As
people with anorexia begin to eat more, they may experience gastrointestinal discom-
fort: Because of a lack of body fat, having more food in the gastrointestinal system may
compress a section of the duodenum (a part of the intestine) that is on top of an impor-
tant artery (Adson et al., 1997). The discomfort goes away as she recovers.
Medical Hospitalization
The bodily effects of eating disorders—particularly anorexia—can be directly life-
threatening. When medical problems related to eating disorders become severe,
a medical hospitalization rather than a psychiatric hospitalization may be necessary.
Medical hospitalization generally occurs in response to a medical crisis, such as a heart
problem, gastrointestinal bleeding, or significant dehydration. The goal of medical
hospitalization is to treat the specific medical problem and stabilize the patient’s health.
Medication
Generally, medications do not help people with anorexia gain weight (Crow et al.,
2009; Walsh et al., 2006). However, once the patient’s normal weight is restored,
selective serotonin reuptake inhibitors (SSRIs) may help prevent the person from
developing anorexia again (Barbarich et al., 2004).
For bulimia, antidepressants—particularly SSRIs—may reduce some symptoms
of the eating disorder. Compared to placebos, SSRIs can help decrease bingeing,
vomiting, and weight and shape concerns, although other symptoms may still persist—
including a fear of normal eating (Bacaltchuk et al., 2000; Mitchell et al., 2001). SSRIs
Eating Disorders 319
may also reduce symptoms of comorbid depression. The SSRI Prozac ( fluoxetine) is
the most widely studied medication for bulimia, and the FDA has approved it to treat
this disorder. Studies of the effects of Prozac on bulimia typically last no longer than
16 weeks, however, so it isn’t clear how long the medication should be taken (de Zwaan
et al., 2004). Moreover, as with other disorders, the beneficial effects of medication
used to treat eating disorders typically stop soon after the medication is discontinued.
Targeting Psychological Factors:
Cognitive-Behavior Therapy
CBT is the most widely studied treatment of eating disorders that directly targets psy-
chological factors, and it is considered the treatment of choice (Pike et al., 2004). CBT
for eating disorders focuses primarily on changes in thoughts, feelings, and behaviors
that are related to eating, food, and the body, at least in the initial stages. At the outset
of treatment, the patient and therapist discuss who monitors the patient’s weight and at
what point inpatient treatment would be recommended and pursued (Pike et al., 2004).
CBT for Anorexia
CBT can be effective in reducing symptoms of anorexia and has been shown to
prevent relapses (Pike et al., 2003). CBT for anorexia focuses on identifying and
changing thoughts and behaviors that impede normal eating and that maintain
the symptoms of the disorder. Cognitive restructuring can decrease the patient’s
irrational thoughts (such as the belief that starving means having self-control) and
help the patient to develop more realistic thoughts (for example, that appropriate
eating indicates the ability to care for herself ). The therapist also helps the patient
to develop more adaptive coping strategies (Bowers & Ansher, 2008; Garner et al.,
1997; Wilson & Fairburn, 2007), such as expressing anger or disappointment
directly to other people rather than hiding or denying such “ negative” feelings.
Treatment may also involve psychoeducation (about the disorder and its effects),
training in self-monitoring (to notice hunger cues and become aware of prob-
lematic behaviors), and relaxation training (to decrease anxiety that arises with
increased eating). Because low weight can affect cognitive functioning, irrational
thoug ht s m ay not change subst ant ia l ly unt i l the pat ient’s weig ht increa ses
( McIntosh et al., 2005).
CBT for Bulimia
The benefits of CBT for bulimia are well documented (Agras, Crow, et al., 2000;
Ghaderi, 2006; Walsh et al., 1997). When used as a treatment for bulimia, CBT
focuses on the thoughts, feelings, and behaviors that: (1) prevent normal eating; and
(2) promote bingeing, purging, and other behaviors that are intended to offset the
calories eaten during a binge. CBT also addresses thoughts, feelings, and behaviors
that are related to body image and appearance and that maintain the symptoms of
bulimia. In addition to focusing on symptoms of the disorder, CBT may address
issues associated with perfectionism, low self-esteem, and mood (Wilson & Fairburn,
2007). CBT for bulimia uses many of the same methods as CBT for anorexia: psy-
choeducation, cognitive restructuring, self-monitoring, and relaxation. In addition,
treatment may employ a method used to treat obsessive-compulsive disorder (OCD):
exposure with response prevention (discussed in Chapter 7). For bulimia, this method
generally involves exposing the patient to anxiety-provoking stimuli, such as foods
she would typically eat only during a binge. Patients are asked to consume a mod-
erate amount of the binge food during a therapy session (the exposure), and the
response prevention involves not purging or responding in another usual way to com-
pensate for the calories taken in.
For people with bulimia, exposure with
response prevention might involve foods
normally eaten only during a binge but eating
them in controlled portions in a normal way.
To
m
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ll
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320 C H A P T E R 1 0
Efficacy of CBT for Treating Eating Disorders
Most people with eating disorders who improve significantly with CBT do so within
the first month of treatment (Agras, Crow, et al., 2000). However, although CBT
helps decrease their bingeing, purging, and dieting behaviors, up to 50% of patients
retain some symptoms after the treatment ends (Lundgren et al., 2004). One study of
48 patients who completely abstained from bingeing and purging after CBT found
that 44% had relapsed 4 months later (Halmi et al., 2002). Various factors predicted
which people relapsed, including more eating rituals, more food-related thoughts,
and less motivation to change; stressful life events can also precipitate relapses (Grilo
et al., 2012). Although CBT may be the treatment of choice and helps many people
with eating disorders, it clearly isn’t a panacea.
Targeting Social Factors
Given the important role that social factors play in contributing to eating disorders, it
is not surprising that various effective treatments directly target these factors. Treat-
ments that target social factors include interpersonal therapy, family therapy, group-
based inpatient treatment programs, and prevention programs.
Interpersonal Therapy
A manual-based form of interpersonal therapy (IPT) has been applied to eating
disorders; this version of IPT includes 4 to 6 months of weekly therapy (Fairburn,
1998; Wilfley et al., 2012). In any form of IPT, the focus is on problems in relation-
ships that contribute to the onset, maintenance, and relapse of the disorder (Frank &
Spanier, 1995; Klerman & Weissman, 1993). Although IPT was originally developed
to treat depression, the central idea behind IPT for eating disorders is that as prob-
lems with relationships resolve, symptoms decrease, even though the symptoms are
not addressed directly by the treatment (Tantleff-Dunn et al., 2004).
How does IPT work to treat eating disorders? The hypothesized mechanism
is as follows: (1) IPT reduces longstanding interpersonal problems; (2) the result-
ing improvement of relationships makes people feel hopeful and empowered and
increases their self-esteem; and, (3) these changes lead people to change other aspects
of their lives, such as disordered eating; moreover, they lead to less concern about
appearance and weight and, therefore, less dieting and bingeing (Fairburn, 1997).
Although IPT for anorexia has not yet been well researched, many studies have
shown that IPT is an effective alternative to CBT for bulimia (Apple, 1999; Fairburn,
1997, 2005; Tanofsky-Kraff & Wilfley, 2010).
Family Therapy
The most widely used family-oriented treatment for anorexia is called the Maudsley
approach (Dare & Eisler, 1997; le Grange & Eisler, 2009; Lock, Le Grange, et al.,
2001), named after the hospital in which the treatment originated. This approach,
most effective for young women and girls who live with their parents, does not view
the family as responsible for causing problems and in fact makes no assumptions about
the causes of the disorder. Instead, the Maudsley approach focuses on: (1) helping
parents view the patient as distinct from her illness; and (2) supporting the parents
as they figure out how to lead their daughter to eat appropriately. The therapist asks
the parents to unite to feed their daughter, despite her anxiety and protests. Once her
weight is normal and she eats without a struggle, they gradually return control to her,
and other family issues—including general ones of adolescent development—become
the focus (Lock, 2004). The initial phase of treatment requires an enormous com-
mitment on the part of the family: A parent must be home continuously to monitor
the daughter’s eating. Clearly, the Maudsley approach is not feasible for all families.
This mother is serving dinner to her daughter;
in a type of family treatment for people with
anorexia known as the Maudsley approach,
the first step is to empower the parents to
figure out how best to lead their daughter to
resume normal eating.
A
lt
re
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d
o
/G
e
tt
y
I
m
ag
e
s
Maudsley approach
A family treatment for anorexia nervosa
that focuses on supporting parents as they
determine how to lead their child to eat
appropriately.
Eating Disorders 321
But research results indicate that it is perhaps the most effective treatment for adoles-
cents and young adults with anorexia (Keel & Haedt, 2008).
In addition, systems therapy is one type of family therapy provided to young women
and girls with eating disorders. In this therapy, the family is viewed as a system;
when one member changes, change is forced on the rest of the system (Bowen, 1978;
Minuchin, 1974). Maladaptive family interactional patterns and structures are seen as
the problem and are the focus of change. With family systems therapy, the therapist
may not specifically address the patient’s eating and food issues.
Psychiatric Hospitalization
In contrast to medical hospitalizations, psychiatric hospitalizations (also called
inpatient treatment) for eating disorders are often planned in advance, and they usu-
ally take place in units or free-standing facilities that specialize in treating people
with eating disorders. Psychiatric hospitalization is recommended when less intensive
treatments have failed to change disordered eating behaviors sufficiently. The hospital
environment is a 24-hour community in which patients attend many different types
of group therapy, including groups focused on body image, coping strategies, and
relationships with food. These groups can decrease the isolation and shame patients
may feel and give patients an opportunity to try out new ways of relating. Hospital-
ized patients also receive individual therapy
and usually some type of family therapy;
patients may also receive medication.
The short-term goals of psychiatric
hospitalization for anorexia and bulimia
include increasing the person’s weight to
the normal range, establishing a normal
eating pattern (three full meals and two
snacks per day), curbing excessive exercise,
and beginning to change irrational, mal-
adaptive thoughts about food, weight, and
body shape. For people who purge or oth-
erwise try to compensate for their caloric
intake, an additional goal is to stop or at
least reduce such compensatory behaviors.
Psychiatr ic hospitalization can im-
prove eating and help to change distorted
thoughts about food, weight, and body.
But, in many cases, these positive changes
are not enduring. Twelve months after discharge from a psychiatric hospital, 30–50%
of patients relapse (Helverskov et al., 2010; Pike, 1998). Consider that in 1 year,
Marya Hornbacher was hospitalized three times.
Various explanations have been proposed for the high relapse rate. One is that
some patients only accept the intensive treatment for health reasons or because of
pressure from family members—and once out of the hospital, they are not willing to
continue the changes they began.
A second reason for the high relapse rate after psychiatric hospitalization is that some
patients do not receive appropriate outpatient care after they leave the hospital. This lack of
care makes it more difficult for them to learn how to sustain their changed eating, weight,
and views about their bodies when they are not in a supervised therapeutic environment.
A third reason for the high relapse rate focuses on economic pressures from insur-
ance companies, which have cut the approved length of hospital stays for people with
eating disorders (and for people with psychological disorders in general). Psychiatric
Which tray of food is most typical of the type of lunch that would be served to someone
who is receiving intensive treatment for an eating disorder? Answer: The photo on the left;
the goal is for the person to learn to eat three “normal” nutritionally sound meals per day,
plus snacks.
GETTING THE PICTURE
@
S
to
ck
b
ro
ke
r/
S
u
p
e
rS
to
ck
@
D
ie
te
r
H
ei
n
e
m
a
n
n
/W
e
st
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d
6
1
/C
o
rb
is
322 C H A P T E R 1 0
hospitalizations have become increasingly short, which reduces the amount of endur-
ing change that can realistically be accomplished during a stay.
Prevention Programs
Many mental health clinicians and researchers seek to prevent eating disorders, par-
ticularly for people most at risk (Coughlin & Kalodner, 2006; Shaw et al., 2009):
namely, people who have some symptoms of an eating disorder but do not meet all
the diagnostic criteria. Prevention programs often seek to challenge maladaptive be-
liefs about appearance and food and to decrease overeating, fasting, and avoidance of
some types of foods (Stice et al., 2013). Prevention programs may take place in a sin-
gle session or in multiple sessions, may take the form of presentations or workshops,
or may even be provided via the Internet (Zabinski et al., 2001, 2004).
Feedback Loops in Treating Eating Disorders
With all eating disorders, successful treatment should resolve medical crises and nor-
malize eating and nutrition, directly or indirectly. For a person with anorexia, this
means increasing her eating. Better nutrition leads to improved brain functioning
(neurological factor) and cognitive functioning (psychological factor). For a person
with bulimia, it means normalizing her meals—making sure that she is not only
eating adequately throughout the day but also getting enough of the various food
groups. Eating in this way will decrease the likelihood of extreme hunger, binges, or
eating that feels out of control (psychological factor) (Shah et al., 2005).
SP
N
Treatments Targeting
Psychological Factors
CBT: Psychoeducation,
cognitive restructuring,
self-monitoring,
relaxation, exposure
with response
prevention
Treatments Targeting
Social Factors
IPT
Family therapy
(including Maudsley
approach for anorexia)
Group therapy
Psychiatric
hospitalization
Treatments Targeting
Neurological and Other
Biological Factors
Nutritional counseling
Medical hospitalization
Medication: SSRIs
Changes weight,
nutrition, medical
functioning, and
neural activity
Changes thoughts,
feelings, and behaviors
Decreases shame and
isolation
Decreases familial
focus on appearance
Improves social and
family interactions
FI G U RE 10.7 • Feedback Loops
in Treating Eating Disorders
Eating Disorders 323
Anorexia Nervosa
• The hallmark of anorexia nervosa is a sig-
nificantly low body weight along with an
intense fear of gaining weight or using
various methods to prevent weight gain,
plus distortions in body image. DSM-5
specifies two types of anorexia: restricting
and binge eating/purging.
• Anorexia can lead to signif icant medical
problems: muscle wasting (particularly of
heart muscle), low heart rate, low blood
pressure, loss of bone density, and decreased
metabol ism. Other symptoms include
irritability, headaches, fatigue, and restless-
ness. All methods of purging—vomiting,
diuretics, laxatives, and enemas—can cause
dehydration because they primarily elimi-
nate water, not calories, from the body.
Bulimia Nervosa
• Bu l i m i a ner vo s a i s ch a r ac ter i z ed by
recurrent episodes of binge eating fol-
lowed by inappropriate efforts to prevent
weight gain.
• All purging methods can cause dehydra-
tion, which leads to electrolyte imbalances
and possibly death. Chronic vomiting can
lead to enlarged parotid and salivary glands
and can erode dental enamel. Chronic
laxative use can lead to permanent loss of
intestinal functioning.
Binge Eating Disorder and “Other”
Eating Disorders
• Binge eating disorder is character ized
by a pattern of feeling out of control dur-
ing episodes of eating in which the person
eats more than most people would eat
in the same period of time and circum-
stances, without subsequent purging.
• Binge eating disorder is more common
that anorexia and bulimia combined.
• People with significantly disturbed eating
who do not meet the criteria for the other
eating disorders may be diagnosed with a
nonspecific “other” eating disorder.
Understanding Eating Disorders
• Cause-and-effect relationships among the
factors associated with eating disorders
are diff icult to establish. This diff iculty
ar ises because the behaviors and their
immediate consequences create neurolog-
ical (and other biological), psychological,
and social changes.
SUMMING UP
In most cases, enduring changes in eating result from changes in the way the
person thinks about food and her beliefs about weight, appearance, femininity, and
control. CBT may contribute to these enduring changes (psychological factor). In
addition, the support of family and friends and the improved quality of these rela-
tionships, which may come from IPT or family therapy (social factor), can help the
patient more realistically evaluate her appearance, weight, and body shape. Improved
family interaction patterns can increase mood and satisfaction with relationships,
which can decrease the level of attention that the person pays to cultural pressures
toward an ideal body shape (psychological factor). The feedback loops involved in
treating eating disorders are shown in Figure 10.7.
Suppose your local hospital establishes an eating disorders treatment program. Based on
what you have learned in this chapter, what services should it offer, and why? If your friend,
who has bulimia nervosa, asked your advice about what type of treatment she should get,
how would you respond, and why?
Thinking Like A Clinician
Follow-up on Marya Hornbacher
Marya Hornbacher wrote her f irst memoir, Wasted, when she was 23 years old.
Within a year of its publication, she was diagnosed with a rapid-cycling form of bi-
polar disorder. (See Chapter 5 for a discussion of bipolar disorder.) Hornbacher spent
the next 10 years struggling with alcoholism and bipolar disorder; her struggles are
recounted in her subsequent memoir, Madness: A Bipolar Life (2008). Although the
flagrant symptoms of eating disorders were mostly behind her at the close of Wasted,
in her later memoir, she reported occasional periods of restricting or purging as she
struggled with manic episodes. She recounts that these periods of disordered eating
were attempts to regulate her extreme moods. Her experiences highlight the fre-
quent comorbidity among people with eating disorders.
324 C H A P T E R 1 0
• Neurological factors associated with eating
disorders include:
° unusually low activit y in the frontal
and temporal lobes as well as reduced
gray and white matter;
° reduced responsiveness to serotonin,
a neurotransmitter involved in mood,
anxiety, and binge eating; and
° a tendency for eating disorders to run
in families, as well as evidence of sub-
stantial her itabilit y, which indicates
that genes play a role.
• Psychological factors related to eating dis-
orders include:
° irrational thoughts and excessive concerns
about weight, appearance, and food;
° binge eating as a result of the abstinence
violation effect;
° positive and negative reinforcement of
symptoms of eating disorders;
° certain personality traits, such as per-
fectionism and low self-esteem;
° disinhibited eating, especially in re-
strained eaters; and
° comorbid psychological disorders in fe-
male adolescents, particularly depression.
• Social factors related to eating disorders
include:
° family members and friends who pro-
v ide a model for e at i n g, concer n s
about weight, and focus on appearance
through their own behaviors;
° cultural factors, which play a key role,
as evidenced by the increased prevalence
over time of bulimia and concern about
weight that is part of anorexia; and
° conf licting gender roles in Wester n
societies and a tendency to view wom-
en’s bodies as objects and search for
bodily flaws (objectification theory).
Treating Eating Disorders
• The treatments that target neurological
and other biological factors include:
° nutritional counseling to improve eat-
ing (and correct erroneous information
about food and weight);
° medical hospitalization for signif icant
medical problems related to the disorder;
and
° medicat ion, in par t icu lar SSR Is, to
address some symptoms of the eating
disorder and of anxiety and depression.
• The primary treatment that targets psy-
chological factors is CBT, which is the
treatment of choice for eating disorders.
CBT addresses ma ladaptive thoughts,
feel i n g s , a nd beh av ior s t h at i mpede
nor ma l eating, promote bingeing and
purging, and lead to body image dissatis-
faction. CBT may include exposure with
response prevention and help patients
develop new coping strategies.
• Treat ment s t h at t a rget soc ia l f actor s
include:
° interpersonal therapy, which is designed
to improve the patient’s relationships;
° f a m i l y t h e r a p y, p a r t i c u l a r l y t h e
Maudsley approach, which can be help-
ful for adolescents with anorexia who
live at home;
° psychiatric hospitalization, which pro-
vides supervised mealtimes to increase
normal eating, and a range of therapeu-
tic groups to address various psycholog-
ical and social factors, plus individual
therapy and possibly medication;
° prevention programs.
Bulimia nervosa (p. 297)
Anorexia nervosa (p. 297)
Eating disorders (p. 297)
Binge eating (p. 300)
Purging (p. 300)
Binge eating disorder (p. 305)
Partial cases (p. 307)
Subthreshold cases (p. 307)
Abstinence violation effect (p. 311)
Restrained eating (p. 313)
Objectification theory (p. 316)
Maudsley approach (p. 321)
More Study Aids
For additional study aids related
to this chapter, including quizzes
to make sure you’ve retained
everything you’ve learned and a
Student Video Activity exploring
one young woman’s struggle with
bulimia nervosa, go to: www.
worthpublishers.com/launchpad/
rkabpsych2e.
Photodisc
Key Terms
Eating Disorders 325
327
CHAPTER 11
Gender and Sexual
Disorders
aura and Mike have been married for a couple of years. They
generally get along well, but lately their relationship has been
strained. They both work long hours and are tired when they
get home. They spend weekends doing household chores or sitting
in front of the television or their computers. Laura and Mike aren’t
spending much quality time together, and their sex life has become
nonexistent. Their relationship has changed so much since they first
started dating, when they were attracted to each other and enjoyed
sexual relations. What went wrong, and what can they do to improve
their relationship?
By its very nature, human sexuality emerges from a confluence of
neuropsychosocial factors. Neurologically, sexuality relies on the ac-
tions of hormones and brain activity. Psychologically, sexuality arises
from the desire to be sexual with a particular person, in a certain sit-
uation, at a specific moment. Fantasies and thoughts, body image, the
subjective sense of being male or female—all these factors and others
influence sexuality. Similarly, concerns about reproduction, infertil-
ity, or sexually transmitted diseases and past experiences related to
sex, such as sexual abuse or rape, also affect a person’s sexuality.
Moreover, sexuality is ultimately social: It involves relation-
ships. In fact, even during solitary masturbation someone’s thoughts
and fantasies usually involve other people. Sexuality is influenced
by general emotional satisfaction with a partner, moral and religious
teachings about sexuality, and cultural views of appropriate sexual
behavior (Malatesta & Adams, 2001). Such conditions and circum-
stances are ultimately rooted in social factors.
Gender Dysphoria
What Is Gender Dysphoria?
Understanding Gender Dysphoria
Treating Gender Dysphoria
Paraphilic Disorders
What Are Paraphilic Disorders?
Assessing Paraphilic Disorders
Criticisms of the DSM-5 Paraphilic Disorders
Understanding Paraphilic Disorders
Treating Paraphilic Disorders
Sexual Dysfunctions
An Overview of Sexual Functioning and Sexual
Dysfunctions
Understanding Sexual Dysfunctions
Treating Sexual Dysfunctions
AbnormAlities in sexuAlity And sexuAl behAvior are in-
fluenced by all these neuropsychosocial factors. For instance, a person’s
brain (and, as a result, his or her body) may not respond to sexual stimuli
in the usual way or may respond sexually to stimuli that are not generally
considered to be sexual in nature (such as shoes). Similarly, some people
may have sexual fantasies that disturb them, or they may have difficul-
ties with sexual functioning that lead to distress or problems in their
Flirt/SuperStock. Photo for illustrative purposes only; any individual depicted is a model.
relationships. In addition, families, communities, and cultures determine which sexual
fantasies, urges, and behaviors are considered “deviant” or “abnormal.” These socially
defined sexual “abnormalities” differ across cultures and shift over time. For example,
masturbation and oral sex were once considered to be deviant. More recently, homo-
sexuality was considered a psychological disorder until 1973, when it was removed from
the DSM. Moreover, like most other psychological problems and disorders, normal and
abnormal sexuality and sexual behavior fall on a continuum. However, DSM-5 relies on
the categorical approach to define sex-related and sexual disorders; that is, according to
DSM-5, sexual fantasies, urges, and behaviors are either normal or not normal.
As we’ll see in this chapter, the diagnosis of most—although not all—gender or sexu-
ally related disorders in DSM-5 hinges on the patient’s experience of distress (or, in some
cases, impaired functioning) as a result of the symptoms (First & Frances, 2008). Simply
having unusual or “deviant” sexual fantasies or engaging in unusual sexual behaviors
is not generally sufficient for a diagnosis. Moreover, some disorders ( specifically, some
of the sexual dysfunctions) have predominantly neurological and other biological criteria,
whereas others (the paraphilic disorders and gender dysphoria) have primarily psychological
and social criteria. We examine these disorders in the following sections.
Gender Dysphoria
Last year, Mike got a Facebook status update from Sam, his friend since high school.
Sam announced that he’d become Samantha; he had begun to dress and live as a
woman. The news, and Samantha’s new Facebook photo, took Mike by surprise.
Sam had dated girls occasionally in high school—they’d even gone out on double
dates together—and Sam seemed so “normal.” In the Facebook photo, Mike found
Samantha only vaguely recognizable as having been Sam. Mike didn’t know how
to make sense of Sam’s change. Mike told Laura about Sam’s change to Samantha,
and Mike found himself wondering what life—and sex—had been like for Sam, and
what it was like now for Samantha. What had happened, or would happen, to Sam’s
genitals? What in the world could have driven Sam to want to make such a drastic
change? Mike surfed the Internet for reputable information about Sam’s condition
and discovered that it is called gender dysphoria.
What Is Gender Dysphoria?
Like Sam, a small percentage of people at birth are (usually based on their observable
sex organs) assigned one gender (either female or male) but do not feel comfortable
with the corresponding gender identity. Gender identity is the subjective sense of
What is viewed as normal and abnormal
sexuality is partly based on the cultural views
of appropriate sexual behavior.
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Gender identity
The subjective sense of being male or female
(or having the sense of a more fluid identity,
outside the binary categories of male and
female), as these categories are defined by a
person’s culture.
328 C H A P T E R 1 1
being male or female (or having the sense of a more fluid identity, outside the binary
categories of male and female), as these categories are defined by a person’s culture. For
instance, people like Sam, who have male sexual anatomy and have been labeled male
since birth, may feel as if they are female. Conversely, some people have been labeled as
female since birth but feel as if they are male. (The gender that a person is assigned at
birth is referred to as the natal gender.) People who feel that their gender identity does
not correspond to their natal gender thus experience cross-gender identification.
Transgender is a broad term sometimes used to describe people whose identifica-
tion and behavior may be at odds with their natal gender but who do not necessar-
ily seek medical treatment to change their sexual characteristics ( Riley et al., 2013).
If such people live as the “opposite gender” (e.g., a natal male dresses in daily life and is
known by others as a female), they are referred to as transsexuals. Transsexuals may seek
medical treatment to attain sexual characteristics that match their experienced gender.
Gender dysphoria is an incongruence between a person’s assigned gender (usually
based on his or her natal gender) and the subjective experience of his or her gender,
and that incongruence causes distress (American Psychiatric Association, 2013).
Gender dysphoria typically begins in childhood; children who are diagnosed with
gender dysphoria usually strongly desire to be the opposite gender of their assigned
one, preferring to dress or play with toys in ways that are typical of children of the
other gender. That is, they wish to behave in accordance with the prototypical gender
role of their experienced gender, not their assigned, natal gender; gender role refers to
the outward behaviors, attitudes, and traits that a culture deems masculine or feminine.
For instance, gender roles for females often allow a wider variety of emotions (anger,
tears, and fear) to be displayed in public than do gender roles for males; in contrast,
gender roles for males often allow more overtly aggressive or
assertive behaviors than do gender roles for females. A person
with gender dysphoria wants to adopt the gender role of the
opposite gender not because of perceived cultural advantages
of becoming the other gender but because the opposite gen-
der role is more consistent with the person’s sense of self.
In children, gender dysphoria is not simply “tomboy-
ishness” in girls or “sissy” behavior in boys. Rather, gen-
der dysphoria reflects a profound sense of identifying with
the other gender, to the point of denying one’s own sex-
ual organs. For instance, natal girls with gender dysphoria
report that they don’t want to develop breasts or menstru-
ate. However, long-term studies of children who have been
diagnosed with gender dysphoria f ind that most of the
children did not continue to have the disorder into adult-
hood (American Psychiatric Association, 2013; Drummond
et al., 2008; Zucker, 2005).
Table 11.1 lists the criteria for gender dysphoria in
children, and Table 11.2 lists the criteria for the disorder
in adolescents and adults. Adolescents and adults may feel
uncomfortable living publicly as their assigned, natal gender.
In fact, these people may be preoccupied by the wish to be
the other gender. They may take that wish further and live,
at least some of the time, as someone of the other gender—
dressing and behaving accordingly, whether at home or in
public. Like Sam, some adults with gender dysphoria have
medical and surgical treatments to assume the appearance
of the other sex; such surgical procedures are called sex reas-
signment surgery (discussed in the section on treatment).
Gender dysphoria
A psychological disorder characterized by an
incongruence between a person’s assigned
gender at birth and the subjective experience
of his or her gender, and that incongruence
causes distress.
Gender role
The outward behaviors, attitudes, and traits
that a culture deems masculine or feminine.
TABLE 11.1 • DSM-5 Diagnostic Criteria for Gender Dysphoria in
Children
A. A marked incongruence between one’s experienced/expressed gender
and assigned gender, of at least 6 months’ duration, as manifested by at
least six of the following (one of which must be Criterion A1):
1. A strong desire to be of the other gender or an insistence that one
is the other gender (or some alternative gender different from one’s
assigned gender).
2. In boys (assigned gender), a strong preference for cross-dressing
or simulating female attire; or in girls (assigned gender), a strong
preference for wearing only typical masculine clothing and a strong
resistance to the wearing of typical feminine clothing.
3. A strong preference for cross-gender roles in make-believe play or
fantasy play.
4. A strong preference for the toys, games, or activities stereotypically
used or engaged in by the other gender.
5. A strong preference for playmates of the other gender.
6. In boys (assigned gender), a strong rejection of typically masculine
toys, games, and activities and a strong avoidance of rough-and-
tumble play; or in girls (assigned gender), a strong rejection of typically
feminine toys, games, and activities.
7. A strong dislike of one’s sexual anatomy.
8. A strong desire for the primary and/or secondary sex characteristics
that match one’s experienced gender.
B. The condition is associated with clinically significant distress or
impairment in social, school, or other important areas of functioning.
Reprinted with permission from the Diagnostic and Statistical Manual of Mental Disorders, Fifth
Edition, (Copyright ©2013). American Psychiatric Association. All Rights Reserved.
Gender and Sexual Disorders 329
In order for a person to be diagnosed with gender dysphoria, DSM-5 requires
that the symptoms cause significant distress or impair functioning. However, the dis-
tress experienced by someone with gender dysphoria often arises because of other
people’s responses to the cross-gender behaviors (Nuttbrock et al., 2010; Roberts et al.,
2012). For instance, a natal male child with gender dysphoria may be ostracized or
made fun of by children or even teachers for consistently “playing girl games”—and
thus the child feels distress because of the reactions of others. In contrast, for most
disorders in DSM-5, the distress that the person feels arises directly from the symp-
toms themselves (e.g., distress that is caused by feeling hopeless or being afraid in
social situations).
Li ke the per son in Ca se 11.1, most adolescent s and adu lt s w ith gender
dysphor ia repor t hav ing had symptoms of the d isorder in ch i ldhood— even
though most people who had gender dysphoria in childhood do not have it later
in life.
CASE 11.1 • FROM TH E INSIDE: Gender Dysphoria
In her memoir She’s Not There: A Life in Two Genders (2003), novelist and English professor
Jenny Finney Boylan (who was born male) describes her experiences of feeling, since the age
of 3, as if she were a female in a male body:
Since then, the awareness that I was in the wrong body, living the wrong life, was never
out of my conscious mind—never, although my understanding of what it meant to be a
boy, or a girl, was something that changed over time. Still, this conviction was present
during my piano lesson with Mr. Hockenberry, and it was there when my father and I shot
off model rockets, and it was there years later when I took the SAT, and it was there in the
middle of the night when I woke in my dormitory at Wesleyan. And at every moment I
lived my life, I countered this awareness with an exasperated companion thought, namely,
Don’t be an idiot. You’re not a girl. Get over it.
But I never got over it.
(pp. 19–21)
Teena Brandon was born female, yet felt like
a male on the inside and came to live as a
man, though without having sex reassignment
surgery. As an adult, Brandon was raped
and later killed by young men after they
discovered that Brandon was biologically
female. Brandon’s life was the subject of the
documentary film The Brandon Teena Story
and the feature film Boys Don’t Cry.
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TABLE 11.2 • DSM-5 Diagnostic Criteria for Gender Dysphoria in
Adolescents and Adults
A. A marked incongruence between one’s experienced/expressed gender and assigned gender,
of at least 6 months’ duration, as manifested by at least two of the following:
1. A marked incongruence between one’s experienced/expressed gender and primary and/
or secondary sex characteristics (or in young adolescents, the anticipated secondary sex
characteristics).
2. A strong desire to be rid of one’s primary and/or secondary sex characteristics because
of a marked incongruence with one’s experienced/expressed gender (or in young
adolescents, a desire to prevent the development of the anticipated secondary sex
characteristics).
3. A strong desire for the primary and/or secondary sex characteristics of the other gender.
4. A strong desire to be of the other gender (or some alternative gender different from one’s
assigned gender).
5. A strong desire to be treated as the other gender (or some alternative gender different
from one’s assigned gender).
6. A strong conviction that one has the typical feelings and reactions of the other gender
(or some alternative gender different from one’s assigned gender).
B. The condition is associated with clinically significant distress or impairment in social,
occupational, or other important areas of functioning.
Reprinted with permission from the Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition, (Copyright
©2013). American Psychiatric Association. All Rights Reserved.
330 C H A P T E R 1 1
Most commonly, people with gender dysphoria are het-
erosexual relative to their gender identification. For instance,
natal men who see themselves as women tend to be attracted to
men and thus feel as if they are heterosexual (Blanchard, 1989,
1990; Zucker & Bradley, 1995). However, some are homosex-
ual relative to their gender identification; a natal woman who
sees herself as a man may be sexually attracted to men. And
some people with gender dysphoria are bisexual and some are
asexual—they have little or no interest in any type of sex.
As noted in Table 11.3 (along with other facts about gen-
der dysphoria), gender dysphoria is about three times more
common among natal males than among natal females. One ex-
planation for this difference is that in Western cultures, females
have a relatively wide range of acceptable “masculine” behavior
and dress (think of Diane Keaton’s character in the move Annie
Hall), whereas males have a relatively narrow range of acceptable
“feminine” behavior and dress. A woman dressed in “men’s”
clothes might not even get a second look, but a man dressed in
“women’s” clothes will likely be subjected to ridicule.
Understanding Gender Dysphoria
As summarized in the following sections, we now know that various neurological,
psychological, and social factors are associated with gender dysphoria.
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Females have a wider range of acceptable
“masculine” behavior and dress than males
have of acceptable “feminine” behavior and
dress. Women can wear men’s clothes without
risk of being labeled as deviant, whereas men
who wear women’s clothes (when not as part
of a performance) are often considered to
have something wrong with them.
TABLE 11.3 • Gender Dysphoria Facts at a Glance
Prevalence
• The prevalence of gender dysphoria is very low, estimated at 0.014% or lower.
Comorbidity
• In one survey of 31 patients who were diagnosed with gender dysphoria and had not yet
begun the process of sex reassignment surgery, almost 75% had another psychiatric disorder
at some point in their lives, most often either a mood disorder or a substance-related disorder
(Hepp et al., 2005). However, only 39% had another psychological disorder after they began
the sex reassignment process; this finding suggests that the previous high comorbidity was at
least partly related to living as a gender that did not correspond to a person’s gender identity.
Onset
• Symptoms of cross-gender identity typically begin in childhood.
Course
• If symptoms persist into adulthood, they are likely to remain stable, leading many people
with this disorder to seek sex reassignment surgery.
Gender Differences
• The ratio of natal males to natal females ranges from 2:1 to 6:1.
Cultural Differences
• Cross-gender identification is not considered pathological in all cultures; in some Native
American and traditional African cultures, such people have high status and are seen as
especially spiritual (Jacobs et al., 1997; Langer & Martin, 2004; Roscoe, 1993).
Source: Unless otherwise noted, information is from American Psychiatric Association, 2013.
Gender and Sexual Disorders 331
Neurological Factors
Researchers have begun to document differences in specific brain structures in peo-
ple who have gender dysphoria versus those who do not. In addition, evidence shows
that hormones during fetal development play a role in producing this disorder. Genes
can also play a large role in contributing to this disorder.
Brain Systems and Neural Communication
The brains of transsexuals differ from typical brains in ways consistent with their gender
identity. In particular, Kruijver and colleagues (2000) examined a specific type of neuron
in a brain structure called the bed nucleus of the stria terminalis (which is often regarded as an
extension of the amygdala). Typically, males have almost twice as many of these neurons
as females do. In this study, the number of these neurons in the brains of male-to-female
transsexuals was in the range typically found in female brains, and the number in the
brains of female-to-male transsexuals was in the range typically found in male brains.
How might such brain alterations arise? Research suggests that prenatal expo-
sure to hormones may affect later gender identity (Bradley & Zucker, 1997; Wallien
et al., 2008; Zucker & Bradley, 1995). In particular, maternal stress during pregnancy
can produce hormones that alter brain structure and thereby predispose a person
to gender dysphoria (Zucker & Bradley, 1995). In addition, fetal levels of testoster-
one—measured from amniotic fluid—are positively associated with later stereotypi-
cal “male” play behavior in girls and, to a lesser extent, in boys; the higher the level
of testosterone in the fluid, the more “male” play the children exhibited when they
were between 6 and 10 years old (Auyeung et al., 2009).
Genetics
Coolidge and colleagues (2002) studied 314 children who were either identical or frater-
nal twins and concluded that as much as 62% of the variance in gender dysphoria can arise
from genes! If this result is replicated, it will provide strong support for these researchers’
view that the disorder “may be much less a matter of choice and much more a matter of
biology” (p. 251). However, even in this study, almost 40% of the variance was ascribed
to the effects of nonshared environment, and thus genes—once again—are not destiny.
In short, neurological factors—brain differences, prenatal hormones, and genetic
predispositions—may contribute to gender dysphoria, but the presence of any one of
these factors does not appear to be sufficient to cause this disorder (Di Ceglie, 2000).
Psychological Factors: A Correlation with Play Activities?
In general, studies have found that boys engage in more rough-and-tumble play and
have a higher activity level than do girls. Natal boys with gender dysphoria, how-
ever, do not have as high an activity level as their counterparts without the disorder.
Similarly, natal girls with gender dysphoria are more likely to engage in rough-and-
tumble play than are other girls (Bates et al., 1973, 1979; Zucker & Bradley, 1995).
Both natal boys and natal girls with gender dysphoria are less likely to play with
same-sex peers; instead, they seek out, feel more comfortable with, and feel them-
selves to be more similar to children of the other sex (Green, 1974, 1987).
However, such findings should be interpreted with caution, for two reasons:
(1) These very characteristics are part of the diagnostic criteria for gender dyspho-
ria in children, so it is not at all surprising that these behaviors are correlated with
having the disorder; (2) a diagnosis of gender dysphoria in childhood does not usu-
ally persist into adulthood. Thus, beyond symptoms that are part of the criteria for
gender dysphoria, no psychological factors are clearly associated with the disorder.
Social Factors: Responses From Others
Social factors may be associated with gender dysphor ia, but such factors are
un l ikely to cause the d isorder ( Brad ley & Zucker, 1997; Di Ceg l ie, 20 0 0 ).
332 C H A P T E R 1 1
As shown in Figure 11.1(a), college students rated photographs of natal boys with
gender dysphoria as cuter and prettier than photos of boys without the disorder;
in contrast, Figure 11.1(b) shows that natal girls with gender dysphoria were rated
as less attractive than girls who did not have the disorder (Zucker et al., 1993).
These contrasting ratings of physical appearance may reflect the prenatal influ-
ence of hormones: Natal boys may have been exposed to more female hormones
in the womb, leading to the feminization of their facial features; conversely, natal
girls may have been exposed to more male hormones in the womb, leading to
the masculinization of their facial features. In turn, the feminized or masculin-
ized facial features may lead others to interact differently with people who then
develop this disorder.
Given how little is known about the factors that contribute to gender dysphoria,
we cannot comment on the nature of any feedback loops among them.
Treating Gender Dysphoria
Treatments for gender dysphoria may target all three types of factors.
Targeting Neurological and Other Biological Factors: Altered
Appearance
One way for people w ith gender dysphor ia to ach ieve g reater cong r uence
between the gender they feel themselves to be and their natal gender is to alter
some or all of their biological sexual characteristics. This sort of treatment may
involve taking hormones. In natal women, taking male sex hormones will lower
the voice, stop menstruation, and begin facial hair growth. In natal men, tak-
ing female sex hormones will enlarge breasts and redistribute fat to the hips and
buttocks.
Some people with gender dysphoria go a step further and have sex reassignment
surgery, a procedure in which the genitals and breasts are surgically altered to appear
like those of the other gender. Sex reassignment surgery for natal males involves creat-
ing breasts and removing most of the penis and testes and then creating a clitoris and
vagina. For natal females, surgery involves removing breasts, ovaries, and uterus and
Sex reassignment surgery
A procedure in which a person’s genitals (and
breasts) are surgically altered to appear like
those of the other sex.
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FI G U RE 11.1 • Physical Attractiveness Ratings of Children With Gender Dysphoria
(a) Viewing photographs, college students rated natal boys with gender dysphoria as more attractive than boys
without this disorder. (b) Similarly, natal girls with gender dysphoria were considered to be less attractive than girls
who did not have the disorder (Zucker et al., 1993).
Source: Adapted from Zucker & Bradley, 1995.
Gender and Sexual Disorders 333
then creating a penis. Patients may also have subsequent surgeries to make their facial
features more similar to those of the other gender. However, these surgical treatments
can—like other forms of surgery—be risky and prohibitively expensive.
Sex reassignment surgery is technically more effective for natal men than for
natal women, in part because it is difficult to create an artificial penis that provides
satisfactory sexual stimulation (Steiner, 1985). Regardless of natal gender, however,
most people who have gender dysphoria are satisfied with the outcome of their sex
reassignment surgery, despite possible difficulty in attaining orgasm (Cohen-Kette-
nis & Gooren, 1999; Smith, van Goozen, et al., 2005). However, up to 10% of people
who have this surgery (depending on the study) later regret it (Landen et al., 1998;
Smith van Goozen, et al., 2001). Factors associated with a less positive outcome after
surgery include having unsupportive family members (Landen et al., 1998) and hav-
ing a comorbid psychological disorder (Midence & Hargreaves, 1997; Smith, van
Goozen, et al., 2005).
In an effort to reduce the proportion of people who come to regret having sex
reassignment surgery, those contemplating it are usually carefully evaluated before-
hand regarding their emotional stability and their expectations of what the surgery
will accomplish. A careful diagnostic evaluation and a long period of cross-dressing
are required by most facilities before sex reassignment surgery.
Targeting Psychological Factors: Understanding the Choices
Treatment that targets psychological factors helps people with gender dysphoria
not only to understand themselves and their situation but also to be aware of their
options and goals regarding living publicly as the other gender; treatment also provides
information about medical and surgical options. Such treatment is typically provided
by mental health clinicians specially trained in diagnosing and helping people with
gender dysphoria. These clinicians also help patients identify and obtain treatment for
any other mental health issues, such as depression or anxiety (Carroll, 2000). For those
who choose to live part time or full time as the other gender, the clinician helps them
discover whether doing so is in fact more consistent with how they feel and how they
see themselves. Moreover, the clinician helps the patient with problem solving related
to living as the other gender—such as by identifying and developing possible solutions
to issues that might arise regarding other people’s responses to their changed gender.
Targeting Social Factors: Family Support
Family members of people with gender dysphoria may not understand the disorder
or know how to be supportive; family therapy techniques that focus on communi-
cation and educating the family about gender dysphoria can help family members
develop more effective ways to discuss problems.
In addition, groups for people with gender dysphoria can provide support and
information. Group therapy may also focus on difficulties in relationships or prob-
lems that arise as a result of living as the other gender, such as experiencing sexual
harassment for those newly living as a woman or taunting by men for those newly
living as a man (Di Ceglie, 2000).
Treatment for gender dysphoria typically f irst targets psychological factors—
helping people to determine whether they want to live as the other gender. If they
decide to do so, then treatment targeting social factors comes into play, to address
problems with family members and interactions with other people in general. Follow-
ing this, treatment targeting neurological and other biological factors is provided when
a person wishes to have medical or surgical procedures. After such treatment, clini-
cians may provide additional treatment that targets psychological and social factors.
Caroline Cossey, born Barry Cossey, increasingly
felt during adolescence that although she had
a male body, she was a female inside. When
20 years old, after a couple of years of taking
female hormones and living as a woman,
Cossey had sex reassignment surgery and later
became a model and actress.
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334 C H A P T E R 1 1
When Nico was a boy, he hated playing with the other boys; he detested sports and loved
playing “house” and “dress up” with the girls—except when the girls made him dress up as
“the man” of the group. Sometimes he got to be the princess, and that thrilled him. As a teen-
ager, Nico’s closest friends continued to be females. Although Nico shied away from playing
with boys, he felt himself sexually attracted to them. To determine whether Nico had gen-
der dysphoria, what information would a clinician want? What specific information would
count heavily? Should the fact that Nico is attracted to males affect the assessment? Why
or why not?
Thinking Like A Clinician
Paraphilic Disorders
Mike found that he was disturbed about Sam’s transformation into Samantha in
part because it reminded Mike of his ver y private pastime during his teenage
years: He had secretly “borrowed” some of his older sister’s clothes from her
room, dressed up in them, and adm ired himself in front of the m ir ror. He’d
found this extremely erotic but also terrif ying. He had worried that he’d get
caught and felt that it somehow wasn’t “right.” Throughout his adulthood, Mike
had struggled to overcome his urge to dress in women’s clothes, usually suc-
cessful ly. Dur ing most of his mar r iage to Laura, he’d managed to keep this
urge at bay, and he’d never told her about it. However, once he heard about
Sam, he felt jealous because Samantha dressed as a woman. His urge to dress in
women’s clothes became stronger, which affected his relationship with Laura: He
thought it best to avoid sexual relations with her until he felt more in control of
himself.
Mike had felt alone in his worries and concerns until he discovered online chat
rooms in which people discussed cross-dressing. Now he’s spending a lot of time
“chatting” with other men who like to cross-dress; he bought some women’s clothes
(which he keeps hidden) and puts them on and masturbates when Laura is out. What’s
going on with Mike? To find out, we need to consider another category of sexual
disorders, called paraphilic disorders.
What Are Paraphilic Disorders?
Some people have unusual sexual interests—paraphilias. Specifically, they are sexu-
ally aroused and have fantasies about objects or activities that are not normally asso-
ciated with sexual interests, such as women’s shoes or spying on other people when
they take off their clothes. A paraphilia (from the Greek para-, meaning “beside”
or “beyond,” and philos, meaning “fondness” or “love”) is an intense and persis-
tent sexual interest that is different than the usual fondling or genital stimulation
with “normal physically mature consenting human partners” (American Psychiatric
Association, 2013, p. 685).
Although paraphilias may be unusual, they are not necessarily considered to be
mental disorders. In contrast, according to DSM-5, paraphilic disorders are para-
philias that lead to distress, impaired functioning, or harm—or risk of harm—to the
person or to others. According to DSM-5, the sexual aspect of a paraphilic disorder
is characterized by unusual preferences either in (1) sexual activity (such as activities
involving pain and suffering or an odd variation of what might be considered “court-
ship”—such as exhibitionistic behavior) or (2) the target of the activity (such as chil-
dren or objects).
This way of classifying paraphilic disorders misses an important element that
some of these disorders share—that they involve partners who do not consent to
Paraphilia
An intense and persistent sexual interest that
is different than the usual fondling or genital
stimulation with “normal physically mature
consenting human partners.”
Paraphilic disorder
A category of disorders characterized by
paraphilias that lead to distress, impaired
functioning, or harm—or risk of harm—to the
person or to others.
Gender and Sexual Disorders 335
the activity. Other paraphilic disorders have pain and humiliation as the primary
activity. Thus, in this section, we classify paraphilic disorders according to whether
they involve:
• nonconsenting adults or children,
• nonhuman objects (such as women’s shoes) or body parts, or
• suffering or humiliating oneself or one’s partner; the diagnosis of a paraphilic disor-
der would apply only when such experiences are not part of sexual role-playing.
These fantasies, urges, or behaviors together form a predictable pattern of arousal that
is consistent for the person. In addition, the diagnostic criteria for all paraphilic disor-
ders require that the pattern of arousal (sometimes referred to as an arousal pattern) has
been present for at least 6 months (American Psychiatric Association, 2013). How-
ever, the arousal pattern doesn’t necessarily affect all areas of functioning; people
with a paraphilic disorder may not be impaired at work or even necessarily in their
family life.
Because DSM-5 uses a categorical approach, it must draw a line to separate
“ normal” from “abnormal.” For some paraphilic disorders, DSM-5 draws the line
at the point where the sexual arousal pattern causes significant distress or impairs
functioning. Someone who becomes aroused in response to violent pornography
or in response to particular items of clothing, for instance, would not be diag-
nosed as having a paraphilic disorder unless this arousal pattern caused significant
distress, impaired functioning, or led to harm or a risk of harm. Thus, having a
paraphilia is necessary, but not sufficient, to be diagnosed as having a paraphilic
disorder. For instance, someone might have exhibitionism but not exhibitionistic
disorder.
The specific arousal patterns of the types of paraphilic disorders are listed in
Table 11.4, along with their DSM-5 diagnostic criteria. Paraphilias and paraphilic
disorders are almost exclusively diagnosed in men; the only paraphilic disorder
observed in a significant percentage of women is sexual sadism disorder. Because the
vast majority of people who have the other paraphilic disorders are men, in this sec-
tion we use the masculine pronouns (e.g., him) when discussing patients with these
disorders. (In the section on understanding paraphilic disorders, we will examine
possible reasons for this gender difference.)
Mental health researchers believe that, based on the number of websites and
online chat rooms, the prevalence of paraphilic disorders is higher than had been
previously thought, but the actual prevalence is unknown. Most research on
paraphilic disorders has been conducted with men whose disorders involve non-
consenting people (such as child molesters, rapists, and exhibitionists) and who
have come to the attention of mental health clinicians and researchers through
the cr iminal justice system or at the urging of family members. We examine
that type of paraphilic disorder first and then consider other types of paraphilic
disorders.
Paraphilic Disorders Involving Nonconsenting People
The common feature of the paraphilic disorders discussed in this section is that
the person with the disorder has recurrent sexual fantasies, urges, or behaviors that
involve nonconsenting people of any age. Specifically, if the patient has recurrent
fantasies or urges that involve a nonconsenting person but does not act on them, a diag-
nosis of the paraphilic disorder is given only if the fantasies and urges cause signifi-
cant distress or impair functioning in some area of life (such as leading to difficulties
in relationships). In contrast, if the man did act on those recurrent fantasies and urges
with a nonconsenting person, the diagnosis would be made, even if the patient did
not experience distress or impaired functioning. For instance, someone who “flashes”
336 C H A P T E R 1 1
TABLE 11.4 • Paraphilic Disorders: An Overview and the DSM-5 Diagnostic Criteria
Disorder
Specific Sexual Thoughts
(Fantasies, or Urges)
or Activities to Enhance
Sexual Arousal Digest of DSM-5 Diagnostic Criteria
Exhibitionistic
disorder
Exposing genitals to an
nonconsenting stranger
• Repeated and significant sexual arousal from thoughts or deeds related to showing one’s pri-
vate parts to a nonconsenting person. Must have occurred over at least 6 months.
• The person has either acted on these thoughts or these thoughts impair normal functioning in
some area of life.
Voyeuristic
disorder
Watching someone who is
taking their clothes off or
having sex
• Repeated and significant sexual arousal from thoughts or deeds related to watching a person
who is unclothed, in the process of removing clothing, or having sex; the person being observed
is unaware of this fact. Must have occurred over at least 6 months.
• The person with this arousal pattern is 18 or older.
• The person has either acted on these thoughts or these thoughts impair normal functioning in
some area of life.
Frotteuristic
disorder
Non-violent physical
contact with a
nonconsenting person
• Repeated and significant sexual arousal from thoughts or deeds related to non-violent physical
contact with a nonconsenting person. Must have occurred over at least 6 months.
• The person has either acted on these thoughts or these thoughts impair normal functioning in
some area of life.
Pedophilic
disorder
Sexual activity with a
child who has not reached
puberty
• Repeated and significant sexual arousal from thoughts or deeds related to sexual activity
involving a child who has not yet reached puberty (typically under age 13). Must have occurred
over at least 6 months.
• The person has either acted on these thoughts or these thoughts impair normal functioning in
some area of life.
• The person is at least 5 years older than the object of the sexual fantasy or activity and is at
least 16.
Sexual Sadism
Disorder
Sexual arousal from
giving psychological or
physical pain
• Repeated and significant sexual arousal from thoughts or deeds related to the physical or emo-
tional suffering of another person. Must have occurred over at least 6 months.
• The person has either acted on these thoughts or these thoughts impair normal functioning in
some area of life.
Sexual
Masochism
Disorder
Sexual arousal from being
made to suffer
• Repeated sexual arousal from thoughts or deeds related to being hurt, humiliated, or suffering
in some other way. Must have occurred over at least 6 months.
• These thoughts or activities impair normal functioning in some area of life.
Fetishistic
Disorder
Sexual arousal from an
object (shoes, underwear)
• Repeated and significant sexual arousal from an object(s) or a specific nongenital body part.
Can be demonstrated either in imagination, desire or action. Must have occurred over at least
6 months.
• The fetish items are not limited to objects used in cross-dressing or self-stimulation (such as
vibrators).
• These thoughts or activities impair normal functioning in some area of life.
Transvestic
Disorder
Sexual arousal from
dressing in the clothes of
the opposite gender
• Repeated and significant sexual arousal from thoughts or deeds related to cross-dressing. Must
have occurred over at least 6 months.
• These thoughts or activities impair normal functioning in some area of life.
Paraphilic disorders include unusual sexual fantasies, urges, and activities that can be classified into three types: Those that involve nonconsenting
partners or children (in blue); those that involve suffering or humiliating oneself or a partner (in red); and those that involve nonhuman animals
or objects (in green). Note that sexual sadism involves nonconsenting people; nevertheless, DSM-5 groups sexual sadism disorder with sexual
masochism disorder, rather than with the other paraphilic disorders that involve nonconsenting people. Note also that the specifics of the criterion
related to distress, impaired functioning, or acting on the sexual thoughts vary across the paraphilic disorders, depending in part on whether the
disorder involves nonconsenting individuals.
Source: Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition, American Psychiatric Publishing, 2013.
Gender and Sexual Disorders 337
Exhibitionistic disorder
A paraphilic disorder in which sexual fantasies,
urges, or behaviors involve exposing one’s
genitals to an unsuspecting person.
Voyeuristic disorder
A paraphilic disorder in which sexual fantasies,
urges, or behaviors involve observing someone
who is in the process of undressing, is nude, or
is engaged in sexual activity, when the person
being observed has neither consented to nor is
aware of being observed.
others, who molests children, or who sadistically sexually assaults victims would be
diagnosed with a paraphilic disorder if the duration criterion—at least 6 months—for
the behavior were met.
Thus, men who engage in criminal sexual behaviors could qualify for the diag-
nosis of a paraphilic disorder, which creates confusion about what constitutes criminal
behavior versus mental illness. However, some psychiatrists point out that paraphilic
disorders should not be diagnosed solely on the basis of sexual behaviors because do-
ing so “blurs the distinction between mental disorder and ordinary criminality”
(First & Frances, 2008, p. 1240). In short, some people with this diagnosis might
commit crimes, but not all people with this diagnosis do so.
Exhibitionistic Disorder: Physically Exposing Oneself
The paraphilic disorder exhibitionistic disorder is characterized by sexual
fantasies, urges, or behaviors that involve a person’s exposing his genitals to an un-
suspecting person (see Table 11.4). To be considered a disorder,
the man must either experience distress or impaired function-
ing as a result of the fantasies and urges—or must have actually
exposed himself to someone who was not a willing observer.
People who expose themselves for money (such as nude danc-
ers or artists’ models) are not considered exhibitionists because
they do so for compensation, not for sexual arousal (McAnulty
et al., 2001).
A man w ith ex h ibit ion ist ic d isorder t y pica l ly gets an
erection and may masturbate while exposing himself. Men
with this disorder commonly report that they don’t intend to
frighten or shock strangers but hope that strangers will enjoy
or be aroused by seeing their genitals (Lang et al., 1987; Lan-
gevin et al., 1979). Men with exhibitionistic disorder may
rehearse beforehand ; they may achieve orgasm dur ing the
exhibitionistic episode or later, when they think about it.
One study found that, over the course of his life, the typical man with this dis-
order had “f lashed” 514 people (Abel et al., 1987). (However, some ver y active
men skew the average; the median number of people f lashed is 34.) Between
2 and 4 % of ma les are thought to have th is d isorder (A mer ican Psych iatr ic
Association, 2013).
Voyeuristic Disorder: Watching Others
Voyeuristic disorder is a paraphilic disorder characterized by sexual fantasies,
urges, or behaviors that involves observing someone who is in the process of undress-
ing, is nude, or is engaged in sexual activity. The person being watched has neither
consented to nor is aware of being observed (see Table 11.4). As with exhibitionistic
disorder, for voyeuristic disorder to be classified as a disorder, the person’s urges and
fantasies must cause distress or impair functioning, or the person must have acted on
those fantasies and urges.
A voyeur rarely has physical contact with the observed person. Moreover, voy-
euristic disorder is distinguished from looking at pornography or watching nude
dancing; voyeuristic disorder involves observing someone who does not know that he
or she is being observed. A man with this disorder might use binoculars to “spy” on a
woman, masturbating while observing her through her window as she undresses,
or might plant hidden cameras and watch the video later or via an Internet feed.
According to DSM-5, this disorder can only be diagnosed in people who are 18 years
old or older, in order not to pathologize what is viewed as a “normal” sexual curios-
ity during puberty and adolescence.
People who are paid to disrobe—either
partially, as is the case with these men,
or fully—are not considered to have
exhibitionistic disorder.
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Frotteuristic Disorder: Touching a Stranger
Frotteuristic disorder (from the French frotter, “to
rub” ) is characterized by recurrent, intense, sexu-
ally arousing fantasies, sexual urges, or behaviors that
involve touching or rubbing against a nonconsent-
ing person (see Table 11.4). As with exhibitionistic
disorder and voyeuristic disorder, the urges and fan-
tasies must cause distress or problems in relation-
ships, or the man must have acted on those fantasies
and urges. This diagnosis has two t ypes: men who
like to rub and men who like to touch (“touchers”).
On crowded public transportation, men with frot-
teuristic disorder try to stand or sit next to attractive
females and rub their genitals against the victims’ buttocks, thighs, or crotch, often
while fantasizing that they are having consensual sex, as Charles, in Case 11.2,
did. When discovered, men with frotteuristic disorder typically f lee from the
train or bus.
CASE 11.2 • FROM TH E OUTSIDE: Frotteuristic Disorder
Charles was 45 when he was referred for psychiatric consultation by his parole officer
following his second arrest for rubbing up against a woman in the subway. According to
Charles, he had a “good” sexual relationship with his wife of 15 years when he began,
10 years ago, to touch women in the subway. A typical episode would begin with his deci-
sion to go into the subway to rub against a woman, usually in her 20s. He would select the
woman as he walked into the subway station, move in behind her, and wait for the train to
arrive at the station. He would be wearing plastic wrap around his penis so as not to stain
his pants after ejaculating while rubbing up against his victim. As riders moved on to the
train, he would follow the woman he had selected. When the door closed, he would begin
to push his penis up against her buttocks, fantasizing that they were having intercourse in
a normal, noncoercive manner. In about half the episodes, he would ejaculate and then go
on to work. If he failed to ejaculate, he would either give up for that day or change trains
and select another victim. According to Charles, he felt guilty immediately after each epi-
sode, but would soon find himself ruminating about and anticipating the next encounter.
He estimated that he had done this about twice a week for the last 10 years and thus had
probably rubbed up against approximately a thousand women.
(Spitzer et al., 2002, pp. 164–165)
Pedophilic Disorder: Sexually Abusing Children
Child sexual abuse is a crime, but the DSM-5 diagnosis for those who fantasize
about, have urges, or actually engage in sexual activity with a child (typically one
who has not yet gone through puberty) is pedophilic disorder (previously called
pedophilia)(see Table 11.4). To be diagnosed with this disorder, the person must
be at least 16 years old and at least 5 years older than the child. Thus, someone
is diagnosed with pedophilic disorder if he has had sexual activity with a child
(and so would also be considered a child molester) or if he has related sexual fanta-
sies or impulses that cause distress or significantly impair his relationships. Some-
one with pedophilic disorder may or may not sexually molest children; a child
molester may or may not be diagnosed with pedophilic disorder, if his related
fantasies, urges, or behaviors have occurred for less than 6 months ( Camilleri &
Quinsey, 2008).
People who have this disorder may engage in sexual behaviors that range from
fondling to oral–genital contact to penetration. Approximately 25% of victims
Frotteuristic disorder
A paraphilic disorder in which recurrent,
intense, sexually arousing fantasies, sexual
urges, or behaviors involve touching or
rubbing against a nonconsenting person.
Pedophilic disorder
A paraphilic disorder in which recurrent
sexually arousing fantasies, sexual urges, or
behaviors involve a child who has not yet gone
through puberty.
These two photos illustrate the key difference
between voyeuristic disorder and frotteuristic
disorder: physical contact. This man on the
left may just be birdwatching, but some
people with voyeuristic disorder may use
binoculars to spy on people who are naked
or engaged in sex. In contrast, frotteuristic
disorder involves physical contact, and a
crowded subway car is the kind of place where
someone with frotteuristic disorder may find
opportunity for physical contact.
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Gender and Sexual Disorders 339
(who are more likely to be girls than boys; McAnult y et al., 2001) are under
6 years of age, 25% are between 6 and 10 years old, and 50 % are between 11 and
13 (Erickson et al., 1988). People with pedophilic disorder often say that they be-
lieve that adult sexual contact with children has positive effects for the child. In
fact, some child molesters with pedophilic disorder report that they didn’t think
they were harming the children they molested but were “sharing pleasure” (Spitzer
et al., 2002). Compared to rapists, people with pedophilic disorder who have mo-
lested children view themselves as less responsible for the abuse and view the child
as more responsible (Stermac & Segal, 1989) —claiming that the child “seduced”
them. Studies suggest that men with pedophilic disorder who are sex offenders
are likely to have at least one other paraphilic disorder (Heil & Simons, 2008;
Raymond et al., 1999).
Sexual Sadism Disorder and Sexual Masochism Disorder:
Pain and Humiliation
Sexual sadism disorder and sexual masochism disorder are two comple-
mentar y sides of a mode of sexual interaction in which actual pain,
suffering, or humiliation creates or enhances sexual excitement. Peo-
ple who do not experience significant distress or impaired function-
ing because of their sadistic or masochistic sexual fantasies, urges, and
behavior and whose sexual partners are consenting adults would not
be diagnosed with either of these disorders. That is, consensual, non-
impairing, and nondistressing BDSM (bondage and discipline, domi-
nance and subm ission, sad ism and masoch ism) fantasies, urges, or
behaviors would not be considered to be a paraphilic disorder (Shindel
& Moser, 2011). In what follows we examine the DSM-5 criteria for
these two disorders.
Sexual Sadism Disorder: Inflicting Pain
A person who becomes sexually aroused by fantasies, urges, and behaviors
that inflict physical or psychological suffering on a nonconsenting person
is said to have sexual sadism disorder (see Table 11.4). Note that sexual
sadism disorder involves acts that actually do, or actually could (in the case
of urges and fantasies) cause someone else to suffer ( versus simulated acts,
where no real suffering occurs). There are two sets of circumstances in
which someone would be diagnosed with sexual sadism disorder: (1) The
recurrent sadistic fantasies or urges cause the person significant distress, as
occurs when a man is horrified to discover that he is consistently aroused
when fantasizing about hurting his partner; or (2) the person has repeat-
edly subjected a nonconsenting partner to sexually sadistic acts, as occurs with sadis-
tic rape, which is also a criminal act.
Any type of rape is a criminal act, and sadistic rape is also a type of sexual sadism
disorder defined in DSM-5. What distinguishes sadistic rape from other forms of
rape is that in the former, the offender becomes sexually aroused by gratuitous
violence or the victim’s suffering or humiliation (Heil & Simons, 2008). In con-
trast, nonsadistic rape occurs when the rapist uses force in order to get his victim to
“ comply” but not because such force is a critical element of his sexual arousal pattern
(Yates et al., 2008).
For people diagnosed with sexual sadism disorder, the sadistic sexual fantasies
often were present in childhood, and the sadistic behavior commonly began in early
adulthood—as occurred with the man in Case 11.3. Sexual sadism disorder is usually
chronic, and the severity of the sadistic behaviors increases over time (American
Psychiatric Association, 2013).
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People who are sexually aroused by sadistic
or masochistic fantasies, urges, or acts
with consenting adults and who are neither
distressed nor impaired by it would not be
considered to have sexual sadism disorder or
sexual masochism disorder.
Sexual sadism disorder
A paraphilic disorder in which recurrent sexually
arousing fantasies, urges, and behaviors inflict,
or would inflict, physical or psychological
suffering on a nonconsenting person.
340 C H A P T E R 1 1
CASE 11.3 • FROM TH E OUTSIDE: Sexual Sadism Disorder
A physician, raised alone by his widowed mother since age 2, has been preoccupied with
spanking’s erotic charge for him since age 6. Socially awkward during adolescence and his
20s, he married the first woman he dated and gradually introduced her to his secret arousal
pattern of imagining himself spanking women. Although horrified, she episodically agreed
to indulge him on an infrequent schedule to supplement their frequent ordinary sexual
behavior. He ejaculated only when imagining spanking [. . .] After 20 years of marriage, her
psychologist instructed her to tell him, “No more.” He fell into despair, was diagnosed with
a major depressive disorder, and wrote a long letter to her about why he was entitled to
spank her. He claimed to have had little idea that her participation in this humiliation was
negatively affecting her mental health (“She even had orgasms sometimes after I spanked
her!”). He became suicidal as a solution to the dilemma of choosing between his or her
happiness and becoming conscious that what he was asking was abusive. He was shocked
to discover that she had long considered suicide as a solution to her marital trap of loving
an otherwise good husband and father who had an unexplained sick sexual need.
(Sadock & Sadock, 2007, pp. 709–710)
Sexual Masochism Disorder: Receiving Pain
Whereas sexual sadism disorder involves hurting others, sexual masochism
disorder is characterized by recurrent sexual arousal in response to fantasies, urges,
or behaviors related to being hurt oneself—specifically, being humiliated or made
to suffer in other ways (see Table 11.4; American Psychiatric Association, 2013). For
a diagnosis of sexual masochism disorder, the sexual fantasies, urges, and behavior
must cause significant distress or impair functioning.
Sexual masochism disorder is diagnosed in both men and women and is, in fact,
the only paraphilic disorder that occurs at measurable rates among women (Levitt
et al., 1994). One study found that about one quarter of women who engage in sexu-
ally masochistic behavior reported a history of sexual abuse during childhood, which
may suggest that the abuse made them more likely to be aroused by masochistic acts
(Nordling et al., 2000). However, these women did not necessarily have sexual mas-
ochism disorder because they did not report that their sexual preferences caused dis-
tress or impaired functioning.
Paraphilic Disorders Involving Nonhuman Objects
Two paraphilic disorders—fetishistic disorder and transvestic disorder—are charac-
terized by persistent sexual fantasies, urges, and behaviors that focus on nonhuman
animals or objects, such as clothing, which lead to signif icant distress or impair
functioning.
Fetishistic Disorder: Sexually Arousing Objects
Fetishistic disorder is the paraphilic disorder characterized by the repeated use
of nonliving objects (such as women’s shoes or undergarments) or nongenital body
parts (such as feet) in sexual fantasies, urges, or behaviors, which in turn leads to
distress or impaired functioning (see Table 11.4). The object or body part—termed
a fetish—may be used to achieve sexual arousal or to maintain an erection with a
partner or alone. For instance, a man with a shoe fetish will become aroused by
seeing or smelling women’s footwear. He may steal women’s shoes and use them
to masturbate (Shiah et al., 2006). When fetishistic disorder is severe, he may be
unable to have sexual relations with a partner unless the fetish is part of the sexual
experience. People with fetishistic disorder generally come to the attention of men-
tal health professionals only after being apprehended for the theft of their fetish.
As usual, in the absence of distress or impaired functioning, a diagnosis of a disorder
should not be made. The man in Case 11.4 gets sexually excited about women’s
underwear.
The hallmark of fetishistic disorder is being
sexually aroused by inanimate objects, such
as footwear or mannequins—or nongenital
body parts.
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Sexual masochism disorder
A paraphilic disorder in which the person
repeatedly becomes sexually aroused by
fantasies, urges, or behaviors related to being
hurt—specifically, being humiliated or made to
suffer in other ways—and this arousal pattern
causes significant distress or impairs functioning.
Fetishistic disorder
A paraphilic disorder in which the person
repeatedly uses nonliving objects or nongenital
body parts to achieve or maintain sexual
arousal and such an arousal pattern causes
significant distress or impairs functioning.
Gender and Sexual Disorders 341
CASE 11.4 • FROM TH E OUTSIDE: Fetishistic Disorder
A single, 32-year-old male freelance photographer presented with the chief complaint
of “abnormal sex drive.” The patient related that although he was somewhat sexu-
ally attracted by women, he was far more attracted by “their panties” . . . His first
ejaculation occurred at 12 via masturbation to fantasies of women wearing panties.
He masturbated into his older sister’s panties, which he had stolen without her knowl-
edge. Subsequently he stole panties from her friends and other women he met socially.
He found pretexts to “wander” into bedrooms of women during social occasions, and
would quickly rummage through their possessions until he found a pair of panties to his
satisfaction. He later used these to masturbate into and then “saved them” in a “private
cache.” The pattern of masturbating into women’s underwear had been his preferred
method of achieving sexual excitement and orgasm from adolescence until the present
consultation . . . he felt anxious and depressed because his social life was limited by his
sexual preference.
(Spitzer et al., 2002, p. 247)
Transvestic Disorder: Cross-Dressing for Sexual Arousal
Transvestic disorder is the diagnosis given to people (almost always men)
who experience sexual arousal when they dress in clothes appropriate for peo-
ple opposite to the person’s assigned gender, and experience distress or impaired
functioning because of it (Table 11.4), as Mike did. (Note that this is in contrast
to people with gender dysphoria, who cross-dress not for sexual arousal but to
make their outward appearance more congruent with their internal experience;
see Table 11.5.) Moreover, men with transvestic disorder use female clothing dif-
ferently than those with a nontransvestic fetish that involves female apparel, such as
an underwear fetish. Men with a nontransvestic fetish may wear female clothes to
achieve sexual arousal, but only if the clothes were previously worn by a woman;
they do not try to appear female, as did Jenny Boylan, in Case 11.1. In contrast,
men with transvestic disorder prefer to wear new female clothes and try to appear
as female, as Mike did.
Transvestic disorder usually begins before age 10 and may involve only one or
two items of clothing, or may involve dressing entirely as the other sex, including
wearing wigs and cross-gender outer clothes (such as coats). Some men who experi-
ence distress may periodically throw away their women’s clothes in the hopes that
their urges and fantasies will subside.
As adults, the cross-dressing typically is not limited to the privacy of the home:
Almost three quarters of men with this disorder who were surveyed reported that
they had appeared in public while dressed as women. Almost two thirds are mar-
ried, often with children; you may assume that they hide their fetish from their
wives, but as with Mr. A. in Case 11.5, the wives often know about the cross-
dressing. Most wives are ambivalent about it, and fewer than one third accept it
(Docter & Prince, 1997).
The man in this photograph doesn’t seem
distressed, so he probably wouldn’t qualify
for a diagnosis of transvestic disorder,
which describes men who dress as women
to become sexually aroused but also are
distressed or impaired by doing so.
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TABLE 11.5 • Transvestic Disorder Versus Gender Dysphoria
Transvestic disorder Gender dysphoria
Gender identity same as natal gender Gender identity different from natal gender
Comfortable with own natal gender Want to be the other gender
Cross-dress for sexual arousal or to feel
“calmer”
Cross-dress for congruence between
appearance and gender identity
Transvestic disorder
A paraphilic disorder in which the person
cross-dresses for sexual arousal and
experiences distress or impaired functioning
because of the cross-dressing.
342 C H A P T E R 1 1
CASE 11.5 • FROM TH E OUTSIDE: Transvestic Disorder
Mr. A., [is] a 65-year-old security guard [married and with grown children], formerly a
fishing-boat captain. . . . His first recollection of an interest in female clothing was putting
on his sister’s [underwear] at age 12, an act accompanied by sexual excitement. He contin-
ued periodically to put on women’s underpants—an activity that invariably resulted in an
erection, sometimes a spontaneous emission, and sometimes masturbation, but was never
accompanied by fantasy. Although he occasionally wished to be a girl, he never fanta-
sized himself as one. He was competitive and aggressive with other boys and always acted
“masculine.” During his single years he was always attracted to girls, but was shy about
sex. Following his marriage at age 22, he had his first heterosexual intercourse.
His involvement with female clothes was of the same intensity even after his marriage.
Beginning at age 45, after a chance exposure to a magazine called Transvestia, he began to
increase his cross-dressing activity. He learned there were other men like himself, and he
became more and more preoccupied with female clothing in fantasy and progressed to period-
ically dressing completely as a woman. . . . Over time [his cross-dressing] has become less erot-
icized and more an end in itself, but it still is a source of some sexual excitement. He always
has an increased urge to dress as a woman when under stress; it has a tranquilizing effect.
If particular circumstances prevent him from cross-dressing, he feels extremely frustrated.
(Spitzer et al., 2002, pp. 257–258)
Assessing Paraphilic Disorders
The paraphilic disorders are usually assessed by examining the now-familiar three types of
factors: neurological (sometimes reflected by bodily responses), psychological, and social.
From a neurological perspective, sexual arousal in men can be measured by a penile
plethysmograph, which is an indirect measure of neurological events. The device is placed on
a man’s penis and measures penile rigidity. The man is then shown “normal” and “devi-
ant” stimuli (such as photos of footwear or whips), and the rigidity of the penis is measured
after each stimulus is presented. If the plethysmograph registers unusual amounts of arousal
when the man views deviant stimuli, compared to stimuli that induce arousal in men
without a paraphilia, this response suggests that he has a paraphilia or paraphilic disorder.
From a psychological perspective, self-reports of arousal are used to assess para-
philic disorders: Men describe what they find sexually arousing, either to a mental
health clinician or in response to a questionnaire.
Finally, from a social perspective, assessment of paraphilic disorders may rely on re-
ports from partners or the criminal justice system, after men are apprehended for enga-
ging in illegal sexual activity such as secretly observing nonconsenting people as they
disrobe or having inappropriate sexual relations with children (McAnulty et al., 2001).
Criticisms of the DSM-5 Paraphilic Disorders
Critics of the set of paraphilic disorders identified in DSM-5 point out that what counts
as “deviant” (or, the flip-side, “normal”) has changed over time. The paraphilic disorders
are, in essence, behaviors and fantasies that Western culture currently labels as deviant—
and such deviance is relative to the current cultural concept of “normal” sexual behavior
or fantasies (Moser & Kleinplatz, 2005). Normal sexual behavior typically has been
defined by the church, the government, or the medical community (McAnulty et al.,
2001; Moser, 2001). In addition, widely different types of attraction are grouped together
(e.g., pedophilic disorder and fetishistic disorder), creating an overly broad category.
Understanding Paraphilic Disorders
Researchers are only just beginning to learn why paraphilic disorders emerge and
persist, and not enough is known to understand how feedback loops might arise
among neurological, psychological, and social factors.
Gender and Sexual Disorders 343
Neurological Factors
Many theorists who have considered the neurological underpinnings of paraphilic
disorders have noted the apparent similarities between these disorders and OCD,
both of which involve obsessions and compulsions. As discussed in Chapter 7, OCD
appears to result from abnormal functioning in a neural system that includes the basal
ganglia (which play a central role in producing automatic, repetitive behaviors) and
the frontal lobes (which normally inhibit such behaviors). In fact, researchers found
that people with pedophilic disorder have very specific cognitive deficits when per-
forming tasks that rely on this neural system (Tost et al., 2004). For example, these
patients were strikingly impaired in inhibiting responses and in working memory—
both of which rely heavily on the frontal lobes (Smith & Kosslyn, 2006).
In addition, evidence suggests that the neurotransmitters that are used in this
neural system, such as dopamine and serotonin, do not function properly in people
who have paraphilic disorders (Kaf ka, 2003). Indeed, SSRIs decrease the sexual fan-
tasies and behaviors related to paraphilic disorders, which is consistent with the view
that neural interactions involved in OCD are also involved in the paraphilic disorders
(Bradford, 2001; Kaf ka & Hennen, 2000; Roesler & Witztum, 2000).
Psychological Factors: Conditioned Arousal
Both psychodynamic and cognitive-behavioral theories have been invoked to explain
paraphilias in general and paraphilic disorders in particular, but research to date does not
generally support either type of explanation (Osborne & Wise, 2005). However, behav-
ioral theory can answer one intriguing question about paraphilias: Why are
almost all people with paraphilias male? An answer may lie in principles of
classical conditioning, which can contribute to paraphilias in part because
of the nature of the male body: The position of the penis and testicles on
the body can easily lead to their being inadvertently stimulated (Munroe
& Gauvain, 2001). This is important because classical conditioning can
occur if the genitals are stimulated right after or at the same time as seeing
or feeling an object (Domjan et al., 2004; Köksal et al., 2004). Consider
this example: A fetish for objects such as women’s shoes can develop when
an unconditioned stimulus that led to sexual arousal became paired with
a conditioned stimulus (women’s shoes). Thus, a boy who coincidentally
saw his mother’s shoes before—intentionally or accidentally—touching his
penis may come to have a conditioned response of sexual arousal to wom-
en’s shoes in the future. In fact, humans—or at least human males—may
be biologically prepared to develop classically conditioned sexual arousal to
some situations or objects (Osborne & Wise, 2005), which would explain
why a pillow fetish is not common.
Classical conditioning may be amplif ied by the Zeigarnik effect
(Deutsch, 1968), which makes people more likely both to recall inter-
rupted activities than ones that they finished and to try to complete interrupted activities
when later allowed to do so. Applied to paraphilias and paraphilic disorders, sexual arousal
that has been associated with an object or situation may be such an interrupted activity:
Sexual arousal at a young age that isn’t allowed expression becomes “interrupted”; the
person is later driven to “complete” the interrupted activity (Munroe & Gauvain, 2001).
Social Factors: More Erotica?
The Zeigarnik effect can also help explain why fewer males in traditional, nonin-
dustrialized societies have paraphilias than do males in Western societies: Western
societies provide many erotic stimuli—in magazines, in movies, on billboards and
television—to which males can become aroused. In turn, males, particularly boys,
Some men who fought in World War II, who
were in their formative years during the war,
spent time with women who wore gas masks,
and such attire became a sexual turn-on for
the men (Kaplan, 1991). If any of these men
experienced significant distress or impaired
functioning as a result of their unusual object
of arousal, they might be considered to have a
fetishistic disorder.
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are thus more likely to be “interrupted,” leading to a desire to complete the task
(Munroe & Gauvain, 2001).
Treating Paraphilic Disorders
Only some people who have paraphilic disorders receive treatment—typically those
who were caught engaging in predatory paraphilic behavior with nonconsenting
people and so were brought into the criminal justice system (where they were clas-
sified as sex offenders). The goal of treatment, which may be ordered by a judge, is to
decrease paraphilic impulses and behaviors by targeting neurological, psychological,
and social factors; research on treatments for paraphilic disorders is not yet advanced
enough to indicate how feedback loops arise as a result of treatment.
Targeting Neurological and Other Biological Factors: Medication
One goal of treatment for men who have engaged in predatory paraphilic behaviors
with nonconsenting people is to decrease or eliminate their sex drive. Chemical cas-
tration refers to the use of medications to achieve this goal. Such medications include
antiandrogen drugs such as medroxyprogesterone acetate (Depo-Provera) and cyprotereone
acetate (Androcur), which decrease testosterone levels. Decreased testosterone levels lead
to decreased sexual urges, fantasies, and behaviors in sex offenders (Bradford, 2000;
Gijs & Gooren, 1996; Robinson & Valcour, 1995). However, these medications don’t
necessarily diminish men’s paraphilic interests along with their sex drive. Moreover,
within a few weeks of stopping the medication, the men again experience the urges
and may engage in the predatory behaviors (Bradford, 2000; Gijs & Gooren, 1996).
In addition, as noted earlier, SSRIs may help decrease the sexual fantasies, urges,
and behaviors in men whose paraphilic disorder has obsessive-compulsive elements.
Thus, a treatment that targets neurological factors can affect thoughts (fantasies),
which are psychological factors.
C U R R E N T C O N T R O V E R S Y
Sex Offenders: Is Surgical Castration
an Ethical Solution?
For some, the surgical castration of sex offenders conjures thoughts
of draconian medieval punishment, whereas for others it reflects
a treatment approach maximally likely to decrease the chances of
recidivism. In the Czech Republic and Slovakia, the procedure
is offered on a voluntary basis to repeat sex offenders who have
been diagnosed with a paraphilic disorder (such as pedophilic
disorder). Each year about 10 men in the Czech Republic un-
dergo the procedure, a 1-hour operation that involves removal of
the tissue that produces testosterone (Bilefsky, 2009). However,
The Committee for the Prevention of Torture of the Council of
Europe has called for an immediate stop to this procedure, on the
basis that it “amounts to degrading treatment” (Pf äfflin, 2010).
Proponents of castration from the Czech Republic argue
that the procedure is medically safe and done only with the
offender’s consent and after an extensive approval process con-
ducted by an independent committee of psychiatric and legal
experts. Further, evidence suggests that the procedure reduces
recidivism rates from 20% (with therapy alone) to between 2 and
5% (Hoy, 2007). One treated sex offender said that having his
testicles removed “was like draining the gasoline from a car hard-
wired to crash” ( Bilefsky, 2009). In other words, surgical castra-
tion has the potential to benefit both society and the offender.
Opponents of the procedure, by contrast, focus on its being
invasive, irreversible, mutilating, and motivated by revenge. Ales
Butala, a Slovenian human rights lawyer, has argued that surgi-
cal castration is unethical because it is not medically necessary
and deprives castrated men of the right to reproduce (Bilefsky,
2009). The Council of Europe has raised doubts about the vol-
untary nature of the intervention, noting that it may be offered
to offenders as an alternative to life in prison. As one critic noted,
“Is that really free and informed consent?”(Bifelsky, 2009).
CRITICAL THINKING Based on what you’ve read in this chapter,
do you think that surgical castration would be an effective and
ethical treatment for those suffering from a chronic paraphilic
disorder with nonconsenting partners? Should it be extended
to other paraphilic disorders such as sexual sadism disorder or
frotteuristic disorder? Why or why not?
(Ken Abrams, Carleton College)
Most men who receive treatment for a paraphilic
disorder do so after coming to the attention of
the criminal justice system, as did this man.
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Gender and Sexual Disorders 345
Targeting Psychological Factors: Cognitive-Behavior Therapy
CBT may be used to treat paraphilic disorders in several ways. For one, it can de-
crease cognitive distortions that promote paraphilic fantasies, urges, and behaviors.
For example, such distortions might include the belief that sexual actions directed
toward nonconsenting people are not harmful. In addition, behavioral methods,
such as extinction, may decrease sexual arousal to paraphilic stimuli while increasing
arousal to normal stimuli (Akins, 2004). Treatment for sex offenders may involve
both medication and CBT (Heilbrun et al., 1998); both types of interventions, when
effective, ultimately reduce problematic arousal patterns, sexual fantasies and urges,
and sexual behaviors toward nonconsenting people.
In addition, treatment may sometimes include relapse prevention training, which
teaches men to identify and recognize high-risk situations and learn strategies to
avoid them. Such training also involves learning new coping skills, such as anger
management or assertiveness (Pithers, 1990). However, such treatments tend not to
reduce subsequent offenses among those sex offenders who are also psychopaths—
people who lack empathy, show little remorse or guilt about hurting others, and shirk
responsibility for their actions (Barbaree, 2005; Langton et al., 2006).
Targeting Social Factors
Some treatments for sex offenders target social factors, for example, by training these
men to empathize with victims in the hopes that they will be less likely to re offend
in the future (Marshall et al., 1996). However, many offenders do not complete
psychosocial treatments (Hanson et al., 2004; Langevin, 2006). Furthermore, such
treatments typically are not very successful (Hanson et al., 2004).
Thinking Like A Clinician
Ben was getting distracted at work because he kept fantasizing about having sexual relations
with young boys. He’d think about a neighbor’s son or a boy in an advertisement. He hadn’t
done anything about his fantasies, but they were getting increasingly hard to ignore.
According to DSM-5, which paraphilic disorder, if any, does Ben have? On what is your deci-
sion based? If Ben wasn’t getting distracted by his fantasies, would your diagnosis change or
stay the same, and why? Do you think that illegal acts (such as child sex abuse or sexual acts
with nonconsenting people generally) should be part of the DSM criteria, as they presently
are? Explain your answer. What treatment options are available to Ben?
Sexual Dysfunctions
Let’s return to Laura and Mike, the married couple whose relationship—and sex life—
had become strained. Laura found that she didn’t particularly miss having sexual rela-
tions with Mike. In fact, Laura didn’t have any sex drive, and the past few times she and
Mike had made love, nothing had “happened” for her—she hadn’t had an orgasm or
even found herself aroused. She couldn’t pinpoint where things had gone astray; she’d
like to feel desire, to want to have sexual relations with her husband, but she just didn’t
know where to start or how to get herself worked up about it. Was there something
wrong with their relationship, or with her? Or is such lack of interest “normal”?
An Overview of Sexual Functioning and
Sexual Dysfunctions
People engage in sexual relations for two general reasons: to create babies (repro-
ductive sex) and for pleasure (recreational sex). The vast majority of sexual acts are
for pleasure, as opposed to procreation. Researchers have def ined the “normal”
346 C H A P T E R 1 1
Sexual dysfunctions
Sexual disorders that are characterized by
problems in the sexual response cycle.
Sexual response cycle
The four stages of sexual response—excitement,
plateau, orgasm, and resolution—outlined by
Masters and Johnson.
progression of sexual pleasure as the human sexual response cycle, discussed in what
follows. Sexual dysfunctions are characterized by problems in the sexual response
cycle. We first examine this cycle and then consider various ways in which it can go
awry for men and women.
The Normal Sexual Response Cycle
What is a normal sexual response? In the 1950s and 1960s, researchers William
Masters and Virginia Johnson sought to answer this question by measuring the sexual
responses of thousands of volunteers. Based on their research, Masters and Johnson
(1966) outlined the sexual response cycle for both women and men as consisting of
four stages (see Figure 11.2):
1. Excitement. Excitement occurs in response to sensory-
motor, cognitive, and emotional stimulation that leads
to erotic sensations or feelings. Such arousal includes
muscle tension throughout the body and engorged
blood vessels, especially in the genital area. In men,
this means that the penis swells; in women, this means
that the clitoris and external genital area swell, and
vaginal lubrication occurs.
2. Plateau. Bodily changes that began in the excitement
phase become more intense and then level off when
the person reaches the highest level of arousal.
3. Orgasm. The arousal triggers involuntary contractions
of internal genital organs, followed by ejaculation in
men. In women, responses range from extended or
multiple orgasms (without falling below the plateau
level) to resolution.
4. Resolution. Following orgasm is a period of relaxation,
of release from tension. For men, this period is often
referred to as a refractory period, during which it is im-
possible to have an additional orgasm. Women rarely
have such limitations and can often return to the ex-
citement phase with effective sexual stimulation.
Although it is convenient to organize these events into
stages, the boundaries between the stages are not clear-cut
(Levin, 1994). In addition, other researchers have noted
that before the excitement phase, the person must f irst
experience sexual attraction, which should lead to sexual
desire, which in turn leads to the first stage of the sexual
response cycle: excitement (Kaplan, 1981). Desire consists
of fantasies and thoughts about sexual activity along with
an inclination or interest in being sexual. Sexual problems can occur when people
experience a diminished—or even a lack of—sexual desire, or when they have dif-
ficulties related to sexual arousal or performance (the last three stages of sexual re-
sponse). Laura appears to lack any sexual desire.
Disorders of sexual dysfunction are often divided into four categories: sexual
desire disorders, sexual arousal disorders, orgasmic disorders, and sexual pain disorders.
Many, if not most, problems in the sexual response cycle have psycholog ical
causes rather than physical causes relating to sex organs. These disorders can arise
in people of various sexual orientations, such as heterosexuals, lesbians, gay men,
or bisexuals.
FI G U RE 11.2 • The Human Sexual
Response Cycle According to Masters
and Johnson (1966), during the normal sexual
response cycle, women and men go through
four stages: excitement, plateau, orgasm, and
resolution. However, women can experience
multiple orgasms without a refractory
period (a), whereas men must experience
a refractory period before a subsequent
orgasm (b).
Source: Masters & Johnson, 1966. For more information
see the Permissions section.
Orgasm
Plateau
Excitement
Time
ResolutionR
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orgasms
One orgasm
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Excitement
and plateau
but no orgasm
Time
Orgasm
Plateau
Excitement
(b) Men
Refractory
period
Refractory
period
R
esolution
Resolution
Gender and Sexual Disorders 347
Sexual Dysfunctions According to DSM-5
A person can have more than one kind of sexual dysfunction, such as occurs
when a man with premature ejaculation becomes ner vous about having sexual
relations and so develops a dysfunction of desire or arousal. Moreover, a sex-
ual dysfunction may have existed for a person’s entire adult life (lifelong) or may
have been acquired after a per iod of nor mal sexual functioning (acquired ), as
happened to Laura. In addition, the dysfunction may occur in all circumstances
( generalized) or only in certain situations, with specific partners or types of stimu-
lation (situational). Table 11.6 lists the DSM-5 sexual dysfunctions and their diag-
nostic criteria.
As noted in Table 11.6, for a sexual dysfunction to be considered a disorder,
the sexual symptoms must cause signif icant distress or problems in relationships
( American Psychiatric Association, 2013). This means that even though a person has
a problem with an aspect of sexual response, he or she would not be diagnosed as
having a sexual dysfunction disorder unless the problem caused marked distress or led
to problems in his or her relationships. Case 11.6 illustrates how sexual dysfunctions
can affect each member of a couple.
TABLE 11.6 • DSM-5 Diagnostic Criteria for Sexual Dysfunctions
Type of Sexual
Dysfunction Female Male
Desire
Female sexual interest/arousal disorder: A lack of sexual
desire for at least 6 months, as shown by at least three
of the following symptoms: (a) reduction of interest in
sex; (b) reduction of sexual thoughts; (c) reduction of
initiating sex and of receptivity to partner’s initiation
of sex; (d) reduction or elimination of sexual enjoyment
in nearly all sexual activity; (e) reduction or elimination
of sexual arousal based on reduced sexual interest/
arousal in response to any internal or external sexual/
erotic cues (e.g., written, verbal, visual); (f) reduced
sensations during sexual activity in almost all or all
sexual encounters.
Male hypoactive sexual desire disorder: A lack of
sexual desire and activity for at least 6 months;
this diagnosis is based on clinical judgment, which
takes into consideration the patient’s age and social
context.
Arousal
Erectile disorder: At least one of these symptoms
must be apparent for at least 6 months during most
sexual activity: (a) challenges in getting an erection;
(b) challenges maintaining erection; (c) significant
decrease in hardness of the erection.
Orgasm
Female orgasmic disorder: During sex, a woman has
one or both of these problems for at least 6 months:
(a) significant delay or lack of orgasm; (b) lessening in the
sensations of orgasm.
Delayed ejaculation: During sex, a man has one
or both of these symptoms for at least 6 months,
without intention: (a) significant delay before
ejaculation; (b) significantly infrequent or lack of
ejaculation.
Premature (early) ejaculation: A condition that occurs
for at least 6 months in which ejaculation occurs less
than a minute after penetration.
Pain
Genito-pelvic pain/penetration disorder: Frequent
problems with one or more of the following
symptoms: (a) vaginal pain during intercourse;
(b) pelvic and/or vulvar pain during attempts at
intercourse; (c) significant anxiety about pain during
intercourse; (d) inability to relax pelvic floor muscles
during penetration.
General Criteria
These symptoms cause distress. The symptoms are not caused by another disorder, medical concern, and are not caused
by problems in the relationship or other stressors.
Note: To be diagnosed with a sexual dysfunction, the person must meet both the criteria for the specific sexual dysfunction and the general criteria.
Source: Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition, American Psychiatric Publishing, 2013.
348 C H A P T E R 1 1
CASE 11.6 • FROM TH E OUTSIDE: Sexual Dysfunctions
Sarah had lost all interest in sex, but she was willing to be sexual for the sake of intimacy,
which she still enjoyed. Her husband, Benjamin, however, had a hard time not taking it
personally that she couldn’t have an orgasm, and began to fixate on the problem, bringing
it up in and out of the bedroom. But all the time and effort he was spending on her arousal
only made her more anxious and less likely to become aroused at all. He started to feel
inadequate as a result and began to find it difficult to maintain his erection. They had gone
on in this way for years, and now were close to a separation.
(Berman et al., 2001, p. 168)
In the following sections, we examine sexual dysfunctions.
Sexual Desire Disorders and Sexual Arousal Disorders
Sexual desire can be thought of as having three major components: (1) a neuro-
logical and other biological component (related to hormones and brain activity,
which lead to a genital response); (2) a cognitive component (related to an in-
clination or desire to be sexual); and (3) an emotional and relational component
(related to being willing to engage in sex with a particular person at a specific
place and time) (Levine, 1988). Difficulty in any of these components can lead
to a sexual desire disorder. However, a discrepancy in the level of desire between
someone and his or her partner does not, in and of itself, constitute a disorder in
sexual desire.
Sexual arousal disorders occur when a person persistently cannot become aroused
or cannot maintain arousal during a sexual encounter. These disorders can arise
when a person has difficulty progressing from desire to excitement. This difficulty
can occur when any of the following persistently interfere: (1) when the pleasurable
stimulation gets interrupted (e.g., when a couple stops their sexual behavior because their
young child enters their bedroom), (2) when other external stimuli interfere (e.g., when a
car alarm goes off outside), or (3) when internal stimuli interfere (e.g., when the person
becomes anxious, afraid, sad, or angry or has thoughts that intrude) (Malatesta &
Adams, 2001).
Like sexual desire, sexual arousal involves neurological and other biological
components (responses to stimuli and stimulation), cognitive components (thoughts),
and emotional components (Rosen & Beck, 1988). And any, or any combination,
of these components can contribute to a problem. For example, a man can have an
adequate erection but think that he is inadequate because he believes that his penis
is not hard enough. Similarly, a woman may respond to the biological sensations of
sexual arousal by being afraid of losing control (Malatesta & Adams, 2001).
Male Hypoactive Sexual Desire Disorder
As specified in DSM-5, one type of problem of desire is male hypoactive sexual
desire disorder, the hallmark of which is a persistent or recurrent lack of erotic or
sexual fantasies or an absence of desire for sexual activity (see Table 11.6). This lack
of desire may or may not be lifelong, and it may occur in all situations (generalized)
or only in particular situations (such as with a specific person), but it must cause dis-
tress. Hypoactive sexual desire focuses primarily on a man’s cognitive (fantasies) and
emotional/relational (desire) state (Malatesta & Adams, 2001). Men with hypoactive
sexual desire disorder may or may not still be willing to engage in sexual behavior
with a partner.
However, a man who is depressed and, as part of the depression, has little or no
sexual desire (a symptom of depression) is not considered to have hypoactive sexual
desire disorder because the low desire is caused by another disorder.
Sexual desire is a multifaceted experience
involving the body, thoughts, emotions, and
another person.
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Male hypoactive sexual desire disorder
A sexual dysfunction characterized by a
persistent or recurrent lack of erotic or
sexual fantasies or an absence of desire for
sexual activity.
Gender and Sexual Disorders 349
Erectile disorder
A sexual dysfunction characterized by a man’s
persistent difficulty obtaining or maintaining
an adequate erection until the end of sexual
activity, or a decrease in erectile rigidity;
sometimes referred to as impotence.
Female sexual interest/arousal disorder
A sexual dysfunction characterized by a
woman’s persistent or recurrent lack of or
reduced sexual interest or arousal; formerly
referred to as frigidity.
Erectile Disorder
Erectile disorder (impotence, in nontechnical language) is an arousal disorder char-
acterized by a persistent difficulty obtaining or maintaining an adequate erection
until the end of sexual activity, or a decrease in erectile rigidity (see Table 11.6;
American Psychiatric Association, 2013). Some men with erectile disorder are able to
have erections during foreplay but not during actual penetration. Others are not able
to obtain a full erection with a new partner or in some situations; still others, such as
Harry, in Case 11.7, have the problem during any type of sexual activity. If the man
is able to have a full erection during masturbation, biological causes are unlikely.
More than half of men over 40 years old have at least some problems in attaining
or maintaining an erection (Feldman et al., 1994), and thus erectile disorder can be
seen as a normal by-product of aging. It is estimated that 300 million men worldwide
will develop erectile disorder by the year 2025, in part because of the increased ag-
ing of the population (cited in Shabsigh et al., 2003). However, psychological factors
can contribute to erectile disorder; it is not always a neurological or other biological
problem or a consequence of normal aging.
CASE 11.7 • FROM TH E OUTSIDE: Erectile Disorder
Harry [had been married for 2 years when] he found out his wife had been involved in
numerous extramarital affairs and divorced her. He said his friends all knew but were
reluctant to tell him. Following the divorce he encountered erectile problems with all
partners—even those to whom he felt close.
(Althof, 2000, p. 261)
Female Sexual Interest/Arousal Disorder
Women who have problems with sexual desire often also have problems with arousal,
and hence DSM-5 groups these desire and arousal problems together in a single dis-
order: female sexual interest/arousal disorder (formerly known as frigidity),
which is a persistent or recurrent lack of or reduced sexual interest or arousal.
Problems regarding interest or arousal may include no interest in any sexual activity,
no erotic or sexual thoughts, hesitation either to respond to a partner’s sexual invitations
or to initiate sexual activity, reduced or no pleasure during most sexual encounters, or a
lack of physical arousal. Any three of these six symptoms (see Table 11.6) are necessary
for this diagnosis. As with all other sexual dysfunctions, the diagnosis of sexual interest/
arousal disorder requires that the problem causes distress or difficulties in relationships
and does not arise exclusively from another psychological or medical disorder.
Laura seems to have such a lack of sexual desire—a lack of any interest in sexual
relations with Mike—and it bothers her that she doesn’t feel desire. As women age,
decreased interest in sex is normal and is probably related to women’s hormonal
shift with menopause: Women who have gone through menopause tend to report
diminished desire (Eplov et al., 2007). In fact, women who enter menopause abruptly
and at an early age because of the surgical removal of their uterus and ovaries are
more likely to report low sexual desire than are their same-age counterparts who
have not yet entered menopause (Dennerstein et al., 2006). In addition, psychologi-
cal and social factors account for a given woman’s distress about decreased desire, and
women in different European countries report different levels of distress in response
to decreased desire (Graziottin, 2007).
Orgasmic Disorders
An orgasmic disorder is diagnosed when a clinician determines that a man or woman
has experienced normal excitement and adequate stimulation for orgasm in normal
circumstances (based on the person’s age and other factors) —but fails to have an
350 C H A P T E R 1 1
orgasm. If a man or woman cannot achieve orgasm with intercourse but can do so
through other types of sexual stimulation, the person is not necessarily considered to
have an orgasmic disorder. Moreover, if orgasmic problems arise as a side effect from
medications (such as SSRIs), a diagnosis of an orgasmic disorder should not be made.
Disorders in this category may have neurological (and other biological), cognitive,
and emotional elements.
Female Orgasmic Disorder
Female orgasmic disorder is diagnosed when a woman’s normal sexual excitement
does not lead to orgasm or her orgasms are significantly less intense (see Table 11.6).
Women who experience occasional difficulty achieving orgasm do not have this dis-
order; the problem with achieving orgasm must be persistent and must exceed what
would be expected based on the woman’s age and sexual experience. Moreover, to be
diagnosed with this disorder, the problem with orgasm should not be caused by inade-
quate sexual stimulation. If a woman experiences orgasm through clitoral stimulation
but not through vaginal intercourse, a diagnosis would not be made; most women
require clitoral stimulation to have an orgasm. As with all other sexual dysfunctions,
female orgasmic disorder is diagnosed only if the problem concerning orgasm causes
distress; many women who rarely or never have orgasms report being satisfied sexu-
ally (American Psychiatric Association, 2013). Approximately 5–24% of women have
female orgasmic disorder (Laumann et al., 1994; Spector & Carey, 1990).
Clinicians distinguish between two types of female orgasmic disorder: gener-
alized and situational. If female orgasmic disorder is generalized, the woman does
not have an orgasm in any circumstance. If female orgasmic disorder is situational,
the woman may have an orgasm but only in certain circumstances, for example,
when masturbating. Lola, described in Case 11.8, has the generalized type of female
orgasmic disorder.
CASE 11.8 • FROM TH E OUTSIDE: Female Orgasmic Disorder
Lola, a 25-year-old laboratory technician, has been married to a 32-year-old cabdriver for
5 years. The couple has a 2-year-old son, and the marriage appears harmonious.
The presenting complaint is Lola’s lifelong inability to experience orgasm. She has never
achieved orgasm, although during sexual activity she has received what should have been
sufficient stimulation. She has tried to masturbate, and on many occasions her husband has
manually stimulated her patiently for lengthy periods of time. Although she does not reach
climax, she is strongly attached to her husband, feels erotic pleasure during lovemaking,
and lubricates copiously. According to both of them, the husband has no sexual difficulty.
Exploration of her thoughts as she nears orgasm reveals a vague sense of dread of
some undefined disaster. More generally, she is anxious about losing control over her
emotions, which she normally keeps closely in check.
(Spitzer et al., 2002, pp. 238–239)
Delayed Ejaculation
Delayed ejaculation is a delay or absence of ejaculation in males; Table 11.6 lists
the specific criteria. Delayed ejaculation is different from female orgasmic disorder
in several respects: (1) Delayed ejaculation typically involves problems ejaculat-
ing with a partner, even though the man can easily ejaculate during masturbation
(Apfelbaum, 1989, 2000); (2) delayed ejaculation typically involves problems ejacu-
lating only during vaginal intercourse (some men, however, cannot ever ejaculate);
and (3) its prevalence (less than 10% of the general male population) is lower than
that of female orgasmic disorder (Spector & Carey, 1990). There is no set definition
of what constitutes a “delay,” and the diagnosis should be made only if the man expe-
riences adequate sexual stimulation.
Female orgasmic disorder
A sexual dysfunction characterized by a
woman’s normal sexual excitement not
leading to orgasm or to her having diminished
intensity of sensations of orgasm.
Delayed ejaculation
A sexual dysfunction characterized by a man’s
delay or absence of orgasm.
Gender and Sexual Disorders 351
Premature (Early) Ejaculation
A second type of orgasm-related problem for men is premature ejaculation, which
is characterized by ejaculation that occurs within a minute of vaginal penetration and
before the male wishes it (Table 11.6; American Psychiatric Association, 2013). Men
with premature ejaculation report not feeling a sense of control over their ejacula-
tion and thus become apprehensive about future sexual encounters. (According to
DSM-5, a man with “early” ejaculation that occurs without vaginal intercourse—
such as with oral sex or anal intercourse—could not be diagnosed with this disorder.)
Premature ejaculation is considered by some to be a couple’s problem, as with
Mr. and Mrs. Albert in Case 11.9. That is, it is a problem only insofar as the couple
prefers the man to ejaculate in a particular phase of his partner’s sexual response
cycle: Some couples try to have both partners achieve orgasm at around the same
time, but this is difficult with premature ejaculation. Other couples do not find early
ejaculation a problem; the partner is sexually stimulated to orgasm in other ways after
the man ejaculates (Malatesta & Adams, 2001).
CASE 11.9 • FROM TH E OUTSIDE: Premature Ejaculation
Mr. and Ms. Albert are an attractive, gregarious couple, married for 15 years, who [are in]
the midst of a crisis over their sexual problems. Mr. Albert, a successful restaurateur, is 38.
Ms. Albert, who since marriage has devoted herself to child rearing and managing the home,
is 35. She reports that throughout their marriage she has been extremely frustrated because
sex has “always been hopeless for us.” She is now seriously considering leaving her husband.
The difficult y is the husband’s rapid ejaculation. Whenever any lovemaking is
attempted, Mr. Albert becomes anxious, moves quickly toward intercourse, and reaches
orgasm either immediately upon entering his wife’s vagina or within one or two strokes.
He then feels humiliated and recognizes his wife’s dissatisfaction, and they both lapse into
silent suffering. He has severe feelings of inadequacy and guilt, and she experiences a mix-
ture of frustration and resentment toward his “ineptness and lack of concern.” Recently,
they have developed a pattern of avoiding sex, which leaves them both frustrated, but
which keeps overt hostility to a minimum. . . . [Mr. Albert’s] inability to control his ejacula-
tion is a source of intense shame, and he finds himself unable to talk to his wife about his
sexual “failures.” Ms. Albert is highly sexual and easily aroused in foreplay but has always
felt that intercourse is the only “acceptable” way to reach orgasm.
In other areas of their marriage, including rearing of their two children, managing the
family restaurant, and socializing with friends, the Alberts are highly compatible. Despite
these strong points, however, they are near separation because of the tension produced
by their mutual sexual disappointment.
(Spitzer et al., 2002, pp. 266–267)
Sexual Pain Disorder: Genito-Pelvic Pain/Penetration Disorder
Some women experience significant pain with sexual activity, particularly with sexual
intercourse. A sexual dysfunction related to consistent pain associated with sexual in-
tercourse for women is genito-pelvic pain/penetration disorder, which is charac-
terized by pain, fear, or anxiety related to the vaginal penetration of intercourse (see
Table 11.6). Vaginismus, recurrent or persistent involuntary spasms of the musculature
of the outer third of the vagina that interfere with sexual intercourse, may occur with
genito-pelvic pain/penetration disorder. These spasms may be so strong that it is impos-
sible to insert the penis into the vagina, or at least not without significant discomfort.
Up to 10–20% of women report recurrent pain with intercourse, though not
necessarily to the degree required for a diagnosis of genito-pelvic pain/penetration
disorder (American Psychiatric Association, 2013; Laumann et al., 1999; Rosen et al.,
1993). When the pain persists, it can lead to problems with desire or excitement. This
disorder is not diagnosed if the problem is caused exclusively by a lack of lubrication.
Lynn in Case 11.10 has genito-pelvic pain/penetration disorder. Table 11.7 provides
more information about the sexual dysfunctions.
Premature (early) ejaculation
A sexual dysfunction characterized by
ejaculation that occurs within a minute of
vaginal penetration and before the man
wishes it, usually before, immediately during,
or shortly after penetration.
Genito-pelvic pain/penetration disorder
A sexual dysfunction in women characterized
by pain, fear, or anxiety related to the vaginal
penetration of intercourse.
352 C H A P T E R 1 1
CASE 11.10 • FROM TH E INSIDE: Genito-Pelvic Pain/Penetration
Disorder
Lynn talks about her experience with symptoms of genito-pelvic pain/penetration disorder.
We’ve been married for nine years and have two great kids. Unfortunately, family respon-
sibilities and high stress jobs really cut into our together time. Exhaustion makes sex seem
like an extra chore—just one more thing to do that we don’t have time to enjoy and now
can’t. I don’t know if it’s from the busy, stressful lifestyle or not, or from being “out of
practice,” but about a year ago intercourse began to really hurt. It started with a burning
sensation some of the time during sex. I found myself getting more anxious that it would
hurt again and it usually did. Trips to the doctor revealed little besides the standard “do
more foreplay or use more lubricant” advice. Now it seems like my body just “tightens
up” and we can hardly have sex at all. Entry is painful and besides burning I feel tightness,
spasms, discomfort and anxiety. The pleasure is gone, and there is only the expectation
of discomfort and frustration. Our marriage is suffering and it feels like a deep chasm is
growing between us as sex has become impossible. My husband and I fight a lot more and
I know he is growing impatient. I don’t want my children to be another statistic of divorce
because of this. I just don’t know what to do.
(Vaginismus.com, 2007)
TABLE 11.7 • Sexual Dysfunctions Facts at a Glance
Prevalence
• According to one survey of 1065 female and 447 male patients in a general medical prac-
tice, 22% of the men and 40% of the women had a “sexual dysfunction” in the preceding
4 weeks (Nazareth et al., 2003), and other studies find similar results (Shifren et al., 2008).
However, the true prevalence of sexual dysfunctions is difficult to determine: Many surveys
either equate sexual dissatisfaction—for any reason—with sexual dysfunction or use crite-
ria that are different from those in DSM-5.
Comorbidity
• People with sexual dysfunctions may also have a co-occurring mood or anxiety disorder
(Atlantis & Sullivan, 2012; Fabre & Smith, 2012) or medical disorder (Tan et al., 2012).
Onset
• A sexual dysfunction may arise from specific circumstances, or it may be lifelong.
Course
• As women age, sexual problems other than desire problems tend to decrease, except for
hormonally induced lubrication problems.
• The opposite is true for men: As they age, their sexual problems tend to increase, usually
because of erectile difficulties that are associated with prostate problems, cardiovascular
problems, or other medical causes (Hackett, 2008; Heiman, 2002b).
Gender Differences
• In one study, the most common problems among men were lack of interest, premature
ejaculation, and performance anxiety. Among women the most common problems were
failure to achieve orgasm and painful intercourse.
Cultural Differences
• Cultural norms about sexuality affect the extent to which a sexual problem leads to enough
distress or relationship difficulties for it to be considered a disorder (Hartley, 2006). For
example, Japanese women have a low prevalence of problems with sexual desire, perhaps
because Japanese women do not consider no or little sexual desire to be a problem
(Kameya, 2001).
Source: Unless otherwise noted, the source for the table material is American Psychiatric Association, 2013.
Gender and Sexual Disorders 353
Criticisms of the Sexual Dysfunctions in DSM-5
Criticisms of the DSM-5 classification of and criteria for sexual dysfunctions focus
on many issues, some of which carry over from the previous edition of DSM (Balon,
2008).In what follows we briefly consider three of these issues:
• The sexual dysfunctions are implicitly based on the progression in Masters and
Johnson’s model of the sexual response cycle. However, this may not be the best
model for understanding sexual dysfunctions in women. As illustrated in the alter-
native female sexual response cycle (Figure 11.3), emotional and physical satisfaction
may include orgasm but not all women need to have an orgasm to feel satisfied.
• The emphasis is on orgasm—in both men and women—as the conclusion of sexual
activity (Tiefer, 1991). Sexual activity that does not end in orgasm is implicitly
considered not satisfying (Kleinplatz, 2001).
• The DSM-5 criteria rest on a cultural definition of “normal” to define abnormal
sexual functioning (Moynihan, 2003). Critics note that the norm promoted by
American culture is that of an adolescent male, ever ready for sexual encounters
and able to have erections on demand (Kleinplatz, 2001). As women and men age,
they are more likely to meet the criteria for a sexual dysfunction even when there is
no real “dysfunction”—only the body’s growing older (Tiefer, 1987, 1991).
Understanding Sexual Dysfunctions
We can view Laura’s lack of sexual desire as being related, at least in part, to Mike’s
sexual difficulties: As Mike became more distant, Laura’s desire for sexual intimacy
with Mike waned. Their experiences highlight the fact that sexuality and any prob-
lems related to it develop through feedback loops among neurological (and other
biological), psychological, and social factors.
Neurological and Other Biological Factors
In this section, we first consider how disease, illness, surgery, and medication can,
directly and indirectly, disrupt normal sexuality. We then turn to the effects of nor-
mal aging, which can produce sexual difficulties.
Sexual Side Effects: Disease, Illness, Surgery, and Medication
Disease or illness can produce sexual dysfunction directly, as occurs with prostate or
cervical cancer, and indirectly, as occurs with diabetes or circulation problems that
seeks or is
receptive to
neurological (and
other biological),
psychological,
social influences
Emotional
intimacy+ +
+ +
+ +
+ +
Emotional and
physical
satisfaction
Sexual desire
and arousal
Sexual neutrality
Sexual stimuli
Sexual arousal
FI G U RE 11.3 • An Alternative Female Sexual Response
Cycle An alternative model of the female sexual response cycle (Basson,
2001)—in the context of relationships—is analogous to a circle. The cycle
starts with sexual neutrality: not feeling very sexual, but with an openness
to seek or be receptive to sexual stimuli. In turn, such sexual stimuli may,
depending on neurological (and other biological), psychological, and social
factors operating at that moment, lead to sexual arousal, which in turn
leads to a sense of desire and further arousal. The desire creates positive
feedback loops (11) that lead to heightened arousal, which then leads to
emotional and physical satisfaction. This satisfaction in turn produces a
sense of emotional intimacy with her partner, making her more likely to
be receptive to or seek out sexual stimuli in the future. She may also feel
spontaneous sexual desire, which leads to positive feedback loops among
the first three phases. Orgasm is not necessary for satisfaction.
Source: Adapted from Basson, 2001.
Prolonged bike riding can sometimes crush
the nerves and arteries to the penis or clitoris,
leading to arousal problems.
R
ic
h
a
rd
P
ri
ce
/G
e
tt
y
I
m
a
g
e
s
354 C H A P T E R 1 1
limit blood flow to genital areas. In addition, surgery can lead to sexual problems:
Half of women who survive major surgeries for gynecological-related cancer develop
sexual difficulties that do not improve over time (Andersen et al., 1989).
Some medications can interfere with normal sexual response, including:
• SSRIs and dopamine-blocking medications such as traditional antipsychotics,
• beta-blockers and other medications that treat high blood pressure,
• anti-seizure medication,
• estrogen and progesterone medications,
• HIV medications, and
• narcotics and sedative-hypnotics.
Alcohol can also disrupt the normal sexual response cycle.
Aging
Researchers have found that normal aging can affect sexual function-
ing among older people (George & Weiler, 1981). For instance, older
women often produce less vaginal lubrication after menopause; when
this dryness is not addressed (for instance, with an over-the-counter
lubricant such as Astroglide or K-Y Jelly), the dryness can cause inter-
course to be painful and lead to genito-pelvic pain/ penetration disorder.
In addition, as men age, their testosterone levels decrease signifi-
cantly, which may lead them to require prolonged tactile stimulation
before they can attain an erection. Older men are likely to experience
reduced penile hardness, decreased urgency to reach orgasm, and a lon-
ger refractory period (Butler & Lewis, 2002; Masters & Johnson, 1966).
In addition to the normal biological changes that arise with age,
older people of both sexes may develop illnesses or diseases that make
sexual activity physically more challenging. They also may take medi-
cations that have side effects that interfere with their sexual response.
However, most older people report that they continue to enjoy sex.
Psychological Factors in Sexual Dysfunctions
Certain beliefs and experiences can predispose people to develop sexual dysfunctions (see
Table 11.8). In addition, a woman may believe that women in general lose their sexual
desire as they age, and a man may believe that “real men” have intercourse at least
twice a day and that only rock-hard erections will satisfy
women (Nobre & Pinto-Gouveia, 2006). Such beliefs can
lead to a self-fulfilling prophecy if they produce the percep-
tion of a dysfunction and that perception in turn leads to
a real dysfunction. For example, a man who believes that
women are only satisfied by very hard erections may de-
velop a problem as he ages: He may notice that his erections
are not as hard as they were when he was younger and then
become self-conscious and preoccupied during sex, which
does in fact lead him to fail to satisfy his partner.
Having been sexually abused as a child also predisposes
a person to develop sexual dysfunctions. Consider the fact
that male victims of childhood sexual abuse are three times
more likely to have problems with their erections and twice
as likely to have problems of desire and premature ejacula-
tion as their peers who did not experience childhood sexual
abuse (Laumann et al., 1999). Similarly, women who were
Men and women often experience changes in
aspects of sexual performance as they get older,
which may disrupt sexual activity. However,
most will still experience pleasure from sexual
activities (Leiblum & Seagraves, 2000).
N
ic
k
D
a
ly
/G
e
tt
y
I
m
ag
e
s
TABLE 11.8 • Predisposing Events for Sexual Dysfunctions
Event Effect
The view that sex is dirty
and sinful
Early learning of such negative attitudes
toward sex and misinformation leads to fears
and inhibitions, which can lead to problems of
desire, arousal, orgasm, and pain.
Early negative
conditioning experiences
In men, premature ejaculation can develop
after hurrying to have an orgasm quickly
for fear of being “caught.” In women, a fear
of pregnancy or being “caught” can lead to
anxiety that contributes to sexual dysfunction.
Sexual trauma
Sexual trauma can produce negative
conditioning and can lead to a fear of sex, as
well as arousal and desire problems.
Sources: Bartoi & Kinder, 1998; Becker & Kaplan, 1991; Kaplan, 1981; Laumann et al., 1999; LoPiccolo
& Friedman, 1988; Masters & Johnson, 1970; Silverstein, 1989.
Gender and Sexual Disorders 355
victims of childhood sexual abuse are more likely than women who were not abused to
report sexual problems (although not necessarily problems that meet the DSM-5 crite-
ria for sexual dysfunctions; Staples et al., 2012).
Psychological factors that precipitate, or trigger, sexual dysfunctions generally
involve the following sorts of preoccupations:
• focusing attention on sex-related fears and worries, which distract and detract
during a sexual encounter;
• feeling uncomfortable with how one’s body may look or feel to a partner (Berman
& Berman, 2001); and
• worrying about nonsexual matters, such as work or family problems.
Once someone has a problem with desire, arousal, orgasm, or pain, he or she may
become anxious that it will happen again, which sets up a self-fulfilling prophecy and
becomes a maintaining factor. For instance, when a
single sexual experience was perceived as a “fail-
ure,” a person may become anxious during sub-
sequent sexual experiences, monitoring his or her
responsiveness (and so thinking about the sexual
response rather than experiencing it) —which in
turn can interfere with a normal sexual response
and create a sexual dysfunction (Bach et al., 1999;
Quinta Gomes & Nobre, 2012).
Social Factors
Although sexuality involves how we see our-
selves, it usually also involves other people.
(Woody Allen once said that his favorite part of
masturbation was the cuddling afterwards. Think
about why this is funny.) The sexual relations of a
couple are influenced by how the partners relate
to each other, specifically: (1) how they express
and resolve a conflict, (2) how they communicate
their needs and desires, their likes and dislikes,
(3) how they handle stress, and (4) how strongly attracted they each are to each other
(Tiefer, 2001). For women in particular, satisfaction with their relationship plays a big
part in sexual desire, arousal, and orgasm (Burri et al., in press). For example, Mike’s
sexual secret led him to pull away from Laura sexually, which led her to think that he
wasn’t interested in sex. From her vantage point, he appeared to have a sexual desire
problem, and she herself then lost interest.
Feedback Loops in Understanding Sexual Dysfunctions
Just as neurological, psychological, and social factors inf luence each other and
contribute to a normal sexual response, feedback loops among these factors can con-
tribute to sexual dysfunctions (see Figure 11.4). Such feedback loops best explain why
some people, and not others, develop sexual dysfunctions. For instance, people’s sexual
beliefs (“I won’t be able to have an orgasm”; psychological factor) can influence other
factors: The beliefs create fears and anxieties that can lead to high levels of sympathetic
nervous system activity (neurological factor), which then interfere with sexual arousal
and orgasm (Apfelbaum, 2001; Kaplan, 1981; Masters & Johnson, 1970). Current prob-
lems in a relationship (social factor) similarly affect sexual functioning, as can having
been sexually abused (Bartoi & Kinder, 1998; DiLillo, 2001; Laumann et al., 1999).
And the influences also run in the opposite direction: If the body does not respond
appropriately, this will affect not only a person’s beliefs but also his or her relationships.
SP
N
©
A
le
x
M
a
re
s-
M
a
n
to
n
/A
G
E
Fo
to
st
o
ck
Je
ff
G
re
e
n
b
e
rg
/P
h
o
to
Ed
it
These young people might just be getting ready
for a special occasion. But being chronically
preoccupied and anxious about something—
including how your body might look or feel to a
partner—while engaged in sexual activity can
interfere with the normal sexual response cycle
and lead to a sexual dysfunction.
356 C H A P T E R 1 1
Familial and cultural views of sexuality (social factors) can also influence sexual func-
tioning: We are all taught about sexuality both directly (what our parents, teachers, reli-
gious leaders, and peers tell us) and indirectly (through observations of family members or
friends and from television, movies, books, and the Internet). Some people are taught that
sexual relations outside of marriage are wrong, whereas other people are taught that sexual
experimentation before marriage is a good thing. Such direct and indirect lessons help
shape each person’s concepts of appropriate or normal sexuality. Depending on what a per-
son learns about sex, he or she may be primed to have sexual difficulties in some situations.
Thus, neurological, psychological, and social factors influence each other in ways
that predispose some people to develop a sexual dysfunction, and that precipitate and
maintain it once it develops.
BehaviorAffect
Brain and Bodily
Systems
GeneticsNeural Communication
NeuroPsychoSocial
NeuroPsychoSocial
Anxiety, fear,
and other
negative
feelings
associated with
sex or with
partner
Negative
conditioning
experiences
For some dysfunctions,
brain areas involved in
anxiety
Illness, disease,
surgical, and
medication side effects
Aging
For some dysfunctions,
neural communication
involved in anxiety
No known major
contribution
Mental Processes and
Mental Contents
Negative thoughts
associated with sex
Negative thoughts
about partner
Hypervigilance about
performance
Gender/Culture
Couple
Poor quality of
relationship
NeuroPsychoSocial
Stressful Life Events
History of sexual abuse
Cultural and familial
views about sex and
appropriate behavior
for each gender
FI G U RE 11.4 • Feedback Loops in Action: Sexual Dysfunctions
Gender and Sexual Disorders 357
Treating Sexual Dysfunctions
After the specif ic nature of a sexual problem has been determined, treatment
can target the relevant factors. Patients may see a sex therapist, usually a men-
tal health clinician who has been trained to assess and treat problems related to
sexuality and sexual dysfunction. Depending on the nature of the problem and
the t ypes of treatments the patient—and his or her partner—are interested in,
treatment may include medication, cognitive-
behavioral therapy, sex therapy (which may pro-
vide specif ic guidance and techniques to treat
sex u a l problem s ), couple s t her apy, or some
ot her t y pe of t her apy ( Moser & Devereu x,
2012).
Targeting Neurological and Other
Biological Factors: Medications
There has been an increasing trend toward the
medicalization of sex therapy, a tendency to tar-
get neurological and other biological factors (see
Table 11.9) and pay less attention to psychological
and social factors. In the 1990s, medical treatments
for erectile dysfunction began in earnest, with the
advent of the drug Viagra and the marketing cam-
paign for it, which brought the topic of erectile
dysfunction from a rarely discussed but relatively
common problem among older men to a topic of
everyday conversation. Viagra (sildenafil citrate) is
one of the class of drugs called phosphodiesterase type
5 inhibitors, or PDE-5 inhibitors. Viagra doesn’t cause
an erection directly; instead, the drug operates by
increasing the flow of blood to the penis only when
LE
M
O
IN
E
/B
S
IP
/S
u
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e
rS
to
ck
K
ev
in
M
a
zu
r/
W
ir
e
Im
ag
e
fo
r
M
T
V
/G
e
tt
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I
m
ag
e
s
Which type of influence—explicit teaching or watching in the media—played a larger role in shaping your
sexuality?
TABLE 11.9 • Medications for Sexual Dysfunctions
Sexual phase Female Male
Desire
Female sexual arousal disorder:
PDE-5 inhibitors when arousal
problems have a medical cause.
Wellbutrin (bupropion) may
counteract diminished desire
that is a side effect of SSRIs
taken for another disorder
Male hypoactive sexual desire
disorder: Testosterone pills or
cream.
Arousal
Erectile disorder: PDE-5
inhibitors
Orgasm
Female orgasmic disorder:
(Medications have not reliably
proved effective in studies that
include a placebo group.)
Delayed ejaculation:
(Medications have not
reliably proved effective
in studies that include a
placebo group.)
Premature ejaculation: SSRIs
Pain
Genito-pelvic pain/penetration
disorder: Estrogen cream for
menopause related dryness;
anti-anxiety medication for
anticipatory anxiety about
penetration.
358 C H A P T E R 1 1
a man is sexually excited. Viagra (and its competitors, such as Cialis) is not a cure but a
treatment for erectile dysfunction, and it is effective only if the man takes a pill before
sexual activity.
Some women with arousal disorders use PDE-5 inhibitors because these medi-
cations can have an analogous effect on the clitoris. However, PDE-5 inhibitors
are most effective with women who—for medical reasons—have reduced blood
flow to the clitoral area, which leads to decreased physical arousal (Berman et al.,
2001). Critics point out that prescribing this type of medication for a woman will
not improve sexual functioning when the problem is with her relationship, not her
anatomy ( Bancroft, 2002).
Targeting Psychological Factors: Shifting Thoughts,
Learning Behaviors
Two types of treatments directly target psychological factors: Sex therapy and psy-
chological therapies—such as CBT or psychodynamic therapy—that address feel-
ings and thoughts about oneself and others and how they may relate to sexual
problems.
One of the goals of treatments that directly target psychological factors re-
lated to sexual dysfunctions is to educate patients about sexuality and the human
sexual response. Another goal is to help patients develop strategies to counter nega-
tive thoughts, beliefs, or attitudes that may interfere with sexual desire, arousal,
or orgasm (Carey & Gordon, 1995). For instance, during sexual activity, some
people are preoccupied with nonsexual thoughts that prevent them from reaching
full arousal or orgasm. These nonsexual thoughts might be work-related worries,
thoughts about household tasks that need to be done, or being alert for someone
who would interrupt the sexual encounter. Cognitive treatment may involve teach-
ing a patient how to filter out such thoughts and (re)focus on the sexual interaction.
The therapist might teach the patient to apply standard cognitive methods to sexual
encounters, such as problem solving (“You could turn the phone off ”) or cognitive
restructuring (“Are you likely to think of a solution to your work problem while
making love? If not, you can let your mind focus on the physical sensations you are
experiencing”).
In addition to addressing ver y specif ic sex-related thoughts and feelings,
the treatment may also address the patient’s view of himself or herself. Some-
times the sense of being dysfunctional or inadequate generalizes from the sex-
ual realm to the whole self, and the person with a sexual dysfunction comes to
have low self-esteem and self-doubts generally. In such cases, the therapy may
use cognitive and behavioral methods to address such dysfunctional thoughts and
feelings.
Treatment that relies on CBT typically involves “homework.” Depending on
the nature of the problem, the homework may be completed by the patient or by the
patient and his or her partner together. Homework for women with female orgasmic
disorder (as well as other sexual dysfunctions) may include masturbation in order to
learn more about which sensations and fantasies facilitate arousal and orgasm (Meston
et al., 2004). For many patients, a first step is to begin to (re)discover pleasurable sen-
sations through specific homework exercises. At the beginning of behavioral treat-
ment, homework may include sensate focus exercises, which increase awareness
of pleasurable sensations while prohibiting genital touching, intercourse, or orgasm;
rather, partners take turns touching other parts of each other’s bodies so that each
can discover what kinds of stimulation feel most enjoyable (Baucom et al., 1998;
LoPiccolo & Stock, 1986).
Sensate focus exercises
A behavioral technique that is assigned as
homework in sex therapy, in which a person
or couple seeks to increase awareness of
pleasurable sensations that do not involve
genital touching, intercourse, or orgasm.
Gender and Sexual Disorders 359
The goals of behavioral techniques are to help patients develop a more relaxed
awareness of their bodies and increase their orgasmic responses and control. Treat-
ment may also involve a realistic look at a person’s or couple’s daily work schedule,
followed by a discussion of how to have sexual encounters during which the partners
are not too tired or distracted.
Targeting Social Factors: Couples Therapy
The sex therapy techniques discussed in the previous section may be implemented
alone (by the person with a sexual dysfunction) or with a partner. Sex therapy may
involve teaching couples specific cognitive and behavioral techniques. However,
implementing such techniques with a partner requires motivation and willing-
ness to be open with the partner about sexual matters and to experiment sexually.
Moreover, how a couple interacts sexually occurs against the backdrop of their
overall relationship. Treatment may focus on the issues in the couple’s relationship
(couples therapy, rather than sex therapy per se) and include teaching communica-
tion, intimacy, and relationship skills (Baucom et al., 1998; Beck, 1995; Heiman,
2002b); such skills include assertiveness, problem solving, negotiation, and con-
flict management. Couples therapy may also address issues of power, control, and
lifestyle as they relate to the sexual dysfunction; for example, the therapist may
employ techniques from systems therapy to focus on assertiveness within the sexual
aspects of the relationship. Treatment for a partner’s sexual dysfunction in a lesbian
or gay couple may also address special issues that affect their sexual relationship,
such as living “in the closet” or sexual intimacy when one partner is HIV positive
(Nichols, 2000).
Feedback Loops in Treating Sexual Dysfunctions
Like successful treatment for any other psychological disorder, successful treat-
ment of sexual dysfunctions ultimately affects all the neuropsychosocial factors (see
Figure 11.5). For instance, CBT for female orgasmic disorder targets psychological
factors (the thoughts, beliefs, and feelings related to sex or orgasm and behaviors such
as masturbation) (Frühauf et al., in press; Heiman, 2002a). In turn, changes in psy-
chological factors lead, through feedback loops, to changes in neurological and other
biological factors (which underlie arousal and orgasm) as well as social factors (the
meaning for both partners of a sexual interaction or an orgasm and the changes in
their relationship). A similar set of feedback loops occurs with CBT for genito-pelvic
pain/penetration disorder (ter Kuile et al., 2007): CBT changes thoughts and feelings
SP
N
Which of the two photos best captures the goal of the first step of sensate focus exercises—
the relaxing bath or a vibrator? Answer: The relaxing bath because the vibrator is most likely
to be used for genital stimulation.
GETTING THE PICTURE
C
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st
o
ck
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ty
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360 C H A P T E R 1 1
about penetration, which in turn changes the responses of the vaginal muscles, mak-
ing vaginal intercourse with a partner possible—which then affects the nature of the
relationship.
Although all the techniques mentioned may alleviate sexual dysfunctions, the
definition of “success” is less clear-cut than for treatments of most other psycho-
logical disorders. As we noted at the beginning of this chapter, sexuality and sexual
dysfunctions typically involve other people, and a treatment that the patient views
as successful may not be perceived that way by the partner. Consider an older man
whose erectile dysfunction was treated with Viagra. He may have been pleased by
his response to the drug treatment, only to discover that his wife was now unhappy
about his sustained erections and more frequent desire for intercourse (Althof et al.,
2006). She, then, might be diagnosed with a sexual desire problem. However, she
might explain that when her husband had difficulty with his erections, he was much
more affectionate, sexually attentive to her, and creative in their sexual interac-
tions. Now he is goal-directed, focusing almost exclusively on intercourse; solving
his erectile dysfunction led to changes in the couple’s sexual relations that were not
viewed as positive by his wife. Treatments—such as medication—that directly target
only one type of factor may seem to resolve the problem for the patient but instead
can (via feedback loops among the three types of factors) have unexpected negative
consequences for the couple.
Treatments Targeting
Neurological and
Other Biological
Factors
Medication: Testosterone,
PDE-5 inhibitors,
estrogen, SSRIs
(depending on the
specific problem)
Changes neural
activity
Increases genital
arousal
Increases control of
orgasm
Changes thoughts,
feelings, and
behaviors
Treatments Targeting
Psychological Factors
Sex therapy and CBT:
Psychoeducation,
sensate focus exercises,
cognitive restructuring,
specific behavioral
techniques
Psychodynamic therapy
Treatments Targeting
Social Factors
Couples therapy:
Communication,
intimacy, and
relationship skills
Sex therapy with couple:
Specific sexual
techniques
Changes couple’s
communication,
sexual interactions,
and general
interaction patterns
FIGURE 11.5 • Feedback Loops in Treat-
ment: Sexual Dysfunctions
Gender and Sexual Disorders 361
SUMMING UP
Gender Dysphoria
• Gender dysphoria is characterized by per-
sistent cross-gender identif ication that
leads to chronic discomfort with one’s
natal sex. Symptoms of gender dyspho-
ria often emerge in childhood, but most
children diagnosed with the disorder no
longer have it when they become adults.
• In children, symptoms of gender dys-
phoria include cross-dressing and oth-
er wise behaving in ways t ypical of the
other gender, such as engaging in other-
gender t ypes of play, choosing other-
gender playmates, and even claiming to
be the other gender. In adults, symptoms
include persistent and extreme discomfort
from living publicly as their natal gender,
which leads many to live (at least some of
the time) as someone of the other gender.
• Some bra in areas in adu lts w ith gen-
der dysphor ia are more sim i lar to the
corresponding brain areas of members of
their desired gender than they are to those
of people who have their natal gender.
• Treatments that target neurological (and
other biological) factors include hormone
treatments and sex reassignment surgery.
Treatments that target psychological factors
include psychoeducation, helping the pa-
tient choose among gender-related lifestyle
options, and problem solving about po-
tential difficulties. Treatments that target
social factors include family education,
support groups, and group therapy.
Paraphilic Disorders
• Paraphi l ic d isorders are character ized
by a predictable sexual arousal pattern
regarding “deviant” fantasies, objects, or
behaviors. Paraphilic disorders can involve
(1) nonconsent i ng adu lt s or ch i ld ren
( exhibitionistic disorder, voyeuristic disor-
der, frotteuristic disorder, and pedophilic
disorder), (2 ) suffering or humiliating
oneself or one’s partner (sexual masoch-
ism disorder and sexual sadism disorder), or
Targeting only a neurological (or other biological)
factor in one partner may not improve the
overall sexual functioning and satisfaction of the
couple.
S
te
ve
K
e
ll
ey
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Chi-Ling and Yinong were in their 30s and had been trying to have a baby for a year. Their sexual
relations were strained: They had sex when the ovulation predictor test kit indicated that they
should, and each month’s attempt and subsequent failure made them anxious. There was no joy
or love in their sexual relations, and most of the time Chi-Ling was barely aroused and lubricated;
she rarely had orgasms anymore. She just wanted Yinong to hurry up and ejaculate, and he was
finding it increasingly difficult to do so. Based on what you have read, do you think that Chi-Ling
or Yinong has a sexual dysfunction, and if so, which one(s)? Support your position. If you could
obtain additional information before you decide, what would you want to know, and why?
Thinking Like A Clinician
362 C H A P T E R 1 1
Gender identity (p. 328)
Gender dysphoria (p. 329)
Gender role (p. 329)
Sex reassignment surgery (p. 333)
Paraphilia (p. 335)
Paraphilic disorders (p. 335)
Exhibitionistic disorder (p. 338)
Voyeuristic disorder (p. 338)
Frotteuristic disorder (p. 339)
Pedophilic disorder (p. 339)
Sexual sadism disorder (p. 340)
Sexual masochism disorder (p. 341)
Fetishistic disorder (p. 341)
Transvestic disorder (p. 342)
Sexual dysfunctions (p. 347)
Sexual response cycle (p. 347)
Male hypoactive sexual desire disorder (p. 349)
Erectile disorder (p. 350)
Female sexual interest/arousal disorder (p. 350)
Female orgasmic disorder (p. 351)
Delayed ejaculation (p. 351)
Premature (early) ejaculation (p. 352)
Genito-pelvic pain/penetration disorder (p. 352)
Sensate focus exercises (p. 359)
(3) arousal by nonhuman objects (fetishis-
tic disorder and transvestic disorder). To be
diagnosed with a paraphilic disorder, either
the person must have acted on these sexual
urges and fantasies or these arousal patterns
must cause the patient significant distress or
impair functioning.
• Critics of the DSM-5 paraphilic disorders
classification note that what is determined
to be sexually “deviant” varies across cul-
tures and over time.
• Research shows that paraphilic disorders
share similarities with OCD. Additional
possible cont r ibut i ng f actor s i nclude
classically conditioned arousal and the
Zeigarnik effect.
• Most frequently, men who receive treat-
ment for paraphilic disorders are ordered
to do so by the cr i m i na l just ice sys-
tem. Treatments that target neurologi-
cal factors decrease paraphilic behaviors
through medication; however, although
the behaviors may decrease, the interests
often do not. Treatments that target psy-
chological factors are designed to change
cognitive distortions about the predatory
sexual behaviors.
Sexual Dysfunctions
• Sexua l dysfunctions are psycholog ica l
disorders characterized by problems in
the human sexual response cycle. The
response cycle traditionally has been re-
garded as having four phases: excitement,
plateau, orgasm, and resolution– –but it
is now commonly regarded as beginning
with sexual attraction and desire.
• Sexual dysfunctions fall into one of four
categories: disorders of desire, arousal, or-
gasm, and pain. To be classified as dysfunc-
tions, they must cause significant distress or
problems in the person’s relationships.
• Sexual desire and arousal disorders involve
three components: cognitive, emotional,
and neurological (and other biological).
Problems with any of these components
can lead to male hypoactive sexual desire
disorder, erectile disorder, or female sex-
ual interest/arousal disorder.
• Sexual orgasmic disorders are character-
ized by persistent problems with the orgas-
mic response after experiencing a normal
excitement phase and adequate stimula-
tion. DSM-5 includes in this categor y:
female orgasmic disorder, delayed ejacula-
tion, and premature ejaculation.
• Genito-pelvic pain/penetration disorder
is characterized by pain with sexual inter-
course and occurs only in women.
• Cr it icism s of the way DSM-5 cla ssi-
fies sexual dysfunction disorders include:
(1) The sexual response cycle may not
apply equally well to women; (2) the end
goal is orgasm, not satisfaction; (3) the
criteria rest on a particular definition of
normal sexual functioning that doesn’t
encompass normal aging.
• Various factors contribute to sexual dys-
functions. Neurological (and other bio-
logical) factors include disease, illness,
surger y or medications, and the normal
aging process.
• Psychological factors include: predispos-
ing factors (such as negative attitudes
toward sex), negative conditioning expe-
riences, and a history of sexual abuse; pre-
cipitating factors, such as anxiety about
sex and distraction because of sexual or
nonsexual matters; and maintaining fac-
tors, such as worrying about future sexual
problems.
• Social factors include the quality of the
partners’ relationship, the partner’s sexual
functioning, a history of abuse, and sexual
mores in the person’s subculture.
• Treatments that target neurological (and
other biological) factors are medications
for erectile dysfunction and for analogous
arousal problems in women.
• Treatments that target psychological fac-
tors include psychoeducat ion, sensate
focus exercises, a nd CBT to cou nter
negative thoughts, beliefs, and behaviors
associated with sexual dysfunction.
• Treatments that target social factors ad-
d ress problem at ic issues in a couple’s
relationship as well as teach the couple
specif ic sex-related cognitive or behav-
ioral strategies.
• Treatments that focus on one type of fac-
tor for a given patient can create complex
feedback loops, which sometimes have
unex pected— a nd perhaps neg at ive —
consequences for the couple.
More Study Aids
For additional study aids related
to this chapter, including quizzes
to make sure you’ve retained
everything you’ve learned and a
Student Video Activity exploring
how men’s and women’s attitudes
toward sex may relate to sexual
dysfunctions, go to: www.
worthpublishers.com/launchpad/
rkabpsych2e.
Fancy Collection/SuperStock
Key Terms
Gender and Sexual Disorders 363
365
12CHAPTER What Are Schizophrenia and Other Psychotic Disorders?
The Symptoms of Schizophrenia
Cognitive Defi cits: The Specifi cs
Distinguishing Between Schizophrenia and
Other Disorders
Schizophrenia Facts in Detail
Understanding Schizophrenia
Neurological Factors in Schizophrenia
Psychological Factors in Schizophrenia
Social Factors in Schizophrenia
Feedback Loops in Understanding Schizophrenia
Treating Schizophrenia
Targeting Neurological Factors in Treating
Schizophrenia
Targeting Psychological Factors in Treating
Schizophrenia
Targeting Social Factors in Treating Schizophrenia
Feedback Loops in Treating Schizophrenia
Schizophrenia and Other
Psychotic Disorders
n 1930, female quadruplets were born in a small midwestern city.
All four survived, which at that time was remarkable. This set of
quadruplets (or quads) was also remarkable in two other ways:
All four developed from a single fertilized egg and so basically were
genetically identical. In addition, all four went on to develop symp-
toms of schizophrenia as young adults. In the psychological literature,
the quadruplets came to be known by pseudonyms they were given
to protect their privacy: Nora, Iris, Myra, and Hester Genain.
The quads were born to parents of limited financial means. Their
father, Henry, was abusive, violent, and alcoholic. He also exhibited
some symptoms of schizophrenia. Their mother, Maud, had been a
nurse. Maud was very strict with the girls, but she was a better parent
than Henry.
By the time the quads were in their early 20s, three had been hos-
pitalized for schizophrenia at least once, and the fourth had symptoms
of schizophrenia. Also around that time, Mrs. Genain was recovering
from bladder surgery, and it was becoming increasingly difficult for her
to care for the young women. The family’s problems were brought to
the attention of researchers at the National Institute of Mental Health
(NIMH), and the family was invited to move to a research and treat-
ment facility in Washington, DC. At the facility, the sisters were
treated, studied, and written about extensively. In fact, the pseudonyms
the quads were given related to the initials of NIMH: Nora, Iris, Myra,
and Hester. Their false last name, Genain, means “dire birth” in Greek.
The facT ThaT all four of The Genain sisTers developed
symptoms of schizophrenia was by no means an inevitable result. For
identical twins, the chance of both twins developing schizophrenia
is about 48% . For identical quads, the odds of all four developing
schizophrenia are about one in six, or 16% (Rosenthal, 1963). The
quads’ story offers possible clues about why all four of them devel-
oped schizophrenia and can help us understand what causes the disor-
der. In this chapter, we discuss the symptoms of schizophrenia, what
is known about its causes, and current treatments for this disorder.
Nora, Iris, Myra, and Hester Genain were identical
quadruplets. All four suffered from schizophrenia,
although this outcome is statistically unlikely. The
symptoms and course of the disorder were different
for each sister, illustrating the range of ways that this
disorder can affect people.
A
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Jason Jaroslav Cook/age fotostock. Photo for illustrative purposes only; any individual depicted is a model.
What Are Schizophrenia and
Other Psychotic Disorders?
Schizophrenia is a psychological disorder characterized by psychotic symptoms—
hallucinations and delusions—that significantly affect emotions, behavior, and, most
notably, mental processes and mental contents. The symptoms of schizophrenia can
interfere with a person’s abilities to comprehend and respond to the world in a normal
way. DSM-5 lists schizophrenia as a single disorder (see Table 12.1), but in its chapter
titled Schizophrenia Spectrum and Psychotic Disorders, it describes a group of disorders
related to and including schizophrenia; research suggests that schizophrenia itself is
not a unitary disorder (Blanchard et al., 2005; Turetsky et al., 2002).
Instead, schizophrenia is a set of related disorders. Research findings
suggest that each variant of schizophrenia has different symptoms,
causes, course of development, and, possibly, response to treatments.
In the following sections we examine in more detail the symptoms of
schizophrenia and other related psychotic disorders.
The Symptoms of Schizophrenia
The criteria for schizophrenia in DSM-5 fall into two clusters:
• positive symptoms, which consist of delusions and hallucinations and
disorganized speech and behavior; and
• negative symptoms, which consist of the absence or reduction of
normal mental processes, mental contents, feelings, or behaviors,
including speech, emotional expressiveness, and/or movement.
Table 12.1 lists the DSM-5 criteria for schizophrenia. After consider-
ing these criteria, we discuss criticisms of these criteria and an alter-
native way to diagnose schizophrenia.
Positive Symptoms
Positive symptoms are so named because they are marked by the
presence of abnormal or distorted mental processes, mental contents,
or behaviors. Positive symptoms of schizophrenia are
• hallucinations (distortions of perception),
• delusions (distortions of thought),
• disorganized speech, and
• disorganized behavior.
These symptoms are extreme. From time to time, we all have hallu-
cinations, such as thinking we hear the doorbell ring when it didn’t.
But the hallucinations experienced by people with schizophrenia
are intrusive—they may be voices that talk constantly or scream at
the patient. Similarly, the delusions of someone with schizophrenia
aren’t isolated, one-time false beliefs (e.g., “My roommate took my
sweater, and that’s why it’s missing”). With schizophrenia and other
psychotic disorders, the delusions are extensive, although they often
focus on one topic (e.g., “My roommate is out to get me, and the fact
that she has taken my sweater is just one more example”).
The positive symptoms of disorganized speech and disorganized be-
havior are apparent from watching or talking to a person who has them;
it’s difficult, if not impossible, to understand what’s being said, and the
person’s behavior is clearly odd (wearing a coat during a heat wave, for
example). We next examine the four positive symptoms in more detail.
TABLE 12.1 • DSM-5 Diagnostic Criteria for
Schizophrenia
A. Two (or more) of the following, each present for a significant
portion of time during a 1-month period (or less if successfully
treated). At least one of these must be (1), (2), or (3):
1. Delusions.
2. Hallucinations.
3. Disorganized speech (e.g., frequent derailment or incoherence).
4. Grossly disorganized or catatonic behavior.
5. Negative symptoms (i.e., diminished emotional expression
or avolition).
B. For a significant portion of the time since the onset of the
disturbance, level of functioning in one or more major areas,
such as work, interpersonal relations, or self-care, is markedly
below the level achieved prior to the onset (or when the onset is
in childhood or adolescence, there is failure to achieve expected
level of interpersonal, academic, or occupational functioning).
C. Continuous signs of the disturbance persist for at least
6 months. This 6-month period must include at least 1 month
of symptoms (or less if successfully treated) that meet
Criterion A (i.e., active-phase symptoms) and may include
periods of prodromal or residual symptoms. During these
prodromal or residual periods, the signs of the disturbance
may be manifested by only negative symptoms or by two or
more symptoms listed in Criterion A present in an attenuated
form (e.g., odd beliefs, unusual perceptual experiences).
D. Schizoaffective disorder and depressive or bipolar disorder
with psychotic features have been ruled out because either
1) no major depressive or manic episodes have occurred
concurrently with the active-phase symptoms, or 2) if mood
episodes have occurred during active-phase symptoms, they
have been present for a minority of the total duration of the
active and residual periods of the illness.
E. The disturbance is not attributable to the physiological
effects of a substance (e.g., a drug of abuse, a medication) or
another medical condition.
F. If there is a history of autism spectrum disorder or a
communication disorder of childhood, the additional diagnosis
of schizophrenia is made only if prominent delusions or
hallucinations, in addition to the other required symptoms of
schizophrenia, are also present for at least 1 month (or less if
successfully treated).
Reprinted with permission from the Diagnostic and Statistical Manual of Mental
Disorders, Fifth Edition, (Copyright ©2013). American Psychiatric Association. All
Rights Reserved.
Schizophrenia
A psychological disorder characterized by
psychotic symptoms that significantly affect
emotions, behavior, and mental processes and
mental contents.
Positive symptoms
Symptoms of schizophrenia that are
characterized by the presence of abnormal or
distorted mental processes, mental contents,
or behaviors.
366 C H A P T E R 1 2
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The man who made this drawing said, “This
belt buckle symbolized safety for me in my
stay in the hospital. I felt no harm would
come to me while I wore it. I also left it visible
to me on my nightstand next to my bed at
night. I thought several times the belt buckle
saved me from whatever was going on. My
belt buckle seemed as though it was wearing
thinner, using up its strength a little at a
time in helping me” (Emmons et al., 1997, p.
183). Although many people have a good luck
charm, the fact that this man believed that his
belt buckle was getting thinner because it was
“using up its strength” suggests that he had a
delusional belief about it.
Hallucinations
As discussed in Chapter 1, hallucinations are sensations so vivid that the per-
ceived objects or events seem real even though they are not. Any of the five senses
can be involved in a hallucination, although auditory hallucinations—specifically,
hearing voices—are the most common type experienced by people with schizo-
phrenia. Pamela Spiro Wagner describes one of her experiences with auditor y
hallucinations:
[The voices] have returned with a vengeance, bringing hell to my nights and days.
With scathing criticism and a constant scornful commentary on everything I do, they
sometimes order me to do things I shouldn’t. So far, I’ve stopped myself, but I might
not always be able to. . . .
(Wagner & Spiro, 2005, p. 2)
Research that investigates possible underlying causes of auditory hallucinations
finds that people with schizophrenia, and to a lesser extent their unaffected siblings,
have difficulty distinguishing between verbal information that is internally gener-
ated (as when imagining a conversation or talking to oneself ) and verbal information
that is externally generated (as when another person is actually talking) (Brunelin
et al., 2007). People with schizophrenia are also more likely to (mis) attribute their
own internal conversations to another person (Brunelin, Combris, et al., 2006); this
misattribution apparently contributes to the experience of auditory hallucinations.
Delusions
People with schizophrenia may also experience delusions— incorrect beliefs that
persist, despite evidence to the contrary. Delusions often focus on a particular theme,
and several types of themes are common among these patients. Persecutory delusions
involve the theme of being persecuted by others. Pamela Spiro Wagner’s persecutory
delusions involved extraterrestrials:
I barricade the door each night for fear of beings from the higher dimensions coming
to spirit me away, useless as any physical barrier would be against them. I don’t
mention the NSA, DIA, or Interpol surveillance I’ve detected in my walls or
how intercepted conversations among these agencies have intruded into TV
shows.
(Wagner & Spiro, 2005, p. 2)
In contrast, delusions of control revolve around the belief that the
person is being controlled by other people (or aliens), who literally
put thoughts into his or her head, called thought insertion:
I came to believe that a local pharmacist was tormenting me by inserting
his thoughts into my head, stealing mine, and inducing me to buy things
I had no use for. The only way I could escape the influence of his deadly
radiation was to walk a circuit a mile in diameter around his drugstore, and
then I felt terrified and in terrible danger.
(Wagner, 1996, p. 400)
Another delusional theme is believing oneself to be significantly more powerful,
knowledgeable, or capable than is actually the case, referred to as grandiose delusions.
Someone with this type of delusion may believe that he or she has invented a new
type of computer when such an achievement by that person is clearly impossible.
Grandiose delusions may also include the mistaken belief that the person is a dif-
ferent—often famous and powerful—person, such as the president or a prominent
religious figure.
Yet another delusional theme is present in referential delusions: the belief that
external events have special meaning for the person. Someone who believes that a
song playing in a movie is in some kind of code that has special meaning just for him
or her, for instance, is having a referential delusion.
Nobel Laureate John Nash (portrayed in the
film, A Beautiful Mind) had entrenched delusions.
©
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Hallucinations
Sensations that are so vivid that the perceived
objects or events seem real, although they
are not. Hallucinations can occur in any of the
five senses.
Delusions
Persistent false beliefs that are held despite
evidence that the beliefs are incorrect or
exaggerate reality.
Schizophrenia and Other Psychotic Disorders 367
Disorganized Speech
People with schizophrenia can sometimes speak incoherently, although they may
not necessarily be aware that other people cannot understand what they are saying.
Speech can be disorganized in a variety of different ways. One type of disorganized
speech is word salad, which is a random stream of seemingly unconnected words. For
example, a patient might say something like, “Pots dog small is tabled.” Another type
of disorganized speech involves many neologisms, or words that the patient makes up:
That’s wish-bell. Double vision. It’s like walking across a person’s eye and reflecting
personality. It works on you, like dying and going to the spiritual world, but landing in
the Vella world.
(Marengo et al., 1985, p. 423)
In this case, “wish-bell” is the neologism; it doesn’t exist, nor does it have an
obvious meaning or function as a metaphor.
Grossly Disorganized Psychomotor Behavior
Another positive symptom (and recall that positive in this context means “present,”
not “good”) of schizophrenia is grossly disorganized or abnormal psychomotor behavior;
the term psychomotor refers to intentional movements, and in this case such behavior
is so unfocused and disconnected from a goal that the person cannot successfully
accomplish a basic task, or the behavior is inappropriate in the situation. Disorganized
behavior can range from laughing inappropriately in response to a serious matter or
masturbating in front of others, to being unable to perform normal daily tasks such as
washing oneself, putting t ogether a simple meal, or even selecting appropriate clothes
to wear.
The categor y of grossly disorganized psychomotor behavior also includes
catatonia (also referred to as catatonic behavior), which occurs when a person does
not respond to the environment or remains in an odd posture or position, with
rigid muscles, for hours. For example, during her early 20s, Iris Genain’s symptoms
included standing in the same position for hours each day.
These positive symptoms—hallucinations, delusions, disorganized speech, and
grossly disorganized psychomotor behavior—constitute four of the f ive DSM-5
symptom criteria for schizophrenia; the f ifth criterion is any negative symptom
( discussed in the following section). Emilio, in Case 12.1, has positive symptoms of
schizophrenia.
CASE 12.1 • FROM TH E OUTSIDE: Schizophrenia
Emilio is a 40-year-old man who looks 10 years younger. He is brought to the hospital, his
twelfth hospitalization, by his mother because she is afraid of him. He is dressed in a rag-
ged overcoat, bedroom slippers, and a baseball cap and wears several medals around his
neck. His affect ranges from anger at his mother (“She feeds me shit . . . what comes out of
other people’s rectums”) to a giggling, obsequious seductiveness toward the interviewer.
His speech and manner have a childlike quality, and he walks with a mincing step and
exaggerated hip movements. His mother reports that he stopped taking his medication
about a month ago and has since begun to hear voices and to look and act more bizarrely.
When asked what he has been doing, he says, “eating wires and lighting fires.” His sponta-
neous speech is often incoherent and marked by frequent rhyming and clang associations
[speech in which sounds, rather than meaningful relationships, govern word choice].
Emilio’s first hospitalization occurred after he dropped out of school at age 16, and since
that time he has never been able to attend school or hold a job. He has been treated with neu-
roleptics [antipsychotic medications] during his hospitalizations but doesn’t continue to take
medication when he leaves, so he quickly becomes disorganized again. He lives with his elderly
mother, but sometimes disappears for several months at a time and is eventually picked up
by the police as he wanders in the streets. There is no known history of drug or alcohol abuse.
(Spitzer et al., 2002, pp. 189–190)
This woman suffers from catatonia, in which
people assume odd postures or poses for
hours at a time. When catatonic, people
cannot care for themselves and require
constant attention.
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Catatonia
A condition in which a person does not
respond to the environment or remains in an
odd posture or position, with rigid muscles,
for hours.
368 C H A P T E R 1 2
Negative Symptoms
In contrast to positive symptoms, negative symptoms are characterized by the absence
or reduction of normal mental processes, mental contents, or behaviors. DSM-5 speci-
fies a number of negative symptoms: diminished emotional expression and avolition.
Diminished Emotional Expression: Muted Expression
Some people with schizophrenia exhibit diminished emotional expression (sometimes
referred to as flat affect), which occurs when a person does not display a large range
of emotion, sometimes speaking robotically and seeming emotionally neutral. Such
people may not express or convey much information through their facial expressions,
body language, tone of voice, and they tend to refrain from making eye contact
(although they may smile somewhat and do not necessarily come off as “cold”).
Avolition: Difficulty Initiating or Following Through
In movies that portray people with schizophrenia, hospitalized patients are often
shown sitting in chairs apparently doing nothing all day, not even talking to others.
This portrayal suggests avolition, which consists of difficulty initiating or follow-
ing through with activities. For example, Hester Genain would often sit for hours,
staring into space, and had difficulty beginning her chores.
Other negative symptoms that are less prominent in schizophrenia are:
• Alogia—speaking less than do most other people. A person with alogia will take a
while to muster the mental effort necessary to respond to a question.
• Anhedonia—a diminished ability to experience pleasure (see Chapter 5).
• Asociality—disinterest in social interactions.
The sets of positive and negative symptoms in DSM-5 grew out of decades of clinical
observations of patients with schizophrenia; these symptoms can generally be observed or
can be inferred by a trained researcher or clinician. According to DSM-5, to be diagnosed
with schizophrenia, the person must have two out of five symptoms (and at least one
symptom must be hallucinations, delusions, or disorganized speech); these symptoms must
be present for at least 1 month continuously and at least one symptom must have been
present for 6 months; the symptoms must significantly impair functioning. However,
research has revealed that cognitive deficits—which are not as easily observed and are not
part of the DSM-5 criteria—also play a crucial role in schizophrenia, as we discuss below.
Cognitive Deficits: The Specifics
Research has revealed that cognitive deficits (also called neurocognitive deficits) often
accompany schizophrenia (Barch, 2005; Green, 2001). It is not clear whether these
deficits cause the disorder, are a necessary or common precondition that makes the
disorder more likely to develop, or are a result of the disorder. Specific deficits are
found in attention, memory, and executive functioning, and they arise in most people
with schizophrenia (Keefe et al., 2005; Wilk et al., 2005).
Deficits in Attention
Cognitive deficits include difficulties in sustaining and focusing attention, which can
involve distinguishing relevant from irrelevant stimuli (Gur et al., 2007). One person with
schizophrenia recounted: “If I am talking to someone they only need to cross their legs or
scratch their heads and I am distracted and forget what I was saying” (Torrey, 2001, p. 29).
Deficits in Working Memory
Another area of cognitive functioning adversely affected in people with schizophre-
nia is working memory, which organizes, temporarily retains, and transforms incoming
information during reasoning and related mental activities (Baddeley, 1986). For
Negative symptoms
Symptoms of schizophrenia that are
characterized by the absence or reduction of
normal mental processes, mental contents, or
behaviors.
Flat affect
A lack of, or considerably diminished,
emotional expression, such as occurs when
someone speaks robotically and shows little
facial expression.
Avolition
A negative symptom of schizophrenia marked
by difficulty initiating or following through
with activities.
Schizophrenia and Other Psychotic Disorders 369
example, if you are trying to remember items you need to buy at the store, you will
probably use working memory to organize the items into easy-to-recall categories.
People with schizophrenia do not organize information effectively, which indicates
that their working memories are impaired.
Deficits in Executive Functioning
Deficits in working memory contribute to problems that people with schizophre-
nia have with executive functions, which are mental processes involved in plan-
ning, organizing, problem solving, abstract thinking, and exercising good judgment
(Cornblatt et al., 1997; Erlenmeyer-Kimling et al., 2000; Kim et al., 2004). The
problems with executive functioning have far-reaching consequences for cogni-
tion in general. For instance, Hester had the most severe symptoms of the Genain
quads, and her deficits in executive functioning were prominent much of the time.
She had difficulty performing household chores that required multiple steps—such
as making mashed potatoes by herself, which required peeling the potatoes, then
boiling them, knowing when to take them out of the water, and mashing them with
other (measured) ingredients. Obviously, deficits in executive functioning can impair
a person’s overall ability to function.
Cognitive Deficits Endure Over Time
Neurocognitive deficits do not necessarily make their first appearance at the same
time that the positive and negative symptoms of schizophrenia first emerge. For
many people who develop schizophrenia, cognitive deficits exist in childhood, well
before a first episode of schizophrenia (Cannon et al., 1999; Ott et al., 2002; Torrey,
2002). In addition to predating symptoms of schizophrenia, cognitive deficits often
persist after the positive and negative symptoms improve (Hoff & Kremen, 2003;
Rund et al., 2004). Thus, at least some of the time these deficits “set the stage” for
the disorder but do not actually cause it. However, as we discuss shortly, in some
cases such deficits may directly contribute to specific symptoms.
The lives of Genain sisters illustrate both the importance of cognitive deficits
and their variety. Hester had the most difficulty academically and was held back in
5th grade because of her poor performance. In contrast, Myra did not exhibit any
significant cognitive deficits, and she graduated from high school, held a job, married,
and had two children. Nora and Iris had moderate levels of cognitive deficits; they
could perform full-time work for periods of time but could not function indepen-
dently for long stretches (Mirsky & Quinn, 1988; Mirsky et al., 1987, 2000).
Limitations of DSM-5 Criteria
Although the DSM-5 criteria provide a relatively reliable way to diagnose schizo-
phrenia, a number of researchers point to drawbacks of those criteria—both of the
specific criteria and of the grouping of positive and negative symptoms (Fauman,
2006; Green, 2001). A more diagnostically and prognostically relevant set of symp-
toms, these researchers suggest, would focus on the extent of cognitive deficits and
the breadth and severity of the DSM-5 symptoms.
Absence of Focus on Cognitive Deficits
Cognitive deficits are not specifically addressed in the DSM-5 criteria, despite their
importance. Although the DSM-5 set of positive symptoms includes disorganized
speech and grossly disorganized psychomotor behavior (see Table 12.1), research
suggests that these two symptoms together form an important cluster, indepen-
dent of hallucinations and delusions. This cluster apparently reflects specific types
of underlying cognitive deficits, which clearly contribute to disorganized thinking.
For instance, cognitive deficits can cause thoughts to skip from one topic to another,
Executive functions
Mental processes involved in planning,
organizing, problem solving, abstract thinking,
and exercising good judgment.
370 C H A P T E R 1 2
topics that are related to each other only tangentially if at all. (This process is referred
to as a loosening of associations.) Thus, disorganized speech arises from disorganized
thinking. Similarly, grossly disorganized psychomotor behavior, such as laughing at
a funeral or putting on four pairs of underwear, can occur because the person’s cog-
nitive deficits prevent him or her from organizing social experiences into categories
covered by general rules of behavior or conventions.
Cognitive deficits can also lead to unusual social behavior or asociality. As we’ll
discuss in more detail later, people with schizophrenia may be socially isolated
and avoid contact with others because such interactions can be overwhelming or
confusing. People with schizophrenia can have difficulty understanding the usual,
unspoken rules of social convention. Also, even after an episode of schizophrenia
has abated, they may not understand when someone is irritated because they do
not notice or correctly interpret the other person’s facial expression or tone of voice
(which are types of cognitive deficits; Clark et al., 2013). When irritation erupts into
anger, it can seem to come out of the blue, frightening and overwhelming people
with schizophrenia. So, they may try to tread a safer path and avoid others as much as
possible. In turn, the poor social skills and social isolation are related to an impaired
ability to work (Dickinson et al., 2007). The disorganized behavior, asociality, and
poor social skills, and perhaps avolition, all are indicators of underlying cognitive
deficits (Farrow et al., 2005).
Deficit/Nondeficit Subtypes
Researchers make a distinction between patients diagnosed with schizophrenia who
have significant cognitive deficits and those who do not (Horan & Blanchard, 2003).
To be considered to have the deficit subtype, a patient must have severe neurocogni-
tive deficits in attention, memory, and executive functioning, as well as the positive
and negative symptoms that are manifestations of these deficits, such as disorganized
speech and grossly disorganized psychomotor behavior. Such patients are generally
more impaired than are other patients with schizophrenia, and their symptoms
are less likely to improve with currently available treatments. They may be more
impaired, at least in part, because parts of their brains do not work together normally;
neuroimaging results show that people with the deficit subtype of schizophrenia (but
not those who have the nondeficit subtype) have abnormalities in their “white matter
tracts”—sets of axons that connect neurons (Voineskos et al., 2013). (They are white
because they are covered with the fatty insulator substance myelin.)
To be considered to have the nondeficit subtype, a patient must have positive symp-
toms, such as hallucinations and delusions, in conjunction with relatively intact cog-
nitive functioning. People with this subtype are generally less impaired, and they
have a better prognosis (McGlashan & Fenton, 1993).
Distinguishing Between Schizophrenia and
Other Disorders
Positive or negative symptoms may arise in schizophrenia or in the context of other
disorders. Clinicians and researchers must determine whether the positive or negative
symptoms reflect schizophrenia, another disorder, or, in some cases, schizophrenia
and another disorder.
Psychotic Symptoms in Schizophrenia, Mood Disorders, and
Substance-Related Disorders
Other psychological disorders, most notably mood disorders and substance-related
disorders, may involve symptoms such as hallucinations and delusions. (Mood dis-
orders with psychotic features are discussed in Chapter 5, and substance-induced
Schizophrenia and Other Psychotic Disorders 371
hallucinations and delusions are discussed in Chapter 9.) The content of these
psychotic symptoms is usually consistent with the characteristics of the mood dis-
order or substance-related disorder, and the psychotic symptoms only arise during a
mood episode or with substance use or withdrawal.
For example, people with mania may become psychotic, developing grandiose
delusions about their abilities. Psychotic mania is distinguished from schizophrenia
by the presence of other symptoms of mania—such as pressured speech or little need
for sleep.
Similarly, psychotically depressed people may have delusions or hallucinations;
the delusions usually involve themes of the depressed person’s worthlessness or the
“badness” of certain body parts (e.g., “My intestines are rotting”). Some negative
symptoms of schizophrenia can be difficult to distinguish from symptoms of depres-
sion: People with schizophrenia or depression may show little interest in activities,
hardly speak at all, give minimal replies to questions, and avoid social situations.
As noted in Table 12.2, although both of these disorders may involve similar
outward behaviors, the behaviors arise from different causes. In general, people with
schizophrenia but not depression do not have other symptoms of depression, such
as changes in weight or sleep or feelings of worthlessness and inappropriate guilt
(American Psychiatric Association, 2013). Of course, people with schizophrenia may
develop comorbid disorders, such as depression.
TABLE 12.2 • Behavioral Symptoms Common to Depression and Schizophrenia
Behavioral symptoms Causes in depression Causes in schizophrenia
Little or no interest in
activities, staring into space
for long periods of time
Lack of pleasure in activities
(anhedonia), difficulty
making decisions
Difficulty initiating behavior
(avolition)
Short or “empty” replies to
questions
Lack of energy Difficulty organizing
thoughts to speak
Social isolation Lack of energy, anhedonia,
feeling undeserving of
companionship
Feeling overwhelmed by
social situations, lack of
social skills
Finally, substance-related disorders can lead to delusions (see Chapter 9), such as
the persecutory delusions that arise from chronic use of stimulants. Substances (and
withdrawal from them) can also induce hallucinations, such as the tactile hallucina-
tions that can arise with cocaine use (e.g., the feeling that bugs are crawling over a
person’s arms). Determining the correct diagnosis can be particularly challenging
when a person has more than one disorder and the symptoms of those disorders
appear similar.
Other Psychotic Disorders
Although mood disorders and substance-related disorders may involve psychotic
symptoms, the diagnostic criteria for these two categories of disorders do not specifi-
cally require the presence of psychotic symptoms. In contrast, the criteria for the dis-
orders collectively referred to as psychotic disorders specifically require the presence of
symptoms related to psychosis; these disorders are part of a spectrum, related to each
other in their symptoms and risk factors but differing in their specific constellations
of symptoms, duration, and severity.
372 C H A P T E R 1 2
Schizophreniform and Brief Psychotic Disorders
In some cases, a person’s symptoms may meet most, but not all, of the criteria for a
diagnosis of schizophrenia. The person clearly suffers from some psychotic symptoms
and has significant difficulty in functioning as a result of his or her psychological
problems. However, the impaired functioning hasn’t been present for the minimum
6-month duration required for a diagnosis of schizophrenia. Two disorders fall into
this class, depending on the specifics of the symptoms and their duration.
Schizophreniform disorder is the diagnosis given when a person’s symptoms
meet all the criteria for schizophrenia except that symptoms have been present for
between 1 and 6 months (American Psychiatric Association, 2013). In addition, daily
functioning may or may not have declined over that period of time. If the symptoms
persist for more than 6 months (and daily functioning has significantly declined), the
diagnosis shifts to schizophrenia.
In contrast, brief psychotic disorder refers to the sudden onset of halluci-
nations, delusions, or disorganized speech or behavior that last between 1 day and
1 month and are followed by full recovery (American Psychiatric Association, 2013).
For this diagnosis, no negative symptoms should be present during the episode.
Rather, brief psychotic disorder is characterized by intense emotional episodes and
confusion, during which the person may be so disorganized that he or she cannot
function safely and independently; he or she also has an increased risk of suicide dur-
ing the episode. Once recovered, people who had this disorder have a good prognosis
for full recovery (Pillman et al., 2002).
Schizoaffective Disorder
Schizoaffective disorder is characterized by the presence of both schizophrenia and
a depressive or manic episode (see Chapter 5). For this diagnosis, the mood episode
must be present during most of the period when the symptoms of schizophrenia are
present; in addition, delusions or hallucinations must be present for at least 2 weeks
when there is no mood episode. Because schizoaffective disorder involves mood epi-
sodes, negative symptoms such as flat affect are less common, and the diagnosis is
likely to be made solely on the basis of positive symptoms. Because of their mood
episodes, people with schizoaffective disorder are at greater risk for committing sui-
cide than are people with schizophrenia (Bhatia et al., 2006; De Hert et al., 2001).
The prognosis for recovery from schizoaffective disorder is somewhat better than
that for recovery from schizophrenia, particularly when stressors or events clearly
contribute to the disorder (American Psychiatric Association, 2013).
Delusional Disorder
A person is diagnosed with delusional disorder when the
sole symptom is delusional beliefs—such as believing that
someone is following you when they actually are at work
on the other side of town—that have persisted for at least
1 month. Clinicians and researchers have identified the fol-
lowing types of delusions in delusional disorder (American
Psychiatric Association, 2013):
• Erotomanic. The belief that another person is in love with
the patient. This delusion usually focuses on romantic or
spiritual union rather than sexual attraction.
• Grandiose. The belief that the patient has a great (but
unrecognized) ability, talent, or achievement.
• Persecutory. The belief that the patient is being spied on,
drugged, harassed, or otherwise conspired against.
Schizophreniform disorder
A psychotic disorder characterized by
symptoms that meet all the criteria for
schizophrenia except that the symptoms have
been present for only 1–6 months, and daily
functioning may or may not have declined
over that period of time.
Brief psychotic disorder
A psychotic disorder characterized by the
sudden onset of positive or disorganized
symptoms that last between 1 day and
1 month and are followed by full recovery.
Schizoaffective disorder
A psychotic disorder characterized by
the presence of both schizophrenia and a
depressive or manic episode.
Delusional disorder
A psychotic disorder characterized by the
presence of delusions that have persisted for
more than 1 month.
Je
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Jo
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il
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Diana Napolis suffered from persecutory
delusions about filmmaker Stephen Spielberg
and singer and actress Jennifer Love Hewitt;
she believed that both were controlling her
brain (Soto, 2003).
Schizophrenia and Other Psychotic Disorders 373
• Somatic. The false belief that something is wrong with the body (such as insects on
the skin) and these delusions are not considered a symptom of another psychologi-
cal disorder, such as obsessive-compulsive disorder (Chapter 7) or body dysmorphic
disorder (Chapter 7).
• Jealous. The belief that the patient’s romantic partner is unfaithful. This belief is
based on tiny amounts of “evidence,” such as the partner’s arriving home a few
minutes late.
People with delusional disorder may appear normal when they are not talking
about their delusions. Their behavior may not be particularly odd nor their func-
tioning other wise impaired. Henr y Genain, the quads’ father, exhibited some
signs of delusional disorder of the jealous type: Soon after he met Maud, the Ge-
nains’ mother, he asked her to marr y him, but she refused. He pestered her for
months, threatening that if she didn’t marry him, neither of them would live to
marr y anyone else. On multiple occasions, he threatened to kill himself or her.
After she consented to marr y him (because his family begged her to), he didn’t
want her to socialize with anyone else, including her family. His jealousy was so
extreme that he didn’t want her to go out of the house because people walking
down the street might smile at her. When the quads were 7 years old, Mrs. Ge-
nain thought of leaving Henry, but he told her, “If you leave me, I will find you
where you go and I’ll kill you” (Rosenthal, 1963, p. 69). She believed him and
stayed with him.
One extremely unusual and rare presentation of delusional symptoms involves
a shared delusion among two or more people (sometimes referred to as folie à deux,
wh ich i s French for “pa i red m ad ne s s” ).
(Techn ica l ly, this is an “other” psychotic
disorder because it doesn’t meet the crite-
ria for any specific disorder in the categor y
of psychotic disorders.) With this variant, a
person develops delusions as a result of his
or her close relationship with another per-
son who has delusions as part of a psychotic
disorder. The person who had the disorder at
the outset is referred to as the primary person
and is usually diagnosed with schizophrenia
or delusional disorder. The delusions of the
primary person may be shared by more than
one other person, as can occur in families
when the primary person is a parent. When
the primar y person’s delusions subside, the
other person’s shared delusions may or may
not also subside.
Schizotypal Personality Disorder
Eccent r ic behav ior s a nd d i f f icu lt y w ith relat ionsh ips a re the ha l l m a rk s of
schizotypal personality disorder, discussed in more detail with the other personal-
ity disorders in Chapter 13. A person with schizotypal personality disorder may
have ver y few if any close fr iends, may feel that he or she doesn’t f it in, and
may experience social anxiety. Schizotypal personality disorder, unlike schizo-
phrenia, does not involve psychotic symptoms. Although schizotypal personality
disorder is thus not technically a psychotic disorder, some research suggests that
it may in fact be a milder form of schizophrenia (Dickey et al., 2002); for this
reason, in DSM-5 the disorder is placed within the schizophrenia spectrum as
Wanda Barzee and her husband, Brian David
Mitchell, kidnapped 14-year-old Elizabeth
Smart in 2002. Mitchell believed he was
God, and Barzee apparently came to share
his belief. Although diagnosing Barzee was
difficult, some doctors who examined her
believed that she suffered from a shared
delusion.
S
a
lt
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a
ke
C
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ty
S
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ff
’s
D
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ag
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s
S
a
lt
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C
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374 C H A P T E R 1 2
TABLE 12.3 • Overview of Schizophrenia Spectrum and Psychotic Disorders
Psychotic disorder Features
Schizophrenia
At least two symptoms—one of which must be delusions,
hallucinations, or disorganized speech—for a minimum of
1 month; continuous symptoms for at least 6 months, during
which time the person has impaired functioning in some
area(s) of life.
Note: Criteria are listed in Table 12.1.
Schizophreniform disorder
Symptoms meet all the criteria for schizophrenia except that
the symptoms have been present for only 1–6 months; daily
functioning may or may not have declined over that period
of time.
Brief psychotic disorder
The sudden onset of positive symptoms, which persist
between a day and a month, followed by a full recovery.
No negative symptoms are present during the episode.
Schizoaffective disorder
Symptoms meet the criteria for both schizophrenia and
mood disorder, with symptoms of schizophrenia present for
at least 2 weeks without symptoms of a mood disorder, and
a mood episode present during most of the period when the
symptoms of schizophrenia are present. Negative symptoms
of schizophrenia are less common with this disorder.
Delusional disorder
The presence of delusions that persist for at least 1 month,
without a diagnosis of schizophrenia.
The various psychotic disorders have in
common the presence of hallucinations
and/or delusions. Although schizotypal
personality disorder is not a psychotic
disorder (because hallucinations and
delusions are absent), this personality
disorder is considered to be on the spectrum
of schizophrenia-related disorders.
C U R R E N T C O N T R O V E R S Y
Attenuated Psychosis Syndrome:
The Diagnosis That Wasn’t
Attenuated psychosis syndrome is a diagnosis that was proposed for
inclusion in DSM-5 but that did not make it in. This condi-
tion is defined by “attenuated” (that is, reduced or weakened)
psychotic symptoms of psychosis. For example, rather than
paranoid delusions, someone may be generally mistrustful,
and rather than hearing voices, someone may hear rumblings
or murmurs.
On the one hand, proponents of adding this diagnosis
thought it would help detect and treat cases of psychotic disor-
ders before they became full blown; therefore, the alternative
name for this disorder was psychotic risk syndrome (McFarlane
et al., 2012; McGorry, 2010, 2012). Psychotic episodes can
create long-lasting disturbances in brain activation, cogni-
tive functioning, and social relations; the proponents of this
diagnosis hoped that identifying and intervening earlier might
reduce the likelihood that “at risk” cases would become full-
blown schizophrenia (McGorry et al., 2002; Wade et al., 2006).
On the other hand, critics charge that identifying people
whose symptoms don’t meet the criteria for positive symptoms
of schizophrenia labels them as “psychotic” when they aren’t
and might never become so (Frances, 2013; Schultze-Lutter et
al., 2013; Tsuang et al., in press). Furthermore, critics argue
that treating such people with antipsychotic medications—
which have signif icant and serious side effects—when the
symptoms don’t warrant it would be inappropriate.
C RITI C AL TH I N KI N G If this diagnosis—or some version of
it—is adopted in the future, how can we reduce the likeli-
hood that this diagnosis will be used to overlabel and overtreat
people with attenuated symptoms?
( James Foley, College of Wooster)
well as within the personality disorders; we have listed its criteria in Chapter 13
( American Psychiatric Association, 2013). With this personality disorder, prob-
lems in relationships may become evident by early adulthood, marked by dis-
com for t when relating to others as wel l as by being stif f or inappropr iate in
relationships. Table 12.3 summarizes the key features of schizophrenia spectrum
and psychotic disorders.
Schizophrenia and Other Psychotic Disorders 375
Schizophrenia Facts in Detail
In this section we discuss additional facts about schizophrenia.
Prevalence
The world over—from China or Finland to the United States or New Guinea—
approximately 1% of the population will develop schizophrenia (Gottesman, 1991;
Perälä et al., 2007).
Schizophrenia is one of the top five causes of disability among adults in
developed nations, ranking with heart disease, arthritis, drug use, and HIV
(Murray & Lopez, 1996). In the United States, about 5% of people with
schizophrenia (about 100,000 people) are homeless, 5% are in hospitals,
and 6% are in jail or prison (Torrey, 2001). In contrast, 34% of people
with this disorder live independently (see Figure 12.1).
Comorbidity
Over 90 % of people w ith schizophren ia a lso suf fer f rom at least one
other psychological disorder (and, as the numbers below suggest, often two
or more other disorders; Sands & Har row, 1999). Substance-related disor-
ders, mood disorders, and an xiet y disorders are the most com mon comorbid
disorders:
• Mood disorders. Approximately 50% of people with schizophrenia also have some
type of mood disorder, most commonly depression (Buckley et al., 2009; Sands &
Harrow, 1999). As noted earlier, according to DSM-5, some of these people may
have schizoaffective disorder.
• Anxiety disorder. Almost half of people with schizophrenia also have panic attacks
( Goodwin et al., 2002) and anxiety disorders (Cosoff & Hafner, 1998).
• Substance use disorders. Up to 60% of people with schizo-
phrenia have a substance abuse problem that is not related
to tobacco (Swartz et al., 2006). Moreover, 90% of those
with schizophrenia smoke cigarettes (Regier et al., 1990),
and they tend to inhale more deeply than do other smokers
(Tidey et al., 2005).
Researchers have also noted that even before their posi-
tive symptoms emerged, some people with schizophrenia
abused drugs, particularly nicotine (cigarettes), marijuana,
amphetamines, phencyclidine (PCP), mescaline, and lyser-
gic acid diethylamide (LSD) (Bowers et al., 2001; Weiser
et al., 2004). For example, a study of Swedish males found
that those who used marijuana in adolescence were more
likely later to develop schizophrenia. The more a person
used marijuana, the more likely he or she was to develop
schizophrenia, particularly if the drug was used more than
50 times (Moore et al., 2007; Zammit et al., 2002).
However, keep in mind that the correlation between
using marijuana and subsequent schizophrenia does not
show that the drug causes schizophrenia. For example, per-
haps marijuana use leads to schizophrenic symptoms only in
those who were likely to develop the disorder anyway, or a predisposition to develop
schizophrenia also might make drug use attractive (Kahn et al., 2011). It is also pos-
sible that marijuana “tips the scales” in those who are vulnerable but who would
not develop schizophrenia if they did not use the drug (Large et al., 2011). Or per-
haps some other factor affects both substance abuse and subsequent schizophrenia
34%
25%
18%
7.5%
6%
5%
5%
Living
independently:
750,000
In supervised living
(group homes, etc.):
400,000
In nursing homes:
165,000
In jails and prisons:
135,000
In hospitals:
100,000
In shelters and
on the streets:
100,000
Living with a
family member:
550,000
FI G U RE 12.1 • Distribution of the
2.2 Million Americans With
Schizophrenia
A
ra
ld
o
D
i C
ro
ll
a
la
n
za
/R
e
x
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ve
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n
Guitarist Peter Green (lying down), cofounder
of the rock group Fleetwood Mac, developed
schizophrenia after using LSD frequently.
Although Green attributes his illness to his
drug abuse, researchers cannot yet definitively
state that such abuse causes schizophrenia
in people who might not otherwise develop
the disorder.
376 C H A P T E R 1 2
(Bowers et al., 2001). Researchers do not yet know enough to be able to choose
among these possibilities, and true experiments designed to investigate them would
obviously be unethical.
Course
Typically, schizophrenia develops in phases. In the premorbid phase, before symptoms
develop, some people may display personality characteristics or cognitive deficits that
later evolve into negative symptoms (MacCabe et al., 2013). However, it is important
to note that the vast majority of people who are odd or have eccentric tendencies do
not develop schizophrenia. During the prodromal phase, which is between the
onset of symptoms and the time when the minimum criteria for a disorder are met.
In the active phase, a person has full-blown positive (and possibly negative) symp-
toms that meet the criteria for the disorder. If the positive symptoms have subsided
but negative symptoms persist, the full criteria for schizophrenia are no longer met;
the person can be said to be in the residual phase, which in-
dicates that there is a residue of (negative) symptoms but the
pronounced positive symptoms have faded away. As shown
in Table 12.4, over time, the person may fully recover, may
have intermittent episodes, or may develop chronic symp-
toms that interfere with normal functioning.
Although most of the Genain sisters were not able to live
independently, like many other people with schizophrenia
(Levine et al., 2011), the symptoms of the Genain sisters gen-
erally improved (Mirsky et al., 2000). Iris and Nora were
able to work part time as volunteers; in their 40s and beyond,
these two sisters were able to live outside a hospital setting
(Mirsky et al., 2000; Rosenthal, 1963).
Gender Differences
Men are more likely to develop schizophrenia than are women; 1.4 men develop
the disorder for every woman (McGrath, 2006). Moreover, men are more likely to
develop the disorder in their early 20s whereas women are more likely to develop
the disorder in their late 20s or later. Compared to men, women usually have fewer
negative symptoms (American Psychiatric Association, 2013; Maric et al., 2003) and
more mood symptoms (Maurer, 2001), and they are less likely to have substance
abuse problems or to exhibit suicidal or violent behavior (Seeman, 2000). Moreover,
women generally function at higher levels before their illness develops.
Culture
Two findings bear on the role of culture and schizophrenia. First, across various
countries, schizophrenia is more common among people in urban areas and lower
socioeconomic classes than among people in rural areas and higher socioeconomic
classes (Freeman, 1994; Mortensen et al., 1999), as we’ll discuss in more detail later
in this chapter. Moreover, there are ethnic differences in prevalence rates in the
United States: Blacks are twice as likely as Whites or Latinos to be diagnosed with
schizophrenia (Dassori et al., 1995; Keith et al., 1991). These prevalence differences
may reflect the influence of a variety of moderating variables, such as biases in the use
of certain diagnostic categories for different ethnic groups.
Second, people with schizophrenia in non-Western countries are generally
better able to function in their societies than are their Western counterparts, and
thus they have a better prognosis. We’ll discuss possible reasons for this finding in the
Understanding Schizophrenia section on social factors.
Table 12.5 provides a summary of facts about schizophrenia.
TABLE 12.4 • 10-Year and 30-Year Course of Schizophrenia
10 years later 30 years later
Completely recovered 25% 25%
Much improved, relatively
independent
25% 35%
Improved but requiring extensive
support network
25% 15%
Hospitalized, unimproved 15% 10%
Dead, mostly by suicide 10% 15%
Source: Torrey, 2001, p. 130.
Prodromal phase
The phase that is between the onset of
symptoms and the time when the minimum
criteria for a disorder are met.
Active phase
The phase of a psychological disorder (such
as schizophrenia) in which the person exhibits
symptoms that meet the criteria for the
disorder.
Schizophrenia and Other Psychotic Disorders 377
Table 12.5 • Schizophrenia Facts at a Glance
Prevalence
• Approximately 1% of people worldwide have schizophrenia (Gottesman, 1991; Tandon et al., 2008).
Comorbidity
• Over 90% of people with schizophrenia also have at least one other disorder. The most frequent comorbid disorders are mood, anxiety,
and substance use disorders.
Onset
• Men are more likely to develop the disorder in their early 20s, whereas women are more likely to develop it in their late 20s or later.
Course
• About two thirds of people who have had one episode will go on to have subsequent episodes.
• About one third of people with schizophrenia become chronically ill, without much reduction of symptoms; for most others, the
symptoms subside.
Gender Differences
• Schizophrenia affects men more frequently than women (1.4 : 1 male-to-female ratio; McGrath, 2006), and—as noted above—women tend
to develop the disorder at older ages than do men.
• Women have fewer negative symptoms than do men.
Cultural Differences
• Schizophrenia is more common among people in urban areas and in lower socioeconomic groups (Freeman, 1994; Saha et al., 2005).
• In non-Western countries, people with schizophrenia generally function better in society than do those in Western countries (Hopper et al., 2007).
• In a given country, immigrants are almost twice as likely to develop schizophrenia as are native-born residents (Saha et al., 2005).
• Within the United States, Latinos and Whites are less likely to be diagnosed with schizophrenia than are Blacks (Zhang & Snowden, 1999).
Source: Unless otherwise noted, citations for above table are: American Psychiatric Association, 2000, 2013.
Does one of the two countries shown in these photos (China and the United States) have a higher
prevalence of schizophrenia, and if so, which one? Answer: These two countries, and other countries
worldwide, have the same general prevalence rate—about 1%.
GETTING THE PICTURE
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378 C H A P T E R 1 2
TABLE 12.6 • Factors Associated With a Better
Prognosis for People With Schizophrenia
People with schizophrenia who significantly improve often
have one or more of the following characteristics:
• They functioned at a relatively high level before their first
episode.
• The symptoms had a sudden onset.
• They developed symptoms later in life.
• They have a family history of mood disorders, not schizophrenia.
• They have symptoms of paranoia or the nondeficit subtype,
with relatively good cognitive functioning.
• They have fewer negative symptoms.
• They are aware of their symptoms and recognize that the
symptoms are caused by an illness.
• They are women.
Sources: 1991; Fenton & McGlashan, 1994; Green, 2001.
Prognosis
In general, the long-term prognosis for schizophrenia follows the rule
of thirds:
• one third of patients improve significantly;
• one third basically stay the same, having episodic relapses and some
permanent deficits in functioning, but are able to hold a “sheltered”
job—a job designed for people with mild to moderate disabilities; and
• one third become chronically and severely disabled by their illness.
Table 12.6 summarizes factors associated with a better prognosis in
Western countries. However, this table does not indicate a crucial fact
about the prognosis for people with schizophrenia: Over the course of
their lives, people with schizophrenia are more likely than others to
die by suicide or to be victims of violence. In what follows we examine
these risks in greater detail.
Suicide
People with schizophrenia have a higher risk of dying by suicide than
do other people: As Table 12.4 shows, as many as 10–15% of people
with schizophrenia commit suicide (Caldwell & Gottesman, 1990; Siris, 2001).
Those with paranoid symptoms are at the highest risk for suicide. Perhaps paradoxi-
cally, patients at risk for committing suicide are those who are most likely to be aware
of their symptoms: They have relatively few negative symptoms but pronounced
positive symptoms; they tend to be highly intelligent, have career goals, are aware
of their deterioration, and have a pattern of relapsing and then getting better, with
many episodes; and—like other people who die by suicide—they are more likely to
be male than female (Fenton, 2000; Funahashi et al., 2000; Siris, 2001). Ironically,
some of these factors—a high level of premorbid functioning, few negative symp-
toms, and an awareness of the symptoms and their effects—are associated with a bet-
ter prognosis (see Table 12.6). As researchers have identified these risk factors, they
have used them to focus suicide prevention efforts.
Violence
A small percentage of people with schizophrenia commit violent acts. Risk factors
associated with violent behavior include being male, having comorbid substance
abuse, not taking medication, and having engaged in criminal behavior or having
had psychopathic tendencies before schizophrenia developed (Hunt et al., 2006;
Monahan et al., 2001; Skeem & Mulvey, 2001; Tengström et al., 2001).
Rather than being violent, people with schizophrenia are much more likely to
be victims of violence. One survey found that almost 20% of people with a psychotic
disorder had been victims of violence in the previous 12 months. Those who were
more disorganized and functioned less well were more likely to have been victimized
(Chapple et al., 2004), perhaps because their impaired functioning made them easier
“marks” for perpetrators.
Thinking Like A Clinician
Suppose you are a mental health clinician working in a hospital emergency room in the
summer; a woman is brought in for you to evaluate. She’s wearing a winter coat, and in
the waiting room, she talks—or shouts—to herself or an imaginary person. You think that
she may be suffering from schizophrenia. What information would you need in order to make
that diagnosis? What other psychological disorders could, with only brief observation, appear
similar to schizophrenia?
Schizophrenia and Other Psychotic Disorders 379
Understanding Schizophrenia
Despite the low odds that all four of the Genain quads would develop schizophrenia,
it did happen. Why? The neuropsychosocial approach helps us to understand the fac-
tors that lead to schizophrenia and how these factors influence each other. As we shall
see, although neurological factors (including genes) can make a person vulnerable to
the disorder, psychological and social factors also play key roles—which may help ex-
plain not only why all four Genain quads ended up with schizophrenia but also why
the disorder affected them differently.
The quads shared virtually all the same genes, looked alike, and, at least in their early
years, were generally treated similarly, especially by Mrs. Genain. However, Hester was
smaller and frailer than the others; she weighed only 3 pounds at birth and could not always
keep up with her sisters. Because of Hester’s difficulties, it wasn’t always possible to treat the
four girls the same, and so Mr. and Mrs. Genain sometimes treated them as two pairs of
twins: Nora and Myra were paired together (they were seen as most competent), and Iris—
who in fact was almost as competent as Nora and Myra—was paired with Hester.
In the following we will examine the specific neurological, psychological, and
social factors that give rise to schizophrenia and then examine how these factors
affect one another.
Neurological Factors in Schizophrenia
Perhaps more than for any other psychological disorder, neurological factors play a
crucial role in the development of schizophrenia. These factors involve brain systems,
neural communication, and genetics.
Brain Systems
People who have schizophrenia have abnormalities in the structure and function
of their brains. The most striking example of a structural abnormality in the brains
of people with schizophrenia is enlarged ventricles, which are cavities in the center of
the brain that are filled with cerebrospinal fluid (Vita et al., 2006). Larger ventricles
means that the size of the brain itself is reduced. Thus, people who
later develop schizophrenia have brains that are smaller than normal
even before they develop the disorder. This occurs, in part, because
their brains never grew to “full” size. In addition, research suggests
that schizophrenia causes parts of the brain to shrink (DeLisi et al.,
1997; Gur et al., 1997; Rapoport et al., 1999).
In 1981, the Genain sisters, then 51 years old, returned to NIMH
for a 3-month evaluation; during that time, they were taken off their
medications. CT scans of the quads showed similar brain abnor-
malities in all four sisters (Mirsky & Quinn, 1988). However, even
though they were basically genetically identical, their performance
on neuropsychological tests varied: Nora and Hester showed more
evidence of neurological difficulties, and they were more impaired
in their daily functioning when not taking medication. Thus, once
again, we see that genes are not destiny and that brain function can-
not be considered in isolation. The brain is a mechanism, but how
it performs depends in part on how it is “programmed” by learning
and experience—which are psychological factors.
In the following sections, we consider the likely role of specific brain abnormali-
ties and possible causes of such abnormalities, and then we examine telltale neurolog-
ical, bodily, or behavioral signs that may indirectly reveal that a person is vulnerable
to developing the disorder.
These brain scans of identical twins show,
for one of them, the enlarged ventricles that
typically are associated with schizophrenia.
The twin on the right has schizophrenia, and
the twin on the left does not.
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380 C H A P T E R 1 2
A Frontal Lobe Defect?
Based on the specific cognitive deficits exhibited by people with schizophrenia,
many researchers have hypothesized that such people have impaired frontal lobe
functioning. The root of this impairment may lie in the fact that the human brain
has too many connections among neurons at birth, and part of normal matura-
tion is the elimination, or pruning, of unneeded connections (Huttenlocher, 2002).
Research results suggest that an excess of such pruning takes place during adoles-
cence for people who develop schizophrenia: Too many of the neural connections
in the frontal lobes are eliminated, which may account for some of the neurocogni-
tive deficits that typically accompany this disorder (Pantelis et al., 2003; Walker et
al., 2004).
Impaired Temporal Lobe and Thalamus?
Enlarged ventricles are associated with decreased size of the temporal lobes. This is
significant for people with schizophrenia because the temporal lobes process auditory
information, some aspects of language, and visual recognition (Levitan et al., 1999;
Sanfilipo et al., 2002). Abnormal functioning of the temporal lobes may underlie
some positive symptoms, notably auditory hallucinations, in people with schizophre-
nia. The thalamus, which transmits sensory information to other parts of the brain,
also appears to be smaller and to function abnormally in people with schizophrenia
(Andrews et al., 2006; Guller et al., 2012). Abnormal functioning of the thalamus
is associated with difficulties in focusing attention, in distinguishing relevant from
irrelevant stimuli, and in particular types of memory difficulties, all of which are
cognitive deficits that can arise with schizophrenia.
Abnormal Hippocampus?
The hippocampus—a subcortical brain structure crucially involved in storing new
information in memory—is smaller in people with schizophrenia and their first-
degree relatives (parents and siblings) than in control participants (Seidman et al.,
2002; Vita et al., 2006). This abnormal characteristic may contribute to the deficits
in memory experienced by people with schizophrenia (Olson et al., 2006; Yoon et
al., 2008).
Interactions Among Brain Areas
Some researchers propose that schizophrenia arises from disrupted interactions
among the frontal lobes, the thalamus, and the cerebellum—which may act as a time-
keeper, synchronizing and coordinating signals from many brain areas (Andreasen,
2001; Andreasen et al., 1999). According to this theory, the thalamus fails to screen
out sensory information, which overwhelms subsequent processing—and thus the
form and content of the person’s thoughts become confused.
Possible Causes of Brain Abnormalities
How might these brain abnormalities arise? Researchers have identified several pos-
sible causes, some of which could affect the developing brain of a fetus or a newborn:
• maternal malnourishment during pregnancy, particularly during the first trimester
(Brown, van Os, et al., 1999; Wahlbeck et al., 2001).
• maternal illness during the 6th month of pregnancy. During fetal development,
neurons travel to their final destination in the brain and establish connections with
other neurons (in a process called cell migration). If the mother catches the flu or
another viral infection in the second trimester, this may disrupt cell migration
in the developing fetus’s brain, which causes some neurons to fall short of their
intended destinations. Because the neurons are not properly positioned, they form
different connections than they would have formed if they had been in the correct
locations—leading to abnormal neural communication (Brown, Begg, et al., 2004;
Green, 2001; McGlashan & Hoffman, 2000). In general, an immune challenge to
Schizophrenia and Other Psychotic Disorders 381
the developing fetus in turn can affect brain development (Meyer, 2013; Watanabe
et al., 2010).
• oxygen deprivation, which can ar ise from prenata l or bir th-related med ica l
complications (McNeil et al., 2000; Zornberg et al., 2000). Studies have shown
that people with schizophrenia who did not receive enough oxygen at specific
periods before birth have smaller hippocampi than do people with schizophrenia
who were not deprived of oxygen during or before birth (van Erp et al., 2002)—
which may be related to memory problems.
Biological Markers
When a neurological, bodily, or behavioral characteristic distinguishes people with
a psychological disorder (or people with a first-degree relative with the disorder)
from people who do not have the disorder, it is said to be a biological marker for
the disorder. One biological marker for schizophrenia, but not other non-psychotic
psychological disorders, is difficulty maintaining smooth, continuous eye movements
when tracking a light as it moves across the visual field; such tracking is called smooth
pursuit eye movements (Holzman et al., 1984; Iacono et al., 1992). This difficulty re-
flects underlying neurological factors and is associated with irregularities in brain
activation while people visually track moving objects (Hong et al., 2005). Although
it is not clear exactly why people with schizophrenia and their family members have
this specific difficulty, researchers believe that it can help to identify people who are
at risk to develop schizophrenia. Figure 12.2 shows the results of smooth pursuit eye
movement recordings for the Genain sisters.
Another biological marker for schizo-
phrenia is sensory gating (Freedman et
al., 1996), which is assessed as follows:
Participants hear two clicks, one immedi-
ately after the other. Normally, the brain
responds less strongly to the second click
than to the f irst. However, people with
schizophrenia and their first-degree rela-
tives don’t show the normal large drop in
the brain’s response to the second click.
This has been interpreted as a manifes-
tation of the difficulties that people with
schizophrenia can have in f iltering out
unimportant stimuli.
A third t ype of biological marker for schizophrenia has been reported by
researchers who performed careful analyses of home movies of children who were
later diagnosed with schizophrenia (Grimes & Walker, 1994; Walker et al., 1993).
They found that children who went on to develop schizophrenia were different
from their siblings: They made more involuntary movements, such as writhing or
excessive movements of the tongue, lips,
or arms. This tendency for involuntary
movement was particularly evident from
birth to age 2 but could be seen even
through adolescence in people who later
developed the disorder (Walker et al.,
1994). Moreover, those who displayed
more severe movement s of th is t y pe
later developed more severe symptoms
of schizophrenia (Neumann & Walker,
1996).
FI G U RE 12.2 • Genain
Sisters’ Smooth Pursuit Eye
Movements The Genain sisters completed
this test in 1981. The results show that Nora
and Hester had more irregularities in their eye
movements, and they also performed more
poorly on some of the neuropsychological
tests, which indicates that they were more
neurologically impaired.
Source: Courtesy of Dr. Deborah Levy, McLean Hospital,
Belmont, MA.
Nora
1 sec
Myra
Iris
Hester
Biological marker
A neurological, bodily, or behavioral
characteristic that distinguishes people with
a psychological disorder (or a first-degree
relative with the disorder) from those without
the disorder.
The child in this photo went on to develop
schizophrenia. Notice the child’s unusual hand
postures (indicating involuntary movement).
Studies of home movies of children who later
developed schizophrenia revealed many such
involuntary movements, particularly of the
tongue, lips, or arms. W
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382 C H A P T E R 1 2
Neural Communication
Schizophrenia is likely to involve a complex interplay of many brain systems, neuro-
transmitters, and hormones.
Dopamine
One neurotransmitter that is clearly involved in schizophrenia is dopamine. The dopamine
hypothesis proposes that an overproduction of dopamine or an increase in the number or
sensitivity of dopamine receptors is responsible for schizophrenia. According to this hy-
pothesis, the excess dopamine or extra sensitivity to this neurotransmitter triggers a flood of
unrelated thoughts, feelings, and perceptions. Delusions are then attempts to organize these
disconnected events into a coherent, understandable experience (Kapur, 2003).
Consistent with the dopamine hypothesis, neuroimaging studies of people with schizo-
phrenia have found abnormally low numbers of dopamine receptors in their frontal lobes
(Okubo et al., 1997), as well as increased production of dopamine (possibly to compensate
for the reduced numbers of receptors in the frontal lobes) in the striatum (parts of the basal
ganglia that produce dopamine; Heinz, 2000). Nevertheless, research has definitively doc-
umented that the dopamine hypothesis was an oversimplification (McDermott & de Silva,
2005). Dopamine affects, and is affected by, other neurotransmitters that, in combination
with the structural and functional abnormalities of various brain areas, give rise to some of
the symptoms of schizophrenia (Vogel et al., 2006; Walker & Diforio, 1997).
Serotonin and Glutamate
Medications that affect serotonin levels can decrease both positive and negative symptoms in
people with schizophrenia. However, this finding does not imply that serotonin levels per se
are the culprit. Research studies suggest complex interactions among serotonin, dopamine,
and glutamate (Andreasen, 2001). For example, serotonin has been shown to enhance the
effect of glutamate, which is the most common fast-acting excitatory neurotransmitter in the
brain (Aghajanian & Marek, 2000). Studies have found unusually high levels of glutamate in
people with schizophrenia, particularly in the frontal lobe (Abbott & Bustillo, 2006; van Elst
et al., 2005); such an excess of glutamate may disrupt the timing of neural activation in the
frontal lobe, which in turn may impair cognitive activities (Lewis & Moghaddam, 2006).
Stress and Cortisol
Research findings suggest that stress can contribute to schizophrenia because stress affects the
production of the hormone cortisol, which in turn affects the brain. In fact, children who are at
risk for developing schizophrenia react more strongly to stress, and their baseline levels of corti-
sol are higher than those of other children (Walker et al., 1999). The relationship between stress,
cortisol, and symptoms of schizophrenia has also been noted during adolescence, the time when
prodromal symptoms often emerge: A 2-year longitudinal study of adolescents with schizotypal
personality disorder found that cortisol levels—and symptoms of schizophrenia—increased over
the 2 years (Walker et al., 2001). Even after adolescence, people with schizophrenia have higher
levels of stress-related hormones, including cortisol (Zhang et al., 2005).
Thus, people who develop schizophrenia appear to be unusually biologically reactive
to stressful events. A hypothesized mechanism for this relationship is that the biological
changes and stressors of adolescence promote higher levels of cortisol, which may then af-
fect dopamine activity. The relationship between cortisol and schizophrenia is supported
by research indicating that anti-inflammatory medications (such as aspirin or other types of
drugs referred to as COX-2 inhibitors), which indirectly reduce the levels of cortisol, reduce
the symptoms of schizophrenia (Keller et al., 2013).
Effects of Estrogen
We noted earlier that when women develop schizophrenia, they often have different
symptoms than men do, and they tend to function better. Such findings have led to the
estrogen protection hypothesis (Seeman & Lang, 1990). According to this hypothesis, the hor-
mone estrogen, which is present at higher levels in women than in men, protects against
Schizophrenia and Other Psychotic Disorders 383
symptoms of schizophrenia via its effects on serotonin and dopamine. This protec-
tion may explain why women typically develop the disorder later in life than do men.
Evidence for the estrogen protection hypothesis comes from two sources. One is the
finding that women with schizophrenia who had higher levels of estrogen also had
better cognitive functioning (Hoff et al., 2001). The other is the finding that constant
doses of estrogen provided by a skin patch (in addition to antipsychotic medication)
reduced the positive symptoms of women with severe schizophrenia more than did
antipsychotic medication without supplementary estrogen (Kulkarni et al., 2008).
Genetics
Various twin, family, and adoption studies indicate that genes play a role in
schizophrenia (Aberg et al., 2013; Tienari et al., 2006; Wicks et al., 2010;
Wynne et al., 2006). The more genes a person shares with a relative who has
schizophrenia, the higher the risk that that person will also develop schizophre-
nia (see Table 12.7). However, even for those who have a close relative with
schizophrenia, the chance of developing the disorder is still relatively low: More
than 85% of people who have one parent or one sibling (who is not a twin)
with the disorder do not go on to develop it themselves (Gottesman & Moldin,
1998)—and this percentage is even higher for people with a grandparent, aunt,
or uncle (second-degree relatives) with the disorder (Gottesman & Erlenmeyer-
Kimling, 2001). Nonetheless, a family history of schizophrenia is still the stron-
gest known risk factor for developing the disorder ( Hallmayer, 2000).
If the cause of schizophrenia were entirely genetic, then when one identi-
cal twin developed the disorder, the co-twin would also develop the disorder;
that is, the co-twin’s risk of developing schizophrenia would be 100%. But this
is not what happens; the actual risk of a co-twin’s developing schizophrenia
ranges from 46 to 53% (in different studies), as shown in Table 12.7.
Which of the two women pictured would have a lower risk of developing schizophrenia (or have
less severe symptoms if she had the disorder), assuming all the factors are the same for both of
them except age? Answer: The younger woman, because her estrogen levels are higher, which is a
protective factor.
GETTING THE PICTURE
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TABLE 12.7 • Degree of Relatedness and Risk
of Developing Schizophrenia
Family member(s) with
schizophrenia
Risk of developing
schizophrenia
First cousin 2%
Half-sibling 6%
Full sibling 9%
One parent 13%
Two parents 46%
Fraternal twin 14–17%
Identical twin 46–53%
Sources: Gottesman, 1991; Kendler, 1983.
384 C H A P T E R 1 2
However, identical twins have the same predisposition for developing schizophre-
nia, although only one of them may develop it. This means that even if only one
twin in a pair develops the disorder, the children of both twins (the one with the dis-
order and the one without) have the same genetic risk of developing it. That is, both
the affected and the unaffected twin transmit the same genetic vulnerability to their
offspring (Gottesman & Bertelsen, 1989).
As evident from the studies of twins, genes alone do not determine whether
someone will develop schizophrenia; rather, the interaction between genes and
environment is crucial (Owen et al., 2011). For example, in one illustrative study,
researchers tracked two groups of adopted children: those whose biological moth-
ers had schizophrenia and those whose biological mothers did not (considered the
control group). None of the adoptive parents of these children had schizophrenia,
but some adoptive families were dysfunctional—and the children often experienced
stress (Tienari et al., 1994, 2006). In the control group, the incidence of schizo-
phrenia was no higher than in the general population, regardless of the character-
istics of the adoptive families. In contrast, the children whose biological mothers
had schizophrenia and whose adoptive families were dysfunctional were much more
likely to develop schizophrenia than were the children whose biological mothers
had schizophrenia but whose adoptive families were not dysfunctional. Thus, better
parenting appeared to protect children who were genetically at risk for developing
schizophrenia.
Psychological Factors in Schizophrenia
We have seen that schizophrenia is not entirely a consequence of brain structure, brain
function, or genetics. As the neuropsychosocial approach implies, schizophrenia arises
from a combination of different sorts of factors. For example, the neurocognitive
deficits that plague people with schizophrenia also affect how they perceive the social
world, and their perceptions affect their ability to function in that world (Sergi et al.,
2006). If we understand their experiences, their behaviors may not appear so bizarre.
However, not every person with schizophrenia experiences each type of difficulty
we discuss in the following sections (Walker et al., 2004).
Mental Processes and Cognitive Difficulties: Attention,
Memory, and Executive Functions
We’ve already noted problems with attention, working memory, and executive func-
tion in schizophrenia. Let’s now consider how such problems may contribute to the
disorder.
The difficulties with attention—specifically in being able to focus on rele-
vant stimuli and ignore irrelevant stimuli—occur even when the person is taking
medication and isn’t psychotic (Cornblatt et al., 1997). This attentional prob-
lem can make it hard for people with schizophrenia to discern which stimuli are
important and which aren’t; such people may feel overwhelmed by a barrage of
stimuli. This leads to problems in organizing what they perceive and experience,
which would contribute to their difficulties with perception and memory (Sergi
et al., 2006).
Another cognitive problem common to people with schizophrenia is that they
often don’t realize that they are having unusual experiences or behaving abnormally;
this inability is referred to as a lack of insight. Thus, they are unaware of their dis-
order or the specif ic problems it creates for themselves and others ( Amador &
Gorman, 1998) and see no need for treatment (Buckley et al., 2007). In Case 12.2,
psychologist Fred Frese discusses his lack of insight into his own schizophrenia and
its effects.
Schizophrenia and Other Psychotic Disorders 385
CASE 12.2 • FROM TH E INSIDE: Schizophrenia
Psychologist Fred Frese describes his history with schizophrenia:
I was 25 years old, and I was in the Marine Corps at the time, and served two back to back
tours in the Far East, mostly in Japan. And when I came back I was a security officer in
charge of a Marine Corps barracks with 144 men. And we had responsibilities for security
for atomic weapons . . . and a few other duties. About 6 months into that assignment,
I made a discovery—to me it was a discovery—that somehow the enemy had developed a
new weapon by which they could psychologically hypnotize certain high-ranking officials.
And I became very confident that I had stumbled onto this discovery. And because it was
a psychological sort of thing I would share this with a person who would be likely to know
most about this kind of stuff and that was the base psychiatrist. So I called him up and he
agreed to see me right away, and I went down and told him about my discovery, and he
listened very politely and when I got finished to get up and leave there were these two
gentlemen in white coats on either side of me—either shoulder. And I often say I think
one of them looked like he might be elected governor of Minnesota somewhere along the
way. But they escorted me down into a seclusion padded room [sic]. And within a day or
two I discovered that they had me labeled as paranoid schizophrenic. Of course I immedi-
ately recognized that the psychiatrist was under the control of the enemies with their new
weapons. I spent about 5 months mostly in Bethesda, which is the Navy’s major hospital,
and was discharged with a psychiatric condition. However, that was my discovery that I
was diagnosed with . . . schizophrenia. The way the disorder works is, I didn’t have a disor-
der, I had “made this discovery”. So it was a number of years before I came to this conclu-
sion that there was something wrong here and I was hospitalized about ten times, almost
always involuntarily . . . over about a 10-year period of time.
(WCPN, 2003).
To develop a sense of the consequences of having such cognitive difficulties,
imagine the experience of a man with these deficits who tries to go shopping for
ingredients for dinner. He may find himself in the supermarket, surrounded by hun-
dreds of food items; because of his attentional problems, each item on a shelf may
capture the same degree of his attention. Because of deficits in executive functioning,
he loses track of why he is there—what was he supposed to buy? And if he remem-
bers why he is there (“I need to get chicken, rice, and vegetables”), he may not be
able to exercise good judgment about how much chicken to buy or which vegetables.
Or, because of the combination of his cognitive deficits, he may find the whole task
too taxing and leave without the dinner ingredients.
Beliefs and Attributions
Cognitive deficits that are present before symptoms occur affect what the person
comes to believe. For example, because children with such cognitive deficits may
do poorly in school and often are socially odd, they may be ostracized or teased by
their classmates; they may then come to believe that they are inferior and proceed
to act in accordance with that belief, perhaps by withdrawing from others (Beck &
Rector, 2005).
In addition, if people with schizophrenia have delusional beliefs, the delusions
almost always relate to themselves and their extreme cognitive distortions (e.g., “The
FBI is out to get me”). These distortions influence what they pay attention to and
what beliefs go unchallenged. People with schizophrenia may be inflexible in their
beliefs or may jump to conclusions, and their actions based on their beliefs can be
extreme (Garety et al., 2005). Moreover, they may be very confident that their (false)
beliefs are true (Moritz & Woodward, 2006). For example, a man with paranoid
schizophrenia might attribute a bad connection on a cell phone call to interference
by FBI agents or aliens; he searches for and finds “confirming evidence” of such in-
terference (“There’s a bad connection when I call my friend and they want to listen
in, but there’s no static when I call for a weather report and there’s no need for them
Psychologist Fred Frese was diagnosed with
paranoid schizophrenia in 1965 when he
was a Marine Corps security officer. He was
hospitalized many times over the next 10 years
but was able to earn a Ph.D. in psychology in
1978. Over the past 35 years, he has written
about mental illness from both sides of the
experience, been an advocate for the mentally
ill, and served as Director of Psychology at
Western Reserve Psychiatric Hospital.
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386 C H A P T E R 1 2
to listen in”). Disconfirming evidence—that cell phone service is weak in the spot
where he was standing when he made the call to his friend—is ignored (Beck &
Rector, 2005).
Similarly, people with schizophrenia who have auditory hallucinations do not
generally try to discover where the sounds of the hallucinations are coming from.
For example, they don’t check whether the radio is on or whether people are talking
in the hallway. They are less likely to question the reality of an unusual experience
(that is, whether it arises from something outside themselves) and so do not correct
their distorted beliefs ( Johns et al., 2002).
Negative symptoms can also give rise to unfounded beliefs; specifically, people
who have negative symptoms generally overestimate the extent of their deficits and
are particularly likely to have low expectations of themselves. Although such low
expectations could indicate an accurate assessment of their abilities, research suggests
that this is generally not the case. When cognitive therapy successfully addresses the
negative self-appraisals of people with schizophrenia, their functioning subsequently
improves (Rector et al., 2003). This finding suggests that the negative self-appraisals
are distorted beliefs that became self-fulfilling prophecies (Beck & Rector, 2005).
Emotional Expression
Another psychological factor is the facial expressions of people with schizophre-
nia, which are less pronounced than those of people who do not have the disor-
der ( Brozgold et al., 1998). Moreover, people with schizophrenia are less accurate
than control participants in labeling the emotions expressed by faces they are shown
(Penn & Combs, 2000; Schneider-Axmann et al., 2006). Part of the explanation for
problems related to emotional expression may be the cognitive deficits. Because they
cannot “read” nonverbal communication well, they are confused when someone’s
words and subsequent behavior are at odds; people with schizophrenia are likely to
miss the nonverbal communication that helps most people make sense of the appar-
ent inconsistency between what others say and what they do (Greig et al., 2004).
In fact, even biological relatives of people with schizophrenia tend to have problems
understanding other people’s nonverbal communication ( Janssen et al., 2003), which
suggests that neurological factors are involved.
Social Factors in Schizophrenia
We’ve seen that schizophrenia often includes difficulty in understanding and navi-
gating the social world. We’ll now examine this difficulty in more detail and also
consider the ways that economic circumstances and cultural factors can influence
schizophrenia.
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How do you interpret these facial
expressions? Do you see surprise, anger, fear
and disgust? People with schizophrenia may
have difficulty accurately “reading” other
people’s emotional expressions, which can
make social interactions confusing and lead
them to respond inappropriately.
Schizophrenia and Other Psychotic Disorders 387
Understanding the Social World
Each of us develops a theory of mind—a theory about other people’s mental states
(their beliefs, desires, feelings) that allows us to predict how they will behave in a
given situation. People with schizophrenia have difficulty with tasks that require
an accurate theory of mind ( Russell et al., 2006) and may thus find relating to oth-
ers confusing. Because people with schizophrenia have difficulty interpreting emo-
tional expression in others, they don’t fully understand the messages people convey.
The symptoms of paranoia and social withdrawal in people with schizophrenia may
directly result from this social confusion (Frith, 1992). To a person with schizophre-
nia, other people can seem to behave in random and unpredictable ways. Thus, it
makes sense that such a person tries to explain other people’s seemingly odd behavior
(persecutory delusion) or else tries to minimize contact with others because their
behavior seems inexplicable.
Despite the fact that they were basically genetically identical, the Genain quads
did not have the same level of social skills or ability to navigate the social world. For
instance, Myra had markedly better social skills and social desires than her sisters, and
was able to work as a secretary for most of her life—a job that requires social aware-
ness and social skills (Mirsky et al., 2000).
Stressful Environments
Orphanages are notoriously stressful environments, which may be one reason why
being raised in an orphanage increases the likelihood of later developing schizophre-
nia in those who are genetically vulnerable. In fact, children born to a parent with
schizophrenia are more likely to develop schizophrenia as adults if they were raised
in an institution than if they were raised by the parent with schizophrenia (Mednick
et al., 1998).
Stress also contributes to whether someone who recovered from schizophre-
nia will relapse (Gottesman, 1991). Almost two thirds of people hospitalized with
schizophrenia live with their families after leaving the hospital. These families can
create a stressful environment for a person with schizophrenia, especially if the family
is high in expressed emotion. The concept of high expressed emotion (high EE)
is not aptly named: It’s not just that the family with this characteristic expresses emo-
tion in general but rather that family members express critical and hostile emotions
and are overinvolved (for example, by frequently criticizing or nagging the patient to
change his or her behavior; Wuerker et al., 2002). In fact, hospitalized patients who
return to live with a family high in EE are more likely to relapse than patients who
do not return to live with such a family (Butzlaff & Hooley, 1998; Kavanagh, 1992).
The Genain quads certainly experienced significant stress, and their family would be
considered high in EE.
The relationship between high EE and relapse of schizophrenia is a correla-
tion. High EE probably does not cause schizophrenia in the f irst place, but it
may contribute to a relapse. However, it is also possible that the causality goes
the other way—that people whose symptoms of schizophrenia are more severe
between episodes elicit more attempts by their family members to try to minimize
the positive or negative symptoms. And then these behaviors lead the family to be
classified as high in EE. This explanation may apply, in part, to the Genain family:
Among the four sisters, Hester’s symptoms were the most chronic and debilitating.
She received the most physical punishment, including being whipped and having
her head dunked in water, often in response to behaviors that her father wanted
her to stop.
Researchers have also discovered ethnic differences in how patients perceive
critical and intrusive family behaviors. Among Black American families, for instance,
Theory of mind
A theory about other people’s mental states
(their beliefs, desires, and feelings) that allows
a person to predict how other people will
react in a given situation.
High expressed emotion (high EE)
A family interaction style characterized by
hostility, unnecessary criticism, or emotional
overinvolvement.
388 C H A P T E R 1 2
behaviors by family members that focus on problem solving are associ-
ated with a better outcome for the person with schizophrenia, perhaps
because such behaviors are interpreted as reflecting caring and concern
(Rosenfarb et al., 2006). Thus, what is important is not the family behav-
ior in and of itself but how such behavior is perceived and interpreted by
family members.
Immigration
A well-replicated finding is that schizophrenia is more common among
immigrants than among people who stayed in the immigrants’ original
country and people who are natives in the immigrants’ adopted coun-
tr y (Cantor-Graae & Selten, 2005; Lundberg et al., 2007; Veling et
al., 2012). This higher rate of schizophrenia among immigrants occurs
among people who have left a wide range of countr ies and among
people who find new homes in a range of European countries. In fact,
one meta-analysis found that being an immigrant was the second larg-
est risk factor for schizophrenia, after a family history of this disorder
( Cantor-Graae & Selten, 2005). Both first-generation immigrants—
that is, those who left their native countr y and moved to another
country—and their children have relatively high rates of schizophre-
nia; this is especially true for immigrants and their children who have
darker skin color than the natives of the adopted countr y, which is
consistent with the role of social stressors (discrimination in particu-
lar) in schizophrenia (Selten et al., 2007). For instance, the increased
rate of schizophrenia among African-Caribbean immigrants to Britain
(compared to British and Caribbean residents who are not immigrants)
may arise from the stresses of immigration, socioeconomic disadvan-
tage, and racism ( Jarvis, 1998). Researchers have sought to rule out
potential confounds such as illness or nutrition, and have found that
such factors do not explain the higher risk of schizophrenia among immigrants.
Case 12.3 describes the symptoms of schizophrenia of an immigrant from Haiti to
the United States.
CASE 12.3 • FROM TH E OUTSIDE: Schizophrenia
Within a year after immigrating to the United States, a 21-year-old Haitian woman
was referred to a psychiatrist by her schoolteacher because of hallucinations and
withdrawn behavior. The patient was fluent in English, although her first language
was Creole. Her histor y revealed that she had seen an ear, nose, and throat special-
ist in Haiti after her family doctor could not find any medical pathology other than a
mild sinus infection. No hearing problems were noted and no treatment was offered.
Examination revealed extensive auditory hallucinations, flat affect, and peculiar delu-
sional references to voodoo. The psychiatrist wondered if symptoms of hearing voices
and references to voodoo could be explained by her Haitian background, although the
negative symptoms seem unrelated. As a result, he consulted with a Creole-speaking,
Haitian psychiatrist.
The Haitian psychiatrist inter viewed the patient in English, French, and Creole.
Communication was not a problem in any language. He discovered that in Haiti, the
patient was considered “odd” by both peers and family, as she frequently talked to her-
self and did not work or participate in school activities. He felt that culture may have
influenced the content of her hallucinations and delusions (i.e., references to voodoo) but
that the bizarre content of the delusions, extensive hallucinations, and associated nega-
tive symptoms were consistent with the diagnosis of schizophrenia.
(Takeshita, 1997, pp. 124–125)
Schizophrenia occurs more frequently among
immigrants and their children than among
people who live in their native country.
The various stresses of the immigration
process, including financial problems and
discrimination, may account, at least in part,
for this increased risk. The people in this
photo are beginning the process of becoming
legal immigrants.
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Schizophrenia and Other Psychotic Disorders 389
In Case 12.3, notice that, a lthough the women had odd and prodroma l
behaviors in Haiti, her full-blown symptoms did not emerge until she immigrated
to the United States. These symptoms could have emerged when she got older
even if she had stayed in Haiti. As compelling as single cases can be, full-scale
studies—with adequate controls—must play a central role in helping us under-
stand psychological disorders.
Economic Factors
Another social factor associated with schizophrenia is socioeconomic status. A
disproportionately large number of people with schizophrenia live in urban ar-
eas and among lower economic classes (Hudson, 2005; Mortensen et al., 1999).
As discussed in Chapter 2, researchers have offered two possible explanations
for this association between the disorder and economic status: social selection
and social causation (Dauncey et al., 1993). The social selection hypothesis
proposes that people who are mentally ill “drift” to a lower socioeconomic level
because of their impairments (and hence social selection is sometimes called so-
cial drift). Consider a young woman who grows up in a middle-class family and
moves to a distant city after college, and where, after she graduates, she supports
herself reasonably well working full time. She subsequently develops schizo-
phrenia but refuses to return home to her fam ily, who cannot af ford to send
her much money. Her income now consists pr imar ily of meager checks from
governmental programs—barely enough to cover food and housing in a poor
section of town where rent is cheapest. She has drifted from the middle class to
a lower class.
Another possible explanation is the social causation hypothesis: The daily
stressors of urban life, especially for the poor, trigger mental illness in people who
are vulnerable ( Freeman, 1994; Hudson, 2005). Social causation would explain
cases of schizophrenia in people who grew up in a lower social class. The stressors
these people experience include poverty or financial insecurity, as well as living in
neighborhoods with higher crime rates. Both hypotheses—social selection and social
causation—may be correct.
Cultural Factors: Recovery in Different Countries
Although the prevalence of schizophrenia is remarkably similar across countries
and cultures, the same cannot be said about recover y rates. Some studies report
that people in developing countries have higher recover y rates than do people
in industrialized countries (Kulhara & Chakrabarti, 2001), although this was
not found in all earlier studies (Edgerton & Cohen, 1994; von Zerssen et al.,
1990).
If the results from the more recent studies can be replicated, what might ac-
count for this cultural difference? The important distinction may not be the level
of industrial and technological development of a country but how individualist its
culture is. Individualist cultures stress values of individual autonomy and independence.
In contrast, collectivist cultures emphasize the needs of the group, group cohesion, and
interdependence. Collectivist cultures may more readily help people with schizo-
phrenia be a part of the community at whatever level is possible. And in fact, people
with schizophrenia in collectivist cultures, such as those of Japan, Hong Kong, and
Singapore, have a more favorable course and prognosis than people with schizo-
phrenia in individualist cultures such as the United States (Lee et al., 1991; Tsoi &
Wong, 1991).
Social selection hypothesis
The hypothesis that people who are mentally
ill “drift” to a lower socioeconomic level
because of their impairments; also referred to
as social drift.
Social causation hypothesis
The hypothesis that the daily stressors of
urban life, especially as experienced by people
in a lower socioeconomic class, trigger mental
illness in those who are vulnerable.
390 C H A P T E R 1 2
The collectivist characteristics of a culture may help a patient to recover for
several reasons. Consider that people in collectivist countries may:
• be more tolerant of people with schizophrenia and therefore less likely to be
critical, hostile, and controlling toward them. In particular, the families of pa-
tients with schizophrenia may be more likely to have lower levels of expressed
emotion, decreasing the risk of relapse and leading to better recoveries (El-
Islam, 1991).
• elevate the importance of community and, in so doing, provide a social norm that
creates more support for people with schizophrenia and their families.
• have higher expectations of people with schizophrenia—believing that such
people can play a functional role in society—and these expectations become a self-
fulfilling prophecy (Mathews et al., 2006).
Thus, collectivism—and the strong family values that usually accompany it—may
best explain the better recovery rates in less developed countries, which are gener-
ally more collectivist (Weisman, 1997). In fact, for Latino patients, increasing their
perception of the cohesiveness of the family is associated with fewer psychiatric
symptoms and less distress (Weisman et al., 2005).
Feedback Loops in Understanding Schizophrenia
No individual risk factor by itself accounts for a high percentage of the cases of
schizophrenia. Genetics, prenatal environmental events (such as maternal mal-
nutrition and maternal illness), and birth complications that affect fetal develop-
ment (neurological factors) can increase the likelihood that a person will develop
schizophrenia. But many people who have these risk factors do not develop the
disorder. Similarly, cognitive deficits (psychological factors) can contribute to the
disorder because they create cognitive distortions, but such factors do not actu-
ally cause schizophrenia. And a dysfunctional family or another type of stress-
ful environment (social factors), again, can contr ibute to, but do not cause,
schizophrenia.
As usual, in determining the origins of psychopathology, no one factor reigns
supreme in producing schizophrenia; instead, the feedback loops among the three
types of factors provide the best explanation (Mednick et al., 1998; Tienari et al.,
2006). To get a more concrete sense of the effects of the feedback loops, consider
the fact that economic factors (which are social) can influence whether a preg-
nant woman is likely to be malnourished, which in turn affects the developing
fetus (and his or her brain). And various social factors create stress (and not sim-
ply among immigrants or among children raised in an orphanage—but for all of
us). The degree of stress a person experiences (a psychological factor) in turn can
trigger factors that affect brain function, including increased cortisol levels. Com-
ing full circle, as shown in Figure 12.3, these psychological and neurological fac-
tors are affected by culture (a social factor), which influences the prognosis, how
people with schizophrenia are viewed, and how they come to view themselves
( psychological factors).
The Genain quads illustrate the effects of these feedback loops. A family his-
tory of schizophrenia as well as prenatal complications made the quads neurologically
vulnerable to developing schizophrenia. They were socially isolated, were teased
by other children, and experienced physical and emotional abuse. Had the Genain
quads grown up in a different home environment, with parents who treated them
differently, it is possible that some of them might not have developed schizophrenia,
and those who did might have suffered fewer relapses.
SP
N
Schizophrenia and Other Psychotic Disorders 391
Mental Processes and
Mental Contents
Behavior
Brain Systems
GeneticsNeural Communication
Stressful Life Events
NeuroPsychoSocial
NeuroPsychoSocialNeuroPsychoSocial
Cognitive deficits
Poor insight
Negative beliefs
about self and
abilities
Disorganized
speech and
behavior
Diminished
emotional
expression
Frontal lobes
Temporal lobes
Thalamus
Hippocampus
Dopamine
Serotonin
Glutamate
Cortisol
Estrogen
Impaired theory of
mind
Growing up in an
orphanage
Family
High expressed
emotion
Gender/Culture
Immigration
Discrimination
Differential recovery
rates across cultures
Inherited
vulnerability for
schizophrenia
spectrum
disorders
Affect
FI G U RE 12.3 • Feedback Loops in
Understanding Schizophrenia
Using the neuropsychosocial approach, explain in detail how the three types of factors and
their feedback loops may have led all four Genain sisters to develop schizophrenia—and
formulate a hypothesis to explain why they had some different symptoms.
Thinking Like A Clinician
Treating Schizophrenia
The Genain sisters were treated at NIMH and then subsequently in hospitals, residen-
tial settings, and community mental health centers. During the early years of the quads’
illness, antipsychotic medications were only just beginning to be used, and treatments
that target psychological and social factors have changed substantially since then. Today,
392 C H A P T E R 1 2
treatment for schizophrenia occurs in steps, with different symptoms and problems tar-
geted in each step (Green, 2001):
STEP 1: When the patient is actively psychotic, first reduce the positive symptoms.
STEP 2: Reduce the negative symptoms.
STEP 3: Improve neurocognitive functioning.
STEP 4: Reduce the person’s disability and increase his or her ability to function in
the world.
As we’ll see, the last step is the most challenging.
Targeting Neurological Factors in Treating Schizophrenia
At present, interventions targeting neurological factors generally focus on the first
two steps of treatment: reducing positive and negative symptoms. However, some
such treatments address on the third step: improving cognitive function.
Medication
Doctors began to use medication to treat symptoms of schizophrenia in the 1950s, with
the development of the first antipsychotic (also called neuroleptic) medication, thorazine.
Since then, various antipsychotic medications have been developed, and two general
types of these medications are now used widely, each with its own set of side effects.
Traditional Antipsychotics
Thorazine (chlorpromazine) and other similar antipsychotics are dopamine antagonists,
which effectively block the action of dopamine. Positive symptoms— hallucinations
and delusions—diminish in approximately 75–80% of people with schizophrenia who
take such antipsychotic medications (Green, 2001). Since their development, traditional
antipsychotics have been the first step in treating schizophrenia. When taken regularly,
they can reduce the risk of relapse: Only 25% of those who took antipsychotic medica-
tion for 1 year had a relapse, compared to 65–80% of those not on medication for a year
(Rosenbaum et al., 2005). Traditional antipsychotics quickly sedate patients; above and
beyond such sedation, psychotic symptoms start to improve anywhere from 5 days to 6
weeks after the patient begins to take the medication (Rosenbaum et al., 2005).
Some of the side effects of traditional antipsychotics create problems when a person
takes them regularly for an extended period of time. For example, patients can develop
tardive dyskinesia, an enduring side effect that produces involuntary lip smacking and
odd facial contortions as well as other movement-related symptoms. Although tardive dys-
kinesia typically does not go away even when traditional antipsychotics are discontinued,
its symptoms can be reduced with another type of medication. Other side effects of tradi-
tional antipsychotics include tremors, weight gain, and a sense of physical restlessness.
Atypical Antipsychotics: A New Generation
More recently, doctors have been able to use a different class of medications to
treat schizophrenia: Atypical antipsychotics (also referred to as second- generation
antipsychotics) affect dopamine and serotonin. Examples of atypical antipsychotics
include Risperdal (risperidone), Zyprexa (olanzapine), and Seroquel (quetiapine).
Atypical antipsychotics also can reduce comorbid symptoms of anxiety and depression
(Marder et al., 1997). Like traditional antipsychotics, they decrease the likelihood of
relapse, at least for 1 year (which is the longest period studied; Csernansky et al., 2002;
Lauriello & Bustillo, 2001). However, any benefits of newer antipsychotics must be
weighed against medical costs: Side effects include changes in metabolism that cause
significant weight gain and increased risk of heart problems, and these side effects
can become so severe or problematic that some people won’t or shouldn’t continue to
use these medications (McEvoy et al., 2007). In addition, atypical antipsychotics, like
traditional antipsychotics, sometimes cause tardive dyskinesia (Woods et al., 2010).
This man is exhibiting signs of tardive
dyskinesia—involuntary lip smacking and
odd facial grimaces that can be an enduring
side effect of long-term use of antipsychotic
medication.
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Tardive dyskinesia
An enduring side effect of traditional
antipsychotic medications that produces
involuntary lip smacking and odd facial
contortions as well as other movement-
related symptoms.
Atypical antipsychotics
A relatively new class of antipsychotic
medications that affects dopamine and
serotonin activity; also referred to as second-
generation antipsychotics.
Schizophrenia and Other Psychotic Disorders 393
Either type of antipsychotic medication is considered “successful” when it significantly
reduces symptoms and the side effects can be tolerated. However, sometimes medication is
not successful because it isn’t really given a fighting chance: Patients often stop taking their
prescribed medication without consulting their doctor, which is referred to as noncompliance.
Many people who stop taking their medication—whether in consultation with their doctor
or not—cite significant unpleasant side effects as the main reason (Lieberman et al., 2005).
Discontinuing Medication
Given how often patients stop taking their medication (up to two thirds in one study;
Lieberman et al., 2005), we need to understand the effects of discontinuing medication:
When people with schizophrenia discontinue their medication, they are more likely to
relapse. One study found that among those who were stable for over 1 year and then
stopped taking their medication, 78% had symptoms return within 1 year after that, and
96% had symptoms return after 2 years (Gitlin et al., 2001). And even up to 5 years after
discharge, patients who had been hospitalized for schizophrenia and then discontinued their
medication were five times as likely to relapse as those who didn’t (Robinson et al., 1999).
Brain Stimulation: ECT
Electroconvulsive therapy (ECT) was originally used to treat schizophrenia but gener-
ally was not successful. Although currently used only infrequently to treat this disorder,
a course of ECT may be administered to people with active schizophrenia who are not
helped by medications. ECT may reduce symptoms, but its effects are short lived; fur-
thermore, “maintenance” ECT—that is, regular although less frequent treatments—may
be necessary for long-term improvement (Keuneman et al., 2002). Three of the Genain
sisters—Nora, Iris, and Hester—received numerous sessions of ECT before antipsychotic
medication was available. After ECT, their symptoms improved at least somewhat but,
usually within months, if not weeks, worsened again until the symptoms were so bad
that a course of ECT was again administered (Mirsky et al., 1987; Rosenthal, 1963).
In experimental studies with small numbers of patients, transcranial magnetic
stimulation (TMS) appears to decrease hallucinations, at least in the short term
(Brunelin, Poulet et al., 2006; Poulet et al., 2005). However, not all studies have
found this positive effect (McNamara et al., 2001; Saba et al., 2006). The specifics of
ECT and TMS administration are discussed in Chapter 5.
Targeting Psychological Factors in Treating Schizophrenia
Treatments for schizophrenia that target psychological factors address three of
the four general treatment steps; they (1) reduce psychotic symptoms through
cognitive-behavior therapy (CBT); (2) reduce negative symptoms of schizophrenia
through CBT; and (3) improve neurocognitive functioning (and quality of life)
through psychoeducation and motivational enhancement (Tarrier & Bobes, 2000).
Cognitive-Behavior Therapy
CBT addresses the patient’s symptoms and the distress they cause. Treatment may
initially focus on understanding and managing symptoms, by helping patients to:
• learn to distinguish hallucinatory voices from people actually speaking,
• highlight the importance of taking effective medications,
• address issues that interfere with compliance, and
• develop more effective coping strategies.
When a therapist uses CBT to address problems arising from delusions, he or she
does not try to challenge the delusions themselves but instead tries to help the patient
move forward in life, despite these beliefs. For instance, if a man believes that the CIA is
after him, the CBT therapist might focus on the effects of that belief: What if the CIA
were following him? How can he live his life more fully, even if this were the case?
394 C H A P T E R 1 2
Patient and therapist work together to implement new coping strategies and monitor
medication compliance. In fact, such uses of CBT not only improve overall functioning
(Step 4) but also can decrease positive (Pfammatter et al., 2006; Rector & Beck, 2002a,
2002b) and negative symptoms (Grant et al., 2012; Turkington et al., 2006).
Treating Comorbid Substance Abuse: Motivational Enhancement
Because many people with schizophrenia also abuse drugs or alcohol, recent research
has focused on developing treatments for people with both schizophrenia and sub-
stance use disorders; motivational enhancement is one facet of such treatment. As we
discussed in Chapter 10, patients who receive motivational enhancement therapy
develop their own goals, and then clinicians help them meet those goals. For peo-
ple who have both schizophrenia and substance use disorders, one goal might be to
take medication regularly (Lehman et al., 1998). For people who have two disorders,
treatment that targets both of them appears to be more effective than treatment that
targets one or the other alone (Barrowclough et al., 2001).
Targeting Social Factors in Treating Schizophrenia
Treatments that target social factors address three of the four general treatment steps: They
identify early warning signs of positive and negative symptoms through family education
and therapy; when necessary, such treatments involve hospitalizing people who cannot care
for themselves or are at high risk of harming themselves or others. These treatments also
reduce certain negative symptoms through social skills training and improve overall func-
tioning (and quality of life) through community-based interventions. Community-based
interventions include work-related and residential programs (Tarrier & Bobes, 2000).
Family Education and Therapy
By the time a person is diagnosed with schizophrenia, family members typically
have struggled for months—or even years—to understand and help their loved one.
Psychoeducation for family members can provide practical information about the illness
and its consequences, how to recognize early signs of relapse, how to recognize side effects
of medications, and how to manage crises that may arise. Such education can decrease
relapse rates (McWilliams et al., 2012; Pfammatter et al., 2006). In addition, family-based
treatments may provide emotional support for family members (Dixon et al., 2000).
Moreover, family therapy can create more adaptive family interaction patterns:
In 1989, my older sister and I joined Mom in her attempts to learn more about managing
symptoms of her illness. Mom’s caseworkers met with us every 6 to 8 weeks for over 8 years.
Mom, who had never been able to admit she had an illness, now told us that she did not want
to die a psychotic. This was one of the many positive steps that we observed in her recovery.
Over the years, other family members have joined our group. . . . With the help of the treat-
ment team, we can now respond effectively to Mom’s symptoms and identify stress-producing
situations that, if left unaddressed, can lead to episodes of hospitalization. With Mom’s help we
have identified the different stages of her illness. In the first stage, we listed withdrawal, con-
fusions, depression, and sleeping disorder. Fifteen years ago when mom reported her symp-
toms to me, I just told her everything would be okay. Today we respond immediately. For
8 years she has maintained a low dosage of medications, with increases during times of stress.
(Sundquist, 1999, p. 620)
Family therapy can also help high EE families change their pattern of interaction,
so that family members are less critical of the patient, which can lower the relapse rate
from 75% to 40% (Leff et al., 1990).
Group Therapy: Social Skills Training
Given the prominence of social deficits in many people with schizophrenia, clinicians
often try to improve a patient’s social skills. Social skills training usually occurs in a
group setting, and its goals include learning to “read” other people’s behaviors, learning
Substance abuse is a common problem for
people with schizophrenia. In such cases,
motivational enhancement may be part of a
treatment program.
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Schizophrenia and Other Psychotic Disorders 395
what behaviors are expected in particular situations, and responding to others in a
more adaptive way. Social skills training teaches these skills by breaking complex social
behaviors into their components: maintaining eye contact when speaking to others,
taking turns speaking, learning to adjust how loudly or softly to speak in different situ-
ations, and learning how to behave when meeting someone new. The leader and mem-
bers of a group take turns role-playing these different elements of social interaction.
In contrast to techniques that focus specifically on behaviors, cognitive techniques
focus on group members’ irrational beliefs about themselves, their knowledge of social
conventions, the beliefs that underlie their interactions with other people, and their ideas
about what others may think; such beliefs often prevent people with schizophrenia from
attempting to interact with others. Each element of the training is repeated several times,
to help patients overcome their neurocognitive problems when learning new material.
Inpatient Treatment
Short-term or long-term hospitalization is sometimes necessary for people with
schizophrenia. A short-term hospital stay may be required when someone is having
an acute schizophrenic episode (that is, is actively psychotic, extremely disorganized,
or otherwise unable to care for himself or herself ) or is suicidal or violent. The goal
is to reduce symptoms and stabilize the patient. Once hospitalized, the patient will
probably receive medication and therapy. The patient may participate in various ther-
apy groups, such as a group to discuss side effects of medications. Once the symptoms
are reduced to the point where appropriate self-care is possible and the risk of harm is
minimized, the patient will probably be discharged. Long-term hospitalization may
occur only when treatments have not significantly reduced symptoms and the patient
needs full-time intensive care.
Legal measures have made it diff icult to hospitalize people against their will
( Torrey, 2001). A lthough these tougher standards protect people from being
hospitalized simply because they do not conform to common social conventions (see
Chapter 1), they also have downsides: People who have a disorder that by its very nature
limits their ability to comprehend that they have an illness may not receive appropriate
help until their symptoms have become so severe that they are dangerous to them-
selves or others, or they are unable to take care of themselves adequately. Early inter-
vention for ill adults who do not want help but do not realize that they are ill is legally
almost impossible today. This issue will be discussed in more detail in Chapter 16.
Minimizing Hospitalizations: Community-Based Interventions
In Chapter 1 we noted that asylums and other forms of 24-hour care, treatment, and
containment for those with severe mental illness have met with mixed success over the
past several hundred years. Traditionally, people with chronic schizophrenia were likely
to end up in such institutions. However, beginning in the 1960s, with the widespread
use of antipsychotic medications, the U.S. government established the social policy of
deinstitutionalization—trying to help those with severe mental illness live in their com-
munities rather than remain in the hospital. Not everyone thinks that deinstitution-
alization is a good idea, at least not in the way it has been implemented. The main
problem is that the patients were sent out into communities without adequate social,
medical, or financial support. It is now common in many U.S. cities to see such people
on street corners, begging for money or loitering, with no obvious social safety net.
The good news is that some communities have adequately funded programs to
help people with chronic schizophrenia (and other chronic and debilitating psycho-
logical disorders) live outside institutions. Community care (also known as asser-
tive community treatment) programs allow mental health staff to visit patients in their
homes at any time of the day or night (Mueser, Bond, et al., 1998). Patients who
receive such community care report greater satisfaction with their care; however,
such treatment may not necessarily lead to better outcomes (Killaspy et al., 2006).
Community care
Programs that allow mental health care
providers to visit patients in their homes at
any time of the day or night; also known as
assertive community treatment.
Deinstitutionalization was mandated without
adequate funding for communities to take
care of people with schizophrenia and other
serious mental illnesses. One result has been
increased poverty and homelessness among
people with such disorders.
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Residential Settings
Some people with schizophrenia may be well enough not to need hospitalization but are
still sufficiently impaired that they cannot live independently or with family members.
Alternative housing for such people includes a variety of supervised residential settings.
Some of these patients live in highly supervised housing, in which a small number of people
live with a staff member. Residents take turns shopping for and making meals. They also
have household chores and attend house meetings to work out the normal annoyances of
group living. Those able to handle somewhat more responsibility may live in an apartment
building filled with people of similar abilities, with a staff member available to supervise
any difficulties that arise. As patients improve, they transition to less supervised settings.
Vocational Rehabilitation
Various types of programs assist people with schizophrenia to acquire job skills; such pro-
grams are specifically aimed at helping patients who are relatively high functioning but
have residual symptoms that interfere with functioning at, or near, a normal level. For
instance, patients who are relatively less impaired may be part of supported employment pro-
grams, which place people in regular work settings and provide an onsite job coach to
help them adjust to the demands of the job itself and the social interactions involved in
having a job (Bustillo et al., 2001). Examples of supported employment jobs might in-
clude work in a warehouse, packaging items for shipment or restocking items in an office
or a store (“Project search,” 2006). Those who are more impaired may participate in shel-
tered employment, working in settings that are specifically designed for people with emo-
tional or intellectual problems who cannot hold a regular job. For example, people in such
programs may work in a hospital coffee shop or create craft items that are sold in shops.
What predicts how well a patient with schizophrenia can live and work in the
world? Researchers have found that a person’s ability to live and perhaps work outside
a hospital is associated with a specific cognitive function: his or her ability to use
working memory (Dickinson & Coursey, 2002).
Details of the treatment that the Genain sisters received are only available for their
time at NIMH in the 1950s, when less was known about the disorder and how to treat
it effectively. During the sisters’ stay at NIMH, therapists tried to reduce the parents’
level of emotional expressiveness and criticism; however, such attempts do not appear
to have been effective. After their departure from NIMH, the sisters lived in a variety
of settings: Nora lived first with Mrs. Genain and subsequently in a supervised apart-
ment with Hester. Iris was less able to live independently and lived in the hospital, in
supervised residential settings, or at home with Mrs. Genain; she died in 2002. Myra,
long divorced, generally lived independently; after Mrs. Genain died in 1983, Myra
moved into her mother’s house with her older son. Like Iris, Hester spent many years
in the hospital and then with Mrs. Genain. She lived with Nora in a supervised apart-
ment until she died in 2003 (Mirsky & Quinn, 1988; Mirsky et al., 1987, 2000).
Feedback Loops in Treating Schizophrenia
To be effective, treatment for people with schizophrenia must employ interventions
that induce interactions among neurological, psychological, and social factors (see
Figure 12.4). When successful, medication (treatment targeting neurological factors)
can reduce the positive and negative symptoms and even help improve cognitive func-
tioning. These changes in neurological and psychological factors, in turn, make it pos-
sible for social treatments, such as social skills training and vocational rehabilitation, to
be effective. If patients are not psychotic and have improved cognitive abilities, they
can better learn social and vocational skills that allow them to function more effectively
and independently. Moreover, to the extent that the patients function more effectively,
they may experience less stress, which reduces cortisol levels—which in turn affects
neurological functioning. And such improved neurological functioning can further
facilitate cognitive functioning, which helps the patients live in the social world.
SP
N
Schizophrenia and Other Psychotic Disorders 397
Suppose you are designing a comprehensive treatment program for people with schizophrenia.
Although you’d like to provide each program participant with many types of services, budget-
ary constraints mean that you have to limit the types of treatments your program offers.
Based on what you have read about the treatment of schizophrenia, what would you defi-
nitely include in your treatment program, and why? Also list the types of treatment you’d like
to include if you had a bigger budget.
Thinking Like A Clinician
Treatments Targeting
Neurological Factors
Medication: traditional
and atypical
antipsychotics
ECT
Changes neural
activity
Changes thoughts,
feelings, and
behaviors
Decreases family
conflict and stress
and family members’
critical behavior
Improves social
interactions and
ability to work and live
more independently
Treatments Targeting
Social Factors
Family therapy and
education
Social skills training
Residential treatment
Vocational rehabilitation
CBT
Motivational
enhancement
Treatments Targeting
Psychological Factors
FI G U RE 12.4 • Feedback
Loops in Treating
Schizophrenia
What Are Schizophrenia and Other
Psychotic Disorders?
• According to DSM-5, schizophrenia is
characterized by two or more positive and
negative symptoms, at least one of which
must be hallucinations, delusions, or dis-
organized speech; these symptoms must
be present for a minimum of 6 months
and must significantly impair functioning.
• Positive symptoms are delusions, halluci-
nations, disorganized speech, and disorga-
nized behavior.
• Negative symptoms include diminished
emotional expression, avolition, alogia,
anhedonia, and asociality.
• Resea rch st ud ies have i nd icated that
cognitive def icits accompany symptoms
of schizophrenia. Such def icits include
problems with attention, working mem-
ory, and executive functioning.
• Symptoms of schizophrenia can appear
to overlap with those of other disorders,
notably mood disorders and substance use
disorders.
• Schizophrenia, schizophreniform disorder,
brief psychotic disorder, schizoaffective dis-
order, and delusional disorder, along with
SUMMING UP
398 C H A P T E R 1 2
Schizophrenia (p. 366)
Positive symptoms (p. 366)
Hallucinations (p. 367)
Delusions (p. 367)
Catatonia (p. 368)
Negative symptoms (p. 369)
Flat affect (p. 369)
Avolition (p. 369)
Executive functions (p. 370)
Schizophreniform disorder (p. 373)
Brief psychotic disorder (p. 373)
Schizoaffective disorder (p. 373)
Delusional disorder (p. 373)
Prodromal phase (p. 377)
Active phase (p. 377)
Biological marker (p. 382)
Theory of mind (p. 388)
High expressed emotion (high EE) (p. 388)
Social selection hypothesis (p. 390)
Social causation hypothesis (p. 390)
Tardive dyskinesia (p. 393)
Atypical antipsychotics (p. 393)
Community care (p. 396)
Key Terms
schizotypal personality disorder, are part of a
spectrum of schizophrenia-related disorders.
• Schizophrenia occurs in approximately 1%
of the population worldwide. Men have an
earlier onset of the disorder than do women.
• Up to 15% of people with schizophrenia
commit suicide. People with this disorder
who behave violently are most likely to
have a comorbid disorder that is associated
with violent behavior, such as a substance
use disorder. People with schizophrenia
are more likely than other people to be
victims of violence.
Understanding Schizophrenia
• Various neurological factors are associated
with schizophrenia:
° Abnormalities in brain structure and
function have been found in the frontal
and temporal lobes, the thalamus, and
the hippocampus. Moreover, certain
brain areas do not appear to interact
with each other properly. People with
schizophrenia are likely to have en-
larged ventricles.
° These brain abnormalities appear to be a
result of, at least in some cases, maternal
malnourishment, illness during preg-
nancy, and/or fetal oxygen deprivation.
° Schizophrenia is associated with abnor-
malities in dopamine, serotonin, and
glutamate activity, as well as a height-
ened stress response and increased cor-
tisol production.
° Genetics is still the strongest predic-
tor that a given person will develop
schizophrenia. Genetics alone, though,
cannot explain why a given person de-
velops the disorder.
• Psychological factors that are associated
with schizophrenia and shape the symp-
toms of the disorder include:
° cognitive deficits (in attention, working
memory, and executive functioning);
° dysfunctional beliefs and attributions;
° diff iculty conveying and recognizing
emotions.
• Various social factors are also associated
with schizophrenia:
° an impaired theor y of m ind, which
makes it diff icult to understand other
people’s behavior, which in turn means
that other people’s behavior appears to
be unpredictable;
° a stressful home environment, such as
being raised in an orphanage or by a
parent with schizophrenia;
° the stresses of immigration—particu-
larly for people l ikely to encounter
discrimination—and economic hard-
ship; and
° the individualist nature of the culture,
which is associated with lower recovery
rates for people with schizophrenia.
Treating Schizophrenia
• Treatments that target neurological fac-
tor s i nclude t r ad it ion a l a nd at y pica l
antipsychotics:
° When these medications do not sig-
nificantly decrease positive symptoms,
ECT may be used;
° Many pat ient s d iscont inue med ica-
tion because of side effects. People who
stop taking medication are much more
likely to relapse.
• Treatments that target psychological fac-
tors include CBT to help patients better
manage their psychotic symptoms and
motivational enhancement to decrease
comorbid substance abuse.
• Treatments that target social factors include
family education, family therapy to im-
prove the interaction pattern among family
members, and group therapy to improve
social skills.
More Study Aids
For additional study aids related to this chapter, including quizzes
to make sure you’ve retained everything you’ve learned and a
Student Video Activity exploring one woman’s struggle with
hallucinations due to schizophrenia, go to: www.worthpublishers.
com/launchpad/rkabpsych2e.
Barbara Chase/Creatas/Jupiter Images/Getty Images
Schizophrenia and Other Psychotic Disorders 399
401
CHAPTER 13
Personality Disorders
achel Reiland wrote a memoir called Get Me Out of Here,
about living with a personality disorder. In the opening of the
book, Reiland remembers Cindy, the golden-haired grade-
school classmate who was their teacher’s favorite. At the end of a
painting class, Cindy’s painting was beautiful, with distinctive trees.
Rachel’s painting looked like a “putrid blob.” Rachel then recounts:
I seethed with jealousy as Mrs. Schwarzheuser showered Cindy with
compliments. Suddenly, rage overwhelmed me. I seized a cup of
brown paint and dumped half of it over my picture. Glaring at Cindy,
I leaned across the table and dumped the other half over her drawing.
I felt a surge of relief. Now Cindy’s picture looked as awful as mine.
“Rachel ! ” M r s. Schwa rzheuser yel led. “You’ve completely
destroyed Cindy’s beautiful trees. Shame on you. You are a horrible
little girl. The paint is everywhere—look at your jeans. . . .”
I felt my body go numb. My legs, arms, and head were weightless.
Floating. It was the same way I felt when Daddy pulled off his belt
and snapped it. Anticipation of worse things to come—things I had
brought on myself because I was different.
“In all my years, I’ve never seen a child like you. You are the worst
little girl I’ve ever taught. Go sit in the corner, immediately.”
Shame on Rachel. That language I understood. And deserved. . . .
Mrs. Schwarzheuser was right. I was horrible.
(2004, pp. 1–2)
Diagnosing Personality Disorders
What Are Personality Disorders?
Understanding Personality Disorders in General
Treating Personality Disorders: General Issues
Odd/Eccentric Personality Disorders
Paranoid Personality Disorder
Schizoid Personality Disorder
Schizotypal Personality Disorder
Treating Odd/Eccentric Personality Disorders
Dramatic/Erratic Personality Disorders
Antisocial Personality Disorder
Borderline Personality Disorder
Understanding Borderline Personality Disorder
Histrionic Personality Disorder
Narcissistic Personality Disorder
Fearful/Anxious Personality Disorders
Avoidant Personality Disorder
Dependent Personality Disorder
Obsessive-Compulsive Personality Disorder
Understanding Fearful/Anxious Personality
Disorders
Treating Fearful/Anxious Personality Disorders
Follow-up on Rachel Reiland
Reiland’s actions towaRd cindy that day were troublesome
and troubling, but many children have episodes of feeling intensely
jealous and angry toward others and then “act out” those feelings. Such
episodes don’t necessarily indicate that a child, or the adult he or she
grows up to be, has a disorder.
But some children and teenagers exhibit problems with relation-
ships that persist into adulthood—problems that interfere with an aspect
of daily life, such as work or family life. These problems have existed
for so long that they seem to be a part of who the person is, a part of his
or her personality. Such persistent problems are central to personality
disorders, a category of psychological disorders characterized by an
enduring pattern of inflexible and maladaptive thoughts, emotional
responses, interpersonal functioning, and impulse control problems that
arise across a range of situations and lead to distress or dysfunction.
Personality disorders
A category of psychological disorders
characterized by an enduring pattern of
inflexible and maladaptive thoughts, emotional
responses, interpersonal functioning, and
impulse control problems that arise across
a range of situations and lead to distress or
dysfunction.
Tiziana Nanni/Getty Images. Photo for illustrative purposes only; any individual depicted is a model.
Diagnosing Personality Disorders
It’s not unusual for children to act out in school, as Rachel Reiland did. But as chil-
dren get older, they mature. In Reiland’s case, she went on to do well academically
in high school and college, but in the nonacademic areas of her life, things didn’t go
as well. While in high school, she developed anorexia nervosa. In high school and
college, she frequently got drunk and had numerous casual sexual encounters. More-
over, she hadn’t yet grown out of the maladaptive childhood patterns of behavior that
got her into so much trouble.
In her mid-20s, Reiland unintentionally became pregnant when dating a man
named Tim. They decided to marry and did so, even though she had a miscar-
riage before the wedding. They then had two children, first Jeffrey and 2 years later,
Melissa. It seemed that Reiland had straightened out her life and that her childhood
problems were behind her.
She temporarily stopped working while the children were young. When they
were 2 and 4years old, Reiland found herself overwhelmed—alternately angry and
needy. One day during this period of her life, her husband called to say he’d be late at
work and wouldn’t be home until 6 or 7 P.M. She responded by asking whether his
coming home late was her fault. Reiland recounts their ensuing exchange:
“I didn’t say it’s your fault, honey. It’s just that . . . well, I’ve got to get some stuff
done.” I began to twist the phone cord around my finger, tempted to wrap it around
my neck.
“I’m a real pain in the ass, aren’t I? You’re pissed, aren’t you?” Tim tried to keep his
patience, but I could still hear him sigh.
“Please, Rachel. I’ve got to make a living.”
“Like I don’t do anything around here? Is that it? Like I’m some kind of stupid
housewife who doesn’t do a god-damned thing? Is that what you’re getting at? ”
Another sigh.
“Okay. Look, sweetheart, I’ve got to do this presentation this afternoon because it’s
too late to cancel. But I’ll see if I can reschedule the annuity guy for tomorrow. I’ll be
home by four o’clock, and I’ll help you clean up the house.”
“No, no, no!”
I was beginning to cry.
“What now?”
“God, Tim. I’m such an idiot. Such a baby. I don’t do a thing around this house, and
here I am, wanting you to help me clean. I must make you sick.”
“You don’t make me sick, sweetheart. Okay? You don’t. Look, I’m really sorry, but
I’ve got to go.”
The tears reached full strength. The cry became a moan that turned to piercing
screams. Why in the hell can’t I control myself? The man has to make a living. He’s such a good
guy; he doesn’t deserve me—no one should have to put up with me!
“Rachel? Rachel? Please calm down. Please! Come on. You’re gonna wake up the
kids; the neighbors are gonna wonder what in the hell is going on. Rachel?”
“[Screw you!] Is that all you care about, what the neighbors think? [Screw] you,
then. I don’t need you home. I don’t want you home. Let this [damn] house rot; let the
[damn] kids starve. I don’t give a shit. And I don’t need your shit!”
(2004, pp. 11–12)
When Tim responds by saying he’s going to cancel all his appointments and can be
home in a few minutes, she sobs, “You must really hate me . . . you really hate me,
don’t you?” (Reiland, 2004, p. 12).
Reiland’s behavior seems extreme, but is it so extreme that it indicates a
personality disorder, or is it just an emotional outburst from a mother of young
children who is feeling overwhelmed? In order to understand the nature of Reiland’s
Rachel Reiland
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402 C H A P T E R 1 3
problems and see how a clinician determines whether a person’s problems
merit a diagnosis of personality disorder, we must focus on personality, and
contrast normal versus abnormal variations of personality.
When you describe your roommate or new friends to your parents,
you usually describe his or her personality—enduring characteristics that
lead a person to behave in relatively predictable ways across a range of situ-
ations. Similarly, when you imagine how family members will react to bad
news you’re going to tell them, you are probably basing your predictions
of their reactions on your sense of their personality characteristics. Such
characteristics—or personality traits—are generally thought of as being on a
continuum, with a trait’s name, such as “ interpersonal warmth,” at one end
of the continuum and its opposite, such as “ standoffishness,” at other end of
the continuum. Each person is unique in terms of the combination of his
or her particular personality traits—and how those traits affect his or her
behavior in various situations.
In this section we examine in more detail the DSM-5 category of
personality disorders and then the specific personality disorders that it contains.
What Are Personality Disorders?
Some people consistently and persistently exhibit extreme versions of personality traits,
such as being overly conscientious and rule-bound or, like Reiland, being overly emo-
tional and quick to anger. In some cases, extreme traits are also
inflexible—the person cannot easily control or modulate them.
Such extreme and inflexible traits can become maladaptive and
cause distress or dysfunction— characteristics of a personality dis-
order. In the following we examine the definition of personality
disorders more closely.
As Table 13.1 notes, personality disorders reflect persistent
thoughts, feelings, and behaviors that are significantly different
from the norms in the person’s culture. Specifically, these dif-
ferences involve the ABCs of psychological functioning:
• affect, which refers to the range, intensity, and changeability
of emotions and emotional responsiveness and the ability to
regulate emotions;
• behavior, which refers to the ability to control impulses and
interactions with others; and
• cognition (mental processes and mental contents), which refers
to the perceptions and interpretations of events, other people,
and oneself.
The differences in the ABCs of psychological functioning are
relatively inflexible and persist across a range of situations, which
highlights how central these maladaptive personality traits are to
the way the person functions. This rigidity across situations in
turn leads to distress or impaired functioning, as it did for Sarah, in
Case 13.1. To be diagnosed with a personality disorder, the mal-
adaptive traits typically should date back at least to early adulthood
and should not primarily arise from a substance- related or medical
disorder or another psychological disorder (American Psychiatric Association, 2013).
We can now answer the question of whether Reiland’s difficulties were more
than those of an overwhelmed mother of young children: Her problems indicate that
she has a personality disorder.
B
il
ly
E
. B
a
rn
e
s/
P
h
o
to
E
d
it
Personality disorders are characterized by
a pattern of inflexible and maladaptive
thoughts, feelings, and behaviors that arise
across a range of situations. This woman
might be diagnosed with a personality
disorder if she consistently got angry
with little provocation and had difficulty
controlling her anger in a variety of settings.
Personality
Enduring characteristics that lead a person to
behave in relatively predictable ways across a
range of situations.
TABLE 13.1 • DSM-5 General Diagnostic Criteria for a
Personality Disorder
A. An enduring pattern of inner experience and behavior that deviates
markedly from the expectations of the individual’s culture. This
pattern is manifested in two (or more) of the following areas:
1. Cognition (i.e., ways of perceiving and interpreting self, other
people, and events).
2. Affectivity (i.e., the range, intensity, lability, and appropriateness
of emotional response).
3. Interpersonal functioning.
4. Impulse control.
B. The enduring pattern is inflexible and pervasive across a broad range
of personal and social situations.
C. The enduring pattern leads to clinically significant distress or
impairment in social, occupational, or other important areas of
functioning.
D. The pattern is stable and of long duration, and its onset can be
traced back at least to adolescence or early adulthood.
E. The enduring pattern is not better explained as a manifestation of
consequence of another mental disorder.
F. The enduring pattern is not attributable to the physiological effects
of a substance (e.g., a drug of abuse, a medication) or another
medical condition (e.g., head trauma).
Reprinted with permission from the Diagnostic and Statistical Manual of Mental Disorders,
Fifth Edition, (Copyright ©2013). American Psychiatric Association. All Rights Reserved.
Personality Disorders 403
CASE 13.1 • FROM TH E OUTSIDE: Personality Disorder
Sarah, a 39-year-old single female, originally requested therapy at . . . an outpatient clinic, to
help her deal with chronic depression and inability to maintain employment. She had been
unemployed for over a year and had been surviving on her rapidly dwindling savings. She was
becoming increasingly despondent and apprehensive about her future. She acknowledged dur-
ing the intake interview that her attitude toward work was negative and that she had easily be-
come bored and resentful in all of her previous jobs. She believed that she might somehow be
conveying her negative work attitudes to prospective employers and that this was preventing
them from hiring her. She also volunteered that she detested dealing with people in general. . . .
Sarah had a checkered employment history. She had been a journalist, a computer tech-
nician, a night watch person, and a receptionist. In all of these jobs she had experienced her
supervisors as being overly critical and demanding, which she felt caused her to become
resentful and inefficient. The end result was always her dismissal or her departure in anger.
Sarah generally perceived her co-workers as being hostile, unfair, and rejecting. However,
she would herself actively avoid them, complaining that they were being unreasonable and
coercive when they tried to persuade her to join them for activities outside of work. For
example, she would believe that she was being asked to go for drinks purely because her
co-workers wanted her to get drunk and act foolishly. Sarah would eventually begin to take
“mental health” days off from work simply to avoid her supervisors and colleagues.
(Thomas, 1994, p. 211)
A lthough personalit y disorders are considered to be relatively
stable, at least from adolescence into adulthood, research suggests
that (as shown in Figure 13.1) these disorders are not as enduring as
once thought (Clark, 2009; Zanarini et al., 2005); rather, symptoms
can improve over time for some people (Grilo et al., 2004; Johnson
et al., 2000).
As a group, people with personality disorders obtain less education
(Torgersen et al., 2001) and are more likely never to have married or to
be separated or divorced (Torgersen, 2005) than people who don’t have
such disorders. Personality disorders are associated with suicide: Among
people who die by suicide, about 30 % apparently had a personality
disorder; among people who attempt suicide, about 40% apparently have
a personality disorder (American Psychiatric Association Work Group
on Suicidal Behaviors, 2003).
Assessing Personality Disorders
Personality disorders can be difficult to diagnose in a first interview, largely because
patients may not be aware of the symptoms. In many cases, people who have a per-
sonality disorder are so familiar with their lifelong pattern of emotional responses,
behavioral tendencies, and mental processes and contents that the ways in which
this pattern is maladaptive may not be apparent to them. In fact, most people with
a personality disorder identify other people or situations as being the problem, not
something about themselves.
Given that many people with personality disorders are not aware of the nature
of their problems, clinicians may diagnose a patient with a personality disorder based
both on what the patient says and on patterns in the way he or she says it (Skodol,
2005). For instance, Sarah, in Case 13.1, probably had specific complaints about
her coworkers, but the key information lies in the pattern of her complaints—in her
claim that most of her coworkers, in various companies, were hostile and rejecting.
Multiple patient visits may be required to identify such a pattern and to diagnose a
personality disorder, more such visits than is usually needed to diagnose other types
of disorders. And more than with other diagnoses, clinicians must make inferences
about the patient in order to diagnose a personality disorder. However, clinicians
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Schizotypal personality disorder
Borderline personality disorder
Avoidant personality disorder
Obsessive-compulsive personality
disorder
FI G U RE 13.1 • Stability of
Personality Disorders Within 2 years
of being diagnosed with a personality disorder,
around one quarter to one third of the people
in one study no longer met the diagnostic
criteria for 12 consecutive months (Grilo et al.,
2004). This finding indicates that personality
disorders are not as stable as once thought.
Source: Grilo et al., 2004. For more information see the
Permissions section.
404 C H A P T E R 1 3
must be careful not to assume that their inferences are correct
without further corroboration (Skodol, 2005).
To help assess persona lit y disorders, clinicians and
researchers may interview the patient and also have patients
complete personality inventories or questionnaires. To diag-
nose a personality disorder, the clinician may also talk with
someone in the patient’s life, such as a family member—who
often describes the patient ver y differently than does the
patient (Clark, 2007; Clifton et al., 2004). The picture that
emerges of someone with a personality disorder is a pattern of
chronic interpersonal difficulties or chronic problems with self,
such as a feeling of emptiness (Livesley, 2001).
According to DSM-5, when clinicians assess personality
disorders, they should take into account the person’s culture,
ethnicity, and social background. For instance, a woman who
appears to be unable to make any decisions independently
(even about what to make for dinner) and constantly defers to
family members might have a personality disorder. However, for some immigrants,
this pattern of behavior may be within a normal range for their ethnic or religious
group. When immigrants have problems that are related to the challenges of adapting
to a new culture or that involve behaviors or a worldview that is typical of people with
their background, a personality disorder shouldn’t be diagnosed. A clinician who isn’t
familiar with a patient’s background should get more information from other sources.
DSM-5 Personality Clusters
DSM-5 lists 10 personality disorders, grouped into three clusters. Each cluster of per-
sonality disorders shares a common feature. Cluster A personality disorders are
characterized by odd or eccentric behaviors that have elements related to those of
schizophrenia. Cluster B personality disorders are characterized by emotional,
dramatic, or erratic behaviors that involve problems with emotional regulation.
Cluster C personality disorders are characterized by anxious or fearful behav-
iors. We will discuss the specific disorders in each cluster as we progress through this
chapter. Table 13.2 provides an overview of facts about personality disorders in general.
In the subsequent discussions of individual personality disorders, you may notice
that adding the prevalence rates for the various disorders gives a higher total than the
overall prevalence rate of 14% listed in Table 13.2 on the next page. This mathemati-
cal discrepancy is explained by the high comorbidity, also noted in the table: Half of
people who have a personality disorder will be diagnosed with at least one other per-
sonality disorder (and, in some cases, with more than one other personality disorder).
Criticisms of the DSM-5 Category of Personality Disorders
The category of personality disorders, as defined in DSM-5 (and in DSM-IV), has been
criticized on numerous grounds. One criticism is that DSM-5 treats personality disor-
ders as categorically distinct from normal personality (Widiger & Lowe, 2008). In con-
trast, most psychological researchers currently view normal personality and personality
disorders as being on continua. In DSM-5 terms, two people might differ only slightly
in the degree to which they exhibit a personality trait, but one person would be
considered to have a personality disorder and the other person would not. A related
criticism is that the DSM-5 criteria for personality disorders create an arbitrary cutoff
on the continuum between normal and abnormal (Morey et al., 2012; Widiger & Trull,
2007). In part to address this point, newly created for DSM-5 is an alternative model
of personality disorders that allows mental health professionals to rate how impaired
patients are in terms of various dimensions (American Psychiatric Association, 2013).
Although a person may exhibit a pattern of
problems that indicates a personality disorder,
clinicians should take into consideration the
person’s ethnicity, social background, and
culture. If the person’s patterns of thoughts,
feelings, and behaviors are characteristic of
people from his or her background, a diagnosis
of a personality disorder is not warranted.
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Cluster A personality disorders
Personality disorders characterized by odd
or eccentric behaviors that have elements
related to those of schizophrenia.
Cluster B personality disorders
Personality disorders characterized by
emotional, dramatic, or erratic behaviors that
involve problems with emotional regulation.
Cluster C personality disorders
Personality disorders characterized by anxious
or fearful behaviors.
Personality Disorders 405
Another criticism pertains to the clusters, which were
organized by superficial commonalities. Research does
not necessarily support the organization of personality
disorders into these clusters (Sheets & Craighead, 2007).
Moreover, some of the specific personality disorders are
not clearly distinct from each other (Trull et al., 2012).
In addition, some personality disorders are not clearly
distinct from other disorders in DSM (Harford et al.,
2013; Widiger & Trull, 2007). The diagnostic criteria for
avoidant personality disorder, for example, overlap con-
siderably with those for social phobia, as we’ll discuss in
the section on avoidant personality disorder. Similarly,
critics point out that the general criteria for personality
disorders (see Table 13.1) could apply to other disorders,
such as persistent depressive disorder and schizophrenia
(Oldham, 2005).
The process by which the DSM-IV/DSM-5 criteria
were determined is another target of criticism. The min-
imum number of symptoms needed to make a diagnosis,
as well as the specific criteria, aren’t necessarily supported
by research results (Widiger & Trull, 2007). Moreover,
different personality disorders require different numbers
of symptoms and different levels of impairment (Livesley,
2001; Skodol, 2005; Westen & Shedler, 2000).
The high comorbidity among personality disorders
invites another criticism: that the specific personality dis-
orders do not capture the appropriate underlying prob-
lems, and so clinicians must use more than one diagnosis to describe the types of
problems exhibited by patients (Widiger & Mullins-Sweatt, 2005). In fact, the most
frequently diagnosed personality disorder is a nonspecific personality disorder that
we’ll call other personality disorder in this chapter; this disorder is often diagnosed along
with an additional personality disorder (Hopwood et al., 2012; Verheul et al., 2007;
Verheul & Widiger, 2004). As with other categories of disorders, the nonspecific
“other” diagnosis is used when a patient’s symptoms cause distress or impair func-
tioning but do not fit the criteria for any of the disorders within the relevant cat-
egory—in this case, one of the 10 specific personality disorders.
Understanding Personality Disorders in General
At one point, Reiland became impatient with her 4-year-old son Jeffrey and “lost it.”
She slapped and then cursed him. As he cried, she commanded him to stop crying.
He didn’t, and she proceeded to spank him so hard that it hurt her hand:
The reality slowly sunk in. I had beaten my child. Just as my father had beaten his. Just as
I swore I never ever would. A wave of nausea rose within me. I was just like my father. Even
my children would be better off without me. There was no longer any reason to stay alive.
(Reiland, 2004, p. 19)
Reiland’s realization was relatively unusual for someone with a personality dis-
order: She recognized in this instance that she had created a problem—she had done
something wrong, although her father never recognized his responsibility. He too
was quick to anger and hit her and her siblings. Do personality disorders run in
families? If so, to what extent do genes and environment lead to personality disor-
ders? How might personality disorders arise?
TABLE 13.2 • An Overview: Personality Disorder Facts at a Glance
Prevalence
• Researchers estimate that up to 14% of Americans will have at least one
personality disorder over the course of their lives (Grant, Hasin, et al., 2004;
Lenzenweger, 2006).
Comorbidity
• Up to 75% of those with a personality disorder will also be diagnosed
with another type of psychological disorder (Dolan-Sewell et al., 2001;
Lenzenweger, 2006). Common comorbid disorders are mood disorders, anxi-
ety disorders, and substance use disorders (Grant, Stinson et al., 2004; John-
son et al., 2006b; Lenzenweger, 2006).
• Approximately 50% of people with a personality disorder will be diagnosed
with at least one other personality disorder (Skodol, 2005).
Onset
• The DSM-5 diagnostic criteria require that symptoms are present by young
adulthood.
• For one personality disorder—antisocial personality disorder—a diagnostic
criterion requires that symptoms are present before age 15.
Course
• Symptoms of personality disorders are often relatively stable, but they may
fluctuate or improve as people go through adulthood.
Gender Differences
• Specific personality disorders have gender differences in prevalence, but there
is no such difference across all personality disorders.
Source: Unless otherwise noted, American Psychiatric Association, 2000.
406 C H A P T E R 1 3
Neurological Factors in Personality Disorders:
Genes and Temperament
Perhaps the most influential neurological factor associated with personality disorders
is genes (Cloninger, 2005; Paris, 2005). Researchers have not produced evidence that
genes underlie specific personality disorders, but they have shown that genes clearly
influence temperament, which is the aspect of personality that reflects a person’s typical
affective state and emotional reactivity (see Chapter 2). Temperament, in turn, plays
a major role in personality disorders. Genes influence temperament via their effects
on brain structure and function, including neurotransmitter activity.
It is possible that the genes that affect personality traits can predispose some peo-
ple to develop a personality disorder (South & DeYoung, 2013). For instance, some
people are genetically predisposed to seek out novel and exciting stimuli, such as
those associated with stock trading, race car driving, or bungee jumping, whereas
other people are predisposed to become easily overstimulated and habitually prefer
low-key, quiet activities, such as reading, writing, or walking in the woods. Such
differences in temperament are the foundation on which different personality traits
are built—and, at their extremes, temperaments can give rise to inflexible person-
ality traits that are associated with personality disorders. Examples include a nov-
elty seeker (temperament) who compulsively seeks out ever more exciting activities
( inflexible behavior pattern), regardless of the consequences, and a person who avoids
overstimulation (temperament) and turns down promotions because the new po-
sition would require too many activities that would be overstimulating (inflexible
behavior pattern).
Reiland may well have inherited a tendency to develop certain aspects of tem-
perament, which increased the likelihood of her behaving like her father in cer-
tain types of situations. However, her genes and her temperament don’t paint the
whole picture; psychological and social factors also influenced how she thought, felt,
and behaved.
Temperament—which is partly genetic—can make a person vulnerable to specific
personality disorders. Which of these two situations—driving a motorcycle fast in traffic or
being nervous about being in a room full of strangers—is more likely to signal a personality
disorder associated with novelty seeking? Answer: Driving a motorcycle fast in traffic.
GETTING THE PICTURE
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Personality Disorders 407
Psychological Factors in Personality Disorders: Temperament and
the Consequences of Behavior
Although an infant may be born with a genetic bias to develop certain temperamental
characteristics, these characteristics—and personality traits—evolve through experi-
ence in interacting with the world. Personality traits involve sets of learned behaviors
and emotional reactions to specific stimuli; what is learned is in part shaped by the
consequences of behavior, including how other people respond to the behavior. The
mechanisms of operant conditioning are at work whenever a person experiences conse-
quences of behaving in a certain way: If the consequences are positive, the behavior is
reinforced (and hence likely to recur); if the consequences are negative, the behavior is
punished (and hence likely to be dampened down).
The consequences of behaving in a specific way not only affect how tempera-
ment develops but also influence a person’s expectations, views of others, and views
of self (Bandura, 1986; Farmer & Nelson-Gray, 2005). Based on what they have
learned, people can develop maladaptive and faulty beliefs, which in turn lead them
to misinterpret other people’s words and actions. These (mis)interpretations reinforce
their views of themselves and the world in a pervasive self-fulfilling cycle, biasing
what they pay attention to and remember, which in turn reinforces their views of
self and others (Beck et al., 2004; Linehan, 1993; Pretzer & Beck, 2005). The conse-
quences of behavior can thereby lead to pervasive dysfunctional beliefs—which can
form the foundation for some types of personality disorders. For instance, at one
point Rachel Reiland states her belief that her husband “doesn’t deserve me—no
one should have to put up with me!” (Reiland, 2004, p. 11). This belief leads her to
be hypervigilant for any annoyance her husband expresses or implies. She’s likely to
misinterpret his actions and comments as confirming her belief that she is undeserv-
ing, and she then alternates lashing out in anger with groveling in grief.
Social Factors in Personality Disorders: Insecurely Attached
Another factor that influences whether a person will develop a personality disorder is
attachment style—the child’s emotional bond and way of interacting with (and think-
ing about) his or her primary caretaker (Bowlby, 1969; see Chapter 1). The attach-
ment style established during childhood often continues into adulthood, affecting
how the person relates to others (Waller & Shaver, 1994). Most children develop
a secure attachment style (Schmitt et al., 2004), which is characterized by a positive
view of their own worth and of the availability of others. However, a significant
minority of children develop an insecure attachment style, which can involve a negative
view of their own worth, the expectation that others will be unavailable, or both
(Bretherton, 1991). People with personality disorders are more likely to have an inse-
cure attachment style (Crawford et al., 2006; Lahti et al., 2012).
People can develop an insecure attachment style for a variety of reasons, such
as childhood abuse (sexual, physical, or verbal), neglect, or inconsistent discipline
( Johnson et al., 2005; Johnson, Cohen, et al., 2006; Paris, 2001). Reiland’s father
abused her physically and verbally, alternating the abuse with bouts of neglect.
However, such social risk factors may lead to psychopathology in general, not per-
sonality disorders in particular (Kendler et al., 2000). A single traumatic event does
not generally lead to a personality disorder (Rutter, 1999).
Feedback Loops in Understanding Personality Disorders
As with other kinds of psychological disorders, no one factor reigns supreme as the under-
lying basis of personality disorders. People must have several adverse factors— neurological,
psychological, or social—to develop a personality disorder, and social adversity will have
the biggest effect on those who are neurologically vulnerable (Paris, 2005).
SP
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Insecure attachment to a parent can make a
child vulnerable to developing a personality
disorder. Insecure attachment can arise from
abuse, neglect, or inconsistent discipline. For
instance, the adult in this photo is neglecting
the child by not getting up to help him/her.
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408 C H A P T E R 1 3
Consider the fact that people with personality disorders tend to have parents with
psychological disorders (Bandelow et al., 2005; Siever & Davis, 1991). The parents’
dysfunctional behavior clearly creates a stressful social environment for children,
and the children may model some of their parents’ behavior (psychological factor).
Moreover, they may also inherit a predisposition toward a specif ic temperament
( neurological factor). Similarly, chronic stress and abuse, such as Reiland experi-
enced, affects brain structure and function (neurological factor; Teicher et al., 2003),
which in turn affects mental processes (psychological factor).
The specific personality disorder a person develops depends on his or her tem-
perament and family members’ reactions to that temperament (Linehan, 1993; Rutter
& Maughan, 1997). For instance, children with difficult temperaments—such as those
that lead a person to be extremely passive—tend to have more conflict with their parents
and peers (Millon, 1981; Rutter & Quinton, 1984), which leads them to experience a
higher incidence of physical abuse and social rejection. These children may then come
to expect (psychological factor) to be treated poorly by others (social factor). Thus, so-
cial factors can amplify underlying temperaments and traits so that they subsequently
form the foundation for a personality disorder (Caspi et al., 2002; Paris, 1996, 2005).
Treating Personality Disorders: General Issues
People with disorders other than personality disorders often say that
their problems “happened” to them—the problems are overlaid on
their “usual” self. They want the problems to get better so that they
can go back to being that usual self, and thus they seek treatment. In
contrast, people with personality disorders don’t see the problem as
overlaid on their usual self; by its very nature, a personality disorder
is integral to the way such people function in the world. And so
people with these disorders are less likely to seek treatment unless
they also have another type of disorder—in which case, they typi-
cally seek help for the other disorder.
Addressing and reducing the symptoms of a personality disorder
can be challenging because patients’ entrenched maladaptive beliefs
and behaviors can lead them to be poorly motivated during treatment
and not inclined to collaborate with the therapist. Treatment for personality disorders
generally lasts longer than does treatment for other psychological disorders. How-
ever, there is little research on treatment for most personality disorders. The next
section summarizes what is known about treating personality disorders in general;
later in the chapter we discuss treatments for the specific personality disorders for
which there are substantial research results.
Targeting Neurological Factors in Personality Disorders
Treatments for personality disorders that target neurological factors include antipsy-
chotics, antidepressants, mood stabilizers, or other medications. Generally, however,
such medications are only effective for symptoms of certain other disorders (such as
anxiety) and are not very helpful for symptoms of personality disorders per se (Paris,
2005, 2008). Nevertheless, some of these medications may reduce temporarily some
symptoms (Paris, 2003; Soloff, 2000).
Targeting Psychological Factors in Personality Disorders
Both cognitive-behavior therapy (CBT) and psychodynamic therapy have been used
to treat personality disorders. Both therapies focus on core issues that are theorized to
give rise to the disorders; they differ in terms of the inferred core issues. Psychody-
namic therapy addresses unconscious drives and motivations, whereas CBT addresses
We don’t know why this couple has ended up
on this couch, but we do know that treating
people who have personality disorders can
be challenging because patients may not see
themselves as having a problem.
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Personality Disorders 409
maladaptive views of self and others and negative beliefs that give rise to the prob-
lematic feelings, thoughts, and behaviors of the personality disorder (Beck et al.,
2004). CBT is intended to increase the patient’s sense of self-efficacy and mastery
and to modify the negative, unrealistic beliefs that lead to maladaptive behaviors.
In addition, because people with personality disorders may not be motivated to
address the problems associated with the disorder, treatment may employ motiva-
tional enhancement strategies to help patients identify goals and become willing to
work with the therapist. Treatment that targets psychological factors has been studied
in depth only for borderline personality disorder; we examine such treatment in the
section discussing that personality disorder.
Targeting Social Factors in Personality Disorders
Guidelines for treating personalit y disorders also stress the importance of the
relationship between therapist and patient, who must collaborate on the goals and
methods of therapy (Critchfield & Benjamin, 2006). In fact, the relationship between
patient and therapist may often become a focus of treatment as the patient’s typical
style of interacting with others plays out in the therapy relationship. This relationship
often provides an opportunity for the patient to become aware of his or her interac-
tion style and to develop new ways to interact with others (Beck et al., 2004).
In addition, family education, family therapy, or couples therapy can provide a
forum for family members to learn about the patient’s personality disorder and to
receive practical advice about how to help the patient—for example, how to respond
when the patient gets agitated or upset. Family therapy can provide support for fami-
lies as they strive to change their responses to the patient’s behavior, thereby chang-
ing the reinforcement contingencies (Ruiz-Sancho et al., 2001).
Moreover, interpersonal or group therapy can highlight and address the mal-
adaptive ways in which patients relate to others. Therapy groups also provide a forum
for patients to try out new ways of interacting (Piper & Ogrodniczuk, 2005). For
example, if a man thinks and acts as if he is better than others, the comments and
responses of other group members can help him understand how his haughty and
condescending way of interacting creates problems for him.
Thinking Like A Clinician
V.J. was 50 years old, never married, and had never been very successful professionally. He
was a salesman and changed companies every few years, either because he was passed over
for a promotion and quit or because he didn’t like the new rules—or the way that the rules
were enforced—at the job. He’d been in love a few times, but it had never worked out. He
chalked it up to difficulty finding the right woman. He had some “friends” who were really
people he’d known over the years and saw occasionally. Most of his positive social interac-
tions happened in chat rooms or texts.
Is there anything about the information presented that would lead you to wonder whether
V.J. might have a personality disorder? If so, what was the information? (And if not, why not?)
Based on what you have read, how should mental health clinicians go about determining whether
V.J. might have a personality disorder or whether his personality traits are in the normal range?
Odd/Eccentric Personality
Disorders
Cluster A personality disorders involve odd or eccentric behaviors and ways of
thinking. Patients who have a Cluster A personality disorder are also likely to de-
velop another psychological disorder that involves psychosis, such as schizophrenia
or delusional disorder (Oldham et al., 1995; see Chapter 12). The three personality
410 C H A P T E R 1 3
disorders in this cluster—paranoid, schizoid, and schizotypal personality disorders—
are on the less severe end of the spectrum of schizophrenia-related disorders; of these
three, only schizotypal personality disorder is considered to be on the schizophrenia
spectrum in DSM-5. We’ll examine each of the three Cluster A personality disorders in
turn and then discuss what is known about the factors that give rise to them and about
how to treat them. Rachel Reiland did not exhibit symptoms
characteristic of this group of personality disorders.
Paranoid Personality Disorder
The essential feature of paranoid personality disorder is
persistent and pervasive mistrust and suspiciousness, accom-
panied by a bias to interpret other people’s motives as hostile
(see Table 13.3). Someone with this personality disorder may
distrust coworkers and family members and may even (incor-
rectly) believe that his or her partner is having an affair, de-
spite the partner’s denials. The patient’s accusations create a
difficult situation for the partner who is not having an affair
but can’t “prove” it to the patient’s satisfaction.
People with paranoid personality disorder are better
able to evaluate whether their suspicions are based on real-
ity than are people with paranoid schizophrenia. Moreover,
the sources of their perceived threats are not likely to be
strangers or bizarre types of signals (such as radio waves), as
is the case with paranoid schizophrenia, but rather known
individuals (Skodol, 2005). If the symptoms arise while a
person is using substances or during a psychotic episode of
schizophrenia or a mood disorder, then paranoid personality
disorder is not diagnosed. As you’ll see in Case 13.2, about
Ms. X., it may not be immediately apparent from a patient’s
report what is “true” and what is a paranoid belief.
CASE 13.2 • FROM TH E OUTSIDE: Paranoid Personality Disorder
Ms. X. is a middle-aged African-American woman who has lived in the area all of her life. She
began seeking treatment . . . after her family members had noted that, to them, she was acting
strangely. Ms. X. stated that she believed that her family members were out to make her crazy
and convince her neighbors of the same. She stated the reason for this was because she was
the “darkest one” in her family. Ms. X. was a fair-skinned black woman. She was born to a dark-
skinned black mother and a white father. She was the darkest sibling of her family. Because of
this, she felt that her family had treated her and her mother unjustly. She stated that as a child,
she was instructed to look after her lighter-skinned older sisters, whom the family held in high
regard. She stated that she did not complete high school because she had to care for her older
sister’s children. She described that she would be instructed to “cook and clean” for them, as
though she were their slave, and be available to them whenever they needed her. . . . Because of
this, [she claimed] she was not able to have a social life. After Ms. X. married, she continued to
receive the same treatment from her sisters. She stated that her children were treated unfairly,
because of their darker skin as well. . . . As she got older, Ms. X. stated that her sisters, who were
part of the elite society, would “embarrass” her while around their socialite friends. She believed
this to be due to her darker skin color. She stated that her sisters convinced her neighbors that
she was a “bad” person, and because of this, her neighbors would do “evil” things to spite her.
Ms. X. met with her sisters to discuss this issue. When confronted, the sisters denied that
they were treating her negatively. They acknowledged that their skin was fairer than hers
but denied that they were treating her in such a way. They believed that their sister was
“delusional.” Ms. X. refused to believe her sisters, and when confronted with the idea that her
family was not in any way harming her, she would shift the conversation to another topic.
(Paniagua, 2001, pp. 135–136)
Paranoid personality disorder
A personality disorder characterized by
persistent and pervasive mistrust and
suspiciousness, accompanied by a bias to
interpret other people’s motives as hostile.
TABLE 13.3 • DSM-5 Diagnostic Criteria for Paranoid
Personality Disorder
A. A pervasive distrust and suspiciousness of others such that their
motives are interpreted as malevolent, beginning by early adulthood
and present in a variety of contexts, as indicated by four (or more) of
the following:
1. Suspects, without sufficient basis, that others are exploiting, harming,
or deceiving him or her.
2. Is preoccupied with unjustified doubts about the loyalty or
trustworthiness of friends or associates.
3. Is reluctant to confide in others because of unwarranted fear that the
information will be used maliciously against him or her.
4. Reads hidden demeaning or threatening meanings into benign
remarks or events.
5. Persistently bears grudges (i.e., is unforgiving of insults, injuries, or slights).
6. Perceives attacks on his or her character or reputation that are not
apparent to others and is quick to react angrily or to counterattack.
7. Has recurrent suspicions, without justification, regarding fidelity of
spouse or sexual partner.
B. Does not occur exclusively during the course of schizophrenia, a bipolar
disorder or depressive disorder with psychotic features, or another
psychotic disorder and is not attributable to the physiological effects of
another medical condition.
Reprinted with permission from the Diagnostic and Statistical Manual of Mental Disorders, Fifth
Edition, (Copyright ©2013). American Psychiatric Association. All Rights Reserved.
Personality Disorders 411
As was the case with Ms. X.’s refusal to believe her
sisters, people with paranoid personality disorder cannot
readily be persuaded that their paranoid beliefs do not re-
flect reality. However, such people can recognize that there
are multiple ways to interpret other people’s reactions and
behaviors.
Although less obvious in the case of Ms. X., other com-
mon characteristics of people with this personality disorder
include a strong desire to be self-sufficient and in control,
which stems from a distrust of others, and a tendency to be
critical of others and blame them for problems that arise.
People with this disorder may also be unable to accept criti-
cism from others. In response to stress, they may become
briefly psychotic, with their paranoid beliefs reaching delu-
sional proportions.
In addition, people with paranoid personality disorder
tend to be difficult to get along with because their suspiciousness frequently leads
them to be secretive or “cold,” argumentative, complaining, or to bear a grudge.
These behaviors often elicit hostility or anger in others, which then confirms the
person’s suspicious beliefs. Table 13.4 provides additional information about paranoid
personality disorder.
To summarize, paranoid personality disorder involves a chronic pattern of
suspiciousness and mistrust that often creates interpersonal problems because of the
guarded ways in which the patient interacts with others. Little is known about the
specific factors that give rise to this personality disorder.
For most people, this kitchen scene would be
an unpleasant but infrequent conflict between
parent and child. But for people with paranoid
personality disorder, such conflict may not be
occasional. People with paranoid personality
disorder distrust others and tend to interpret
other people’s remarks or behaviors as having
malevolent intent. They are likely to maintain
these interpretations despite evidence to the
contrary.
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s
TABLE 13.4 • Paranoid Personality Disorder Facts at a Glance
Prevalence
• Between 2.3% and 4.5% of the general population is estimated to have paranoid personality
disorder.
Comorbidity
• People with paranoid personality disorder may also have another personality disorder, usu-
ally another Cluster A (odd/eccentric) personality disorder (schizoid or schizotypal) or narcis-
sistic, avoidant, or borderline personality disorder.
Onset
• Symptoms can first appear in childhood or adolescence, when the person appears hyper-
sensitive, has difficulties with peers, and has odd thoughts or fantasies or uses language
unconventionally.
Course
• The symptoms of paranoid personality disorder are relatively stable over time (Seivewright
et al., 2002).
Gender Differences
• Based on surveys in the general population, there is no clear gender difference in the preva-
lence of paranoid personality disorder. However, among people with this disorder, men are
more likely than women to come to the attention of mental health professionals (Morey,
Alexander, & Boggs, 2005).
Source: Unless otherwise noted, the source is American Psychiatric Association, 2000, 2013.
412 C H A P T E R 1 3
Schizoid Personality Disorder
Schizoid personality disorder is characterized by a
restricted range of emotions in social interactions and
few—if any—close relationships (American Psychiatric
Association, 2013). Table 13.5 lists the DSM-5 diag-
nostic criteria. People with schizoid personality disor-
der often lack social skills and may not pick up on or
understand the normal social cues required for smooth
social interactions—for instance, they may return some-
one’s smile with a stare. Such difficulties with social cues
can lead to problems in jobs that require interacting with
others; people with this personality disorder generally
are not interested in developing personal relationships.
In addition, people with schizoid personality dis-
order may react passively to adverse events. They may
seem to lack initiative and drift through life. People
with this disorder appear to be emotionless and often
don’t express anger, even when provoked. And, in fact,
they often report that they rarely experience strong
emotions such as joy and anger ( Livesley, 2001). In
contrast to those with paranoid personality disorder, people with schizoid personality
disorder generally aren’t suspicious and are indifferent to other people (Skodol, 2005).
Case 13.3 on the next page describes one woman with schizoid personality disorder,
and Table 13.6 presents some additional facts about schizoid personality disorder.
In sum, schizoid personality disorder involves a chronic pattern of limited emo-
tional expression and diminished social understanding, few relationships, and little
desire for relationships.
TABLE 13.6 • Schizoid Personality Disorder Facts at a Glance
Prevalence
• Approximately 3% of the general population is estimated to have schizoid personality
disorder (Grant, Hasin, et al., 2004).
Comorbidity
• Common comorbid personality disorders are the other Cluster A (odd/eccentric) personality
disorders and avoidant personality disorder. Half of the people diagnosed with schizoid
personality disorder will also be diagnosed with schizotypal personality disorder (McGlashan
et al., 2000).
Onset
• Those who develop schizoid personality disorder were often socially isolated underachievers
who were teased by their classmates as children and adolescents.
Course
• Schizoid personality disorder is relatively stable over time (Seivewright et al., 2002).
Gender Differences
• This personality disorder tends to be diagnosed more often in men than in women.
• Men with this personality disorder are often more impaired than their female counterparts.
Source: Unless otherwise noted, the source is American Psychiatric Association, 2013.
Schizoid personality disorder
A personality disorder characterized by
a restricted range of emotions in social
interactions and few—if any—close
relationships.
TABLE 13.5 • DSM-5 Diagnostic Criteria for Schizoid Personality
Disorder
A. A pervasive pattern of detachment from social relationships and a restricted
range of expression of emotions in interpersonal settings, beginning by early
adulthood and present in a variety of contexts, as indicated by four (or more)
of the following:
1. Neither desires nor enjoys close relationships, including being part of a family.
2. Almost always chooses solitary activities.
3. Has little, if any, interest in having sexual experiences with another person.
4. Takes pleasure in few, if any, activities.
5. Lacks close friends or confidants other than first-degree relatives.
6. Appears indifferent to the praise or criticism of others.
7. Shows emotional coldness, detachment, or flattened affectivity.
B. Does not occur exclusively during the course of schizophrenia, a bipolar disorder
or depressive disorder with psychotic features, or another psychotic disorder
and is not attributable to the physiological effects of another medical condition.
Reprinted with permission from the Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition,
(Copyright ©2013). American Psychiatric Association. All Rights Reserved.
Personality Disorders 413
CASE 13.3 • FROM TH E OUTSIDE: Schizoid Personality Disorder
A 33-year-old woman with three children became a cause of concern to social services be-
cause of her limited caring abilities. Investigations led to two of her children being taken
into [foster] care and, after a further period of 2 years, her third child was also taken away.
At this time she was referred to psychiatric services because she was felt to be isolated
from society and had such poor social function. It proved very difficult to engage her as
she would go to great lengths to avoid contact and it was uncertain to what extent she re-
quired compulsory treatment. Eventually, she was admitted under a compulsory order after
threatening a community worker. . . . After discharge from [the] hospital she was transferred
to supportive housing but resented the frequent monitoring of her progress, which she per-
ceived as intrusion and tried to avoid contact. . . . She functioned better with no contact and
so a transfer was agreed to a supported [apartment] where she would be left undisturbed
apart from one visit each week from a support worker and a full review every 6 months. Af-
ter 2 years she remains well on no treatment and is very happy with her life, which despite
little interaction with other people now includes regular contact with her family.
(Tyrer, 2002, p. 470)
Schizotypal Personality Disorder
People with schizotypal personality disorder have eccentric thoughts, percep-
tions, and behaviors, in addition to having very few close relationships, like those
with schizoid personality disorder (American Psychiatric Association, 2013).
What Is Schizotypal Personality Disorder?
According to the DSM-5 diagnostic criteria, schizotypal personality disorder has
nine symptoms (see Table 13.7). These symptoms can be organized into three dis-
tinct groups (Calkins et al., 2004; Raine, 2006; Reynolds et al., 2000) although
DSM-5 does not do so:
• Cognitive-perceptual
(Criterion A1) ideas of reference, in which the person interprets ordinary events to
have particular meaning for him or her (a milder form of referential delusions,
described in Chapter 12);
(A2) odd beliefs or magical thinking, in which the person believes that he or she
has control over external events, as occurs with superstitious beliefs;
(A3) unusual perceptual experiences, such as feeling “dislocated” from parts of
one’s body or hearing a voice on the radio murmuring one’s name;
(A5) suspiciousness or paranoid ideation, which consists of paranoid beliefs that
are less entrenched than paranoid delusions.
• Interpersonal
(A6) inappropriate or constricted affect, such as showing only a narrow range of
emotions;
(A8) lack of close friends because of a preference for being alone;
(A9) excessive social anxiety that arises because of a general suspiciousness about
other people.
• Disorganized
(A4) odd thinking and speech, such as being overly vague or elaborate or using
words idiosyncratically (as in “My coworker isn’t talkable”);
(A7) behavior or appearance that is odd or eccentric, such as wearing mismatched
or unkempt clothing, avoiding eye contact, or being unable to make conversation.
IK, in Case 13.4, had symptoms that represent all three groups highlighted in
Table 13.7. This personality disorder is on the schizophrenia spectrum (see Chapter 12).
Additional facts about schizotypal personality disorder are listed in Table 13.8.
Schizotypal personality disorder
A personality disorder characterized by
eccentric thoughts, perceptions, and
behaviors, in addition to having very few close
relationships.
TABLE 13.7 • DSM-5 Diagnostic
Criteria for Schizotypal Personality
Disorder
A. A pervasive pattern of social and
interpersonal deficits marked by acute
discomfort with, and reduced capacity
for, close relationships as well as by
cognitive or perceptual distortions and
eccentricities of behavior, beginning by
early adulthood and present in a variety
of contexts, as indicated by five (or
more) of the following:
1. Ideas of reference (excluding delusions
of reference).
2. Odd beliefs or magical thinking
that influences behavior and is
inconsistent with subcultural norms
(e.g., superstitiousness, belief in
clairvoyance, telepathy, or “sixth
sense”; in children and adolescents,
bizarre fantasies or preoccupations).
3. Unusual perceptual experiences,
including bodily illusions.
4. Odd thinking and speech (e.g.,
vague, circumstantial, metaphorical,
overelaborate, or stereotyped).
5. Suspiciousness or paranoid ideation.
6. Inappropriate or constricted affect.
7. Behavior or appearance that is odd,
eccentric, or peculiar.
8. Lack of close friends or confidants
other than first degree relatives.
9. Excessive social anxiety that does not
diminish with familiarity and tends
to be associated with paranoid fears
rather than negative judgments about
self.
B. Does not occur exclusively during
the course of schizophrenia, a bipolar
disorder or depressive disorder with
psychotic features, another psychotic
disorder, or autism spectrum disorder.
Note: Cognitive-perceptual symptoms are in
green, interpersonal symptoms are in blue, and
disorganized symptoms are in red.
Reprinted with permission from the Diagnostic and
Statistical Manual of Mental Disorders, Fifth Edition,
(Copyright ©2013). American Psychiatric Association. All
Rights Reserved.
414 C H A P T E R 1 3
Schizotypal personality disorder differs from schizoid personality disorder in that
the former includes cognitive- perceptual symptoms—such as IK’s ideas of reference
and seeing things with peripheral vision that could not be seen with a direct gaze—
and odd behavior. Nevertheless, research suggests that these two disorders may not
be distinct from each other; half of those with schizoid personality disorder are also
diagnosed with schizotypal personality disorder (McGlashan et al., 2000). Some
researchers propose that schizoid personality disorder may simply be a subtype of
schizotypal personality disorder (Raine, 2006).
Understanding Schizotypal Personality Disorder
We focus on understanding schizotypal personality disorder, the most researched of
the Cluster A personality disorders. As noted in Chapter 12, schizotypal personality
disorder includes less intense manifestation of features of schizophrenia: delusions
and unusual perceptions.
TABLE 13.8 • Schizotypal Personality Disorder Facts at a Glance
Prevalence
• Approximately 0.6–4.6% of the general population has schizotypal personality disorder.
Comorbidity
• Common comorbid personality disorders include other Cluster A personality disorders (McGlashan et al., 2000), as well as borderline, avoidant,
and obsessive-compulsive personality disorders (Raine, 2006).
• Common comorbid psychological disorders are major depressive disorder, social phobia, and panic disorder (Raine, 2006).
Onset
• Symptoms emerge by early adulthood.
• In childhood and adolescence, symptoms may include social isolation and social anxiety, academic underachievement, hypersensitivity, odd
fantasies and thoughts, and idiosyncratic use of language.
Course
• Although schizotypal personality disorder most commonly is stable over time, symptoms may improve for some people (Fossati et al., 2003). In
fact, for almost one quarter of patients, symptoms improve to the point where they no longer meet all the diagnostic criteria (Grilo et al., 2004).
• Among other patients with this disorder, the opposite is true: A small percentage go on to develop schizophrenia or another psychotic disorder
(Grilo et al., 2004).
Gender Differences
• Schizotypal personality disorder is slightly more common among men than women.
Source: Unless otherwise noted, the source is American Psychiatric Association, 2013.
CASE 13.4 • FROM TH E OUTSIDE: Schizotypal Personality Disorder
IK is a 33-year-old man who had both schizotypal personality disorder and obsessive-
compulsive disorder (OCD) for at least 17 years. His schizotypal symptoms included poor
interpersonal relatedness, ideas of reference (not delusional), social anxiety, unusual per-
ceptual experiences (such as seeing things in the periphery, but not there when viewed di-
rectly), constricted affect, and some paranoid ideation (in particular with regard to police
officers, but his father reported that this was unrealistic).
IK’s social skills deficits were primarily conversation skills, inappropriate affect, poor
assertion skills, and lack of eye contact with the therapist and family members. He was
also prone to aggressive outbursts in the home, often breaking objects due to frustration.
(McKay & Neziroglu, 1996, pp. 190–191)
Personality Disorders 415
Neurological Factors in Schizotypal Personality Disorder
Most of the neurological factors that contribute to schizophrenia have also been found to
contribute to schizotypal personality disorder: genes and prenatal environment, such as
maternal illness and malnourishment, and birth complications (Raine, 2006; Torgersen
et al., 2000). In both disorders, researchers have documented similar abnormalities in
brain structure and in neural function (activity of dopamine, serotonin, and glutamate).
These abnormalities are generally not as severe in people with schizotypal personality
disorder as in people with schizophrenia (Buchsbaum et al., 2002; Siever & Davis, 2004).
Genes also play a role: The rates of schizotypal personality disorder are higher
among family members of people with schizophrenia than among the general popu-
lation (Siever & Davis, 2004; Tienari et al., 2003).
Psychological Factors in Schizotypal Personality Disorder
Like people with schizophrenia, those with schizotypal personality disorder tend to
have specific cognitive deficits. These include problems with attention (distinguishing
relevant from irrelevant stimuli), memory, and executive function (used in problem
solving, planning, and judgment) (Voglmaier et al., 2000). According to Beck and col-
leagues (2004), schizotypal personality disorder is unusual among the personality dis-
orders in that the primary distortions are in mental processes (e.g., perceptions) rather
than in mental contents. However, problems with social interactions can arise from
the cognitive deficits: People with this personality disorder tend to have an impaired
theory of mind—and thus have difficulty recognizing emotions in others (Waldeck &
Miller, 2000) and in taking another’s point of view or recognizing another’s mental
state (Langdon & Coltheart, 2001; Miller & Lenzenweger, 2012). Although people
with schizotypal personality disorder have cognitive deficits, they generally have bet-
ter cognitive skills than do people with schizophrenia (Trestman et al., 1995).
People with this personality disorder also often behave in unusual ways, which
can make other people more likely to mistreat them, intentionally or not. Such mis-
treatment may thus confirm their beliefs about themselves and other people. People
with this disorder also pay attention to, remember, and interpret stimuli in ways that
are consistent with their beliefs—and that thus reinforce their isolation from, and
avoidance of, other people.
Social Factors in Schizotypal Personality Disorder
Certain social factors appear to play a relatively large role in the onset of schizo-
typal personality disorder, in contrast to their lesser role in schizophrenia. These
social factors include physical abuse or neglect, insecure attachment to parents, and
discrimination (Berenbaum et al., 2008; Raine, 2006; Wilson & Constanzo, 1996)—
all stressful events. In fact, some of these social factors may be related to each other:
Insecure attachment may, at least in part, result from abuse or neglect. Children who
develop schizotypal personality disorder are more likely to have experienced trauma,
abuse, and neglect than are those who develop most other personality disorders (Yen
et al., 2002). These negative childhood experiences influence patients’ views of other
people as untrustworthy and having malevolent motives.
Feedback Loops in Understanding Schizotypal Personality Disorder
With schizotypal personality disorder, as with schizophrenia, neuropsychosocial fac-
tors create feedback loops. For instance, early social stressors such as neglect and trauma
can contribute to brain abnormalities, particularly if a genetic or other neurological
vulnerability exists before birth. The neurological changes, in turn, contribute to
disturbances in cognitive and emotional functioning (Raine, 2006). These cognitive
and emotional disturbances then can lead to problems in social interactions, which in
turn produces stress (Skodol, Gunderson et al., 2002)—and the stress can then affect
neurological functioning. Moreover, trauma, neglect, and insecure attachment may
give rise to a paranoid attributional style and discomfort with others (Raine, 2006).
SP
N
Neurological factors that are associated with
schizophrenia are associated with schizotypal
personality disorders, such as maternal illness
or malnourishment during pregnancy.
A
J
P
h
o
to
/B
S
IP
/S
u
p
e
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to
ck
O N L I N E
416 C H A P T E R 1 3
Treating Odd/Eccentric Personality Disorders
Very little research has been conducted to evaluate treatments for odd/eccentric
personality disorders. People with any of these sorts of personality disorders tend
not to be interested in treatment and, if urged or coerced into it, are often reluctant
participants at best. Treatment may create significant anxiety for the patient. Thus,
the particular challenge of treating people with odd/eccentric personality disorders
is their tendency not to collaborate with the therapist to develop goals for treatment
(Beck et al., 2004; Farmer & Nelson-Gray, 2005).
Nevertheless, when such patients do participate in CBT, they can develop more
adaptive strategies, such as improved social skills (which makes them less likely to
be conspicuous and in turn leads them to feel safer with others). CBT may also
employ relaxation techniques, exposure to avoided social situations, and cognitive
restructuring of distorted views of self and others, and of dysfunctional beliefs (Beck
et al., 2004; Farmer & Nelson-Gray, 2005).
Most of the medications that effectively treat symptoms of schizophrenia can
also treat symptoms of schizotypal personality disorder, although the medications are
often taken at lower doses (Koenigsberg et al., 2003; Raine, 2006; see Chapter 12).
Thinking Like A Clinician
Shawna has few friends; most of the time she’s quiet and shy, avoiding eye contact. Occasion-
ally, she mentions that her troubles—work, social, and financial—are because of the radia-
tion coming out of the computer. She says it with a straight face, but it’s hard to tell whether
she’s joking. When asked whether she’s being serious, she reluctantly says that she’s not, but
it’s not clear whether she’s being honest. If you were asked to determine whether she has a
personality disorder, what kinds of questions would you ask? Based on what you have read,
what types of answers would distinguish quirky behavior from the truly odd behavior that
characterizes a Cluster A personality disorder? If you determined that her behavior was odd
enough to merit a diagnosis of a Cluster A (odd/eccentric) personality disorder, what would
you look for in order to decide which of those disorders might be the best diagnosis?
Dramatic/Erratic Personality
Disorders
In her memoir, Rachel Reiland recalls an occasion when a minor matter set off an
escalating fight between her and her husband. She raged at him until she realized that
she might drive him away. So she decided to leave him before he had a chance to
leave her. She ran out of the house barefoot and then ran for miles through the city.
After several hours, her husband and children—who had been searching for her—
pulled up their car beside her and brought her home (Reiland, 2004).
Reiland’s response to this fight with her husband exemplifies the typical re-
actions of people with Cluster B personality disorders: impulsive, dramatic, and
erratic behaviors. These disorders arise because of difficulty regulating emotions.
This commonality can sometimes make it difficult to determine which specific
Cluster B personality disorder a given patient has; many of the symptoms specified
in the diagnostic criteria are not unique to a single personality disorder in the clus-
ter (Blais et al., 1999; Zanarini & Gunderson, 1997). People with a dramatic/erratic
personality disorder also tend to have certain additional psychological disorders:
substance-related disorders, mood disorders, anxiety disorders, or eating disorders
(Dolan-Sewell et al., 2001; McGlashan et al., 2000; Skodol et al., 1999; Zanarini et
al., 1998).
Personality Disorders 417
Antisocial Personality Disorder
One day, Reiland was particularly angry, and she put the following note on the front
door: “You need to pick up the kids. I’m upstairs in the attic. Don’t even think of going up
there if you know what’s good for you!” Another note was on the attic door, which was
locked: “I might die anyway, but if you dare come in here, you might all be dead! You don’t
know what I have up here!” (Reiland, 2004, p. 148).
Some might say that Reiland’s behavior—and her apparent lack of concern for
how her husband and children might respond to the notes—had elements of antisocial
personality disorder, which involves a persistent disregard for the rights of others.
As noted in Table 13.9, people with antisocial personality disorder may violate rules
or laws (for example, by stealing) and may lie or act aggressively, hurting others, be-
lieving that they are entitled to break the rules (American Psychiatric Association,
2013). They may also act impulsively, putting themselves or others at risk of harm.
In addition to these behaviors, people with antisocial personality disorder shirk their
responsibilities—they don’t pay their bills or show up for work on time, for instance.
They may also exhibit a fundamental lack of regret for or guilt about their antiso-
cial behaviors, seeming to lack a conscience, a moral sense, or a sense of empathy. In
Reiland’s case, though, holing up in the attic and writing the threatening notes proba-
bly resulted from uncontrollable emotions rather than from a disregard for others.
The diagnostic criteria for antisocial personality disorder are the most behavior-
ally specific of the criteria for personality disorders and even include overt criminal
behaviors (Skodol, 2005). Because of this specificity, antisocial personality disorder is
the most reliably diagnosed personality disorder (Skodol, 2005).
Like other personality disorders, antisocial personality disorder manifests itself
in childhood or adolescence, but DSM-5 is again very specific about antisocial per-
sonality disorder: The symptoms must have arisen by age 15, although the diag-
nosis cannot be made until the person is at least 18 years old; this was true of John
in Case 13.5. The diagnosis for people who exhibit a similar pattern of symptoms
but are younger than 18 is conduct disorder, which is characterized by consis-
tently violating the rights of others (through lying, threatening, and destructive and
aggressive behaviors) or violating societal norms and typically diagnosed in children
and adolescents. (In Chapter 14 we discuss conduct disorder in detail.) Table 13.10
provides additional facts about antisocial personality disorder.
CASE 13.5 • FROM TH E OUTSIDE: Antisocial Personality Disorder
John and his sister were adopted by the same family when they were respectively 1.5 and
3 years of age. From the very beginning, John was severely physically abused by his adop-
tive father as a result of just minor misbehaviors. Furthermore, John felt that he and his sis-
ter were neglected (lack of warmth and attention) by his adoptive parents and that he and
his sister were thought of much less highly by them than their only biological son. From age
10 John and his sister were sexually abused on a regular basis by his adoptive father, and
John was forced to watch when his father raped his sister. He demonstrated more and more
oppositional and angry behavior, and he became a notorious thief. John left junior sec-
ondary technical school prematurely and had many short-term jobs, but he was dismissed
every time because of lack of motivation, disobedience, and/or theft. As a consequence of
his deviant behavior, John was placed in a juvenile correctional and observation institute
when he was 16 years of age. A psychiatric report from this episode described him as a so-
cially, emotionally, morally, and sexually underdeveloped person who was very suspicious
and angry. He projected his discomfort on the outside world. After his release from the
juvenile correctional institute (when he was 18 years of age), John was arrested because of
violent pedophilic rape, theft, and fraud. John was sentenced to forensic psychiatric treat-
ment. But soon after his release, when he was 24, John was sentenced to life imprisonment
because he committed an excessively violent sexual homicide on a 9-year-old boy.
(Martens, 2005, pp. 117–118)
Antisocial personality disorder
A personality disorder diagnosed in adulthood
characterized by a persistent disregard for the
rights of others.
Conduct disorder
A psychological disorder that typically arises
in childhood and is characterized by the
violation of the basic rights of others or of
societal norms that are appropriate to the
person’s age.
TABLE 13.9 • DSM-5 Diagnostic
Criteria for Antisocial Personality
Disorder
A. A pervasive pattern of disregard for
and violation of the rights of others,
occurring since age 15 years, as indicated
by three (or more) of the following:
1. Failure to conform to social norms
with respect to lawful behaviors, as
indicated by repeatedly performing
acts that are grounds for arrest.
2. Deceitfulness, as indicated by repeated
lying, use of aliases, or conning others
for personal profit or pleasure.
3. Impulsivity or failure to plan ahead.
4. Irritability and aggressiveness, as indi-
cated by repeated physical fights or
assaults.
5. Reckless disregard for safety of self or
others.
6. Consistent irresponsibility, as indi-
cated by repeated failure to sustain
consistent work behavior or honor
financial obligations.
7. Lack of remorse, as indicated by being
indifferent to or rationalizing having
hurt, mistreated, or stolen from
another.
B. The individual is at least age 18 years.
C. There is evidence of conduct disorder
with onset before age 15 years.
D. The occurrence of antisocial behavior
is not exclusively during the course of
schizophrenia or bipolar disorder.
Reprinted with permission from the Diagnostic and
Statistical Manual of Mental Disorders, Fifth Edition,
(Copyright ©2013). American Psychiatric Association. All
Rights Reserved.
418 C H A P T E R 1 3
The term psychopath (or sociopath, which was used in the first DSM) has often
been used to refer to someone with symptoms of antisocial personality disorder.
However, psychopathy emphasizes specific emotional and interpersonal character-
istics, such as a lack of empathy, an unmerited feeling of high self-worth, and a refusal
to accept responsibility for one’s actions—as well as antisocial behaviors. The classi-
fication of psychopathy is narrower (i.e., more restrictive, because there are more cri-
teria) than the diagnosis of antisocial personality disorder. In contrast, the diagnosis
of antisocial personality disorder tends to focus more on behaviors—mostly criminal
ones, such as stealing or breaking other laws—than on the personality traits that
may underlie the behaviors. Only a minority of prisoners (15% of male prisoners,
7.5% of female prisoners) meet the specific criteria for psychopathy, but a majority
of prisoners (50–80%) meet the broad behavioral criteria for antisocial personality
disorder (Hare, 2003).
Psychopathy is generally considered to be a more universal concept than anti-
social personality disorder; most cultures recognize a similar cluster of psychopathic
characteristics (Cooke, 1998; Gacono et al., 2001).
Understanding Antisocial Personality Disorder and Psychopathy
The concept of psychopathy has been employed longer than the diagnosis of antisocial
personality disorder. Hence, more research has addressed psychopathy and criminal-
ity than antisocial personality disorder—and the relative lack of research on antisocial
personality disorder makes it difficult to identify the factors that contribute to the
disorder (Ogloff, 2006). Moreover, most research that does examine factors that con-
Antisocial personality disorder is characterized
by an emphasis on criminal behaviors, whereas
psychopathy is more narrowly defined by
personality traits that underlie the behaviors.
B
e
li
n
d
a
Im
ag
e
s/
S
u
p
e
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to
ck
Psychopathy
A set of emotional and interpersonal
characteristics marked by a lack of empathy,
an unmerited feeling of high self-worth, and a
refusal to accept responsibility for one’s actions.
TABLE 13.10 • Antisocial Personality Disorder Facts at a Glance
Prevalence
• Between 1% and 4% of Americans are diagnosed with antisocial personality disorder (Grant,
Hasin, et al., 2004).
• Approximately 60% of male prisoners in a number of countries have antisocial personality
disorder (Moran, 1999).
Comorbidity
• The most common comorbid psychological disorders are anxiety disorders, mood disorders,
substance use disorders, and somatization disorders (Compton, Conway, et al., 2005; Sareen
et al., 2004).
• In a clinical setting, most patients who meet the criteria for antisocial personality disorder
also are diagnosed with at least one other personality disorder, typically another dramatic/
erratic personality disorder (Widiger & Corbitt, 1997).
Onset
• As required by the DSM-5 criteria, symptoms of conduct disorder emerge before age 15, and
specific symptoms of antisocial behavior occur since age 15. The specific antisocial behaviors
then continue into adulthood.
Course
• Antisocial personality disorder has a chronic course, but symptoms may improve as patients
age, particularly in their 40s (Seivewright et al., 2002).
Gender Differences
• Antisocial personality disorder is diagnosed more often in men than in women.
Source: Unless otherwise noted, citations are to American Psychiatric Association, 2013.
Personality Disorders 419
tribute to antisocial personality disorder has studied participants who are or have been
in prisons or jails or who have comorbid substance abuse problems; hence, numerous
confounds prevent us from conclusively identifying the factors that contribute solely
to antisocial personality disorder. Therefore, the following sections examine neuro-
logical, psychological, and social factors—and the feedback loops among them—that
contribute to antisocial personality disorder and/or psychopathy, keeping in mind the
limitations of existing research.
Neurological Factors in Antisocial Personality Disorder and Psychopathy
People with antisocial personality disorder or psychopathy (and the groups have not
been rigorously separated in most of this research) may have abnormal brain structures
as well as abnormal brain function (Pridmore et al., 2005).
First, regarding brain structure, people with antisocial personality disorder or
psychopathy tend to have unusually small frontal lobes (Raine et al, 2000). The
smaller frontal lobes might suggest problems in inhibiting and planning behavior.
Second, regarding brain function, the frontal and temporal lobes of these patients
tend to show less activation than normal during many tasks (Schneider et al., 2000;
Smith, 2000; Völlum et al., 2004). Moreover, these patients exhibit deficits on tasks
that rely on the frontal lobes, such as those requiring planning or discovering that a
rule has been changed (Dolan & Park, 2002). Such deficits probably contribute to
their problems in inhibiting and planning behavior.
Antisocial personality disorder has been linked to genes that regulate dopa-
mine production (Prichard et al., 2007) and also to genes that regulate serotonin
(Lyons-Ruth et al., 2007). Genes that affect dopamine and serotonin may influence
temperament and have been linked to being highly motivated by the possibility
of reward (Gray, 1987), not being strongly motivated by the threat of punishment
(Cloninger et al., 1993; Gray, 1987; Lykken, 1995), and having low frustration
tolerance—which often leads to impulsive be-
havior and a tendency to take shortcuts.
However, effects of genes are modulated by
the environment. Adoption studies have found
that the environment in which a child is raised
influences the risk of criminal behavior or an-
tisocial personality disorder only if the child
is biologically vulnerable, as shown in Table
13.11. When a child’s biological parents were
not criminals, the child’s later criminal behav-
ior was unaffected by environmental influences,
such as the number of foster placements before
adoption or the adoptive parents’ criminality
(Caspi et al., 2002; Mednick et al., 1984).
Psychological Factors in Antisocial Personality Disorder and Psychopathy
Antisocial personality disorder and psychopathy appear to develop, in part, because
of problems with classical and operant conditioning processes. Whereas classical
conditioning and operant conditioning lead most people to learn to avoid encoun-
ters with a painful stimulus (such as a shock), criminals with psychopathic traits do
not learn to avoid painful stimuli. Thus, they cannot easily learn from punishing ex-
periences (Eysenck, 1957) and are likely to repeat behavior associated with negative
consequence, despite receiving punishment, such as a prison sentence (Zuckerman,
1999). And because they are highly motivated by rewarding activities, they are
less inclined to inhibit themselves to avoid punishment; they thus behave in ways
that are impulsive, have difficulty delaying gratification, and have poor judgment
(Silverstein, 2007).
TABLE 13.11 • Percentage of Children Who Later Committed Crimes: The
Role of Biology and Family Environment in Criminality
Biological parents’ criminality
Exposure to environmental forces
associated with criminality High Low
High 40.0% 6.7%
Low 12.1% 2.9%
Note: Environmental forces associated with criminality include variables such as the number of foster
placements before adoption and the adoptive father’s socioeconomic status.
Source: Brock et al., 1996. For more information see the Permissions section.
420 C H A P T E R 1 3
Social Factors in Antisocial Personality Disorder and Psychopathy
One risk factor for conduct disorder and subsequent antisocial personality disorder
is a child’s relationship with his or her parents or primary caretakers. Each parent
or other primary caretaker has a style of interacting with the child from infancy.
Some parents abuse or neglect their children or are inconsistent in disciplining them,
which can lead to an insecure attachment (Bowlby, 1969). These children have a
relatively high risk of developing conduct disorder and later antisocial personality
disorder (Levy & Orlans, 1999, 2000; Ogloff, 2006; Shi et al., 2012). Note, however,
that this finding is simply a correlation and does not necessarily mean that attach-
ment difficulties cause later antisocial behavior; it is possible that some other variable
both interferes with a child’s developing normal attachment and promotes antisocial
behaviors.
Other childhood factors associated with the later development of antiso-
cial personality disorder include poverty, family instability, and—in those who are
genetically vulnerable—adoptive parents’ criminality (Raine et al., 1996).
Feedback Loops in Understanding Antisocial Personality Disorder
and Psychopathy
Various factors create feedback loops that ultimately produce psychopathy or antisocial
personality disorder. Twin and adoption studies reveal that some people have a pre-
disposition toward criminality or associated temperaments (neurological factor), but
the environment in which children grow up (social factor) influences whether that
predisposition is likely to lead to criminal behavior. One study found that children
with conduct disorder who were punished for their offenses were less likely to develop
antisocial personality disorder later in life, confirming the contribution of operant
conditioning to the disorder (Black, 2001).
However, the types of temperaments that are associated with antisocial per-
sonality disorder and psychopathy can impede the types of classical and operant
conditioning processes that promote empathy and discourage antisocial behaviors
(psychological factor; Kagan & Reid, 1986; Martens, 2005; Pollock et al., 1990).
Moreover, the experience of abuse or neglect by parents (social factor) may contrib-
ute to a tendency toward underarousal (Schore, 2003), which in turn leads people to
seek out more arousing (and reckless) activities that may increase their risk of seeing
or experiencing violence ( Jang et al., 2001)—which they may find stimulating, and
which then may reinforce such behavior.
Treating Antisocial Personality Disorder and Psychopathy
Most research on treatment involves people who are diagnosed with psychopathy,
not antisocial personality disorder specifically. Some of the personality traits associ-
ated with psychopathy interfere with a therapeutic collaboration: problems in delay-
ing gratification, lack of empathy, and low frustration tolerance. Psychopathy has a
poor prognosis, and treatments developed thus far are not likely to alter behavior or
reduce symptoms (Gacono et al., 2001; Rice et al., 1992; Serin, 1991). People with
psychopathy who are in prison are likely to commit additional crimes after their
release (Ogloff et al., 1990; Seto & Barbaree, 1999). When a person with psychopa-
thy is violent, managing the patient may be more realistic and appropriate than treating
the patient’s personality problems (Ogloff, 2006).
Ultimately, a challenge in treating people with antisocial personality disorder
is their lack of motivation. Because they aren’t disturbed by their behavior, they are
rarely genuinely motivated to change, which makes any real collaboration between
therapist and patient unlikely; patients often will attend therapy only when re-
quired to do so. Treatment generally focuses on changing overt behaviors (Farmer &
Nelson-Gray, 2005).
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Personality Disorders 421
Borderline Personality Disorder
The term borderline personality originally was used by psychodynamic therapists to de-
scribe patients whose personality was on the border between neurosis and psychosis
(Kernberg, 1967). Now, however, it is generally used to describe the DSM-5 personal-
ity disorder that includes some features of that type of personality: borderline per-
sonality disorder is characterized by volatile emotions, an unstable self-image, and
impulsive behavior in relationships (American Psychiatric Association, 2013). The di-
agnostic criteria for borderline personality disorder are noted in Table 13.12. A key cri-
terion is emotional dysregulation (also known as affective instability), which leads the
person frequently to respond more emotionally than a situation warrants and to display
quickly changing emotions— lability (Glenn & Klonsky, 2009). Another prominent
criterion refers to a relationship pattern of idealizing the other person at the beginning
of the relationship, spending a lot of time with the person and revealing much, thus
creating an intense intimacy. But then positive feelings quickly switch to negative ones,
which leads the person with this disorder to devalue the other person. Rachel Reiland’s
pattern of thoughts, feelings, and behaviors meet the criteria for borderline personality
disorder. Reiland describes the switch in how she viewed other people:
I saw people as either good or evil. When they were “good,” I vaulted them to the top
of a pedestal. They could do no wrong, and I loved them with all of my being. When
they were “bad,” they became objects of scorn and revenge.
Borderline personality disorder
A personality disorder characterized by
volatile emotions, an unstable self-image, and
impulsive behavior in relationships.
C U R R E N T C O N T R O V E R S Y
Should Psychopaths Receive
Treatment?
Psychopathy has a distinctive pattern of interpersonal, behavioral,
and affective symptoms (Hare, 1997). According to Hare (1993,
p. 25), “psychopaths can be described as intraspecies predators
who use charm, manipulation, intimidation and violence to con-
trol others and to satisfy their own selfish needs.” Psychopathy
is a difficult disorder to treat, and individuals with psychopathy
rarely seek treatment unless it is for self-serving purposes such as
probation or parole (Hare, 1993). The question arises, then, as to
whether psychopaths should receive treatment at all.
Studies on the ef f icacy of treatment in psychopathy
have been mixed (Salekin et al., 2010), with some research
reporting higher recidivism rates in psychopaths who received
treatment (Rice et al., 1992). Others have suggested that psy-
chopaths who complete treatment may merely be perfecting
their interpersonal skills to manipulate others (Hare, 1997;
Hart, 1998). For example, Rice et al. (1992) measured the
effects of an intensive treatment program on violent psycho-
pathic and nonpsychopathic forensic patients. After a 10-year
follow-up, the violent recidivism rate was 55% for untreated
psychopaths, and 77% for treated psychopaths. Researchers
have also noted that no effective treatments are available to
treat psychopathy (O’Neill et al., 2003), regardless of the type
of setting (e.g., community), and psychopaths tend to drop out
of treatment programs early (Ogloff et al., 1990).
On the other hand, in a review of three studies designed
to reduce violence and offending behaviors in psychopathic
offenders, Wong et al. (2012) reported positive treatment out-
comes. Olver and Wong (2009) found that psychopathic sex
offenders who completed treatment were less likely to violently
reoffend. Other researchers (D’Silva et al., 2004; Salekin, 2002),
however, have pointed out several methodological flaws in many
of the studies measuring treatment response in psychopathy.
CRITICAL THINKING If you were to treat a psychopath, what
outcome measures could you assess to ensure that therapy was
indeed effective? In your opinion, how should forensic psy-
chologists treat psychopaths: as criminals or individuals with a
mental illness? Why?
(Richard Conti, Kean University)
Treatments for people w ith antisocia l persona l it y d isorder who are not
psychopathic have some success—at least in the short term. These treatments focus
on comorbid substance abuse and aggressive behavior (Henning & Frueh, 1996). The
most effective treatments provide clear rules about behavior—including clear and
consistent consequences for rule violations—and target behavior change and behav-
ioral control, as is addressed with CBT.
422 C H A P T E R 1 3
In relationships with those closest to me, the
“good” and “bad” assessments could alternate
wildly, sometimes from one hour to the next.
The unrealistic expectations of perfection that
came with the good-guy pedestal were destined
to be unfulfilled, which led to disappointment
and sense of betrayal.
(2004, p. 88)
The highly fluid and impulsive behaviors
that are part of borderline personality disorder
occur in part, because of the patient’s strong
responses to emotional stimuli, which may
stem from difficulty understanding emotions
(Peter et al., 2013). For example, if a patient
with borderline personality disorder has to
wait for someone who is late for an appoint-
ment, the patient often cannot understand and
regulate the ensuing powerful feelings of an-
ger, anxiety, or despair, which can last for days.
The person with this personality disorder is
extremely sensitive to any hint of being aban-
doned, which also can cause strong emotions
that are then difficult to bring under control.
When not in the throes of intense emotions, people with borderline personality
disorder may feel chronically empty, lonely, and isolated (Klonsky, 2008). When feel-
ing empty, they may harm themselves in some nonlethal way—such as superficial cut-
ting of skin—in order to feel “something”; such behavior has been called parasuicidal
rather than suicidal because the intention is not to commit suicide but rather to gain
relief from feeling emotionally numb. The parasuicidal behavior usually occurs when
the person is in a dissociated state, often after he or she has felt rejected or abandoned
(Livesley, 2001). More worrying to clinicians, family members, and friends is when
self-harming behavior is a suicide attempt. People with borderline personality disor-
der may have comorbid depression, which frequently contributes to increased suicidal
thoughts, plans, or attempts. When borderline personality disorder symptoms dimin-
ish—including a decrease in emotional sensitivity—depression is likely to improve
(Gunderson et al., 2004). Table 13.13 provides additional facts about borderline per-
sonality disorder. Donna, in Case 13.6, exhibits extreme emotional sensitivity.
CASE 13.6 • FROM TH E OUTSIDE: Borderline Personality Disorder
[A woman, Donna, exhibited] episodes of explosive anger and bitter tirades, along with weekly
(sometimes daily) expressions of bitterness and resentment. Frustrations and disappointments,
which are inevitable within any relationship and would only be annoying inconveniences to
most people, were perceived by Donna as outrageous mistreatments or exploitations. Even
when she recognized that they did not warrant a strong reaction, she still had tremendous
difficulty stifling her feelings of anger and resentment. Her tendency to misperceive innocent
remarks as being intentionally inconsiderate (at times even malevolent) further exacerbated
her propensity to anger. She acknowledged that she would often push, question, and test her
friends and lovers so hard for signs of disaffection, reassurances of affection, or admissions of
guilt, that they would become frustrated and exasperated and might eventually lash out against
her. She would often find herself embroiled in fruitless arguments that she subsequently regret-
ted. She had no long-standing relationships, but there were numerous people who remained
embittered toward her. Three marriages had, in fact, all ended in acrimonious divorce.
(Widiger et al., 2002, p. 443)
People with borderline personality disorder
may engage in parasuicidal behaviors, such
as cutting their arms, to help regulate their
emotions. These scars on a 50-year-old
woman are a result of such parasuicidal
behavior. Self-harming behavior may also
occur in an attempt to commit suicide.
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TABLE 13.12 • DSM-5 Diagnostic Criteria for Borderline Personality Disorder
A pervasive pattern of instability of interpersonal relationships, self-image, and affects,
and marked impulsivity, beginning by early adulthood and present in a variety of contexts,
as indicated by five (or more) of the following:
1. Frantic efforts to avoid real or imagined abandonment. (Note: Do not include suicidal or
self-mutilating behavior covered in Criterion 5.)
2. A pattern of unstable and intense interpersonal relationships characterized by
alternating between extremes of idealization and devaluation.
3. Identity disturbance: markedly and persistently unstable self-image or sense of self.
4. Impulsivity in at least two areas that are potentially self-damaging (e.g., spending,
sex, substance abuse, reckless driving, binge eating). (Note: Do not include suicidal or
self-mutilating behavior covered in Criterion 5.)
5. Recurrent suicidal behavior, gestures, or threats, or self-mutilating behavior.
6. Affective instability due to a marked reactivity of mood (e.g., intense episodic dysphoria,
irritability, or anxiety usually lasting a few hours and only rarely more than a few days).
7. Chronic feelings of emptiness.
8. Inappropriate, intense anger or difficulty controlling anger (e.g., frequent displays of
temper, constant anger, recurrent physical fights).
9. Transient, stress-related paranoid ideation or severe dissociative symptoms.
Reprinted with permission from the Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition, (Copyright
©2013). American Psychiatric Association. All Rights Reserved.
Personality Disorders 423
Understanding Borderline Personality Disorder
The neuropsychosocial approach allows us to appreciate the complexity of borderline
personality disorder. In fact, this approach underlies the most comprehensive analysis
that has been made of the disorder and its treatment (Linehan, 1993).
Neurological Factors: Born to Be Wild?
Considerable research has been reported on the neurological bases of borderline per-
sonality disorder.
Brain Systems The frontal lobes, hippocampus, and amygdala are unusually small in
people with borderline personality disorder (Driessen et al., 2000;Schmahl, Vermetten
et al., 2003; Tebartz van Elst et al., 2003). These structures are part of a network of brain
areas that functions abnormally in people with this disorder. The frontal lobes (which
are involved in regulating emotions and formulating plans) are less strongly activated
in these patients than is normal. Consistent with findings from neuroimaging stud-
ies, numerous studies have shown that people who have borderline personality disorder
have difficulty performing tasks that rely on the frontal lobes (LeGris & van Reekum,
2006); specifically, people with this disorder also have difficulty focusing attention,
organizing visual material, and making decisions (LeGris & van Reekum, 2006).
TABLE 13.13 • Borderline Personality Disorder Facts at a Glance
Prevalence
• Borderline personality disorder occurs in about 2% of the general population, 10% of outpa-
tients, and 20% of inpatients.
• Borderline personality disorder is the most common personality disorder: 30–60% of those
diagnosed with a personality disorder have borderline personality disorder (Adams et al.,
2001; Widiger & Trull, 1993).
• Borderline personality disorder is five times more common among first-degree relatives of
someone with the disorder than in the general population.
Comorbidity
• Common comorbid disorders include mood disorders, substance use disorders, eating
disorders (especially bulimia), and anxiety disorders (Grilo et al., 2004; Gunderson, Weinberg
et al., 2006; Zanarini et al., 2004).
Onset
• As with all other personality disorders, symptoms for borderline personality disorder emerge
in childhood or adolescence.
Course
• People with borderline personality disorder have a high suicide rate, with almost 10% dying
by suicide (Linehan & Heard, 1999; Paris, 1993).
• The early adulthood years of people with this disorder are marked by mood episodes and
serious impulse control problems, including suicide attempts; the risk of suicide peaks during
early adulthood.
• Those who survive into their 20s and 30s are likely to improve within 10 years (Gunderson
et al., 2011; Zanarini et al., 2010).
Gender Differences
• Approximately 75% of those diagnosed with borderline personality disorder are female.
Cultural Differences
• The diagnostic criteria for borderline personality disorder—and its conceptual underpin-
nings—may not apply equally well in all cultures, especially Asian cultures (Lee, 2008).
Source: Unless otherwise noted, citations should be for American Psychiatric Association, 2013.
Although online message boards may provide
support for adolescent girls and young
women, they may also encourage or normalize
the self-harming behavior that is associated
with borderline personality disorder (Whitlock
et al., 2006).
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424 C H A P T E R 1 3
The amygdala (which is involved in the perception and production of strong
emotions, notably fear) is more strongly activated than normal in these patients when
they see faces with negative expressions (Donegan et al., 2003). This finding makes
sense because the frontal lobes normally inhibit the amygdala (LeDoux, 1996); thus,
if the frontal lobes are not working properly, they may fail to keep activation of the
amygdala within a normal range.
In addition, consistent with the unusually small hippocampus, these patients
have impaired visual and verbal memory (LeGris & van Reekum, 2006).
Neural Communication Relatively low levels of serotonin are related to impulsivity,
which is characteristic of borderline personality disorder. Thus, it is not surprising
that these patients have been shown to have abnormal serotonin functioning (Soloff
et al., 2000); in particular, their serotonin receptors are less sensitive than normal,
and thus the effects of serotonin are diminished (Hansenne et al., 2002). In addi-
tion, this dysfunction involving serotonin is apparently greater in women than in
men with the disorder (New et al., 2003; Soloff, Kelly et al., 2003)—and many more
women than men receive this diagnosis.
Thus, people with borderline personality disorder are likely to be neurologically
vulnerable to emotional dysregulation. This vulnerability is usually expressed as a low
threshold for emotional responding, with responses that are often extreme and intense.
In addition, the brains of these people are relatively slow to return to a normal baseline
of arousal.
Genetics Genetic studies reveal a genetic vulnerability to components of this disor-
der, such as impulsivity, emotional volatility, and anxiety (Adams et al., 2001; Heim
& Westen, 2005; Skodol, Siever, et al., 2002).
Psychological Factors: Emotions on a Yo-Yo
The core feature of borderline personality disorder is dysregulation—of emotion,
of sense of self, of cognition, and of behavior (Robins et al., 2001). The behaviors
of people with this disorder can be extreme: In one instant, they will fly into a rage
over some inconsequential thing, but in the next instant, they will break down in
tears and beg for reassurance, as Reiland did. These behaviors may inadvertently be
reinforced by family members’ attention.
People with this disorder often engage in other behaviors that are more directly
self-destructive—including substance use or abuse, binge eating, and parasuicidal
behaviors; they may act in these ways to try to feel better after interpersonal stress
(Paris, 1999). And, in fact, such maladaptive behaviors can be (negatively) reinforc-
ing because they do temporarily relieve emotional pain. (Recall that negative rein-
forcement is different from punishment; removing something aversive is reinforcing.)
Social Factors: Invalidation
Borderline personality disorder also involves interpersonal dysregulation—relation-
ships are typically intense, chaotic, and difficult (Robins et al., 2001). One expla-
nation for the interpersonal problems suggests that they arose in childhood—that
family members and friends were likely to invalidate the patient’s experience (Linehan,
1993). For instance, a parent might tell a child, “You’re too sensitive” or “You’re
overreacting.” During childhood, such chronic dismissals may have led to fear of
rejection and abandonment, if not actual rejection. Such experiences may have sen-
sitized the child, leading him or her subsequently to overreact to the slightest hint of
being invalidated.
In addition, this interpersonal dysregulation may arise in part because of patients’
emotional and cognitive dysregulation (Fonagy & Bateman, 2008). When people
with borderline personality disorder meet someone who is positive or helpful, they
often begin by depending on that person to help calm their emotions, as Reiland
What do you see in this negative expression?
People with borderline personality disorder
tend to have stronger activation of their
amygdalae (a brain structure notably involved
in fear) when viewing faces with negative
expressions. This finding may help explain why
people who have this personality disorder are
especially sensitive to being rejected by others.
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Personality Disorders 425
Mental Processes and
Mental Contents
Hypervigilance for
threats
Affect
Emotional
dysregulation
Behavior
Impulsivity
Stressful Life Events
Abuse or neglect
Unstable
interpersonal
relationships
Genetics
Inherited
tendency for
emotional
dysregulation
and impulsivity
Neural Communication
NeuroPsychoSocial
Serotonin
Brain Systems
Frontal lobes
Amygdala
Hippocampus
NeuroPsychoSocial NeuroPsychoSocial
Family
Invalidation
of patient’s
experiences
Gender/Culture
No known major
contribution
FI G U RE 13.2 • Feedback
Loops in Understanding
Borderline Personality
Disorder
did with her husband. But, paradoxically, once they feel dependent, they fear being
abandoned—which leads them to behave in ways likely to lead to rejection. Friends
and family members may come to respond with caring and concern only when the
patient exhibits self-destructive behaviors (which, in turn, inadvertently reinforces
those behaviors).
Feedback Loops in Understanding Borderline Personality Disorder
Linehan’s (1993) model of borderline personality disorder rests on a series of feed-
back loops (like those illustrated in Figure 13.2): Some children have brain systems
(neurological factor) that lead them to have extreme emotional reactions (psycholog-
ical factor), and their parents may have difficulty soothing them (social factor) when
they are emotionally aroused (Graybar & Boutelier, 2002; Linehan, 1993). Either
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426 C H A P T E R 1 3
because the parents create an invalidating environment (“It’s not as bad as you’re
making it out to be”; social factor) or because they engage in outright abuse or ne-
glect (as occurred with Reiland), the children may become insecurely attached to
their parents. In turn, the children don’t learn to regulate their emotions or behav-
iors (and cognitions) and elicit untoward reactions from others, which then confirms
their view of themselves and others.
This invalidating process, according to Linehan, leaves the person feeling pun-
ished for his or her thoughts, feelings, and behaviors—they are trivialized, dismissed,
disrespected (Linehan & Kehrer, 1993). Such people therefore have a hard time iden-
tifying and labeling their emotions accurately and coming to trust their own ex-
periences and perceptions as valid (psychological factor). They don’t learn effective
problem solving or ways to cope with distress.
Treating Borderline Personality Disorder: New Treatments
Borderline personality disorder is among the most challenging personality disorders
to treat (Robins et al., 2001), in part, because of the patient’s parasuicidal or suicidal
thoughts and behaviors. It can also be challenging because of the intense anger that
a patient may direct at the mental health clinician. In what follows we examine the
various targets of treatment—neurological factors, psychological factors, and social
factors—and pay particular attention to a comprehensive psychological treatment
that is the treatment of choice: dialectical behavior therapy.
Targeting Neurological Factors: Medication
Various medications may be prescribed to people with borderline personalit y
disorder for a comorbid non-personality disorder or to target certain symptoms,
including quickly changing moods, anxiety, impulsive behavior, and psychotic
symptoms (Lieb et al., 2004). An SSRI—compared to a placebo—may diminish
symptoms of emotional lability and anxiety and help with anger management. In
addition, antipsychotics can alleviate psychotic symptoms, and mood stabilizers may
help some symptoms (Binks et al., 2006a). Although medications may reduce the
intensity of some symptoms, medications have limited effect and should not be the
only form of treatment for people with borderline personality disorder (Koenigsberg
et al., 2007).
Targeting Psychological Factors: Dialectical Behavior Therapy
Marsha Linehan, a pioneer in the treatment of borderline personality disorder, ini-
tially treated such patients with CBT, which focuses on identifying and correcting
irrational thoughts and faulty beliefs (Beck et al., 2004; Linehan, 1993)—but this
led some people to drop out of treatment because they felt that the focus on chang-
ing their thoughts and beliefs implicitly criticized and invalidated them (Dimeff &
Linehan, 2001). In response, Linehan (1993) developed a new treatment for people
with borderline personality disorder. From CBT she incorporated skill development
and cognitive restructuring. In addition, in her new therapy, she underscored the
importance of a warm and collaborative bond between patient and therapist; to this
mix she added the following elements:
• An emphasis on validating the patient’s experience. That is, the patient’s thoughts, feel-
ings, and behaviors in a given situation make sense in the context of his or her life,
past experiences, and strengths and weaknesses.
• A Zen Buddhist approach. Patients should see, and then without judgment, accept
any painful realities of their lives. Patients are encouraged to “let go” of emotional
attachments that cause them suffering. Mindfulness, or nonjudgmental awareness,
is the goal (Perroud et al., 2012).
Personality Disorders 427
• A dialectics component. Dialectics refers to a synthesis of opposing elements; in this context,
it refers to the patient’s coming to accept the situation and aspects of it that he or she
does not feel able to change (e.g., validating his or her experience) while at the same
time recognizing that in order to feel better, change must occur (Robins et al., 2001).
Linehan called this treatment dialectical behavior
therapy (DBT), and it entails both group and individ-
ual therapy. The initial priority of DBT is to reduce self-
harming behaviors such as burning or cutting oneself. As
these behaviors are reduced, treatment focuses on other
behaviors that interfere with therapy and with the qual-
ity of life. Therapy also helps patients develop skills to
change what can be changed: their own behavior rather
than the behavior of other people, such as family mem-
bers. In addi tion, treatment helps patients to recognize
aspects of their lives that they can’t change: For instance,
although patients can learn to change the way they be-
have toward their parents, they can’t change the way their
parents behave toward them. Treatment lasts about 1 year.
Researchers have conducted many studies to evaluate
DBT and have noted impressive results for patients with
borderline personality disorder: DBT does decrease suicidal
thoughts and behaviors and leads to lower dropout and hospitalization rates—and it does
so more effectively than other specialized treatments for this disorder (Binks et al., 2006b;
Linehan et al., 2006). DBT has been adapted to treat people with other psychological
disorders that involve impulsive symptoms, such as bulimia (Palmer et al., 2003).
Intensive forms of psychodynamically oriented psychotherapy have also been
shown to be effective for patients with borderline personality disorder (Clarkin et al.,
2007; Gregory & Remen, 2008). Similarly, research indicates that cognitive therapy
and CBT can be effective (Davidson et al., 2006; Wenzel et al., 2006).
Targeting Social Factors: Interpersonal Therapy
Interpersonal therapy (IPT) has been adapted to treat borderline personality disor-
der. The goal of IPT for this personality disorder is to help the patient develop more
adaptive interpersonal skills so that he or she feels and functions better. This therapy
tries to help patients integrate their extreme but opposed feelings about a person:
When they talk about feeling one way about someone (“He’s perfect”), the therapist
tries to discuss opposite feelings as well, underscoring that no individual is all good
or all bad (Markowitz, 2005; Markowitz et al., 2006). A course of IPT for borderline
personality disorder typically lasts about 8 months. Social interactions are also a focus
of the group therapy component of DBT.
Feedback Loops in Treating Borderline Personality Disorder
Successful treatment of borderline personality disorder may target more than one
factor; positive changes in any factor, though, affect other factors via feedback loops
(see Figure 13.3). For example, one goal of DBT is to help patients regulate their
emotions (psychological factor). When the therapy is successful, better emotional
regulation allows patients to calm themselves more effectively when they are anxious
or angry, which directly affects brain mechanisms (neurological factor) and in turn
makes their relationships less volatile (social factors). Similarly, the honest and caring
feedback from others within the therapeutic environment (part of DBT, IPT, CBT,
and intensive psychodynamic therapy) challenges patients to alter their behaviors and
ways of thinking about themselves and their relationships (psychological and social
factors), which in turn decreases their emotional reactivity (neurological and psycho-
logical factors).
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Dialectical behavior therapy (DBT)
A form of treatment that includes elements of
CBT as well as an emphasis on validating the
patient’s experience, a Zen Buddhist approach,
and a dialectics component.
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Dialectical behavior therapy involves both
individual and group therapy; this treatment
validates the patient’s experience, encourages
nonjudgmental awareness, and acceptance of
opposing elements of life.
428 C H A P T E R 1 3
Histrionic Personality Disorder
You may know someone who initially seemed charming, open, enthusiastic—
maybe even flirtatious. After a while, did he or she seem to go to great lengths
to be the center of attention, behaving too dramatically? Did the person have
temper tantrums, sobbing episodes, or other dramatic displays of emotion that
appeared to turn on and off like a light switch? These are the qualities of people
with histrionic personality disorder, who seek attention and exaggerate
their emotions (American Psychiatric Association, 2013).
Rachel Reiland relates her desire to be the center of attention:
I wanted to be the entire focus of any person I was obsessed with. My incessant
hunger for attention had been a part of my life for as long as I could remem-
ber. The burning heartache of emptiness obsessed me even when my peers had
been taken with Barbie dolls and coloring books. I knew even then that these
constant feelings were not normal. . . .
When the object of my longing—the teacher, the coach, the boss—was pres-
ent in the room, I geared everything to that person. I contrived every word, action,
inflection, and facial expression for him. Does he see me laughing? Does he see how funny
everybody thinks I am?
(2004, pp. 335–336)
Reiland’s behavior involved some features of histrionic personality disorder; in what
follows we examine the disorder in more detail.
We don’t know why this woman is so upset.
But in people with histrionic personality
disorder, this type of exaggerated response is
not unusual. Histrionic personality disorder
is characterized by attention-seeking and
dramatic emotions.
R
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Treatments Targeting
Psychological Factors
DBT: CBT techniques
plus validation,
Buddhist mindfulness,
and dialectical
acceptance
Psychodynamic
therapy
(intensive forms)
CBT
Treatments Targeting
Social Factors
DBT: Group therapy
component
IPT: Focus on current
relationships and
effects of patient’s
actions
Treatments Targeting
Neurological Factors
Medication: SSRIs to
treat symptoms of
mood, anxiety, and
anger; mood
stabilizers
Changes neural
activity
Changes thoughts,
feelings, and behaviors
Changes social
interactions
Increases support for
making positive changes
FI G U RE 13.3 • Feedback Loops in Treating
Borderline Personality Disorder
Histrionic personality disorder
A personality disorder characterized by
attention-seeking behaviors and exaggerated
and dramatic displays of emotion.
Personality Disorders 429
What Is Histrionic Personality Disorder?
Table 13.14 lists the diagnostic criteria for histrionic personality disorder. Beyond the
overt attention seeking and dramatic behavior, people with histrionic personality dis-
order may exhibit more subtle symptoms: When they feel bored or empty, they seek
out novelty and excitement; they may have difficulty delaying gratification and tend
to become easily and excessively frustrated by life’s challenges. Being in long-term
relationships with people with histrionic personality disorder can be challenging
because they usually don’t recognize their symptoms—they don’t feel as though they
are overreacting or being overly dramatic or seductive, although they clearly are.
Case 13.7 presents a woman with this personality disorder and Table 13.15 provides
additional facts about the personality disorder.
CASE 13.7 • FROM TH E OUTSIDE: Histrionic Personality Disorder
A 23-year-old single woman was referred for a psychological assessment by her gynecolo-
gist. The patient had been described as “outgoing, effusive, and ‘dressed to kill’.”
She had been experiencing debilitating pain for over half a year, but the pain seemed to
be medically unexplainable. Throughout the interview, she used facial and other nonverbal
expressiveness to dramatize the meaning of her words. In describing her pain, for example,
she said she felt as though “I will absolutely expire” as she closed her eyes and dropped
her head forward to feign death. However, when asked about her pain, she became co-
quettish and was either unable or unwilling to provide details. She talked freely about
topics tangential to the interview, skipping quickly from topic to topic and periodically in-
serting sexual double entendres. She described her family as happy and well- adjusted but
acknowledged conflict with her mother and complained that her older brothers treated
her like a baby. . . . She was not currently in a serious relationship, but stated with a giggle
that most boys “find me very attractive,” adding that they “just want me for my body.” . . .
At the time of the interview, she was working as a dancer at an adult club; she particularly
liked the attention and the money that the job provided.
(Millon & Davis, 2000, p. 237; quoted in Horowitz, 2004, pp. 190–191)
TABLE 13.15 • Histrionic Personality Disorder Facts at a Glance
Prevalence
• Approximately 2% of the general population will have histrionic personality disorder at some point during their lives (Grant, Hasin, et al., 2004).
• Among people seeking treatment in inpatient and outpatient mental health settings, the prevalence of this disorder is 10–15%.
Comorbidity
• Common comorbid personality disorders are borderline, narcissistic, antisocial, and dependent personality disorders (Skodol, 2005).
• Common comorbid psychological disorders are somatic symptom disorders and major depressive disorder.
Onset
• As with other personality disorders, symptoms must emerge by young adulthood.
Course
• Symptoms of histrionic personality disorder may improve over time but rarely completely resolve (Seivewright et al., 2002).
Gender Differences
• Some studies find histrionic personality disorder to occur as frequently in men as in women, but others find that it is diagnosed more frequently in
women.
• Men with histrionic personality disorder may appear “macho” and seek attention for their athletic skills, not their appearance.
Source: Unless otherwise noted, the source is American Psychiatric Association, 2000, 2013.
TABLE 13.14 • DSM-5 Diagnostic
Criteria for Histrionic Personality
Disorder
A pervasive pattern of excessive emotionality
and attention seeking, beginning by early
adulthood and present in a variety of contexts,
as indicated by five (or more) of the following:
1. Is uncomfortable in situations in which he
or she is not the center of attention.
2. Interaction with others is often
characterized by inappropriate sexually
seductive or provocative behavior.
3. Displays rapidly shifting and shallow
expression of emotions.
4. Consistently uses physical appearance to
draw attention to self.
5. Has a style of speech that is excessively
impressionistic and lacking in detail.
6. Shows self-dramatization, theatricality,
and exaggerated expression of emotion.
7. Is suggestible (i.e., easily influenced by
others or circumstances).
8. Considers relationships to be more
intimate than they actually are.
Reprinted with permission from the Diagnostic and
Statistical Manual of Mental Disorders, Fifth Edition,
(Copyright ©2013). American Psychiatric Association. All
Rights Reserved.
430 C H A P T E R 1 3
Distinguishing Between Histrionic Personality Disorder and
Other Disorders
A lthough people with antisocial personalit y disorder, borderline personalit y
disorder, and histrionic personality disorder are all manipulative and impulsive, their
motivations differ: People with histrionic personality disorder desire frequent atten-
tion from others; people with antisocial personality disorder seek power or mate-
rial gain; and people with borderline personality disorder want nurturance (Skodol,
2005). Moreover, although both histrionic and borderline personality disorders in-
volve rapidly shifting emotions, only with the latter are the emotions usually related
to anger.
Reiland’s behavior fit some of the criteria for histrionic personality disorder, in
that some of her dramatic displays seemed to be motivated by a desire for attention.
She might be diagnosed with histrionic personality disorder as a comorbid disor-
der; however, the elements of her behavior that indicate borderline personality dis-
order overshadow the features of histrionic personality disorder. A clinician trying
to make a definitive diagnosis (or diagnoses) would want to find out more about any
thoughts, feelings, or behaviors that might indicate or rule out histrionic personality
disorder. Little formal research has been conducted that illuminates factors that con-
tribute to this personality disorder, and so we next focus on how to treat this person-
ality disorder.
Treating Histrionic Personality Disorder
A goal of treatment for histrionic personality disorder is to help patients recognize
and then modify their maladaptive beliefs and strategies. Specifically, using tech-
niques from CBT or psychodynamic therapy, the therapist tries to help patients
increase their capacity to cope with distress, develop more adaptive ways of respond-
ing to frustration, recognize the negative impact that their actions have on their
relationships, and shift their view of themselves and other people (Beck et al., 2004;
Farmer & Nelson-Gray, 2005). Like other patients with dramatic/erratic personality
disorders, those with histrionic personality disorder often do not remain in treatment
for long; they become bored or frustrated and continue to see other people as the pri-
mary problem.
Narcissistic Personality Disorder
Unlike antisocial and borderline personality disorders, narcissistic personality disor-
der does not involve impulsiveness or self-destructive tendencies but rather a sense of
grandiosity.
What Is Narcissistic Personality Disorder?
People with narcissistic personality disorder have an inflated sense of their own
importance; they expect—and demand—praise and admiration, and they lack em-
pathy (American Psychiatric Association, 2013). This sense of self-importance, how-
ever, masks mixed feelings. On the one hand, they are preoccupied with their own
concerns and expect others to be as well, and they get angry when other people
don’t defer to them. They overvalue themselves and undervalue other people, which
is true of Patricia in Case 13.8. On the other hand, their self-esteem can be frag-
ile, leading them to fish for compliments. They are relatively insensitive to others’
feelings and points of view. Table 13.16 lists the diagnostic criteria for narcissis-
tic personality disorder, and Table 13.17 presents additional information about this
disorder.
Narcissistic personality disorder
A personality disorder characterized by an
inflated sense of self-importance, an excessive
desire to be admired, and a lack of empathy.
TABLE 13.16 • DSM-5 Diagnostic
Criteria for Narcissistic Personality
Disorder
A pervasive pattern of grandiosity
(in fantasy or behavior), need for admiration,
and lack of empathy, beginning by early
adulthood and present in a variety of
contexts, as indicated by five (or more) of
the following:
1. Has a grandiose sense of self-importance
(e.g., exaggerates achievements and tal-
ents, expects to be recognized as superior
without commensurate achievements).
2. Is preoccupied with fantasies of
unlimited success, power, brilliance,
beauty, or ideal love.
3. Believes that he or she is “special” and
unique and can only be understood by,
or should associate with, other special or
high-status people (or institutions).
4. Requires excessive admiration.
5. Has a sense of entitlement (i.e., unrea-
sonable expectations of especially favor-
able treatment or automatic compliance
with his or her expectations).
Reprinted with permission from the Diagnostic and
Statistical Manual of Mental Disorders, Fifth Edition,
(Copyright ©2013). American Psychiatric Association. All
Rights Reserved.
Personality Disorders 431
CASE 13.8 • FROM TH E OUTSIDE: Narcissistic Personality Disorder
Patricia was a 41-year-old married woman who presented at an outpatient mental health
clinic complaining of interpersonal difficulties at work and recurring bouts of depression. She
described a series of jobs in which she had experienced considerable friction with coworkers,
stating that people generally did not treat her with the respect she deserved. . . . Shortly before
her entrance into treatment, Patricia was demoted from a supervisory capacity at her current
job because of her inability to effectively interact with those she was supposed to supervise.
She described herself as always feeling out of place with her coworkers and indicated that
most of them failed to adequately appreciate her skill or the amount of time she put in at
work. She reported that she was beginning to think that perhaps she had something to do with
their apparent dislike of her. Patricia stated several times . . . that the tellers at the bank were
jealous of her status and abilities as a loan officer and that this made them dislike her.
(Corbitt, 2002, pp. 294–295)
Note that Patricia, in Case 13.8, said that people didn’t treat her with the respect that
she felt she deserved and that she didn’t feel adequately appreciated; people with narcis-
sistic personality disorder often report such feelings. Reiland’s symptoms do not meet the
criteria for a diagnosis of narcissistic personality disorder; her problematic behaviors were
often impulsive and self-destructive, and she did not have a stable, inflated sense of self.
As is true for histrionic personality disorder, very little research illuminates fac-
tors that contribute to narcissistic personality disorder—and so we move directly to
examine ways to treat narcissistic personality disorder.
Treating Narcissistic Personality Disorder
Treatment for narcissistic personality disorder is basically the same as treatment for
histrionic disorder: The therapist seeks to help patients recognize and then modify their
maladaptive beliefs and strategies, using techniques of CBT or psychodynamic therapy.
However, as for all patients with personality disorders, those with narcissistic personal-
ity disorder usually do not remain in treatment for long—and typically continue to see
other people as the primary problem rather than their own beliefs or behaviors.
TABLE 13.17 • Narcissistic Personality Disorder Facts at a Glance
Prevalence
• Up to 1% of the general population will have narcissistic personality disorder at some point
in their lifetimes.
Comorbidity
• Common comorbid personality disorders include paranoid personality disorder and the
other Cluster B (dramatic/erratic) personality disorders.
• Common psychological comorbid disorders are substance use disorders and anorexia nervosa.
Onset
• As with other personality disorders, symptoms must emerge by early adulthood.
Course
• People with narcissistic personality disorder may have a hard time adjusting to physical or
occupational limitations that arise with advancing age.
Gender Differences
• Between 50% and 75% of those diagnosed with narcissistic personality disorder are male.
Source: Unless otherwise noted, the source is American Psychiatric Association, 2013.
432 C H A P T E R 1 3
In high school and college, Will acted in school plays. Now in his 30s, he travels a lot, making
presentations for his job, and so has a lot of independence. He likes the freedom of not having
a boss looking over his shoulder all the time, and he enjoys making presentations. Because no
one really knows how many hours he works, he sometimes starts late in the morning or quits
early; then he heads for a bar to down a few beers. Occasionally, he takes whole days off—
after he’s had too much to drink the night before. He’s been through a series of girlfriends,
never staying with one for more than 6 months. Lately, though, his single status has been both-
ering him, and he’s been wondering why there don’t seem to be any decent women out there.
In what ways does Will seem typical of someone with a Cluster B (dramatic/erratic) per-
sonality disorder? In what ways is he unusual? What would you need to know before you
could decide whether he had a dramatic/erratic personality disorder? Which specific person-
ality disorder seems most likely from the description of him, and why? Why is—or isn’t—this
information enough to make a diagnosis?
Thinking Like A Clinician
Fearful/Anxious Personality
Disorders
The personalit y disorders in Cluster C—avoidant, dependent, and obsessive-
compulsive personality disorders—share the feature of anxiety or fear. Although they
have this superficial commonality, there is little overlap among the diagnostic criteria
for these three disorders; this is in sharp contrast to the disorders within Cluster A
(odd/ eccentric) and those within Cluster B (dramatic/erratic), which have overlap-
ping criteria. Nonetheless, people who have anxiety disorders and a comorbid per-
sonality disorder are most likely to have that personality disorder be from Cluster C
(Friborg et al., 2013).
Avoidant Personality Disorder
The predominant characteristic of people with avoidant personality disorder is social
inhibition—extreme shyness—that usually stems from feeling inadequate and being overly
sensitive to negative evaluation (American Psychiatric Association, 2013). People with
avoidant personality disorder are often characterized as shy, isolated, timid, or lonely.
What Is Avoidant Personality Disorder?
The diagnostic criteria for avoidant personality
disorder (see Table 13.18) all relate to the person’s
predominant concern about embarrassing him-
self or herself during social interactions—per-
haps by blushing or crying—and being socially
rejected or humiliated. These fears, in turn, lead
the person to limit social interactions.
People with avoidant personality disorder
are so reluctant to engage in social interac-
tions that they may turn down a promotion
if the position requires increased social con-
tact. And they are often hypervigilant for any
indication of criticism or rejection. These
fears and anxieties may cause them to behave
in tense and fearful ways—for example, not
talking about themselves for fear of what oth-
ers might think—when they do interact with
Avoidant personality disorder
A personality disorder characterized by
extreme shyness that usually stems from
feeling inadequate and being overly sensitive
to negative evaluation.
TABLE 13.18 • DSM-5 Diagnostic Criteria for Avoidant Personality Disorder
A pervasive pattern of social inhibition, feelings of inadequacy, and hypersensitivity to
negative evaluation, beginning by early adulthood and present in a variety of contexts, as
indicated by four (or more) of the following:
1. Avoids occupational activities that involve significant interpersonal contact because of
fears of criticism, disapproval, or rejection.
2. Is unwilling to get involved with people unless certain of being liked.
3. Shows restraint within intimate relationships because of the fear of being shamed or ridiculed.
4. Is preoccupied with being criticized or rejected in social situations.
5. Is inhibited in new interpersonal situations because of feelings of inadequacy.
6. Views self as socially inept, personally unappealing, or inferior to others.
7. Is unusually reluctant to take personal risks or to engage in any new activities because
they may prove embarrassing.
Reprinted with permission from the Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition, (Copyright
©2013). American Psychiatric Association. All Rights Reserved.
Personality Disorders 433
other people. This anxious way of relating to others may inadvertently elicit a mild
version of the very reaction they fear—that others will evaluate them in a negative
light. Among all people with personality disorders, those with avoidant personality
disorder report the lowest quality of life (Cramer et al., 2003; Wilberg et al., 2009).
Case 13.9 describes one person’s experience, and Table 13.19 provides additional facts
about this disorder.
CASE 13.9 • FROM TH E OUTSIDE: Avoidant Personality Disorder
Marcus is a 33-year-old man who recently divorced.
His marriage deteriorated over several years and primarily as the result of his wife’s in-
creasing frustration with his unwillingness to do anything to improve his situation. He is
employed as a warehouse manager and has held the same position for 9 years. He sees
others doing more with their lives and wishes that he could as well. Although he hates that
his wife chose to leave the marriage, he cannot blame her for doing so. Each evening after
work he is filled with feelings of self-contempt and anguish. He would like to go out and be
with other people, but he is certain that no one wants his company. He finds that drink-
ing alcohol and watching television usually takes his mind off this unfulfilling life. Marcus
thinks of committing suicide frequently.
(Rasmussen, 2005, p. 201)
Distinguishing Between Avoidant Personality Disorder and Other
Disorders
If you’re thinking that you’ve read about a disorder that seems similar to avoidant
personality disorder earlier in this textbook, you’re correct. Avoidant personality
TABLE 13.19 • Avoidant Personality Disorder Facts at a Glance
Prevalence
• Approximately 2.5% of the American population has avoidant personality disorder (Grant,
Hasin, et al., 2004).
• Up to 10% of those seen in outpatient clinics have this disorder.
Comorbidity
• Because the diagnostic criteria overlap with those of social phobia, comorbidity between the
two disorders is very high (Shea et al., 2004; Skodol, 2005; Skodol et al., 1995); in one study,
43% of people diagnosed with social phobia were also diagnosed with avoidant personality
disorder (Faravelli et al., 2000).
• Common comorbid personality disorders are dependent personality disorder (because
patients are dependent on the few friends they have), borderline personality disorder, and
the Cluster A (odd/eccentric) personality disorders.
• Common comorbid psychological disorders are mood disorders and anxiety disorders.
Onset
• Based on the diagnostic criteria, symptoms such as shyness or a fear of strangers or new
situations must emerge by early adulthood.
Course
• Two years after diagnosis, approximately 50% of people with avoidant personality disorder improve
enough with treatment that their symptoms no longer meet the criteria (Grilo et al., 2004).
Gender Differences
• Men and women do not consistently differ in their prevalence rates for avoidant personality
disorder (Torgersen, 2005).
Source: Unless specifically noted, citations are to American Psychiatric Association, 2000, 2013.
434 C H A P T E R 1 3
disorder has much in common with social phobia (Chapter 6), and the symp-
toms of the two disorders overlap (Chambless et al., 2008; Tillfors et al., 2004).
However, the criteria for avoidant personality disorder are broader than those for
social phobia, and the symptoms include a more pervasive sense of inadequacy or
inferiority and a reluctance to take risks (Skodol, 2005), as was true of Marcus in
Case 13.9.
When making the diagnosis of avoidant personality disorder, clinicians must take
cultural factors into account (American Psychiatric Association, 2013). For example,
recent immigrants may exhibit symptoms of this disorder, perhaps because of lan-
guage barriers or concerns about safety, and so clinicians must be sure to ask whether
the behavior predates immigration. Because the three fearful/anxious personality
disorders have not been studied in depth, we will discuss the underlying bases for
and treatment of all three disorders after we consider specific features of each of them
separately.
Dependent Personality Disorder
Dependent personality disorder is characterized by submissive and cling y
behaviors, based on fear of separation. The DSM-5 definition notes that the clingy
behaviors are intended to elicit attention, reassurance, and decisive behaviors from
other people (American Psychiatric Association, 2013). These behaviors are not a tem-
porary bid for attention or reassurance (like the behaviors of those with borderline or
histrionic personality disorder) but are part of a chronic pattern of helpless behavior.
People with dependent personality disorder are chronically plagued by self-doubt
and consistently underestimate their abilities (see Table 13.20 for the list of diagnos-
tic criteria). Thus, they have a hard time making all kinds of decisions, from life-
altering ones about what career to pursue to mundane decisions about what clothes
to wear. They prefer to have other people make such choices for them. And because
they are quick to believe they are wrong, they are likely to see any criticism or disap-
proval as proof of their negative beliefs about themselves.
People with dependent personality disorder often don’t learn the skills needed
to function independently and so are, in fact, dependent on others; they have rea-
son to be concerned about living on their
own. When a relationship ends, they typi-
cally leap into another one in order to en-
sure that they are not alone. Even while
in an intimate relationship, they are often
preoccupied with the possibility that the
relationship will end, and they will have
to fend for themselves. People with depen-
dent personality disorder are most comfort-
able in relationships with people who take
the initiative—and take responsibility. Not
surprisingly, then, they often choose over-
protective and dominating people to be
their friends and partners, becoming passive
in those relationships.
Generally, people who have dependent
personality disorder have a limited social
circle, consisting of only a few people on
whom they depend, as is true of Matthew
in Case 13.10. Once they have established
a relat ionsh ip, people w ith dependent
personality disorder are hesitant to disagree
This woman might just be bored, but meetings
like the one shown in this photo make
people with avoidant personality disorder
uncomfortable. Symptoms of avoidant
personality disorder and social phobia overlap,
and people with either disorder are excessively
concerned about being rejected by others
or behaving in a way that leads them to feel
humiliated. However, the social difficulties and
feelings of inadequacy of people with avoidant
personality disorder are generally more
pervasive than those of people with other
types of disorders.
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Dependent personality disorder
A personality disorder characterized by
submissive and clingy behaviors, based on fear
of separation.
TABLE 13.20 • DSM-5 Diagnostic Criteria for Dependent Personality Disorder
A pervasive and excessive need to be taken care of that leads to submissive and clinging
behavior and fears of separation, beginning by early adulthood and present in a variety of
contexts, as indicated by five (or more) of the following:
1. Has difficulty making everyday decisions without an excessive amount of advice and
reassurance from others.
2. Needs others to assume responsibility for most major areas of his or her life.
3. Has difficulty expressing disagreement with others because of fear of loss of support or
approval. (Note: Do not include realistic fears of retribution.)
4. Has difficulty initiating projects or doing things on his or her own (because of a lack of
self-confidence in judgment or abilities rather than a lack of motivation or energy).
5. Goes to excessive lengths to obtain nurturance and support from others, to the point of
volunteering to do things that are unpleasant.
6. Feels uncomfortable or helpless when alone because of exaggerated fears of being unable
to care for himself or herself.
7. Urgently seeks another relationship as a source of care and support when a close
relationship ends.
8. Is unrealistically preoccupied with fears of being left to take care of himself or herself.
Reprinted with permission from the Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition, (Copyright
©2013). American Psychiatric Association. All Rights Reserved.
Personality Disorders 435
with the other person for fear that he or she will withdraw emotional support. In
fact, a person with this personality disorder may go to great lengths to maintain
the support that the other person provides, even tolerating mental or physical abuse
(American Psychiatric Association, 2013).
CASE 13.10 • FROM TH E OUTSIDE: Dependent Personality Disorder
Matthew is a 34-year-old single man who lives with his mother and works as an accountant. He
is seeking treatment because he is very unhappy after having just broken up with his girlfriend.
His mother had disapproved of his marriage plans, ostensibly because the woman was of a
different religion. Matthew felt trapped and forced to choose between his mother and his girl-
friend, and because “blood is thicker than water,” he had decided not to go against his mother’s
wishes. . . . Matthew is afraid of disagreeing with his mother for fear that she will not be sup-
portive of him and he will then have to fend for himself. He criticizes himself for being weak, but
also admires his mother and respects her judgment. . . .He feels that his own judgment is poor.
Matthew works at a job several grades below what his education and talent would
permit. On several occasions he has turned down promotions because he didn’t want
the responsibility of having to supervise other people or make independent decisions. . . .
He has two very close friends whom he has had since early childhood. He has lunch with
one of them every single workday and feels lost if his friend is sick and misses a day.
Matthew is the youngest of four children and the only boy. . . . He had considerable
separation anxiety as a child—he had difficulty falling asleep unless his mother stayed in
the room, mild school refusal, and unbearable homesickness when he occasionally tried
“sleepovers.” . . . He has lived at home his whole life except for 1 year of college, from which
he returned because of homesickness.
(Spitzer, Gibbon et al., 2002, pp. 179–180)
It is important to note that even if a person possesses enough of the characteristics
to meet the diagnostic criteria in Table 13.20, he or she will not be diagnosed with
dependent personality disorder unless these characteristics significantly impair func-
tioning in major areas of life. Table 13.21 provides additional information about this
disorder, although little is known about its etiology.
Obsessive-Compulsive Personality Disorder
Obsessive-compulsive personality disorder is characterized by preoccupations
with perfectionism, orderliness, and self-control, as well as low levels of flexibility
and efficiency (American Psychiatric Association, 2013). This personality disorder
is associated with the least disability (Skodol, Gunderson et al., 2002) and the high-
est obtained educational level (Torgersen et al., 2001). Rachel Reiland describes her
father as having some elements of obsessive-compulsive personality disorder: He was
strict, “coveted control,” and became enraged when events weren’t to his liking.
Reiland herself had some elements of this disorder: “Once upon a time perfectionism
was my noble aspiration. My perfectionism extended beyond academics or career.
I also aspired to be the perfect mother, lover, and friend, always appropriate in all my
emotional expressions” (2004, p. 361).
What Is Obsessive-Compulsive Personality Disorder?
People with obsessive-compulsive personality disorder can get so bogged down in
details that they leave the most important elements to the last minute (see Table 13.22).
For instance, when preparing a presentation, people with this disorder might spend
hours creating a single PowerPoint slide, trying to get it perfect, and end up running out
of time for organizing their talk. They can’t see the forest for the trees. For people with
obsessive-compulsive personality disorder, decision making is a painful, long process;
thus, once they’ve made a decision, they’re not likely to change their minds—which can
Obsessive-compulsive personality
disorder
A personality disorder characterized
by preoccupations with perfectionism,
orderliness, and self-control, as well as low
levels of flexibility and efficiency.
TABLE 13.21 • Dependent Personality
Disorder Facts at a Glance
Prevalence
• The prevalence of dependent personality
disorder in the American population is
less than 1% (Grant, Hasin, et al., 2004).
Comorbidity
• Common comorbid personality disorders
are avoidant, borderline, and histrionic
personality disorders.
• Common psychological disorders are
mood disorders and anxiety disorders.
Onset
• As required by the diagnostic criteria,
symptoms must emerge by young
adulthood.
Course
• Symptoms may improve over time, to the
point where the person no longer meets
the criteria for the disorder (Markowitz et
al., 2005).
Gender Differences
• In the general population, women tend to
be diagnosed with dependent personality
disorder more often than men (Torgersen,
2005).
Source: Unless otherwise noted, citations are to American
Psychiatric Association, 2000, 2013.
Some people with obsessive-compulsive
personality disorder may feel an urge to
perfect a work-related task so strongly that
they have difficulty stopping work.
©
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436 C H A P T E R 1 3
end up making them appear rigid and inflexible. And, like Reiland’s father, when they
are unable to control a situation, they may become angry, irritable, or upset.
Some (but not all) people who are workaholics may have obsessive-compulsive per-
sonality disorder—they may feel uncomfortable on vacations unless they take work along
with them. And some with obsessive-compulsive personality disorder may spend excessive
amounts of time on hobbies or household chores, striving for perfection and adhering to
rules inflexibly. They may hold others to these same unrealistically stringent standards.
The relationships of people with obsessive-compulsive personality disorder are
normally formal and serious; they are preoccupied with logic and intellect, are overly
conscientious, and are intolerant of emotional or “illogical” behavior in others. Typi-
cally, people with obsessive-compulsive personality disorder feel uncomfortable with
others who express emotions easily and openly. People with this disorder are not
likely to express tender feelings or pay compliments. Other people often feel frus-
trated by their rigidity. In turn, people with obsessive-compulsive personality disor-
der have difficulty acknowledging the perspectives of others, as is true of Mr. V in
Case 13.11. Table 13.23 provides additional information about this disorder.
CASE 13.11 • FROM THE OUTSIDE: Obsessive-Compulsive Personality
Disorder
Mr. V, a 25-year-old philosophy graduate student, began twice-weekly psychotherapy. His
presenting complaint was difficulty with completing work effectively, particularly writing
tasks, due to excessive anxiety and obsessionality. . . . When he came for treatment, he was
struggling to make progress on his master’s thesis. Although Mr. V socialized quite a bit,
he reported that intimate relationships often felt “wooden.” He was usually overcommit-
ted, with an endless list of “shoulds” that he would constantly mentally review and remind
himself how much he was failing to satisfy his obligations. A central theme throughout
treatment was his tendency to be self-denigrating, loathing himself as a person deserving
of punishment in some way yet being extremely provocative. . . . He also held very strong
political beliefs, sure that his way of viewing things was superior to others.
(Bender, 2005, p. 413)
TABLE 13.23 • Obsessive-Compulsive Personality Disorder Facts at a Glance
Prevalence
• Approximately 2–8% of the general population has obsessive-compulsive personality dis-
order, making it the most prevalent personality disorder (American Psychiatric Association,
2013; Grant, Hasin, et al., 2004).
Comorbidity
• Most people with obsessive-compulsive disorder (OCD) do not also have obsessive-
compulsive personality disorder.
Onset
• The diagnostic criteria specify that symptoms must emerge by early adulthood.
Course
• Symptoms of up to one third of patients may improve over time to the point that they no
longer meet the diagnostic criteria (Grilo et al., 2004).
Gender Differences
• Twice as many men as women are diagnosed with obsessive-compulsive personality disorder.
Source: Unless otherwise noted, citations should be American Psychiatric Association, 2013.
TABLE 13.22 • DSM-5 Diagnostic
Criteria for Obsessive-Compulsive
Personality Disorder
A pervasive pattern of preoccupation with
orderliness, perfectionism, and mental
and interpersonal control, at the expense
of flexibility, openness, and efficiency,
beginning by early adulthood and present
in a variety of contexts, as indicated by four
(or more) of the following:
1. Is preoccupied with details, rules, lists,
order, organization, or schedules to
the extent that the major point of the
activity is lost.
2. Shows perfectionism that interferes
with task completion (e.g., is unable to
complete a project because his or her
own overly strict standards are not met).
3. Is excessively devoted to work and
productivity to the exclusion of leisure
activities and friendships (not accounted
for by obvious economic necessity).
4. Is overconscientious, scrupulous, and
inflexible about matters of morality,
ethics, or values (not accounted for by
cultural or religious identification).
5. Is unable to discard worn-out or
worthless objects even when they have
no sentimental value.
6. Is reluctant to delegate tasks or to work
with others unless they submit to exactly
his or her way of doing things.
7. Adopts a miserly spending style toward
both self and others; money is viewed
as something to be hoarded for future
catastrophes.
8. Shows rigidity and stubbornness.
Reprinted with permission from the Diagnostic and
Statistical Manual of Mental Disorders, Fifth Edition,
(Copyright ©2013). American Psychiatric Association. All
Rights Reserved.
Personality Disorders 437
Distinguishing Between Obsessive-Compulsive Personality
Disorder and OCD
Obsessive-compulsive personality disorder is distinguished from OCD by the
absence of true obsessions and compulsions. Rather, those with obsessive-compulsive
personality disorder are preoccupied with details—as was Mr. V when writing his
master’s thesis—and are inflexible. Researchers are still trying to determine whether
obsessive- compulsive personality disorder and OCD differ quantitatively or qualita-
tively. Research studies addressing this question have reported mixed findings (Eisen
et al., 2006; Wu et al., 2006). Most people with one of the two disorders do not have
the other (Mancebo et al., 2005).
Understanding Fearful/Anxious Personality Disorders
Vir tua l ly nothing is k nown about the neurolog ica l bases of fear fu l/an x ious
personalit y disorders, but the apparent similarit y between these disorders and
anxiety disorders might indicate that the amygdala is involved. In contrast, psy-
chological factors associated with these disorders have been identif ied—fear and
anxiet y. Temperament can contribute to the development of any of these dis-
orders, especial ly avoidant personalit y disorder ( Joyce et al., 2003; Taylor et
al., 2004). In fact, many of the factors related to social phobia are also associ-
ated with avoidant personality disorder, which makes sense, given the overlap in
the symptoms of the two disorders. Moreover, people with both disorders have
similar negative beliefs about themselves in relation to other people and avoid
social situations for fear of embarrassing themselves (B. Meyer, 2002; Morey et
al., 2003).
Cognitive and behavioral factors apparently contribute to all three fearful/
anxious personality disorders. For all three, patients avoid situations that lead to
discomfort and anxiety: With avoidant personality disorder, patients avoid social
situations; with dependent personality disorder, they avoid making decisions and
having responsibility; and with obsessive-compulsive personality disorder, they avoid
making mistakes and experiencing strong emotions. The avoidance perpetuates the
cognitive distortions because the patients’ fears go unchallenged (Beck et al., 2004;
Farmer & Nelson-Gray, 2005).
Social factors apparently also contribute to these personality disorders. These
factors include anxious or avoidant attachment style, which may have arisen in
childhood as a result of particular interaction patterns with parents (Gude et al.,
2004; Pincus & Wilson, 2001).
Treating Fearful/Anxious Personality Disorders
As for most other personality disorders, there is little research on the treatment of fear-
ful/anxious personality disorders, and what research there is has focused primarily on
avoidant personality disorder. The findings suggest that the best treatment for social
phobia can also help people with avoidant personality disorder—namely, CBT that
uses exposure to avoided stimuli as well as cognitive restructuring of maladaptive
beliefs and strategies (Beck et al., 2004; Emmelkamp et al., 2006; Farmer & Nelson-
Gray, 2005; Reich, 2000). Treatment may also include family or couples therapy to
help family members change their responses to—and thus the consequences of—the
patient’s maladaptive behaviors.
Table 13.24 summarizes the contrasting characteristics of the 10 personality
disorders.
Some workaholics have obsessive-
compulsive personality disorder: They are
perfectionistic and extremely orderly and
organized. However, they can become so
preoccupied with doing a job perfectly that
they are inefficient or can’t complete the task.
Moreover, when problems arise, they can be
rigid and inflexible.
P
h
o
to
d
is
c/
G
e
tt
y
I
m
ag
e
s
438 C H A P T E R 1 3
Thinking Like A Clinician
Juan and his wife, Beatriz, are from Argentina. They have been referred to mental health
services by their family doctor. Beatriz always brings her husband with her to her doctor’s
appointments, and she always wants her husband in the room during the examination, al-
though her English is more than sufficient to express herself and understand the doctor.
Beatriz happened to mention at her last medical visit that she never leaves the house
if Juan isn’t with her. She didn’t see why she should because Juan is happy to go with her
wherever she needs to go. She said that she likes it this way—that she doesn’t feel “stuck” at
home and that Juan pretty much takes care of whatever she doesn’t feel able to do.
What specific areas of Beatriz’s functioning would you want to know more about before
making a diagnosis, and why? What other types of information would you want to have (for
example, about cultural issues), and why? Might Beatriz be suffering from a comorbid psy-
chological disorder that is not a personality disorder? If so, which one, and what would you
need to know to be relatively certain of that?
TABLE 13.24 • The Personality Disorders: A Summary
Personality
disorder Affect Behavior Cognition Social functioning
Odd/eccentric: Cluster A
Paranoid
Easily feels betrayed and angry Hypervigilant for
betrayal
Distrustful/suspicious of others; reads
malevolent meaning into neutral remarks
Generally avoids
relationships
Schizoid
Emotionally constricted, detached Avoids people when
possible
Views relationships as messy and
undesirable
Indifferent to praise
or criticism; generally
avoids relationships
Schizotypal
Generally emotionally constricted but
displays inappropriate affect and anxiety
Avoids people
whenever possible
Perceptual distortions, ideas of reference,
magical thinking
Generally avoids
relationships
Dramatic/erratic: Cluster B
Antisocial
Aggressive feelings toward others,
lack of empathy
Generally poor
impulse control
Believes that he or she is entitled to
break rules
Dominant in
relationships
Borderline
Emotionally expressive, with
inappropriately strong and rapid
reactions
Poor impulse control Dramatic shifts between overvaluing
and undervaluing others; may develop
paranoid thinking under stress
Alternately dominant and
submissive in relationships
Histrionic
Rapidly shifting but shallow emotions Relatively poor impulse
control; strives to be
center of attention
Wants to be the center of attention Dominant in
relationships
Narcissistic
No empathy; haughty toward others Manipulates others Grandiosity Dominant in
relationships
Fearful/anxious: Cluster C
Avoidant
Anxiety in social situations Overcontrol of
behavior
Excessively negative self-opinion;
worries about being rejected or
criticized
Submissive in
relationships, but
generally avoids them
Dependent
Anxiety about possible separation
from others and having to function
independently
Overcontrol of
behavior
Believes that he or she is helpless and
incompetent and so must rely on others
Submissive in
relationships
Obsessive-
compulsive
Constricted in expression of emotion
to others
Overcontrol of
behavior
Perfectionism; rigid thinking;
preoccupation with details, rules, and lists
Dominant and relatively
detached in relationships
Source: Pretzer & Beck, 2005; Skodol, 2005.
Personality Disorders 439
Follow-up on Rachel Reiland
We can say with certainty that Rachel Reiland suffered from borderline personal-
ity disorder. In addition, she displayed significant elements of two other personal-
ity disorders: histrionic personality disorder (her dramatic behaviors may have been
motivated by excessive emotional reactivity and a desire for attention) and obsessive-
compulsive personality disorder (her rigid thoughts and behaviors may have been
motivated by perfectionism). However, it is difficult to determine whether these
aspects of her personality met the criteria for the diagnosis of comorbid personality
disorders. Her symptoms of borderline personality disorder were so pronounced that
they might have masked additional personality disorders.
What happened to Reiland? In her memoir, she notes that she was hospitalized
three times; the first time because of significant suicidal impulses. After discharge from
that first hospitalization, she spent 4 years in intensive outpatient therapy with a psychia-
trist—three times a week during the first 2 years of treatment. She was hospitalized twice
more over the course of her therapy and again developed anorexia for a period of time.
Her symptoms were sufficiently severe that her therapist imposed strict limits on their
interactions; for instance, he banned physical contact of any kind. Although her thera-
pist used psychodynamic therapy, he also incorporated elements of CBT and DBT into
the treatment: The therapist addressed Reiland’s black-and-white thinking and validated
her experiences while trying to help her accept her feelings without judging herself. In
addition to the hospitalizations and outpatient therapy, Reiland tried various medica-
tions, settling on antidepressants that she gradually stopped before her therapy ended.
Her treatment was successful. She wrote her memoir 8 years after her therapy
ended; she developed and sustained the ability to regulate her moods, to control her
impulses, and to have productive and enjoyable relationships.
SUMMING UP
Diagnosing Personality Disorders
• A personality disorder is characterized by
maladaptive personality traits that begin
by young adulthood and continue through
adulthood; these traits are relatively inflex-
ible, are expressed across a wide range of
situations, and lead to distress or impaired
functioning. A personality disorder affects
three areas of functioning: affect, behavior
(including social behavior), and cognition.
• In DSM-5, per son a l it y d i sorder s a re
grouped into three clusters: Cluster A,
characterized by odd or eccentric behav-
iors related to features of schizophrenia;
Cluster B, characterized by dramatic and
erratic behaviors and problems with emo-
tional regulation; and Cluster C, charac-
terized by anxious or fearful behaviors.
• The category of personality disorders in
DSM-5 has been criticized on numerous
grounds.
• The neuropsychosocial approach explains
how persona l it y d isorders develop by
highlighting the interactions among three
sorts of factors:
° Neurological factors primarily involve
the effects of genes on temperament.
° Psychological factors include tempera-
ment, operant conditioning, and dys-
functional beliefs.
° Social factors include insecure attach-
ment that can result from childhood
abuse or neglect.
• Treat ment s for per son a l it y d i sorder s
include medications for comorbid symp-
toms, CBT or psychodynamic therapy,
a nd fa m i ly educat ion a nd therapy, a s
well as couples, interpersonal, and group
therapy.
Odd/Eccentric Personality
Disorders
• The essential feature of paranoid person-
ality disorder is a persistent and pervasive
mistrust and suspiciousness, which is ac-
companied by a bias to interpret other peo-
ple’s motives as hostile. Although paranoid
personality disorder and paranoid schizo-
phrenia both involve suspicious beliefs,
people with the personality disorder have
some capacity to evaluate whether their
suspicions are based on reality.
• Schizoid personality disorder is character-
ized by a restricted range of emotions in
social interactions and few—if any—close
relationships; people with this disorder
have poor social skills. They report rarely
experiencing strong emotions, and they
prefer to be—and function best when—
isolated from others.
• Schizotypal personality disorder is char-
acterized by eccentric thoughts, percep-
tions, and behaviors, as well as by having
very few close relationships. This person-
ality disorder has three groups of symp-
toms: cognitive-perceptual, interpersonal,
and disorganized. Schizotypal personal-
ity disorder is viewed as a milder form of
schizophrenia.
440 C H A P T E R 1 3
• Paranoid, schizoid, and schizotypal per-
sonalit y disorders are on the spectrum
of schizophrenia-related disorders, and
close rel at ive s of people w it h a ny of
these odd/eccentr ic personalit y disor-
ders are more likely to have schizophre-
n ia. Sch izot y pa l per sona l it y d isorder
involves neurological abnormalities that
are less severe than those associated with
schizophrenia.
• People w ith odd /eccent r ic per sona l-
ity disorders are reluctant participants in
treatment. Treatment may address fun-
damental issues, such as isolation and sus-
piciousness. Treatment for schizot ypal
personalit y disorder may include anti-
psychotic medication (although at lower
doses than used for psychotic disorders),
and CBT.
Dramatic/Erratic Personality
Disorders
• The hallmark of antisocial personalit y
disorder is a persistent disregard for the
rights of others, which may lead these
people to violate rules or laws or to act
aggressively.
• The d ia g nost ic cr iter ia for a nt isocia l
per sona l it y d isorder overlap w ith a s –
pect s of ps ychopat hy. However, ps y-
chopathy is defined by a more restrictive
set of cr iter ia, wh ich foc u s on emo –
tional and interpersonal characteristics,
such as a lack of empathy and antisocial
behaviors.
• Psychopathy and antisocial personalit y
disorder arise from feedback loops among
various factors, including genes, lack of
empathy, classical and operant condition-
ing, abuse or neglect or inconsistent dis-
cipline in childhood, parents’ criminal
behavior, and attachment style. Treatment
for psychopathy has generally not been
successful; treatment for antisocial per-
sonality disorder focuses on modifying
specific behaviors and has some degree of
success, at least temporarily, in motivated
people.
• Borderline personality disorder is charac-
terized by volatile emotions, an unstable
self-image, and impulsive behavior in re-
lationships. People with this disorder have
problems with emotional regulation and
may engage in self-harming behaviors or
try to commit suicide.
• Factors that contribute to borderline per-
sonality disorder include the genetic and
neurological underpinnings of emotional
dysregulation, a relatively low threshold
for emotional responsiveness, an easily
changeable sense of self, cognitive distor-
tions, and a history of abuse, neglect, or
feeling invalidated by others. Treatment
for borderline personalit y may include
medication, DBT, CBT, intensive psy-
chodynamic therapy, and IPT.
• The ha l l m a rk of h ist r ion ic per sona l-
ity disorder is attention seeking, usually
through exaggerated emotional displays.
Symptoms may also include a sense of
boredom or emptiness and a low tolerance
for frustration.
• Narcissistic personality disorder is charac-
terized by a grandiose sense of self-impor-
tance and a constant desire for praise and
admiration. People with this disorder may
also feel a sense of entitlement, behave
ar rogantly, and have dif f icult y under-
standing other people’s points of view.
Fearful/Anxious Personality
Disorders
• The hallmark of avoidant personality dis-
order is social inhibition, which usually
stems from feeling inadequate and being
overly sensitive to negative evaluation.
Although similar to social phobia, the cri-
teria for avoidant personality disorder are
more pervasive and involve a more gen-
eral reluctance to take risks. CBT meth-
ods that are used to treat social phobia can
also be effective with avoidant personality
disorder.
• Dependent personality disorder is char-
a c t e r i z e d by s u b m i s s ive a nd c l i n g y
behaviors, based on fear of separation;
these behav ior s are intended to el icit
at tent ion a nd rea s su r a nce, a nd pl ace
responsibilit y for making decisions on
other people. People with dependent per-
sonality disorder are chronically plagued
by self-doubt and consistently underesti-
mate their abilities; in fact, they may not
know how to function independently.
• Obsessive-compulsive personalit y dis-
order i s ch a r acter i zed by preoccupa-
t ions w ith per fect ion ism, orderl iness,
a nd sel f- cont rol a nd by low level s of
f lex ibi l it y and ef f iciency. These r ig id
personality traits may lead these people
to have diff iculty prioritizing and mak-
i ng decision s, a nd t hey a re of ten i n –
t oler a nt of emot ion a l or “ i l log ic a l ”
behavior in others.
Personality disorders (p. 401)
Personality (p. 403)
Cluster A personality disorders (p. 405)
Cluster B personality disorders (p. 405)
Cluster C personality disorders (p. 405)
Paranoid personality disorder (p. 411)
Schizoid personality disorder (p. 413)
Schizotypal personality disorder (p. 414)
Antisocial personality disorder (p. 418)
Conduct disorder (p. 418)
Psychopathy (p. 419)
Borderline personality disorder (p. 422)
Dialectical behavior therapy (DBT) (p. 428)
Histrionic personality disorder (p. 429)
Narcissistic personality disorder (p. 431)
Avoidant personality disorder (p. 433)
Dependent personality disorder (p. 435)
Obsessive-compulsive personality disorder
(p. 436)
Key Terms
More Study Aids
For additional study aids related to this chapter, including
quizzes to make sure you’ve retained everything you’ve
learned and a Student Video Activity exploring the possible
connections between personality disorders and brain
disorders, go to: www.worthpublishers.com/launchpad/
rkabpsych2e.
Image Source Black/Alamy
Personality Disorders 441
443
CHAPTER 14
Neurodevelopmental
and Disruptive Behavior
Disorders
ela and Carlos Enriquez have three children: Javier, Pia, and
Richie. It’s been a very challenging year for the family, full of
heartache; all three children have been having various difficul-
ties at home or at school. Lela and Carlos are trying to figure out
what, exactly, the problems are and what can be done about them.
The most troubling problem concerns their youngest son, Richie.
He’s almost 2 years old, but he has yet to smile at his parents—or
anyone else. He’s not talking, either, and although he seems to un-
derstand what people say to him, he is a bit slow to respond. Whereas
most toddlers are talking in two- or three-word sentences, Richie
doesn’t say even single words. Richie also seems shy in the extreme;
he doesn’t even look people in the eye.
Richie’s older siblings have also been having problems. Javier
is 10 years old, and he’s had both academic and social problems at
school; his teacher suggested that he receive a thorough evaluation.
And his 8-year-old sister, Pia, has been a bit of a puzzle. On her last
report card, her teacher noted that she’s very bright but doesn’t seem
to be working as hard as she could.
Like Richie, Pia, and Javier, many children achieve milestones,
such as walking and talking, later than the average child or have
problems socially or academically. When do such difficulties fall in
the range of normal development, and when do they signal a larger
problem? In this chapter we address this question by exploring two
categories of DSM-5 disorders that typically arise in childhood:
(1) neurodevelopmental disorders, which involve problems with the
brain—the neuro part of the term—and are typically first diagnosed
during infancy, childhood, or adolescence—the developmental part of
the term, and (2) disruptive behavior disorders, also typically first
diagnosed before adulthood. However, we must note that these are
not the only disorders that can affect children; children can also be
diagnosed with many of the disorders discussed in previous chapters.
Intellectual Disability (Intellectual
Developmental Disorder)
What Is Intellectual Disability?
Understanding Intellectual Disability
Treating Intellectual Disability
Autism Spectrum Disorder
What Is Autism Spectrum Disorder?
Understanding Autism Spectrum Disorder
Treating Autism Spectrum Disorder
Specific Learning Disorder: Problems
with the Three Rs
What Is Specifi c Learning Disorder?
Understanding Specifi c Learning Disorder
Treating Dyslexia
Disorders of Disruptive Behavior and
Attention
What Is Conduct Disorder?
What Is Oppositional Defi ant Disorder?
What Is Attention-Defi cit/Hyperactivity Disorder?
Understanding Disorders of Disruptive Behavior
and Attention
Treating Disorders of Disruptive Behavior and
Attention: Focus on ADHD
Luis Mariano González/Getty Images. Photo for illustrative purposes only; any individual depicted is a model.
We begin this chapter by examining intellectual disability—a disorder that
can profoundly affect the lives of children and their families and that may require
special schools or residential placements as well as other special services.
Intellectual Disability (Intellectual
Developmental Disorder)
When either Lela or Carlos calls Richie’s name, he often seems to ignore it. They
can tell that he’s not deaf—he clearly notices street noises and other sounds, and
he startles in response to loud noises. His cognitive abilities are noticeably less
developed than Javier’s and Pia’s were when they were his age; Richie’s intellec-
tual functioning doesn’t seem normal. Could he have intellectual developmental
disorder?
What Is Intellectual Disability?
Intellectual disability (also called intellectual developmental disorder [IDD], and
related to what was previously called mental retardation, a term that is generally no
longer used) is characterized by deficits in cognitive abilities (significantly below
normal), as determined both by standardized intelligence testing and by clinical
assessment, along with impaired adaptive functioning in daily life. Specific deficits
are in academic learning, in social understanding, and in “practical understanding”
(such as knowing how to manage money) and involve a variety of cognitive abili-
ties: reasoning and problem solving, planning, abstract thinking, judgment, and
understanding complex ideas.
Although the DSM-5 criteria themselves do not specify a specific IQ score
cutoff, the part of the manual that discusses the criteria in detail suggests that
impaired intelligence would entail having an IQ score that is at least two standard
deviations below average. On a standard IQ test where the mean is set at 100, an
IQ approximately equal to or less than 70 (plus or minus 5 points) would be two
standard deviations below average.
But DSM-5 is clear that a low IQ by itself is not enough to diagnose IDD; the
child must also have impaired adaptive functioning in daily life as a result of the
cognitive deficits. Adaptive functioning involves three domains, assessed relative to
the person’s age and background:
• conceptual (language, mathematical, reasoning used to solve problems, and judg-
ments in novel situations),
• social (being aware of and having empathy for other people’s experiences and emo-
tions; the capacity for friendship and social judgment and communication), and
• practical ( bei ng able to ca re for onesel f; m a nage money, school, a nd job
responsibilities).
The deficits in intellectual ability and adaptive functioning (see Table 14.1) must
have emerged during childhood and thus cannot be the result of brain trauma in
adulthood.
A lthough a per son’s IQ score may ser ve as a rough g uide to eva luat ing
ment a l abi l it ies, the most i mpor t ant cr iter ion for deter m in ing the level of
intel lect ua l d isabi l it y is the level of impaired adaptive f unction ing. DSM-5
specif ies four levels of severit y of these impairments—mild, moderate, severe,
and profound—which ref lect functioning in conceptual, social, and practical
Intellectual disability
A neurodevelopmental disorder characterized
by cognitive abilities that are significantly
below normal, along with impaired adaptive
functioning in daily life; also called intellectual
developmental disorder and previously
referred to as mental retardation.
TABLE 14.1 • DSM-5 Diagnostic
Criteria for Intellectual Disability
(Intellectual Developmental
Disorder)
A. Deficits in intellectual functions, such
as reasoning, problem solving, planning,
abstract thinking, judgment, academic
learning, and learning from experience,
confirmed by both clinical assessment
and individualized, standardized
intelligence testing.
B. Deficits in adaptive functioning that
result in failure to meet developmental
and socio-cultural standards for personal
independence and social responsibility.
Without ongoing support, the adap-
tive deficits limit functioning in one
or more activities of daily life, such as
communication, social participation, and
independent living, across multiple envi-
ronments, such as home, school, work,
and community.
C. Onset of intellectual and adaptive defi-
cits during the developmental period.
Reprinted with permission from the Diagnostic and
Statistical Manual of Mental Disorders, Fifth Edition,
(Copyright ©2013). American Psychiatric Association. All
Rights Reserved.
444 C H A P T E R 1 4
domains. In general, the greater the severity, the more impaired the person
is likely to be:
• Mild intellectual disability. Most people with intellectual disability fall into this
group. People in this mild range may be able to function relatively inde-
pendently with training but usually need additional help and support during
stressful periods and seem “immature” in social interactions.
• Moderate intellectual disability. Although they are not able to function indepen-
dently, with training and supervision, people in this group may be able to per-
form unskilled work and take basic care of themselves; although able to have
relationships, people in this range may not accurately interpret social cues.
• Severe intellectual disability. A small number of people with intellectual dis-
ability fall into this group. Adults in this group are likely to live with their
family or in a supervised setting and are able to perform simple tasks only with
close supervision. They may be able to speak in simple phrases and do simple
counting. During childhood, they may begin speaking later than other children.
• Profound intellectual disability. The smallest number of people with intellectual
disability fall into this group. People in this group need constant supervision
or help to perform simple tasks and may communicate only nonverbally; they
are likely to have significant neurological problems.
Information from parents and teachers may help the clinician to determine a
person’s ability to function. Depending on IQ and level of adaptive functioning,
someone with IDD may require supervision, ranging from minimal to constant care.
Like Larry in Case 14.1, many of these people have needs and abilities that fall some-
where in the middle.
CASE 14.1 • FROM TH E OUTSIDE: Intellectual Disability
Larry, a 34-year-old man with moderate [intellectual disabilities]. . . had been referred for
complaints of seeing “monsters,” “scary faces,” and “the bogeyman.” He initially appeared
paranoid and delusional, describing the feared bogeyman in detail. An assessment of pos-
sible neurochemical or physical factors that might help explain the recent onset of these
symptoms yielded no significant diagnostic information. . . .
Larry’s perception of monsters was specific to certain situations, such as being alone in
a dark room. . . .
Specifically, when asked to go alone to any dark place [including the dark stairwell in
his group home, where Larry must go to carry out his assigned chore of taking down the
trash], he became agitated, resisted, and made loud statements about monsters and scary
faces. . . .
Larry’s monsters could be attributed to his limited means of communicating his fear of
being alone in the dark. [It appears, then, that Larry has a phobic response to the dark.] . . .
(Nezu et al., 1992, pp. 78, 164)
Larry had two disorders: intellectual disability and a specific phobia. because of
his intellectual disability, he had difficulty explaining his fears. He received CBT for
his phobia, which was successful, and he was then able to go down to the basement
without fear.
Like people of normal intelligence, people with intellectual disability exhibit a
wide variety of personality characteristics: some are passive or easygoing, and others
are impulsive or aggressive; some people with intellectual disability, like Larry, may
have difficulty communicating verbally—which can heighten aggressive or impul-
sive tendencies. People with intellectual disability are more likely than average to be
exploited or abused by others. Table 14.2 lists additional facts about IDD.
Like Sean Penn’s character in the movie
I Am Sam, people with mild intellectual
disability can, with training, learn to function
independently. In this scene Penn is shown with
Michelle Pfeiffer, who plays his lawyer in his
fight to retain custody of his young daughter.
N
ew
L
in
e
C
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C U R R E N T C O N T R O V E R S Y
Changing Mental Retardation to
Intellectual Disability: Will Such a
Switch Be Beneficial?
People with intelligence levels low enough to affect their
daily life have been labeled in various ways over the decades.
The newest change in the DSM-5 is to replace the diagno-
sis of mental retardation with that of intellectual disability. How-
ever, this is not simply a change in label; the criteria have
changed: The diagnosis and its severity are no longer a func-
tion of the assessed intelligence level. (Previously the diag-
nosis and its severity were anchored in IQ scores of various
ranges.) Rather, the diagnosis and its severity are now based
on levels of adaptive functioning—how well the person can
adapt and function—in three domains: conceptual, social,
and practical.
On the one hand, the new name more accurately describes
the disorder in that it is not simply that mental abilities are
delayed (that is “retarded”). Moreover, changing the criteria
to deemphasize IQ scores and emphasize the three domains of
functioning is ultimately more relevant to people’s ability to
function and their need for services.
On the other hand, if the name change has been made in
order to reduce stigma, it could be just a matter of time before
this new diagnosis becomes a stigmatizing label. The diagnosis
may be more descriptive, but is the description accurate? If
the emphasis is more on adaptive functioning than intellectual
level, then using the diagnostic term “intellectual disability”
could be confusing.
CRITICAL TH I N KI NG Do you think that the term intellectual
disability will come to be as stigmatizing as mental retardation?
Why or why not? Is there a better word than intellectual, given
that the diagnosis focuses more on the ability to adapt and
function than on intellect?
( James Foley, College of Wooster)
TABLE 14.2 • Intellectual Disability Facts at a Glance
Prevalence
• Approximately 1% of the general population has intellectual disability; however, prevalence estimates vary depending on the age, the survey
method used, and the particular population studied.
Onset
• Severe and profound intellectual disability are generally identified at birth, although in some cases intellectual disability is caused by a medical condition
later in childhood, such as head trauma.
• Mild intellectual disability is sometimes not diagnosed until relatively late in childhood, although the onset may have been earlier.
Comorbidity
• Compared to the general population, people with intellectual disability are three to four times more likely to have an additional psychological
disorder, cerebral palsy, or epilepsy.
• Among the most common comorbid disorders are major depressive disorder, attention-deficit/hyperactivity disorder, and autism spectrum disorder.
Course
• The diagnosis is typically lifelong for moderate to severe intellectual disability, but beneficial environmental factors can improve adaptive func-
tioning for those with mild intellectual disability to the point where they no longer meet all the criteria for the disorder.
• Educational opportunities, support, and stimulation can improve the level of functioning.
Gender Differences
• Intellectual disability occurs more frequently in males, with a male-to-female ratio of about 1.5 to 1.
Cultural Differences
• Although the criteria for intellectual disability used in many other countries are similar to those used in the United States, they are not always the
same; such differences may account for the higher prevalence rates in some other countries, such as 4.5% in France (Oakland et al., 2003).
Source: Unless otherwise noted, the source for information is American Psychiatric Association, 2013.
446 C H A P T E R 1 4
TABLE 14.3 • Genetic Causes of Intellectual Disability
Cause of intellectual disability Genetic abnormality
Down syndrome Abnormality in chromosome 21
Rett’s disorder (females only) Abnormality in X chromosome (which is lethal for male fetuses)
Fragile X ( the most common cause of
inherited intellectual disability)
Repetition of a piece of genetic code on the X chromosome that becomes progressively more
severe in each generation
Prader-Willi and Angelman syndromes Deletion on chromosome 15 that has different consequences depending on which parent’s genes
contribute the deletion
Phenylketonuria (PKU) A genetically based defect in an enzyme, phenylalanine hydroxylase, that leads to a failure to
convert phenylalanine to tyrosine. Unconverted phenylalanine is toxic to brain cells, leading to
intellectual disability, which can be prevented if PKU is identified (through a blood test at birth)
and the person adheres to a diet that restricts phenylalanine.
Congenital hypothyroidism Inadequate production of thyroid hormone caused by a genetic mutation. The fetus gets thyroid
hormone from the mother, but after birth, the deficiency leads to defects in the developing brain.
If hypothyroidism is not detected within the first 3 months of life, the damage cannot be reversed,
even with thyroid hormone replacement.
Source: For more information see the Permissions section.
Understanding Intellectual Disability
Many neurological events can lead to intellectual disability, some of which reflect
the fact that the fetus was exposed to certain types of substances (such as drugs or
a virus) or to other stimuli (such as radiation); such harmful substances and stimuli
are referred to as teratogens. Intellectual disability may also result from particu-
lar complications during labor (such as occurs when a newborn receives insufficient
oxygen during birth) or from exposure to high levels of lead prenatally or during
childhood.
Neurological Factors: Teratogens and Genes
One type of teratogen is environmental toxins, to which a fetus typically is exposed
through the placenta after the toxin has entered the mother’s bloodstream. Examples
of environmental toxins include synthetic chemicals such as methyl mercur y,
polychlorinated biphenyls (PCBs), and pesticides. Exposure to these toxins in the
first trimester of pregnancy can disrupt early developmental processes of the central
nervous system (Lanphear et al., 2005). Intellectual disability may also
arise because of a variety of genetic abnormalities, listed in Table 14.3.
The cognitive and behavioral def icits observed in people with
intellectual disability occur because the brain does not process infor-
mation appropriately, often because of abnormal brain structure. For
example, fetal alcohol syndrome is a set of birth defects caused by the
mother’s alcohol use during pregnancy. (Alcohol is a teratogen.) People
who have this syndrome have an unusually small head size, which occurs
in part because the frontal lobes are smaller than normal—specifically
the portions involved in planning, carrying out tasks, and controlling
impulsive behavior (Riley & McGee, 2005). All of these activities are
difficult for many children with fetal alcohol syndrome.
A lthough severe or profound intellectual disabilit y often involves global
abnormalities, each case of mild or moderate IDD may have a unique prof ile of
specific impaired abilities, related to the particular cause of the disability.
Teratogens
Substances or other stimuli that are harmful
to a fetus.
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The characteristic facial features associated
with fetal alcohol syndrome include small
eyes; a smooth philtrum—the space between
the upper lip and the nose; and a thin upper lip.
Neurodevelopmental and Disruptive Behavior Disorders 447
Psychological Factors: Problem Behaviors
People with intellectual disability often engage in two types of problematic be-
haviors that are not specifically mentioned in the DSM-5 criteria: (1) stereotyped
behaviors (also referred to as stereotypies), which are repetitive behaviors that don’t
serve a function, such as hand flapping, slight but fast finger and hand motions, and
body rocking; and (2) self-injurious behaviors, such as hitting the head against some-
thing and hitting or biting oneself. People with intellectual disability who exhibit
both stereotypic behaviors and self-injurious behaviors have greater deficits in non-
verbal social skills than those with only one type of problematic behavior (Matson
et al., 2006).
Other problematic behaviors that often go along with intellectual disabil-
it y include consistently choosing to interact with objects rather than people,
inappropriately touching others, and resisting physical contact or affection.
Social Factors: Understimulation
If an infant is severely understimulated (e.g., the child is not played with enough) or is
undernourished, he or she may subsequently develop intellectual disability (Dennis,
1973; Dong & Greenough, 2004; Skeels & Dye, 1939). For example, children raised
in orphanages where they are essentially warehoused, ignored and neglected, may
develop this disorder.
In sum, most cases of intellectual disability arise primarily from neurological
factors—teratogens or genes—that produce abnormal brain structure and function,
which then cause cognitive deficits. Children with intellectual disability may exhibit
stereotyped or self-injurious behaviors.
Treating Intellectual Disability
Intellectual disability cannot be “cured,” but interventions can help people with
IDD to function more independently in daily life. Such interventions are designed
to improve specific skills and abilities, such as the person’s ability to communicate.
But more than that, clinicians try to prevent intellectual disability from arising in the
first place. Prevention efforts seek to avert or reduce the factors that cause intellectual
disability.
Targeting Neurological Factors: Prevention
Because the key causes of intellectual disability are neurological, this type of factor
is the target of prevention efforts. For example, one successful prevention effort
focuses on phenylketonuria (PKU). Since the 1950s, virtually all newborns in the
United States have received a test to detect whether they have PKU, which addresses
a problem metabolizing the enzyme phenylalanine hydroxylase. For newborns who
test positive, lifelong dietary modifications can prevent any brain damage, thereby
preventing intellectual disability.
Another successful prevention effort addresses childhood exposure to lead,
which can trigger brain abnormalities. Lead was banned as an ingredient in paint
in 1978; laws were passed that required landlords and homeowners to inform any
prospective renters or buyers of any known lead paint on the property. Begin-
ning in the 1970s, lead was also phased out as an additive to gasoline. As a result
of these measures, lead exposure—and lead-induced intellectual disability—has
decreased.
There are no neurological treatments for intellectual disabilit y, although
symptoms of comorbid disorders and some self-injurious behaviors may respond to
medication (Unwin & Deb, 2011).
When this child gets excited, she engages in
the stereotyped behavior of hand flapping.
Other stereotyped behaviors exhibited by
people with intellectual disability include
rocking back and forth and repeatedly moving
a finger.
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Stereotyped behaviors
Repetitive behaviors—such as body rocking—
that do not serve a function; also referred to
as stereotypies.
448 C H A P T E R 1 4
Targeting Psychological and Social Factors: Communication
Given the deficits and heterogeneous symptoms that accompany intellectual dis-
ability, no single symptom is the focus of all psychological and social treatments.
Rather, psychological and social treatments depend on the person’s specific con-
stellation of symptoms and comorbid disorders. In some cases, treatment targets
significant communication deficits. Such treatment may teach nonvocal com-
munication, for example, using a technique called the Picture Exchange
Communication System (PECS) (Bondy & Frost, 1994). With this system,
children learn to give a picture of the desired item to someone in exchange
for that item.
Targeting Social Factors: Accommodation in the Classroom—It’s
the Law
With the passage of the Americans with Disabilities Act in 1990 and the subse-
quent Individuals with Disabilities Education Act (IDEA) in 1997, eligible children
with disabilities between the ages of 3 and 21 are guaranteed special education and
related services that are individually tailored to the child’s needs, at no cost to the
parents. An individualized education program (IEP) specifies educational goals as well
as supplementary services or products that should be used to help the student benefit
from the regular curriculum. Each child with disabilities receives a comprehensive
evaluation, and the child is placed in the least restrictive environment that responds
to his or her needs.
For many children, one goal of the IEP is to facilitate inclusion—
placing students with disabilities in a regular classroom, with guidelines for
any accommodations that the regular classroom teacher or special education
teacher should make. Note that mainstreaming is not the same as inclusion;
mainstreaming simply refers to placing a child with disabilities into a regular
classroom, with no curricular adjustments to accommodate the disability.
Legal mandates have brought people with intellectual disability
(and other disabilities) out from the shadows of institutional living into
society: Depending on the severity of their retardation, they live in com-
munities, hold jobs, and have families.
Is intellectual disability an appropriate diagnosis for Richie Enriquez?
It may well be, but in the next section, we’ll examine a set of disorders
that might better account for these problems.
Clare just graduated from college and started working in a center for adults with various in-
tellectual disabilities. She is trying to get to know each client—his or her strengths and weak-
nesses. The clients with intellectual disability are classified in the moderate-to-severe range.
Based on what you’ve learned, what can—and can’t—you assume about those clients? Why
might people with mild or profound intellectual disability not be at the center?
Thinking Like A Clinician
Autism Spectrum Disorder
Richie Enriquez exhibits some behaviors that are not typical of people diagnosed
with intellectual disability: He avoids making eye contact, hardly smiles, and can
spend hours playing with a glittery plastic ball. When his mother takes a toy away
from him, perhaps because it’s time for lunch, he has a nuclear-sized temper tantrum:
“He screams, he cries, he hits his head against the wall. . . . I don’t know what to
Like this girl with Down syndrome, youngsters
with mild to moderate intellectual disability
may be placed in regular classrooms, either
as part of inclusion (in which the teacher
makes specific accommodations based on
the child’s special needs) or mainstreaming
(in which the teacher doesn’t make specific
accommodations).
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Inclusion
The placement of students with disabilities in
a regular classroom, with guidelines for any
accommodations that the regular classroom
teacher or special education teacher should
make.
With the Picture Exchange Communication
System, a child who has intellectual disability
with poor verbal communication skills can
make his or her desires known: The child
presents a card with the picture of the desired
object to another person, who then may give
the actual object to the child.
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Neurodevelopmental and Disruptive Behavior Disorders 449
do. When I try to hold him, to comfort him, it seems to make things even worse.
I’ve never seen a child like him.” His father notes that “if the evening routine—din-
ner, bath, three books, bed—varies, if I forget to read the third book, Richie freaks
out, rocking himself and screaming. And he has no interest in playing with Javier
and Pia—even though they try so hard to get him to play or to laugh.” From these
descriptions, Richie’s behaviors sound like symptoms of autism spectrum disorder.
What Is Autism Spectrum Disorder?
Autism spectrum disorder (ASD) is characterized by deficits in communication
and social interaction skills, as well as stereotyped behaviors and narrow interests. The
term spectrum is used because people with the disorder may differ in the severity of the
symptoms and in their developmental level relative to their chronological age. The
term autism by itself does not capture the range of variations that can occur. As noted
in Table 14.4, the DSM-5 criteria include problems with social communication and
interaction: difficulty with normal back-and-forth conver-
sations or even initiating social interaction, poor eye con-
tact, difficulty using facial expressions and body language
as a means of communication, difficulty understanding
the social communication of others, and difficulty devel-
oping and maintaining age-appropriate relationships.
Like children with intellectual disability (but unlike
other children), children with ASD (1) are much more or
much less reactive to sensory stimuli, (2) engage in very
repetitive play, and (3) often display stereotyped behaviors
(such as flapping their hands). These children insist on re-
peating the same behaviors or activities for much longer pe-
riods than other children do. People with ASD also become
distressed when certain routines are not carried out or com-
pleted, as was Richie when his father varied the evening ac-
tivities in any way; to calm themselves down, they may rock
themselves, as did Richie. To diagnose ASD, these symp-
toms must impair the ability to function on a daily basis.
ASD is caused pr imar ily by neurological abnor-
malities and dysfunctions (Ecker et al., 2012; Kundert &
Trimarchi, 2006). Symptoms of ASD usually become evi-
dent during infancy or early childhood, and many chil-
dren also have comorbid intellectual disability, which
may be true of Richie. Children for whom intellectual
disability is the only psychological disorder usually look
people in the eye, and they tend to respond when hearing
their names and to smile at other people. In contrast, chil-
dren with ASD—with or without intellectual disability—
generally avoid eye contact and shy away from social
interactions. (DSM-IV, the previous version of DSM,
contained two separate disorders—autistic disorder and a
milder form, Asperger’s disorder—that have been combined
in DSM-5, in part because research suggests that they
have related symptoms and etiology; Towbin et al., 2002.)
People with ASD tend to be oblivious to—and so ap-
pear to ignore—others. Younger children with ASD appear
to be uninterested in making friends. Some older children
may want to make friends, but they don’t understand the
basic rules of social interaction; thus, their attempts are
Autism spectrum disorder (ASD)
A neurodevelopmental disorder characterized
by deficits in communication and social
interaction skills, as well as stereotyped
behaviors and narrow interests.
TABLE 14.4 • DSM-5 Diagnostic Criteria for Autism Spectrum
Disorder (ASD)
A. Persistent deficits in social communication and social interaction across
multiple contexts, as manifested by the following, currently or by history
(examples are illustrative, not exhaustive; see text):
1. Deficits in social-emotional reciprocity, ranging, for example, from
abnormal social approach and failure of normal back-and-forth conver-
sation; to reduced sharing of interests, emotions, or affect; to failure to
initiate or respond to social interactions.
2. Deficits in nonverbal communicative behaviors used for social interac-
tion, ranging, for example, from poorly integrated verbal and nonverbal
communication; to abnormalities in eye contact and body language or
deficits in understanding and use of gestures; to a total lack of facial
expressions and nonverbal communication.
3. Deficits in developing, maintaining, and understanding relationships,
ranging, for example, from difficulties adjusting behavior to suit various
social contexts; to difficulties in sharing imaginative play or in making
friends; to absence of interest in peers.
B. Restricted, repetitive patterns of behavior, interests, or activities, as
manifested by at least two of the following, currently or by history
(examples are illustrative, not exhaustive; see text):
1. Stereotyped or repetitive motor movements, use of objects, or speech
(e.g., simple motor stereotypes, lining up toys or flipping objects,
echolalia, idiosyncratic phrases).
2. Insistence on sameness, inflexible adherence to routines, or ritualized
patterns of verbal or nonverbal behavior (e.g., extreme distress at small
changes, difficulties with transitions, rigid thinking patterns, greeting
rituals, need to take same route or eat same food every day).
3. Highly restricted, fixated interests that are abnormal in intensity or
focus (e.g., strong attachment to or preoccupation with unusual objects,
excessively circumscribed or perseverative interests).
4. Hyper- or hyporeactivity to sensory input or unusual interest in sensory
aspects of the environment (e.g., apparent indifference to pain/temperature,
adverse response to specific sounds or textures, excessive smelling or touch-
ing of objects, visual fascination with lights or movement).
C. Symptoms must be present in the early development period (but may not
become fully manifest until social demands exceed limited capacities, or
may be masked by learned strategies in later life).
Reprinted with permission from the Diagnostic and Statistical Manual of Mental Disorders, Fifth
Edition, (Copyright ©2013). American Psychiatric Association. All Rights Reserved.
450 C H A P T E R 1 4
unlikely to be successful. To understand how symptoms of ASD translate into daily life,
consider the following list of “peculiarities” that a mother compiled about her 4-year-
old son, George, before he was diagnosed with autism (Moore, 2006, pp. 94–95):
• He talks [by reciting] quotations and by imitating adult speech.
• Has poor social interaction. Doesn’t know how to play with others.
• Avoids eye contact with strangers.
• He is very excitable (easily aroused, not easy to calm).
• He complains about strong stimuli, such as the sun, loud noises.
• Abnormalities of attention, including the ability to shut people out and be
absorbed in something trivial for a long time.
• Loves nature, will stand and look at the moon for as long as he is allowed,
despite freezing weather.
• Has a strong aversion to strangers, groups, and crowds.
• Obsessive.
• Ritualistic.
• Lines up [Lego bricks or matches them by color, but] doesn’t build. Always destroys.
• Occasionally plays with feces.
• Doesn’t dress or undress—just beginning to put on trousers and coat.
• Could recognize simple words at twenty months.
• Has a strong reaction to colors.
• Never asks questions except where is Mummy, Daddy, Sam.
• Only just starting to correlate facial expressions of others to emotion.
These behaviors might not be that unusual for a 1-year-old, but they are definitely not
typical for a 4-year-old. The items on George’s mother’s list span the problem areas that
are the hallmarks of ASD: impaired communication and social interactions and restricted
and repetitive behaviors. Some of these problem areas—symptoms of ASD—overlap with
symptoms of schizophrenia that arises during childhood: playing with feces, not dressing
oneself, and becoming very upset in response to unwanted change. However, symptoms
of ASD are present in early childhood (e.g., before age 3), as was true of George, and
symptoms of childhood schizophrenia typically emerge later, after normal development.
DSM-5 also specifies three levels of severity of ASD, each of which is associated
with different levels of required support. The least severe level requires some support,
and the most severe level requires very substantial support.
When assessed with an intelligence test that measures both verbal and visual abili-
ties, many people with ASD are also diagnosed as having intellectual disability. When
researchers use an intelligence test that does not rely on verbal instructions or responses,
however, intelligence scores of people with ASD are often significantly higher—in or
above the average intelligence range (Dawson, Mottron, et al., 2005). Moreover, unlike
people who have intellectual disability, people with ASD may not be impaired in all
domains (although, as a rule, the impairments are general enough to be considered
pervasive). In fact, about 20% of people with ASD have pockets of unique skills relating
to art, music, numbers, or calendars, such as the ability to identify the day of the week
on which a given date fell, even when the date is many years in the past (Hermelin,
2001); such people are sometimes referred to as autistic savants. James, the person de-
scribed in Case 14.2, has a remarkable ability to remember information he has heard.
George, on the left, is the oldest of three boys
and has ASD; his middle brother, Sam, also
has ASD; his youngest brother does not. The
brothers, and their mother, Charlotte, are
shown here.
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CASE 14.2 • FROM TH E OUTSIDE: Autism Spectrum Disorder
James was the third of four children, born following an uncomplicated pregnancy and la-
bor. His health during the first 3 months of life was good, but shortly thereafter his mother
expressed concern because of his sensitivities to light and sound, his failure to make an an-
ticipatory response to being picked up, his fluctuating moods between inconsolable crying
and extreme passiveness, and his failure to look at her when she fed him. She reported that
he preferred lying in his crib, staring at the mobile, to being held or played with. Because
his motor milestones appeared at the appropriate times, James’s pediatrician reassured his
Neurodevelopmental and Disruptive Behavior Disorders 451
TABLE 14.5 • Autism Spectrum Disorder Facts at a Glance
Prevalence
• Up to 1% of the population has ASD, but among children and adolescents (which is a younger cohort), the estimate is closer to 2% (Blumberg
et al., 2013).
• The reported prevalence of ASD is increasing (Atladóttir, 2007; Hertz-Picciotto & Delwiche, 2009), at least in part because of earlier diagnosis of
the disorder (Parner et al., 2008).
Onset
• Symptoms usually arise during infancy (Ozonoff et al., 2008).
• However, symptoms may not be recognized until the second year of life (or earlier, if symptoms are severe).
Comorbidity
• Between 50% and 70% of people with ASD also have intellectual disability (Sigman et al., 2006). However, some researchers believe the high comor-
bidity is an overestimate (Edelson, 2006), particularly because people with ASD tend to have higher IQs when tested using nonverbal IQ tests.
Course
• Children with ASD often improve in some areas of functioning during the elementary school years (Shattuck et al., 2007).
• During adolescence, some children’s symptoms worsen, whereas other children’s symptoms improve (Fountain et al., 2012).
Gender Differences
• Males are four times more likely than females to develop ASD.
Source: Unless otherwise noted, the source for information is American Psychiatric Association, 2013.
mother that his development was fine. By age 16 months, James had not begun to babble or
say single words, and spent most of his time in a corner, repetitively moving toy cars back and
forth. At 20 months, other symptoms emerged: he developed unusual hand movements and
body postures; his obliviousness to people increased; he reacted to even the most subtle inter-
ruption in his routine or other changes in the world with extreme disorganization and panic;
he developed a fascination with light switches and with studying tiny bits of paper and twigs.
At 4 years, James had not yet begun to speak socially to others, but could identify by
name many numbers and all of the letters of the alphabet. . . He persisted in lining up
objects in the most complex patterns, but could never use objects appropriately. . . At about
the age of 4-1/2 years, he began to echo long and complicated sentences, some of which his
mother reported he may have heard days or even weeks before. He was able to complete
puzzles designed for 8- and 9-year olds quickly, but was unable to reproduce a line or circle.
At about age 5, James made his first spontaneous statement. His mother reported that
he had been looking at the sky and said, “It looks like a flower.” He did not speak again for
8 months, but then began talking in full sentences. . . When he met strangers, he mechani-
cally introduced himself without ever establishing eye contact, and then rushed on to ask
what the person’s birthday, anniversary, and social security number were, often appearing
to pause long enough to get the answers. Years later, upon re-meeting the person, he was
able to recite back these facts.
(Caparulo & Cohen, 1977, pp. 623–624; case printed in Sattler, 1982, p. 474)
For the most part, people with ASD do not go through childhood milestones
(language, social, or motor) in a normal fashion. They may speak with a monotone
voice, and the rhythm of their speech may be odd. Moreover, they often have a
variety of problems with attention and may be impulsive or aggressive. Typically,
children with ASD have only one narrow interest, such as the names of subway sta-
tions. Richie probably has intellectual disability and ASD: intellectual disability best
explains his general cognitive slowing, which is not limited to social interactions. His
other odd behaviors—such as avoidance of eye contact, lack of social interest in his
siblings, and extreme preoccupation with his ball—are best accounted for by ASD.
Table 14.5 provides additional facts about ASD.
452 C H A P T E R 1 4
Understanding Autism Spectrum Disorder
ASD appears to be rooted primarily in neurological factors, which interact with
psychological and social factors. The symptoms themselves involve a range of
psychological and social factors.
Neurological Factors
ASD is associated with significant abnormalities in brain structure and function.
Brain Systems
The connections among brain areas appear abnormal in ASD (Minshew & Williams,
2007). Moreover, brain areas in the same immediate region appear to communicate
excessively, whereas distant areas appear not to communicate enough (Courchesne
& Pierce, 2005); in particular, the frontal lobes apparently do not communicate
effectively with other brain areas (Murias et al., 2006). In addition, parts of the fron-
tal lobes often are less active than normal, which is consistent with the documented
deficits in executive function in ASD (Silk et al., 2006).
Genetics
How might these abnormalities arise? Genes appear to play a role. Researchers have
long observed that ASD tends to run in families; 8% of siblings of affected children
will also have the disorder (compared to at most 0.2% of the general population;
Muhle et al., 2004). Additional evidence comes from twin studies: Monozygotic
twin pairs are up to nine times more likely to have the disorder than are dizygotic
twin pairs (Bailey et al., 1995; Hallmayer et al., 2011; Le Couteur et al., 1996).
However, researchers have not located a single gene that gives rise to ASD (Weiss
et al., 2008). Instead, most forms of ASD probably result from interactions among
genes—perhaps 15 or more of them (Santangelo
& Tsatsanis, 2005).
Psychological Factors: Cognitive
Deficits
Neurolog ica l factors produce psycholog ica l
symptoms, particularly cognitive deficits in shift-
ing attention and in mental flexibility (Chawarska
et al., 2010 ; Ozonoff & Jensen, 1999). These
def icit s u nderl ie the ex t reme d i f f icu lt y i n
transitioning from one activity to another that
people with more severe forms of ASD experi-
ence. These deficits also underlie a tendency to
focus on details at the expense of the broader
picture (Frith, 2003).
Another problem is difficulty recognizing
facia l ex pressions of emot ions ( Ser ra et a l.,
2003; Tye et al., 2013). For example, in one
study researchers used EEG to assess 3 – and
4 -year-olds’ brain act iv it y wh i le they were
show n photog raphs of faces that either ex-
pressed fear or had neutral expressions. Chil-
dren who did not have ASD had greater brain
activity in response to the fear expressions than
to the neutral expressions—but children with
ASD responded to both types of facial expres-
sions with the same pattern of brain activit y
(Dawson et al., 2004).
What is a person with ASD most likely to focus on in this picture? Answer: People
with ASD tend to focus on an object’s details, such as the doors of the bus in this
drawing, and can overlook the “big picture,” such as the fact that this drawing is
of a city.
GETTING THE PICTURE
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Neurodevelopmental and Disruptive Behavior Disorders 453
Jason McElwain, at 17, was manager of his
high school’s basketball team. At the final
home game, which his team was losing, with
4 minutes to go, he was allowed to play. Here
he is being cheered by his teammates and the
crowd after he went on to score 20 points
and win the game. Jason was diagnosed with
autism when he was 2 years old; he didn’t begin
speaking until he was 5 years old (Associated
Press, 2006). As he grew older, his social skills
improved (McElwain & Paisner, 2008).
A
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People with ASD also have difficulty viewing the world from another person’s
perspective—with using a theory of mind, which is a theory about other people’s
mental states (their beliefs, desires, and feelings) that allows each of us to predict how
others will react in a given situation (Tager-Flusberg, 1999). Because a theory of
mind requires thinking about somebody else, by definition, this ability involves both
psychological and social factors.
Social Factors: Communication Problems
The earliest indications of ASD arise in interactions with other people: Children with
ASD don’t respond to their own name or to parents’ voices (Baranek, 1999); in addition,
they pay attention to other people’s mouths, not their eyes (Dawson, Webb, & McPart-
land, 2005). Moreover, their cognitive deficits in communication and in the ability to
recognize faces and emotions, both in voices (Rutherford et al., 2002) and in facial ex-
pressions (Bölte & Poustka, 2003), make social interactions confusing and unpredictable.
Even older children with ASD who have developed some
communication skills may still have deficits that prevent normal
conversation. And, despite adequate verbal skills, adults with ASD
often don’t understand elements of conversation involving a back-
and-forth exchange of information and interest in the other person,
and so cannot interact normally.
Treating Autism Spectrum Disorder
There is no cure for ASD, and no one type of intervention is help-
ful for all those with the disorder. Treatment of ASD generally
focuses on increasing communication skills and appropriate social
behaviors. The treatments that are most effective are time intensive
(at least 25 hours per week), require strong family involvement, are
individualized for each child, and begin as early in the child’s life as
possible (Rogers, 1998). Early treatment depends on early diagnosis
of the disorder; to ensure early diagnosis, the American Academy of
Pediatrics recommends that all children receive screening tests for
ASD before the age of 2 ( Johnson et al., 2007).
Targeting Neurological Factors
No treatments successfully target the neurological factors that underlie autism
spectrum disorders. Medication may help treat symptoms of comorbid disorders or
of agitation or aggression. The medications most likely to be prescribed are antipsy-
chotics and SSRIs (des Portes et al., 2003).
Targeting Psychological Factors: Applied Behavior Analysis
The technique most widely used to modify maladaptive behaviors associated with ASD is
called applied behavior analysis, which uses shaping to help people learn complex be-
haviors. The key idea is that a complex behavior is broken down into short, simple actions
that are reinforced and then ultimately strung together. For example, many children with
ASD eat with their hands and resist eating with utensils, which can create problems when
they eat with classmates or when the family goes out to eat. Thus, learning to use a spoon
is one behavior that is often shaped via applied behavior analysis. Initially, the therapist
looks for any spoon-related behavior—such as a glance at the spoon or the child’s moving
a hand near the spoon—and responds with verbal reinforcement (“That’s right, there is
the spoon, good job”) and perhaps some concrete reward, such as a small candy. After a
few successful attempts at approaching the spoon, the child is reinforced for picking up the
spoon, then for putting the spoon in the mouth, and finally for using it with food. Parents
of children with ASD are encouraged to use this method at home.
Theory of mind
A theory about other people’s mental states
(their beliefs, desires, and feelings) that allows
a person to predict how other people will
react in a given situation.
Applied behavior analysis
A technique used to modify maladaptive
behaviors by reinforcing new behaviors
through shaping.
454 C H A P T E R 1 4
Targeting Social Factors: Communication
Treatment for ASD that addresses social factors often focuses, in one way or another,
on facilitating communication and interpersonal interactions. For example, when a
child with ASD has severe communication difficulties, treatment may include the
use of PECS, a picture system for facilitating communication. For people who have
high-functioning ASD, treatment may focus on training appropriate social behaviors
through social skills groups or through individual instruction and modeling—
observing others engaging in appropriate social behavior and then role-playing such
behaviors (Bock, 2007). For instance, when Richie enters elementary school, he
might attend a social skills group for selected kindergarteners and first-graders; the
psychologist who leads such groups explicitly teaches the children appropriate social
behavior—such as making eye contact and asking and answering questions—and
has the children practice with each other. Parents are asked to continue social skills
training at home by modeling desired social behaviors and reinforcing their children
for improved behavior (Kransny et al., 2003).
In addition, various training programs have been developed to help people with ASD
who do not also have intellectual disability; such programs help them perceive and inter-
pret social cues—facial expressions and body language—more accurately. In fact, com-
puter games have been developed to provide such training (Golan & Baron-Cohen, 2006).
The center where Clare works also has clients with ASD. Based on what you have learned,
what is the most important information that Clare should know about people with this dis-
order and why? How might Clare use her knowledge about ASD when she is working with the
center’s clients?
Thinking Like A Clinician
Specific Learning Disorder:
Problems with the Three Rs
Richie Enriquez’s older brother, Javier, is in the 4th grade. Javier’s teacher has noted
that his reading ability doesn’t seem up to what it should be. Javier is a bright boy,
but when the students take turns reading aloud, Javier isn’t able to read as well as his
classmates. Javier generally has things he wants to say in class—sometimes raising
his hand so high and waving it so energetically that he practically hits the heads of
nearby children. His comments often show a keen understanding of what the teacher
has said, and his apparent reading problem seems to be at odds with his general intel-
ligence. Could Javier have a learning disorder?
What Is Specific Learning Disorder?
Specific learning disorder is characterized by well below average skills in reading,
writing, or math, based on the expected level of performance for the person’s age,
general intelligence, cultural group, gender, and education level. For the diagnosis to
be made, the deficits must significantly interfere with school or work performance
or daily living (when supports and services are not provided). Table 14.6 lists the
DSM-5 criteria for specific learning disorders.
DSM-5 lists three categories of specific learning disorder (American Psychiatric
Association, 2013):
• Reading, often referred to as dyslexia, characterized by difficulty with accuracy,
speed, or comprehension when reading, to the point that the difficulty interferes
with academic achievement or activities of daily functioning that involve reading.
Specific learning disorder
A neurodevelopmental disorder characterized
by skills well below average in reading,
writing, or math, based on the expected level
of performance for the person’s age, general
intelligence, cultural group, gender, and
education level.
Dyslexia
A learning disorder characterized by
difficulty with reading accuracy, speed, or
comprehension that interferes with academic
achievement or activities of daily functioning
that involve reading.
Neurodevelopmental and Disruptive Behavior Disorders 455
• Written expression, characterized by poor spelling, signif icant grammatical or
punctuation mistakes, or problems with writing in a clear and organized manner.
• Mathematics, sometimes referred to as dyscalculia, characterized by difficulty under-
standing the relationships among numbers, memorizing arithmetic facts, accurately
and fluently making calculations, and reasoning effectively about math problems.
Nancy, in Case 14.3, has a specific learning disorder that involves reading. Additional
facts about specific learning disorder are presented in Table 14.7.
CASE 14.3 • FROM TH E INSIDE: Specific Learning Disorder (Reading)
Nanc y Lelewer, author of Something’s Not Right: One Family’s Struggle W ith Learning
Disabilities (1994), describes what having a learning disorder was like for her:
I began public elementary school in the early 1940s. . . . Reading was taught exclusively
by a whole-word method dubbed “Look, Say” because of its reliance on recognizing indi-
vidual words as whole visual patterns, rather than focusing on letters or letter patterns.
In first grade, I listened to my classmates, and when it was my turn, I read the pictures,
not the words, “Oh Sally! See Spot. Run. Run. Run.” When we were shown flash cards and
responded in unison to them, I mouthed something.
Then came our first reading test. The teacher handed each student a sheet of paper,
the top half of which was covered with writing. I looked at it and couldn’t read a word. . . .
The room grew quiet as the class began to read.
As I stared at the page, total panic gripped me. My insides churned, and I began to perspire
as I wondered what I was going to do. As it happened, the boy who sat right in front of me was
the most able reader in my class. Within a few minutes, he had completed the test and had
pushed his paper to the front of his desk, which put it in my full view. . . . [I copied his answers
and] passed the test and was off on a track of living by my wits rather than being able to read.
The “wits track” is a nerve-wracking one. I worried that the boy would be out sick on
the day we had a reading test. I worried that the teacher might change the location of my
desk. I worried that I would get caught copying another student’s answers. I knew that
something was wrong with me, but I didn’t know what. Why couldn’t I recognize words
that my classmates read so easily?
(pp. 15–17)
TABLE 14.6 • DSM-5 Diagnostic Criteria for Specific Learning Disorder
A. Difficulties learning and using academic skills, as indicated by the presence of at least one of the following symptoms that have persisted for at
least 6 months, despite the provision of interventions that target those difficulties:
1. Inaccurate or slow and effortful word reading (e.g., reads single words aloud incorrectly or slowly and hesitantly, frequently guesses words, has
difficulty sounding out words).
2. Difficulty understanding the meaning of what is read (e.g., may read text accurately but not understand the sequence, relationships, inferences,
or deeper meanings of what is read).
3. Difficulties with spelling (e.g., may add, omit, or substitute vowels or consonants).
4. Difficulties with written expression (e.g., makes multiple grammatical or punctuation errors within sentences; employs poor paragraph organi-
zation; written expression of ideas lacks clarity).
5. Difficulties mastering number sense, number facts, or calculation (e.g., has poor understanding of numbers, their magnitude, and relationships;
counts on fingers to add single-digit numbers instead of recalling the math fact as peers do; gets lost in the midst of arithmetic computation
and may switch procedures).
6. Difficulties with mathematical reasoning (e.g., has severe difficulty applying mathematical concepts, facts, or procedures to solve quantitative problems).
B. The affected academic skills are substantially and quantifiably below those expected for the individual’s chronological age, and cause significant
interference with academic or occupational performance, or with activities of daily living, as confirmed by individually administered standardized
achievement measures and comprehensive clinical assessment. For individuals age 17 years and older, a documented history of impairing learning
difficulties may be substituted for the standardized assessment.
C. The learning difficulties begin during school-age years but may not become fully manifest until the demands for those affected academic skills exceed the
individual’s limited capacities (e.g., as in timed tests, reading or writing lengthy complex reports for a tight deadline, excessively heavy academic loads).
D. The learning difficulties are not better accounted for by intellectual disabilities, uncorrected visual or auditory acuity, other mental or neurologi-
cal disorders, psychosocial adversity, lack of proficiency in the language of academic instruction, or inadequate educational instruction.
Reprinted with permission from the Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition, (Copyright ©2013). American Psychiatric Association. All Rights Reserved.
456 C H A P T E R 1 4
Specific learning disorder may cast a long shadow over many areas of life for
many years. People with a learning disorder are 50 % more likely to drop out of
school than are people in the general population, and work and social relationships
are more likely to suffer (American Psychiatric Association, 2000). These people are
also more likely than average to suffer from poor self-esteem.
Understanding Specific Learning Disorder
Like intellectual disability and ASD, specific learning disorder is primarily caused by
neurological factors. But psychological and social factors also play a role.
Neurological Factors
Among the three domains of specific learning disorder, dyslexia has been studied the
most extensively. Evidence is growing that impaired brain systems underlie this dis-
order and that genes contribute to these impaired systems.
Brain Systems
In most forms of dyslexia, the brain systems involved in auditory processing do not
function as well as they should (Marshall et al., 2008; Ramus et al., 2003). The results
of many neuroimaging studies have converged to identify a set of brain areas that is
disrupted in people who have dyslexia (Shaywitz et al., 2006). First, two rear areas in
the left hemisphere are not as strongly activated during reading tasks in people with
dyslexia as they are in people who read normally. One of these areas is involved in con-
verting visual input to sounds (Friedman et al., 1993), and the other area, at the junc-
tion of the parietal and occipital lobes, appears to be used to recognize whole words,
TABLE 14.7 • Specific Learning Disorder Facts at a Glance
Prevalence
• Between 5% and 15% of school-age children in the United States are estimated to have this
disorder.
Onset
• Symptoms of specific learning disorder and its diagnosis typically occur in elementary
school, when the relevant academic skills are needed.
Comorbidity
• Common comorbid disorders include depressive disorders and attention- deficit/hyper-
activity disorder.
Course
• With early identification and intervention, some children with dyslexia can overcome their
difficulties; for others, difficulties in reading fluency, comprehension, and spelling may
persist into adulthood.
Gender Differences
• Between 60% and 75% of people with dyslexia are male; however, it may be that males are
more likely to be diagnosed because of their disruptive behavior, which calls attention to
their difficulties.
Cultural Differences
• In the United States, Hispanic children are least likely to be diagnosed with a learning disor-
der, perhaps because language barriers make it more difficult to diagnose (Boyle et al., 2011).
Source: Unless otherwise noted, the source for information is American Psychiatric Association, 2013.
Neurodevelopmental and Disruptive Behavior Disorders 457
based on their visual forms (Cao et al., 2006; McCandliss et al., 2003). Second, two
other brain areas are more strongly activated in people with dyslexia than in people
who read normally. These areas appear to be used in carrying out compensatory strate-
gies, which rely on stored information instead of the vision–sound conversion process.
Genetics
A specific learning disorder in reading is moderately to highly heritable (Hawke
et al., 2006; Schulte-Körne, 2001), and at least four specific genes are thought to
affect the development of this disorder (Fisher & Francks, 2006; Marino et al., 2007).
Some of these genes affect how neurons become connected during brain develop-
ment (Rosen et al., 2007), and some may affect the functioning of neurons or influ-
ence the activity of neurotransmitters (Grigorenko, 2001).
Psychological Factors
Some children with a specific learning disorder succeed in situations where others
fail. For example, they might persevere in solving a difficult puzzle. Why? In order
to address this question, researchers interviewed college students with a specific
learning disorder and asked about their experiences as young children (Miller, 2002).
These people reported a number of psychological factors that played important
roles in shaping their motivation to overcome their disorder; these factors included
self-determination, recognizing particular areas of strength, identifying the learning
disability, and developing ways to cope with it.
Social Factors
Social factors play a role in shaping motivation to persist in the face of a learning
disorder (Miller, 2002). Other people, such as parents and teachers, were important
in supporting and encouraging children who later succeeded in overcoming their
learning disabilities. In addition, certain social environments—such as attending a
low-quality school or coming from a disadvantaged family—apparently can contrib-
ute to at least some forms of dyslexia (Shaywitz et al., 2006; Wadsworth et al., 2000).
Treating Dyslexia
As with the other childhood disorders discussed thus far in this chapter, neurological
factors generally are not directly targeted for treatment (unless the treatment is for a
comorbid disorder). Dyslexia has been the subject of the most research on treatment,
and researchers have reported successful interventions for this disorder.
One technique for helping people with dyslexia is phonological practice, which con-
sists of learning to divide words into individual sounds and to identify rhyming words.
Another technique focuses on teaching children the alphabetic principle, which governs
What do (left to right) singer Jewel, TV star Patrick Dempsey, martial artist Billy Blanks, business mogul Richard Branson, and actress Keira Knightley
have in common? They all have dyslexia, but it has not stopped them from attaining success in their fields.
T
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458 C H A P T E R 1 4
the way in which letters signal elementary speech sounds (Shaywitz et al., 2004). In fact,
various forms of training using these techniques have been shown not only to improve
performance but also to improve the functioning of brain areas that were impaired prior
to the training (Gaab et al., 2007; Simos et al., 2007; Temple et al., 2003).
Nikhil recently graduated from college and is about to start working in the Teach for America
program. He’s been assigned to teach at an inner-city school. Nikhil was a math major in
college and doesn’t know much about learning disabilities. However, he was a peer tutor in
college and saw that some people had a really hard time understanding different elements of
math. Based on what you’ve read, what information should Nikhil know (and hopefully will
be taught as part of his training) about specific learning disorder before he walks into a class-
room, and why should he learn this material?
Thinking Like A Clinician
Disorders of Disruptive Behavior
and Attention
In addition to Javier Enriquez’s apparent difficulties reading, his teacher has com-
mented—not very positively—on Javier’s high energy level. He doesn’t always stay in
his chair during class, and when he’s working on a group project, other kids seem to
get annoyed at him: “He can get ‘in their face’ a bit.” Javier’s mother, Lela, and his
father, Carlos, acknowledge that Javier is a very active, energetic boy. But Carlos says,
“I was that way when I was a kid, but I grew out of it as I got older.” Javier’s teacher
recently mentioned the possibility of his having attention-def icit/ hyperactivity
disorder.
In contrast, Javier’s sister, 8-year-old Pia, is definitely not energetic. Like her
brother, Pia is clearly bright, but her teacher says she seems to “space out” in class.
The teacher thinks that Pia simply does not apply herself, but her parents wonder
whether she’s underachieving because she’s bored and understimulated in school. At
home, Pia has defied her parents increasingly often—not doing her chores or per-
forming simple tasks they ask her to do. At other times, Pia is off in her own world,
“kind of like an absent-minded professor.” Is Pia’s behavior in the normal range, or
does it signal a problem? If so, what might the problem be?
And what about Javier’s behavior—is it in the normal range? Most children are
disruptive some of the time. But in some cases, the disruptive behavior is much more
frequent and obtrusive and becomes a cause for concern. Even if disruptive behaviors
do not distress the children who perform them, they often distress other people or
violate social norms (Christophersen & Mortweet, 2001). The most common rea-
son that children are referred to a mental health clinician is because they engage in
disruptive behavior at home, at school, or both (Frick & Silverthorn, 2001). The
clinician must distinguish between normal behavior and pathologically disrup-
tive behavior and, if the behavior falls outside the normal range, determine which
disorder(s) might be the cause.
Three disorders are associated with disruptive behavior: conduct disorder, oppositional
defiant disorder, and attention deficit/hyperactivity disorder (which is characterized mainly
by problems with attention but sometimes by disruptive behavior as well). Although
DSM-5 does not put attention-def icit/hyperactivity disorder in the category of
disruptive disorders (but rather puts it in category of neurodevelopmental disorders),
we discuss it here both because the symptoms can include disruptive behavior and
because symptoms of these three disorders commonly—though not always—occur
together.
Neurodevelopmental and Disruptive Behavior Disorders 459
What Is Conduct Disorder?
The hallmark of conduct disorder is a violation of the basic rights of others or of
societal norms that are appropriate to the person’s age (American Psychiatric Associa-
tion, 2013). As outlined in Table 14.8, 15 types of behaviors are listed in the diagnostic
criteria for conduct disorder; these behaviors are sorted into four categories.
DSM-5 requires the presence of at least 3 out of the 15 types of behavior within
the past 12 months and at least 1 type of such behavior must have occurred during
the past 6 months. Although the diagnosis requires impaired functioning in some
area of life, it does not require distress.
Just as the criteria for antisocial personality disorder (Chapter 13) focus almost
exclusively on behavior that violates the rights of others, so do the criteria for con-
duct disorder. However, people diagnosed with conduct disorder also often have out-
bursts of anger, recklessness, and poor frustration tolerance. Most people diagnosed
with conduct disorder are under 18 years old; if the behaviors persist into adulthood,
the person usually meets the criteria for antisocial personality disorder.
Like people with antisocial personality disorder, people with conduct disorder
appear to lack empathy and concern for others, and they don’t exhibit genuine re-
morse for their misdeeds. In fact, when the intent of another person’s behavior is
Children with conduct disorder exhibit a
pattern of violating the rights of others, such
as frequently hurting other children, as is the
girl in this photograph.
R
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ck
Conduct disorder
A psychological disorder that typically arises
in childhood and is characterized by the
violation of the basic rights of others or of
societal norms that are appropriate to the
person’s age.
TABLE 14.8 • DSM-5 Criteria for Conduct Disorder
A. A repetitive and persistent pattern of behavior in which the basic rights of others or major
age-appropriate societal norms or rules are violated, as manifested by the presence of at
least three of the following 15 criteria in the past 12 months from any of the categories
below, with at least one criterion present in the past 6 months:
Aggression to People and Animals
1. Often bullies, threatens, or intimidates others.
2. Often initiates physical fights.
3. Has used a weapon that can cause serious physical harm to others (e.g., a bat, brick,
broken bottle, knife, gun).
4. Has been physically cruel to people.
5. Has been physically cruel to animals.
6. Has stolen while confronting a victim (e.g., mugging, purse snatching, extortion, armed
robbery).
7. Has forced someone into sexual activity.
Destruction of Property
8. Has deliberately engaged in fire setting with the intention of causing serious damage.
9. Has deliberately destroyed others’ property (other than by fire setting).
Deceitfulness or Theft
10. Has broken into someone else’s house, building, or car.
11. Often lies to obtain goods or favors or to avoid obligations (i.e., “cons” others).
12. Has stolen items of nontrivial value without confronting a victim (e.g., shoplifting, but
without breaking and entering; forgery).
Serious Violations of Rules
13. Often stays out at night despite parental prohibitions, beginning before age 13 years.
14. Has run away from home overnight at least twice while living in the parental or
parental surrogate home, or once without returning for a lengthy period.
15. Is often truant from school, beginning before age 13 years.
B. The disturbance in behavior causes clinically significant impairment in social, academic, or
occupational functioning.
C. If the individual is age 18 years or older, criteria are not met for antisocial personality disorder.
Reprinted with permission from the Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition, (Copyright
©2013). American Psychiatric Association. All Rights Reserved.
460 C H A P T E R 1 4
ambiguous, a person with conduct disorder is likely to misconstrue the other’s mo-
tives as threatening or hostile and then feel justified in his or her own aggressive
behavior. People with conduct disorder typically blame others for their inappropriate
behaviors (“He made me do it”).
DSM-5 specifies three levels of intensity for the symptoms of conduct disorder:
mild (few behaviors or causing minimal harm), moderate, and severe (many behaviors
or causing signif icant harm). Symptoms may progress from mildly disruptive to
severely disruptive.
People with conduct disorder are also likely to use—and abuse—substances at an
earlier age than are people without this disorder. Similarly, they are more likely to
have problems in school (such as suspension or expulsion), legal problems, unplanned
pregnancies and sexually transmitted diseases, and physical injuries that result from
fights. Because of their behavioral problems, children with conduct disorder may
live in foster homes or attend special schools. They may also have poor academic
achievement and score lower than normal on verbal intelligence tests. Problems
with relationships, financial woes, and other psychological disorders may persist into
adulthood ( Colman et al., 2009).
When clinicians assess whether conduct disorder might be an appropriate diagnosis
for a person, they will of course talk with him or her; however, the nature of conduct
disorder is such that a child or an adult patient may not provide complete information
about his or her behavior. Thus, when diagnosing a child, clinicians try to obtain addi-
tional information from other sources, usually school officials or parents, although even
these people may not know the full extent of a child’s conduct problems. By the same
token, when diagnosing adults, clinicians try to obtain additional information from
family members, peers, or coworkers. Usually, the behaviors that characterize conduct
disorder are not limited to one setting but occur in a variety of settings: in school or
work, at home, in the neighborhood. This was true for Brad, as described in Case 14.4.
CASE 14.4 • FROM TH E OUTSIDE: Conduct Disorder
Brad was [a teenager and] small for his age but big on fighting. For him, this had gone
beyond schoolyard bullying. He had four assault charges during the previous 6 months,
including threatening rape and beating up a much younger boy who was mentally chal-
lenged. The family was being asked to leave their apartment complex because of Brad’s
aggressive behavior and several stealing incidents. Other official arrests included burglar-
ies and trespassing. Brad had participated in a number of outpatient services, including
anger management classes in which he had done well, but obviously he was not applying
what he had learned to everyday life. He was referred to [a treatment] program by the
juvenile court judge.
Prior to placement, Brad had lived with his mother and older brother. Their family
life had been characterized by many disruptions, including contact with several abusive
father figures and frequent moves. Brad’s older brother also had a record with the juvenile
authorities, but his offenses were confined to property crimes and the use of alcohol. He
had graduated from an inpatient substance abuse program. Brad and his brother had a
history of physical fighting. Prior to the boys’ births, Mrs. B had had two children removed
from her custody by state protective services. Mrs. B was very protective of Brad. She felt
that the police and schools had it “in for him” and regularly defended him as having been
provoked or blamed falsely. Although she was devastated at having Brad removed from
her home, Mrs. B reported that she could no longer deal with Brad’s aggression.
(Chamberlain, 1996, pp. 485–486)
DSM-5 uses the timing of onset to define two types of conduct disorder, which
typically have different courses and prognoses:
• adolescent-onset type, in which no symptoms were present before age 10; and
• childhood-onset type, which is more severe and in which the first symptoms appeared
when the child was younger than 10 years old.
Neurodevelopmental and Disruptive Behavior Disorders 461
As noted in Table 14.9, various characteristics of con-
duct disorder that develop in childhood are different from
those of the conduct disorder that develops in adolescence.
In the following sections we examine them in more detail.
Adolescent-Onset Type
For people with adolescent-onset type, the symptoms of
conduct disorder emerge after—but not before—puberty,
considered in DSM-5 to occur at 10 years of age. The dis-
ruptive behaviors are not likely to be violent and typically
include minor theft, public drunkenness, and property
offenses rather than violence against people and robbery,
which are more likely with childhood-onset type (Moffitt
et al., 2002). The behaviors associated with adolescent-onset
type conduct disorder can be thought of as exaggerations of
normal adolescent behaviors (Moffitt & Caspi, 2001). With
this type, the disruptive behaviors are usually transient, and
adolescents with this disorder are able to maintain relation-
ships with peers. This type of conduct disorder has been
found to have a small sex difference; the male to female
ratio is 1.5 to 1 (Moffitt & Caspi, 2001).
Childhood-Onset Type
Research has shown that people with the childhood-
onset type of conduct disorder can be further divided into
two categories: Those who are callous and/or unemotional
(Caputo et al., 1999; Frick et al., 2000), which are fea-
tures of psychopathy (discussed in Chapter 13), and those
who are not.
Childhood-Onset Type, Neither Callous nor
Unemotional
People with childhood-onset conduct disorder who are
not callous and display feelings of guilt or remorse for
their deeds are less likely to be aggressive in general; when
they are aggressive, it is usually as a reaction to a perceived
or real threat—it is not premeditated (Frick et al., 2003).
People with this sort of conduct disorder have difficulty
regulating their negative emotions: They have high levels
of emotional distress (Frick & Morris, 2004; Frick et al., 2003), and they react more
strongly to other people’s distress and to negative emotional stimuli generally (Loney
et al., 2003; Pardini et al., 2003).
In addition, such people process social cues less accurately than normal and so are
more likely to misperceive such cues and respond aggressively when (mis)perceiv-
ing threats (Dodge & Pettit, 2003). Because of their problems in regulating negative
emotions, they are more likely to act aggressively and antisocially in impulsive ways
when distressed. They often feel bad afterward but still can’t control their behavior
(Pardini et al., 2003). Children with this disorder may fall into a negative interaction
pattern with their parents: When a parent brings up the child’s past or present mis-
conduct, the child becomes agitated and then doesn’t appropriately process what the
parent says, becomes more distressed, and impulsively behaves in an aggressive man-
ner. The parent may respond with aggression (verbal or physical), creating a vicious
cycle (Gauvain & Fagot, 1995).
TABLE 14.9 • Conduct Disorder Facts at a Glance
Prevalence
• Studies find a wide range of prevalence rates in the general population
(2–10%), depending on how the study was conducted and the exact com-
position of the population studied. Approximately 10% of Americans will be
diagnosed with conduct disorder during their lives (Nock et al., 2006).
Onset
• According to DSM-5, when symptoms arise before age 10, the diagnosis
is childhood-onset type; when there are no symptoms before age 10, it is
adolescent-onset type.
Comorbidity
• With the childhood-onset type, common comorbid disorders include oppo-
sitional defiant disorder and attention-deficit/hyperactivity disorder (both
discussed later) (Costello et al., 2003); some studies estimate that up to
90% of children with conduct disorder exhibit symptoms of attention-defi-
cit/hyperactivity disorder (Frick & Muñoz, 2006).
Course
• The earlier the onset and the more severe the disruptive behaviors, the
worse the prognosis (Barkley et al., 2002; Frick & Loney, 1999).
• People with childhood-onset conduct disorder are likely to develop
additional symptoms of the disorder by puberty and continue to have the
disorder through adolescence.
• People with the childhood-onset type are more likely than those with the
adolescent-onset type to be diagnosed with antisocial personality disorder
in adulthood.
Gender Differences
• During their lives, about 12% of American males and 7% of American females
will have had symptoms that meet the criteria for conduct disorder (Nock et
al., 2006). Although more males than females are diagnosed with this disorder
(both types), the sex difference is more marked for the childhood-onset type,
with 10 males diagnosed for each female (Moffitt & Caspi, 2001).
• Males with conduct disorder tend to be confrontationally aggressive (fighting,
stealing, vandalism, and school-related problems); females tend to be noncon-
frontational (lying, truancy, running away, substance use, and prostitution).
Source: Unless otherwise noted, the source for information is American Psychiatric Association, 2013.
462 C H A P T E R 1 4
Childhood-Onset Type, With Callous and Unemotional Traits
Although not consider a “subtype” in DSM-5, the manual allows mental health
professionals to specify when someone with childhood-onset conduct disorder
has callous and unemotional features (specified in DSM-5 as with limited prosocial
emotions). This group of people has some unique characteristics: Like adults with
psychopathy, these young people seek out exciting and dangerous activities, are
relatively insensitive to threat of punishment, and are strongly oriented toward
the possibility of reward (Frick et al., 2003; Pardini et al., 2003). Moreover, they
react less strongly to threatening or distressing stimuli (Frick et al., 2003; Loney
et al., 2003).
Re s e a r che r s pr o p o s e t h a t t he d e c r e a s e d s e n s it i v it y t o
punishment— associated with low levels of fear—underlies the unique
constellation of callousness and increased aggression (Frick, 2006;
Pardini et al., 2006). People with this sort of conduct disorder are not
concerned about the negative consequences of their violent behav-
iors. And being insensitive to punishment, they don’t learn to refrain
from certain behaviors and thereby fail to internalize social norms or
develop a conscience or empathy for others (Frick & Morris, 2004;
Pardini, 2006; Pardini et al., 2003). In fact, people with conduct dis-
order with callous and unemotional traits are less likely to recognize
emotional expressions of sadness (Blair et al., 2001). This variant of
conduct disorder has the highest heritability and is associated with
more severe symptoms (Viding et al., 2005).
What Is Oppositional Defiant Disorder?
The defining characteristics of oppositional defiant disorder are
angr y or irritable mood, def iance or argumentative behavior, or
vindictiveness. As noted in Table 14.10, for a diagnosis of opposi-
tional defiant disorder, DSM-5 requires that the person exhibit four
out of eight symptoms, many of which are confrontational behav-
iors, such as arguing with authority figures, intentionally annoying
others, and directly refusing to comply with an authority figure’s or
adult’s request, which were true of Josh, in Case 14.5. (However,
according to DSM-5, such behavior with a sibling is not grounds for
diagnosing the disorder.) Young children with oppositional defiant
disorder may have intense and frequent temper tantrums. Pia did
not comply with her parents’ requests to complete her chores or help
with other tasks; her teacher has commented on a similar behavior
pattern at school.
These behaviors must have occurred for at least 6 months,
more frequently than would be expected for the person’s age and
developmental level, and must impair functioning.
CASE 14.5 • FROM TH E OUTSIDE: Oppositional Defiant Disorder
At school and with friends, Josh behaves like a perfectly normal ten-year-old boy. At home,
however, it’s a very different story. Josh pushes every limit possible. He often swears at
his parents and harasses his siblings. Forget about asking Josh to do things around the
house—he refuses to do even the most routine chores without serious resistance toward
his parents. Communication between Josh and his parents consists of a series of argu-
ments, leaving them all exhausted, angry, and tense.
(Bernstein, 2006, p. 2)
Oppositional defiant disorder
A disorder that typically arises in childhood
or adolescence and is characterized angry or
irritable mood, defiance or argumentative
behavior, or vindictiveness.
TABLE 14.10 • DSM-5 Diagnostic Criteria for
Oppositional Defiant Disorder
A. A pattern of angry/irritable mood, argumentative/ defiant
behavior, or vindictiveness lasting at least 6 months as
evidenced by at least four symptoms from any of the follow-
ing categories, and exhibited during interaction with at least
one individual who is not a sibling.
Angry/Irritable Mood
1. Often loses temper.
2. Is often touchy or easily annoyed.
3. Is often angry and resentful.
Argumentative/Defiant Behavior
4. Often argues with authority figures or, for children and
adolescents, with adults.
5. Often actively defies or refuses to comply with requests
from authority figures or with rules.
6. Often deliberately annoys others.
7. Often blames others for his or her mistakes or misbehavior.
Vindictiveness
8. Has been spiteful or vindictive at least twice within the
past 6 months.
B. The disturbance in behavior is associated with distress in the
individual or others in his or her immediate social context
(e.g., family, peer group, work colleagues), or it impacts nega-
tively on social, educational, occupational, or other important
areas of functioning.
C. The behaviors do not occur exclusively during the course of a
psychotic, substance use, depressive, or bipolar disorder. Also, the
criteria are not met for disruptive mood dysregulation disorder.
Reprinted with permission from the Diagnostic and Statistical Manual of Mental
Disorders, Fifth Edition, (Copyright ©2013). American Psychiatric Association. All
Rights Reserved.
Neurodevelopmental and Disruptive Behavior Disorders 463
The disruptive behaviors of oppositional defiant disorder are different in sev-
eral important ways from those characterizing conduct disorder. Oppositional defiant
disorder involves only a subset of the symptoms of conduct disorder—the overtly
defiant behaviors—and these are often verbal. The disruptive behaviors of opposi-
tional defiant disorder are:
• generally directed toward authority figures;
• not usually violent and do not usually cause severe harm; and
• in children, often exhibited only in specific situations with parents or other adults
the children know well (Christophersen & Mortweet, 2001).
The clinician must obtain information from others when assessing disruptive behav-
iors and must keep in mind any cultural factors that might influence which sorts of
behaviors are deemed acceptable or unacceptable.
According to DSM-5, if a person meets the diagnostic criteria for both oppo-
sitional defiant disorder and conduct disorder, both disorders would be diagnosed.
Table 14.11 lists additional facts about oppositional defiant disorder.
TABLE 14.11 • Oppositional Defiant Disorder Facts at a Glance
Prevalence
• Estimates of prevalence rates for this disorder vary widely, from 1% to 11%, depending on the
specific population investigated and the specific research methods used.
Onset
• Symptoms usually emerge before 8 years of age, although they may become evident as
late as 13.
• The onset progresses gradually, over months or even years, until the symptoms reach the
point where the diagnostic criteria are met. Symptoms are typically observed at home
before occurring in other contexts.
Comorbidity
• Up to 90% of children with oppositional defiant disorder also exhibit symptoms of
attention-deficit/hyperactivity disorder (Frick & Muñoz, 2006).
Course
• Most people with the childhood-onset type of conduct disorder were previously diagnosed
with oppositional defiant disorder (Whittinger et al., 2007); however, most people with opposi-
tional defiant disorder do not go on to develop conduct disorder.
Gender Differences
• Before puberty, more males than females are diagnosed with oppositional defiant disorder.
After puberty, there is no sex difference in prevalence.
• Males exhibit more persistent and more confrontational symptoms than females do.
Cultural Differences
• Different cultures may have different norms concerning what defiant behaviors are considered
inappropriate or unacceptable.
Source: Unless otherwise noted, the source for information is American Psychiatric Association, 2013.
Children with oppositional defiant disorder
typically are verbally aggressive with
authority figures but are not generally violent.
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What Is Attention-Deficit/Hyperactivity Disorder?
People who have oppositional def iant disorder or conduct disorder intend to
defy rules, authority figures, or social norms, and hence behave disruptively. But
people may unintentionally behave disruptively because they have another disorder,
464 C H A P T E R 1 4
attention-deficit/hyperactivity disorder (ADHD), which is characterized by six
or more symptoms of inattention, hyperactivity, and/or impulsivity (five or more in
people 17 years old or greater). People diagnosed with this disorder vary in which set
of symptoms is most dominant; some primarily have difficulty maintaining attention,
whereas others primarily have difficulty with hyperactivity and impulsivity. Still
others have all three types of symptoms. To meet the criteria for the diagnosis (see
Table 14.12), the symptoms must impair functioning in at least two settings, such
as at school and at work or at work and at home, and some symptoms must have
been present by age 12. The impulsivity and hyperactivity are most noticeable and
Attention-deficit/hyperactivity
disorder (ADHD)
A disorder that typically arises in childhood
and is characterized by inattention,
hyperactivity, and/or impulsivity.
TABLE 14.12 • DSM-5 Diagnostic Criteria for Attention-Deficit/Hyperactivity Disorder
A. A persistent pattern of inattention and/or hyperactivity-impulsivity that interferes with functioning or development, as characterized by (1) and/or (2):
1. Inattention: Six (or more) of the following symptoms have persisted for at least 6 months to a degree that is inconsistent with developmental
level and that negatively impacts directly on social and academic/occupational activities:
Note: For older adolescents and adults (age 17 and older), at least five symptoms are required.
a. Often fails to give close attention to details or makes careless mistakes in schoolwork, at work, or during other activities (e.g., overlooks or
misses details, work is inaccurate).
b. Often has difficulty sustaining attention in tasks or play activities (e.g., has difficulty remaining focused during lectures, conversations, or
lengthy reading).
c. Often does not seem to listen when spoken to directly (e.g., mind seems elsewhere, even in the absence of any obvious distraction).
d. Often does not follow through on instructions and fails to finish schoolwork, chores, or duties in the workplace (e.g., starts tasks but quickly
loses focus and is easily sidetracked).
e. Often has difficulty organizing tasks and activities (e.g., difficulty managing sequential tasks; difficulty keeping materials and belongings in
order; messy, disorganized work; has poor time management; fails to meet deadlines).
f. Often avoids, dislikes, or is reluctant to engage in tasks that require sustained mental effort (e.g., schoolwork or homework; for older adoles-
cents and adults, preparing reports, completing forms, reviewing lengthy papers).
g. Often loses things necessary for tasks or activities (e.g., school materials, pencils, books, tools, wallets, keys, paperwork, eyeglasses, mobile
telephones).
h. Is often easily distracted by extraneous stimuli (for older adolescents and adults, may include unrelated thoughts).
i. Is often forgetful in daily activities (e.g., doing chores, running errands; for older adolescents and adults, returning calls, paying bills, keeping
appointments).
2. Hyperactivity and impulsivity: Six (or more) of the following symptoms have persisted for at least 6 months to a degree that is inconsistent
with developmental level and that negatively impacts directly on social and academic/occupational activities:
Note: For older adolescents and adults (age 17 and older), at least five symptoms are required.
a. Often fidgets with or taps hands or feet or squirms in seat.
b. Often leaves seat in situations when remaining seated is expected (e.g., leaves his or her place in the classroom, in the office or other work-
place, or in other situations that require remaining in place).
c. Often runs about or climbs in situations where it is inappropriate. (Note: In adolescents or adults, may be limited to feeling restless.)
d. Often unable to play or engage in leisure activities quietly.
e. Is often “on the go,” acting as if “driven by a motor” (e.g., is unable to be or uncomfortable being still for extended time, as in restaurants,
meetings; may be experienced by others as being restless or difficult to keep up with).
f. Often talks excessively.
g. Often blurts out an answer before a question has been completed (e.g., completes people’s sentences; cannot wait for turn in conversation).
h. Often has difficulty waiting his or her turn (e.g., while waiting in line).
i. Often interrupts or intrudes on others (e.g., butts into conversations, games, or activities; may start using other people’s things without ask-
ing or receiving permission; for adolescents and adults, may intrude into or take over what others are doing).
B. Several inattentive or hyperactive-impulsive symptoms were present prior to age 12 years.
C. Several inattentive or hyperactive-impulsive symptoms are present in two or more settings (e.g., at home, school, or work; with friends or rela-
tives; in other activities).
D. There is clear evidence that the symptoms interfere with, or reduce the quality of, social, academic, or occupational functioning.
E. The symptoms do not occur exclusively during the course of schizophrenia or another psychotic disorder and are not better explained by another
mental disorder (e.g., mood disorder, anxiety disorder, dissociative disorder, personality disorder, substance intoxication or withdrawal.
Reprinted with permission from the Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition, (Copyright ©2013). American Psychiatric Association. All Rights Reserved.
Neurodevelopmental and Disruptive Behavior Disorders 465
disruptive in a classroom setting. Javier’s difficulty staying in his chair at school, which
disrupted the class, may have reflected this disorder. In Case 14.6, an adult recounts
how he recognized his own ADHD.
CASE 14.6 • FROM THE INSIDE: Attention Deficit/Hyperactivity Disorder
Attention-deficit disorder (ADD) was the term used in the third edition of the DSM. In his book
Driven to Distraction: Recognizing and Coping with Attention Deficit Disorder from Childhood
Through Adulthood, psychiatrist Edward Hallowell recounts what happened when he learned
about the disorder:
I discovered I had ADD when I was thirty-one years old, near the end of my training in child
psychiatry at the Massachusetts Mental Health Center in Boston. As my teacher in neuro-
psychiatry began to describe ADD in a series of morning lectures during a steamy Boston
summer, I had one of the great “Aha!” experiences of my life.
“There are some children,” she said, “who chronically daydream. They are often very
bright, but they have trouble attending to any one topic for very long. They are full of
energy and have trouble staying put. They can be quite impulsive in saying or doing what-
ever comes to mind, and they find distractions impossible to resist.”
So there’s a name for what I am! I thought to myself with relief and mounting excite-
ment. There’s a term for it, a diagnosis, an actual condition, when all along I’d thought I
was just slightly daft. . . . I wasn’t all the names I’d been called in grade school—“a day-
dreamer,” “lazy,” “an underachiever,” “a spaceshot”—and I didn’t have some repressed
unconscious conflict that made me impatient and action-oriented.
What I had was an inherited neurological syndrome characterized by easy distractibil-
ity, low tolerance for frustration or boredom, a greater-than-average tendency to say or
do whatever came to mind . . . and a predilection for situations of high intensity. Most of
all, I had a name for the overflow of energy I so often felt—the highly charged, psyched-
up feeling that infused many of my waking hours in both formative and frustrating ways.
(Hallowell & Ratey, 1994, pp. ix–x)
Symptoms of hyperactivity may be different in females than in males: Girls who
have hyperactive symptoms may talk more than other girls or may be more emo-
tionally reactive, rather than hyperactive with their bodies (Quinn, 2005). Some
researchers propose that ADHD is underdiagnosed in girls, who are less likely to
have behavioral problems at school and so are less likely to be referred for evalua-
tion (Quinn, 2005). In fact, female teenagers with ADHD are likely to be diagnosed
with and treated for depression before the ADHD is diagnosed (Harris International,
2002, cited in Quinn, 2005).
Because the sets of symptoms of ADHD vary, clinicians find it useful to clas-
sify ADHD into different forms (“presentations” to use the DSM-5 term). The
predominantly hyperactive/impulsive form is associated with disruptive behaviors, ac-
cidents, and rejection by peers, whereas the inattentive form of ADHD is associated
with academic problems that are typical of deficits in executive functions: difficulty
remembering a sequence of behaviors, monitoring and shifting the direction of at-
tention, organizing material to be memorized, and inhibiting interference during
recall. Some patients may have a combination of the two types of symptoms.
However, symptoms may change over time; as some children get older, the par-
ticular set of symptoms they exhibit can shift, most frequently from hyperactive/
impulsive to the type that has a combination of the two sets of symptoms (Lahey,
Pelham, et al., 2005). Children with ADHD often have little tolerance for frustra-
tion, as was true of Edward Hallowell in Case 14.6; such children tend to have temper
outbursts, changeable moods, and symptoms of depression. Once properly diagnosed
and treated, such symptoms often decrease.
Problems with attention are likely to become more severe in group settings,
where the person receives less attention or rewards, in settings when sustained
attention is necessar y, or when a task is thought to be boring—which is what
This girl may simply be in a talkative mood.
But girls with the hyperactive form of ADHD
tend to talk more than girls without the
hyperactive form of ADHD.
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happened to Javier. Various psychological and social factors can reduce symptoms,
including:
• frequent rewards for appropriate behavior;
• close supervision;
• being in a new situation or setting;
• doing something interesting; and
• having someone else’s undivided attention.
Socially, people with ADHD may initiate frequent shifts in the topic of a con-
versation, either because they are not paying consistent attention to the conversa-
tion or because they are not following implicit social rules. People with symptoms
of hyperactivity may talk so much that others can’t get a word in edgewise, or they
may inappropriately start conversations. These symptoms can make peer relationships
difficult. In addition, symptoms of impulsivity can lead to increased risk of harm. As
the child heads into adulthood, hyperactive and impulsive symptoms tend to decrease
but not disappear. Symptoms of inattention, however, do not tend to decrease as
much. Additional facts about ADHD are presented in Table 14.13.
TABLE 14.13 • Attention-Deficit/Hyperactivity Disorder Facts at a Glance
Prevalence
• The estimated prevalence of ADHD in school-aged children increased from 6% in 1997 to almost 10% in 2007 (National Center for Health
Statistics, 2008; Visser et al., 2010).
• Prevalence among American adults is about 4% (Kessler, Adler, et al., 2006).
Comorbidity
• Common comorbid disorders include mood and anxiety disorders, learning disorders, and oppositional defiant disorder (American Psychiatric
Association, 2013; Larson et al., 2011).
• Up to half of children with ADHD also have oppositional defiant disorder.
• Children with hyperactive and impulsive symptoms are more likely to be diagnosed with oppositional defiant disorder or conduct disorder than are
those with inattentive symptoms (Christophersen & Mortweet, 2001).
Onset
• Children are not usually diagnosed before age 4 or 5 because the range of normal behavior for preschoolers is very wide.
• In younger children, the diagnosis is generally based more on hyperactive and impulsive symptoms than on inattention symptoms.
Course
• Symptoms of ADHD become obvious during the elementary school years, when attentional problems interfere with schoolwork.
• By early adolescence, the more noticeable signs of hyperactivity—difficulty sitting still, for example—typically diminish to a sense of restlessness
or a tendency to fidget.
• Almost a third of childhood cases carry over into adulthood (Barbaresi et al., in press).
Gender Differences
• Males are more likely—in one survey, more than twice as likely—to be diagnosed with ADHD, particularly the hyperactive/impulsive type,
although this gender difference may reflect a bias in referrals to mental health clinicians rather than any actual difference in prevalence (National
Center for Health Statistics, 2008).
Cultural Differences
• In the United States, non-Hispanic White children are more likely to be diagnosed with ADHD than are Hispanic or Black children (Havey et al.,
2005; Stevens et al., 2005).
• Worldwide, the prevalence of the disorder among children averages about 5% (Polanczyk & Rohde, 2007), although some studies find higher preva-
lence rates (Bird, 2002; Ofovwe et al., 2006); variability across countries can be explained by the different thresholds at which behaviors are judged
as reaching a symptomatic level, as well as somewhat different diagnostic criteria (Bird, 2002).
Source: Unless otherwise noted, the source for information is American Psychiatric Association, 2000.
Neurodevelopmental and Disruptive Behavior Disorders 467
Understanding Disorders of Disruptive Behavior and
Attention
Given the high comorbidity and overlap of symptoms among the three disorders—
conduct disorder, oppositional defiant disorder, and ADHD—we’ll focus on the
disorder that is best understood, ADHD. Studies of factors related to oppositional
defiant disorder and conduct disorder probably include participants who also have
ADHD, which makes it difficult to determine which factors are uniquely associated
with oppositional defiant disorder and conduct disorder and not ADHD.
Neurological Factors
Research has revealed that people who have ADHD have abnormal brain structure
and function, and research also has begun to characterize the roles of neurotransmit-
ters and genes in these brain abnormalities.
ADHD: Brain Systems and Neural Communication
The behavioral problems that characterize people with ADHD may arise in part from
impaired frontal lobe functioning. This hypothesis is consistent with the fact that people
with ADHD often cannot perform functions well that rely on the frontal lobes, such
as various executive functions (e.g., formulating and following plans; Kiliç et al., 2007)
and estimating time accurately, which affects their ability to plan and follow through
on commitments (Barkley et al., 2001; McInerney & Kerns, 2003; Riccio et al., 2005).
Studies have shown that children and adolescents with this disorder have smaller
brains than do children and adolescents without the disorder, and the deficit in size is
particularly marked in the frontal lobes (Schneider, Retz et al., 2006; Sowell et al., 2003;
Valera et al., 2007). Indeed, particular parts of the frontal lobes have been shown to be
relatively small in adults with ADHD (Durston et al., 2004; Hesslinger et al., 2002).
Although research findings implicate the frontal lobes, they also indicate that it
is not the sole culprit that underlies ADHD. In particular, people with ADHD also
have smaller cerebellums, which is noteworthy because this brain structure is crucial
to attention and timing; in fact, the smaller this structure, the worse the symptoms of
ADHD are (Castellanos et al., 2002; Mackie et al., 2007).
Studies have also shown that ADHD is not a result of impaired function-
ing in any single brain area but rather emerges from how different areas interact.
Neuroimaging studies have revealed many patterns of abnormal brain functioning in
people who have ADHD (Rubia et al., 2007; Stevens et al., 2007; Vance et al., 2007).
In general, neural structures involved in attention tend not to be activated as strongly
(during relevant tasks) in people with this disorder as in people without it (Stevens et
al., 2007; Schneider, Retz, et al., 2006; Vance et al., 2007). However, virtually every
lobe in the brains of people with ADHD has been shown not to function
normally during tasks that draw on their functions (Mulas et al., 2006;
Vance et al., 2007).
Moreover, abnormal brain functioning can influence the autonomic
nervous system (see Chapter 2): ADHD (and some types of conduct dis-
order) has been associated with unusually low arousal in response to nor-
mal levels of stimulation (Crowell et al., 2006), a response that could
explain some of the stimulation-seeking behavior seen in people with
this disorder. That is, these people could engage in stimulation-seeking
behavior in order to obtain an optimal level of arousal.
People with ADHD have lower-than-normal levels of dopamine—
which is a key neurotransmitter used in the frontal lobes and in many
other brain areas. However, the overall pattern of difficulties that char-
acterizes ADHD suggests problems with multiple neurotransmitters—
i nclud i n g seroton i n a nd norepi neph r i ne — t h at a re i nvolved i n
Bored in class? For a child with ADHD, it may
be even worse than for these kids. ADHD is
associated with low levels or arousal to normal
levels of stimulation. For a child with ADHD,
when a teacher or the material discussed
isn’t “exciting” or interesting, time in the
classroom can feel particularly understimulating
and boring.
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coordinating and organizing cognition and behavior (Arnsten, 2006; Volkow et al.,
2007). Given the number of brain areas that are involved, problems with multiple
neurotransmitters are probably associated with the disorder.
ADHD and Genetics
Genes may be one reason why people with ADHD have abnormal brain systems and
disrupted neural communication. Indeed, not only does this disorder run in fami-
lies, but also parent and teacher reports indicate that it is highly correlated among
monozygotic twins (with correlations ranging from 0.60 to 0.90). In addition, a large
set of data reveals that this disorder is among the most heritable of psychological dis-
orders (Martin et al., 2006; Stevenson et al., 2005; Waldman & Gizer, 2006).
However, as with most other psychological disorders that are influenced by genes,
a combination of genes—not a single gene—probably contributes to it ( Faraone et al.,
2005). In fact, over a dozen different genes have so far been identified as possibly contrib-
uting to this disorder (Guan et al., 2009; Swanson et al., 2007; Waldman & Gizer, 2006).
Moreover, as usual, genes are not destiny: The effects of the genes depend in part
on the environment. For example, children whose mothers smoked while pregnant
are much more likely to develop ADHD than are children whose mothers did not
smoke (Braun et al., 2006), and this relationship appears to be particularly strong for
children who have a specific gene (Neuman et al., 2007).
Psychological Factors: Recognizing Facial Expressions,
Low Self-Esteem
In addition to problems with attention and executive function, people with ADHD
may have other, perhaps less obvious, difficulties. In particular, as with ASD, people
with ADHD have difficulty recognizing emotions in facial expressions (Demopoulos
et al., 2013)—but not all emotions; they have problems recognizing anger and sadness
in particular. Why? The answer isn’t known, but one suggestion is that these people
might have had very negative experiences with others who are sad or angry, and these
unpleasant experiences motivate them to tune out such expressions (Pelc et al., 2006).
In addition, children with ADHD appear to have an attributional style that leaves them
vulnerable to low self-esteem. In one study (Milich, 1994), children with ADHD initially
overestimated their ability to succeed in a challenging task, and—when confronted with
failure—boys with ADHD became more frustrated and were less likely to persist with the
challenging task than were boys in a control group. Moreover, in another study (Collett &
Gimpel, 2004), children with ADHD attributed the cause of negative events to global and
stable characteristics about themselves (“I am a failure”) rather than external, situational
factors (“That was a very hard task”). Conversely, children with ADHD were more likely
than children without a psychological disorder to attribute positive events to external,
situational causes. These attribution patterns were observed regardless of whether children
were taking medication for ADHD. Such patterns are often seen in people who experi-
ence low self-esteem (Sweeney et al., 1986; Tennen & Herzberger, 1987).
Low self-esteem among those with ADHD isn’t restricted to children. One study
compared college students with and without ADHD and matched them to control
participants who had comparable demographic variables and grade-point averages.
Students with ADHD reported lower self-esteem and social skills than did students
without ADHD (Shaw-Zirt et al., 2005). Other studies report lower self-esteem
among adolescents with ADHD (Slomkowski et al., 1995).
Social Factors: Blame and Credit
The low self-esteem of children with ADHD may also be related to social factors,
in particular to their parents’ attributions: Although parents don’t necessarily blame
their children for ADHD-related behaviors, they don’t give their children as much
credit for positive behaviors as do parents of children without ADHD ( Johnston &
What does this man’s expression mean? For
people with ADHD, it might not be clear
that he’s not happy to see a visitor. People
with ADHD can have difficulty noticing and
understanding certain social cues; specifically,
they may not recognize the facial expressions
that correspond to anger and sadness.
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Neurodevelopmental and Disruptive Behavior Disorders 469
Freeman, 1997). The parents of children with ADHD tend to attribute children’s
positive behaviors to random situational factors.
In addition, social factors can indirectly influence the development of this disor-
der. For example, children typically are raised in homes selected by their parents—
based on various social factors, such as parents’ financial status, proximity to extended
family, and community resources. If children are raised in a house where lead paint
has been applied, they may be more vulnerable to ADHD. In fact, children whose
hair contains higher levels of lead (which is a measure of exposure to lead, perhaps
from lead paint in one’s home environment) are more likely to have ADHD than are
children who have lower levels of lead in their hair (Tuthill, 1996). Even children
who were exposed to very low levels of lead in their environment are more likely to
develop ADHD than are children who were not exposed (Nigg, 2006b).
Feedback Loops in Understanding Attention-Deficit/
Hyperactivity Disorder
In this section, we examine how the different factors related to ADHD create feed-
back loops (see Figure 14.1). Current research suggests that psychological and social
factors contribute to the development of ADHD in people whose genes lead them to
be neurologically vulnerable to the disorder.
Consider the finding that children with ADHD are less accurate at recognizing sad
and angry facial expressions (Pelc et al., 2006). Such deficits, particularly difficulty in rec-
ognizing anger, are associated with more interpersonal problems. These results suggest that
when peers or adults (typically parents or teachers) show—rather than tell—their displea-
sure to a child who has ADHD, that child is less likely to perceive (psychological factor)
the social cue (social factor) than is a child who does not have the disorder. This difficulty
in perceiving others’ displeasure in turn creates additional tension for both the child and
those who interact with him or her. In fact, children with ADHD are more likely than
those without the disorder to be rejected by their peers (Mrug et al., 2009). Moreover,
other people’s responses to the child’s behavior (social factor) in turn influence how the
child comes to feel about himself or herself (psychological factor; Brook & Boaz, 2005).
Other research results suggest that the family environment is associated with
ADHD. In particular, family conf lict is higher in families that include a child
with ADHD than in control families (Pressman et al., 2006). However, do family
environments that are higher in conflict play a role in causing a child to develop
ADHD? Or do the symptoms of the disorder—inattention, hyperactivity, or im-
pulsivity—create more tension in the family? Or do difficulties associated with the
disorder, such as difficulty in recognizing angry or sad facial expressions, increase
family tension? It may be that all these possible influences occur.
Treating Disorders of Disruptive Behavior and Attention:
Focus on ADHD
Treat ment s for d isorder s of d isr upt ive behav ior a nd at tent ion a re usua l ly
comprehensive, targeting more than one type of factor and sometimes all three types
of factors. And children with ADHD may be legally entitled to special services and
accommodations in school. Specific treatments for ADHD focus both on attentional
symptoms and, when present, on hyperactivity/impulsivity symptoms.
Targeting Neurological Factors: Medication
Medication for ADHD often treats symptoms of both ADHD and also comor-
bid oppositional defiant disorder or conduct disorder. One type of medication for
ADHD targets dopamine, which plays a key role in the functioning of the frontal
lobes ( Solanto, 2002). Many of these medications are stimulants, which may sound
counterintuitive because people with ADHD don’t seem to need more stimulation.
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However, these stimulants increase attention and reduce general activity level and
impulsive behavior. Although the mechanism that produces these effects is not entirely
understood, the medications appear to have their effects by disrupting the reuptake of
dopamine, leaving more dopamine in the synapse and thus correcting at least some of
the imbalance in this neurotransmitter that has been observed in the brains of people
with ADHD (Volkow et al., 2005). In addition, this disorder may arise in part because
the person is understimulated and hence seeks additional stimulation; by providing
stimulation internally, the medications reduce the need to seek it externally.
Stimulant medications for ADHD may contain methylphenidate (such as Ritalin,
Concerta, and Focalin) or an amphetamine (such as Adderall) and are available in
relatively short-acting formulas (requiring two or three daily doses) and in a timed-
release formula (requiring only one dose per day). Methylphenidate is also available
Affect
Stressful Life Events Family
NeuroPsychoSocialNeuroPsychoSocial
Easily
distressed
Mental Processes and
Mental Contents
Difficulty focusing and
sustaining attention
Difficulty recognizing
facial expression of
anger and sadness
Low self-esteem
Maladaptive
attributional style
Parents’
attributions
Gender/Culture
No known major
contribution
Behavior
Impulsive and/or
hyperactive
behaviors
NeuroPsychoSocial
Genetics
Inherited vulnerability
for ADHD
Brain Systems
Frontal lobes
Abnormalities that
arise from exposure
to teratogens
Underresponsive
autonomic nervous
system
Neural Communication
Multiple neurotransmitters
Interpersonal problems
FI G U RE 14.1 • Feedback
Loops in Understanding
Attention-Deficit/
Hyperactivity Disorder
Neurodevelopmental and Disruptive Behavior Disorders 471
as a daily skin patch. About 65–75% of people with ADHD who receive stimulants
improve (compared to 4–30% of controls who receive placebos), and the side effects
are not severe for most people (Pliszka, 2007; Pliszka et al., 2006). In fact, stimulants
have been shown to improve the functioning of various brain areas that are impaired
in this disorder (Bush et al., 2008; Clarke et al., 2007; Epstein et al., 2007).
Another medication for ADHD is atomoxetine (Strattera); it is a noradrenaline reup-
take inhibitor, not a stimulant. Atomoxetine has effects and side effects similar to those
of the stimulant medications (Kratochvil et al., 2002) and currently is the medication of
choice for people with both ADHD and substance abuse.
Medications for ADHD reduce impulsive behaviors, which seems to decrease
related aggressive behaviors (Frick & Morris, 2004). This effect can have wide-
ranging consequences. As noted earlier, the symptoms of ADHD can give rise to
feedback loops with a child’s family or with peers, and these feedback loops can cause
disruptive behaviors to escalate. Successful treatment with medication disrupts these
feedback loops, reducing the frequency and intensity of disruptive behaviors, which
in turn leads family members and peers not to become as irritated and angry, which
thereby reduces their undercutting the child’s self-esteem (Frick & Muñoz, 2006;
Hinshaw et al., 1993; Jensen et al., 2001).
Targeting Psychological Factors: Treating Disruptive Behavior
Treatments that target psychological factors have been developed for all three disrup-
tive disorders. These treatments usually employ behavioral and cognitive methods to
address disruptive behaviors. One reason for such behaviors is that children with any
of these disorders tend to have low frustration tolerance and difficulty in working for
delayed—rather than immediate—reward. Thus, behavioral methods may focus on
helping such children restrain their behavior and accept a delayed reward. Specific
techniques include a reinforcement program that uses concrete rewards, such as a toy,
and social rewards, such as praise or special time with a parent. These methods slowly
increase the delay until the child receives either a concrete reward (“Now you can
have that toy”) or a social reward (“You did a great job, I’m proud of you”), which
should motivate the child to control behavior for a delayed reward in the future
(Sonuga-Barke, 2006).
Behavioral methods for treating all three disorders may also be used to modify social
behaviors, such as not responding to others aggressively or not interrupting others. For
example, when children enter preschool or kindergarten, this may be the first time they
have to sit quietly for a length of time and wait for a turn to participate. Often the teacher
will ask children to raise a hand and wait until called on to answer a question. A child with
ADHD will be more likely than other children to speak out of turn or to keep vigorously
waving a raised hand, trying to get the teacher’s attention. A program of rewarding the
child for increasingly longer times of not speaking out or waving frantically can teach the
child to behave with more restraint, which can ease relations with classmates.
Cognitive methods seek to enhance children’s social problem-solving abilities.
Specifically, the therapist helps the child interpret social cues in a more realistic way—
for instance, acknowledging that the other person may not have hostile motives when
he asked you to move your backpack—and develop more appropriate social goals
and responses (Dodge & Pettit, 2003). Through skills-building, modeling, and role-
playing, the treatment also helps the child to learn how to inhibit angry or impulsive
reactions and to learn more effective ways to respond to others. The therapist praises
the child’s successes in these areas. To enhance the generalizability of the new skills
to life outside the therapy session, parents and teachers may be asked to help with
role-playing and modeling and to use praise in their contacts with the child. CBT for
adults with ADHD (which focuses on helping the person with planning, organiza-
tion, and coping with distractions) is also effective (Safren et al., 2010).
To help increase a child’s frustration
tolerance—which is typically low in children
with a disruptive disorder—parents may
institute a reinforcement program that
rewards the child for restraining himself or
herself.
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472 C H A P T E R 1 4
This little boy seems to be enjoying a leap
on the couch, but is it inappropriate?
Parents of children with ADHD are taught
contingency management training to develop
realistic goals for their child’s behavior, to
institute appropriate behavior modification
plans, and to respond consistently to the
child’s misbehavior.
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Contingency management
A procedure for modifying behavior by
changing the conditions that led to, or are
produced by, it.
Targeting Social Factors: Reinforcement in Relationships
Most of the treatments that target social factors are designed to help parents—and
teachers, when necessary—to use operant conditioning principles to shape a child’s
prosocial behavior and decrease defiant or impulsive behavior.
Contingency Management: Changing Parents’ Behavior
Contingency management is a procedure for modifying behavior by changing the
conditions that lead to, or are produced by, the behavior. Treatment may target par-
ents of children with ADHD to help them set up a contingency management program
with their child—particularly in cases in which the parents have been inconsistent in
their use of praise (and other reinforcers) or punishment (Frick & Muñoz, 2006).
The first step of contingency management training with parents is psychoeducation—
teaching the parents that the symptoms are not the result of intentional misbehavior but
part of a disorder (Barkley, 1997, 2000). The subsequent training then is intended to:
1. change parents’ beliefs about the reasons for their child’s behavior so that parents
approach their child differently and develop realistic goals for their child’s behavior;
2. help parents to institute behavior modification, which includes paying attention
to desired behaviors, being consistent and clear about directions, and developing
reward programs; and
3. teach parents to respond consistently to misbehavior.
Parent training targets social factors—interactions between parents and child.
Changes in the way parents think about and interact with their child, in turn, change
the child’s ability to control behavior (psychological factor). Parent training may be
the best treatment for families who have children with mild ADHD or preschoolers
with ADHD (Kratochvil et al., 2004).
Parent Management Training
Parent management training is designed to combine contingency management tech-
niques with additional techniques that focus on improving parent–child interactions
generally—improving communication and facilitating real warmth and positive
interest in the parent for his or her child (Kazdin, 1995).
Multisystemic Therapy
Multisystemic therapy (Henggeler et al., 1998) is based on family systems therapy and
focuses on the context in which the child’s behavior occurs: with peers, in school, in the
neighborhood, and in the family. This comprehensive treatment may involve family and
couples therapy, interventions with peers, CBT with the child, and an intervention in
the school (such as meeting with the child’s teacher or directly assisting in the classroom
to help the child manage his or her behavior). The specific techniques employed are tai-
lored to change systems in the child’s life in order to manage his or her behavior better.
Feedback Loops in Treating Attention-Deficit/Hyperactivity
Disorder
At first glance, medication might seem to have its effects solely through neurological
mechanisms, but this isn’t so. Taking medication (neurological factor) not only leads
to increased control of attention and hyperactive or impulsive behaviors, but it is also
associated with higher levels of self-esteem (psychological factor; Frankel et al., 1999),
which can lead a child not to seek attention as vigorously. Moreover, such increased
control of attention and behavior also improves social functioning (social factor;
Chacko et al., 2005). And better social functioning feeds back to improve self-esteem.
Other feedback loops originate from programs for parents or the family (which
target social factors); such interventions in turn create feedback loops with psycho-
logical factors—improving the child’s thoughts, feelings, and behaviors. Figure 14.2
illustrates feedback loops among the various factors that are used to treat ADHD.
SP
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Neurodevelopmental and Disruptive Behavior Disorders 473
SUMMING UP
Intellectual Disability (Intellectual
Developmental Disorder)
• The diagnosis of intellectual disabilit y
typically involves both cognitive deficits
that are signif icantly below normal and
impaired daily functioning in conceptual,
social, and/or practical areas. Some people
with intellectual disability— particularly
at the severe or profound level—may have
difficulty communicating verbally.
• Neurological factors are the primary di-
rect cause of most cases of intellectual
disability—usually a genetic abnormal-
ity or prenatal exposure to a teratogen,
which in turn alters brain structure and
function.
• Many types of intellectual disability can
be prevented, such as those related to
PKU and lead poisoning.
• Inter ventions are designed to improve
t he per son’s f u nct ion i n g by i nc rea s –
ing his or her communication and daily
living skills.
• Legally, children with an intellectual dis-
ability are entitled to special education
and related services, tailored to their indi-
vidual needs.
Nikhil has some first-hand familiarity with oppositional defiant disorder and conduct disor-
der: He went to a large middle school and large high school, where some kids always acted up
and got into trouble. And during high school and college, some of his friends and then one of
his roommates had ADHD. Even though Nikhil may think he knows something about disrup-
tive behavior disorders and ADHD, based on what you have read, what information about
these disorders should he be given before he begins to teach, and why?
Thinking Like A Clinician
FI G U RE 14.2 • Feedback
Loops in Treating
Attention-Deficit/
Hyperactivity Disorder
Changes neural activity
Treatments Targeting
Psychological Factors
CBT: Modeling, reinforcement
programs, social problem solving
Treatments Targeting
Social Factors
Contingency management
Parent management training
Multisystemic therapy
Changes thoughts,
feelings, and behaviors
Decreases family conflict and
family members’ critical
behavior
Increases positive attention
and support for making
positive changes
Changes social interactions
Treatments Targeting
Neurological Factors
Medication: Stimulants such as
methylphenidate or atomoxetine
474 C H A P T E R 1 4
Autism Spectrum Disorder
• Autism spectrum disorder (ASD) involves
two types of problems: (1) significant def-
icits in communication and social interac-
tion skills and (2) stereotyped behaviors
or narrow interests.
• M a n y p e o p l e w i t h A S D a l s o h a v e
comorbid intel lect ua l d isabi l it y when
tested w ith convent iona l intel l igence
tests; on tests that do not rely on verbal
abilities, people with ASD tend to score in
the average range or higher.
• Neurological factors that underlie ASD
include abnormal connections and com-
munication among different brain areas.
• Psychological symptoms of ASD include
def icits in shifting attention, in mental
flexibility, and an impaired theory of mind.
• Social symptoms of ASD include problems
in recognizing emotion in the voices and
faces of others and in understanding the
give and take of social communication.
• Treatment for ASD that targets psycho-
logical factors includes applied behavior
analysis to modify maladaptive behaviors.
Treatments that target psychological and
social factors focus on teaching the person
to recognize conventional social cues, to
read the emotional expressions of others,
and to communicate, as well as how to
initiate and respond in social situations.
Specific Learning Disorder: Problems
with the Three Rs
• Specific learning disorder is characterized
by well-below-average skills in reading,
writing, or math, based on the expected
level of performance for the person’s age,
general intelligence, cultural group, gen-
der, and education level. DSM-5 includes
three types of learning disorders related
to: reading (dyslexia), written expression,
and mathematics (dyscalculia).
• Dyslexia appears to result from disrup-
tions in brain systems that process lan-
g uage and that process visua l stimuli.
Treatment for dyslexia may involve vari-
ous cognitive techniques to compensate
for reading difficulties.
Disorders of Disruptive Behavior
and Attention
• Conduct disorder is characterized by a
violation of the basic rights of others or of
societal norms that are appropriate to the
person’s age. Conduct disorder involves
four t y pes of behav ior: agg ression to
people and animals, destruction of prop-
erty, deceitfulness or theft, and serious
violation of rules. The disorder may begin
in childhood or adolescence. Conduct
d isorder is com mon ly comorbid w ith
attention-deficit/hyperactivity disorder.
• Childhood-onset conduct disorder with
cal lous and unemotional traits has the
h ig he st her it abi l it y a mong t he va r i-
ous types of conduct disorder; this vari-
ant is also associated with more severe
symptoms.
• Oppositional def iant disorder is char-
acter ized by ang r y or ir r itable mood,
def iance or argumentative behavior, or
vindictiveness. The behaviors are usually
Intellectual disability (p. 444)
Teratogens (p. 447)
Stereotyped behaviors (p. 448)
Inclusion (p. 449)
Autism spectrum disorder (ASD) (p. 450)
Theory of mind (p. 454)
Applied behavior analysis (p. 454)
Specific learning disorder (p. 455)
Dyslexia (p. 455)
Conduct disorder (p. 460)
Oppositional defiant disorder (p. 463)
Attention-deficit/hyperactivity disorder
(ADHD) (p. 465)
Contingency management (p. 473)
More Study Aids
For additional study aids related
to this chapter, including quizzes
to make sure you’ve retained
everything you’ve learned and a
Student Video Activity exploring
the case of one boy with autism
spectrum disorder, go to: www.
worthpublishers.com/launchpad/
rkabpsych2e.
Photodisc
not v iolent, nor do they cause severe
harm, and they often occur only in cer-
tain contexts.
• Attention-deficit/hyperactivity disorder
(ADHD) is characterized by inattention,
hyperactivity, and/or impulsivity.
• Oppositional def iant disorder, conduct
disorder, and ADHD are highly comor-
bid, making it difficult to sort out factors
that contribute uniquely to one of the
disorders.
• Neurological factors that contribute to
A DH D include f ronta l lobe problems
and genes. Too little dopamine and im-
balances in other transmitters also play
a role.
• Psycholog ica l f actor s a ssociated w ith
ADHD include low self-esteem and dif-
f iculty recognizing facial expressions of
anger and sadness.
• Social factors that contribute to ADHD
i nclude pa rent s’ not g iv i ng ch i ld ren
enough credit for their positive behaviors.
• Treatment targeting neurological factors
in A DHD involves medication—t ypi-
cally methylphenidate or atomoxetine.
Treatments targeting psychological factors
include behavioral methods to increase a
person’s ability to tolerate frustration and
to delay reward, and cognitive methods
to enhance social problem-solving abil-
ity. Treatments that target social factors
include group therapy and comprehensive
treatments such as contingency manage-
ment, parent management training, and
multisystemic therapy.
Key Terms
Neurodevelopmental and Disruptive Behavior Disorders 475
477
CHAPTER 15
Neurocognitive Disorders
rs. B. was an 87-year-old woman at the time that she was
referred for neuropsychological testing. Mrs. B. wasn’t always
able to get to the toilet in time to urinate, her hearing and
vision weren’t as good as they had been and, because of an inner-ear
problem, she sometimes lost her balance and fell. A neuropsychologist
was asked to determine the nature of Mrs. B.’s problems— specifically
the extent to which a neurocognitive disorder might account for
at least some of her difficulties. The neuropsychologist noted that
Mrs. B.:
had moved from another state several months earlier at the urging
of her daughter, who had been receiving reports from neighbors and
relatives that she was unable to care for herself or her home and was
increasingly suspicious and argumentative. Her first residence in her
new community was . . . a nursing home, but it soon became apparent
that she was functioning at a higher level than other residents and she
moved to a small board-and-care home [a small residential facility
for elders who need round-the-clock help with daily functioning
and personal care]. With only a few persons in the home and a low
resident-to-staff ratio, this seemed a good arrangement for an older
person who needed an intermediate level of assistance. Mrs. B. appar-
ently thought otherwise.
She often refused to admit staff to her room or to accept assis-
tance with activities such as bathing, despite an unsteady gait and
several recent falls. She had arguments with other residents that some-
times escalated into shouting matches. A private-duty companion was
hired to assist her for several hours a day and to take her on excursions
outside of the home. This was helping somewhat, but accusations and
arguments continued at an unsettling rate. Mrs. B. sometimes seemed
to forget plans that she had agreed to and was occasionally tearful
and sad.
(La Rue & Watson, 1998, pp. 6, 10)
Normal Versus Abnormal Aging and
Cognitive Functioning
Cognitive Functioning in Normal Aging
Psychological Disorders and Cognition
Medical Factors That Can Affect Cognition
Delirium
What Is Delirium?
Understanding Delirium: A Side Effect?
Treating Delirium: Rectify the Cause
Dementia (and Mild Versus Major
Neurocognitive Disorders)
What Is Dementia?
Understanding Dementia
Treating Dementia
Diagnosing Mrs. B.’s Problems
Neurocognitive disorders
A category of psychological disorders in which
the primary symptom is significantly reduced
cognitive abilities, relative to a prior level
of functioning; also referred to as cognitive
disorders.
What might account for mrs. B.’s disruptive behavior
and memory problems? One possibility is that she had a neurocogni-
tive disorder. According to DSM-5, neurocognitive disorders are
a category of psychological disorders in which the primary symptom
is significantly reduced cognitive abilities relative to a prior level of
functioning. These disorders are also referred to as cognitive disorders.
LAURENT/ANNETTE/BSIP/age fotostock. Photo for illustrative purposes only;
any individual depicted is a model.
Because such deficits reflect a reduction of a previous ability, they cannot be present
at birth. (The neurodevelopmental disorders discussed in Chapter 14 involve deficits
either since birth or at some point during childhood.)
Impaired cognitive abilities are not unique to neurocognitive disorders. Many of the
disorders discussed in previous chapters involve a change in cognitive functioning: People
who are depressed or anxious can have impaired attention, concentration, and memory;
those with a psychotic disorder have impaired perception and judgment; and substance
use disorder can lead to a wide variety of cognitive impairments (Balash et al., 2013). The
cognitive changes associated with these other disorders, however, are secondary to the
symptoms that characterize the disorders: depressed mood, anxiety and fear, psychotic
symptoms, or behaviors related to substance abuse.
In contrast, with neurocognitive disorders, the changes in cognitive
functioning—in mental processes—constitute the primary set of symp-
toms. Patients may (or may not) also have unusual behavior, mood, or
mental contents. Usually, the undesired cognitive changes arise from a
medical disease such as Parkinson’s disease, a medical condition such as a
stroke, or the use of or withdrawal from a psychoactive substance (which
may include exposure to a toxic substance).
Neurocognitive disorders are almost exclusively caused by neurologi-
cal factors (hence their name), and thus this chapter does not contain any
Feedback Loops sections or figures. Although psychosocial treatments may
buffer or delay the ways that the disorders impair functioning or cause
distress, they do not generally feed back to affect the neurological factors
that lead to the disorder.
In most cases, these disorders afflict older adults rather than younger
adults. So, part of the job of diagnosing these disorders is to distinguish their symp-
toms from changes that occur with normal aging. In what follows we first examine the
changes in cognitive functioning that occur during the normal aging process, which
will allow us to contrast these effects with those described in subsequent sections.
Normal Versus Abnormal Aging
and Cognitive Functioning
The neuropsychologist assessing Mrs. B. needed to determine whether her distur-
bances in memory, mood, and behavior were normal for an 87-year-old, particularly
one with a variety of medical problems. And, if her memory, mood, and behavior
weren’t in the normal range, given her circumstances, what, specifically, were her
diff iculties? And what could account for them? The neuropsychologist initially
assessed Mrs. B. using a clinical interview (discussed in Chapter 3), observing her as
well as noting her responses to questions:
Mrs. B. arrived promptly for her appointment, accompanied by her private-duty nurse.
She was well-groomed and alert but ambulated slowly, leaning against the railing on
the wall to maintain her balance; she was also unsteady on rising and standing from a
chair. She was fluent and willing to talk at great length about her situation, although her
speech was often repetitive and tangential. Mood was . . . positive during the interview.
She denied hallucinations, delusions, or suicidal ideation but admitted to some depres-
sion, which she felt had improved somewhat on antidepressant medication. She was
able to describe some aspects of her experience at the [nursing home] and gave several
examples of the types of things that annoyed her at the current board-and-care home.
(La Rue & Watson, 1998, p. 6)
Mrs. B. was able to remember aspects of her nursing home experience that
she didn’t like, but she forgot other types of information, such as her upcoming
This woman might just be thinking, but she
also could be worrying. In fact, many older
adults are concerned that they might have
a neurocognitive disorder because these
disorders more frequently afflict the elderly
than the young. Clinicians need to be able to
distinguish these disorders from the normal
aging process.
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478 C H A P T E R 1 5
plans. In the normal course of events, however, various cognitive functions tend
to decline with advancing age. Even healthy older adults have some cognitive
deficits, compared to their younger selves, and these must be taken into account
when attempting to determine whether an older person has a disorder. Thus,
the neuropsychologist must assess whether Mrs. B.’s functioning has declined
and, if so, whether this decline is beyond what occurs with the normal aging
process. In this section, we examine what happens to cognitive functioning dur-
ing normal aging and then examine the neurological factors that can disrupt
cognitive functioning.
Cognitive Functioning in Normal Aging
Most—although not all—aspects of cognitive functioning remain relatively stable
during older adulthood.
Intelligence
Let’s first examine intelligence, which can be divided into two types (Cattell, 1971):
Crystallized intelligence relies on using knowledge to reason in familiar ways;
such knowledge has “crystallized” from previous experience. For example, an avid
fisherman can use knowledge gleaned from prior experience to reason about where
fish are likely to be lurking in a stream. Normally, crystallized intelligence remains
stable or actually increases with age, even among older adults; crystallized intel-
ligence is often assessed by tests that measure verbal ability, and these tests often
allow ample time for people to respond to questions. In contrast, fluid intelligence
relies on the ability to create novel strategies to solve new problems, without rely-
ing solely on familiar approaches. For example, fluid intelligence would be required
to devise a new way to catch fish without a hook, line, and sinker—perhaps using a
shirt or basket as a net. Fluid intelligence relies on executive functions, which include
the abilities to think abstractly, to plan, and to exert good judgment. Fluid intel-
ligence is typically assessed with tests of visual-motor skills, problem solving, and
perceptual speed (Salthouse, 2005). As adults age, their scores on most measures of
fluid intelligence decline.
Crystallized intelligence
A type of intelligence that relies on using
knowledge to reason in familiar ways; such
knowledge has “crystallized” from previous
experience.
Fluid intelligence
A type of intelligence that relies on the
ability to create novel strategies to solve new
problems, without relying solely on familiar
approaches.
Which photo best illustrates crystallized intelligence? Answer: The photo on the left. If a person has
been fishing for years, this knowledge would contribute to the crystalized intelligence used to decide
where best to try to catch fish (with a pole). If a fishing pole were not available, reasoning about novel
ways to catch fish—such as by using a basket as a net—would draw on fluid intelligence.
GETTING THE PICTURE
G
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©
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Fo
to
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Neurocognitive Disorders 479
Normal cognitive decline must be judged in relation to each person’s own base-
line. An older adult who starts out with a high IQ and has functioned well will
probably be able to continue to function well even with the normal decline of aging.
In contrast, the functioning of someone who has a lower IQ initially (such as in the
low normal range, an IQ between 85 and 100) will be affected more dramatically—
perhaps to the point where his or her ability to function independently is curtailed
(Harvey, 2005a).
Memory
Memory is not a single ability, and various aspects of it are affected in different ways
by aging.
The elderly (generally considered to be people aged 65 and older;
World Hea lth Organ izat ion [W HO] , 20 09 ) tend to have problem s
reca l l ing prev iously stored in for mat ion. To recall in for mat ion is to
become aware of that information after voluntarily attempting to “look
it up” in memor y. In contrast, healthy older people often have little
difficulty with recognition; to recognize information requires first per-
ceiving it and then compar ing it to information previously stored in
memor y to determine whether the perceived information matches the
stored information.
For example, older people sometimes have trouble recalling the names
of common objects on demand. Thus, they might say, “I went to the store
to buy a ‘thingamajig’ this morning.” Despite difficulty recalling the names
of objects, cognitively healthy older people can describe the object or rec-
ognize the correct word when someone else says it, and may even recall
the correct word a few minutes later when talking about something else
(Nicholas et al., 1985).
However, in spite of these difficulties, healthy older people can often recall tem-
porarily forgotten names of common things when given cues or hints. Moreover,
with normal aging, the ability to recall personal information is preserved; people can
recall important episodes from their past.
Processing Speed, Attention, and Working Memory
People generally process information more slowly as they reach old age. One ex-
planation for this slowed processing speed is that the myelin sheaths coating the
axons of neurons degrade or disappear, which then causes the neurons’ signals to
dissipate—and hence communication among brain areas is impaired (Andrews-
Hanna et al., 2007).
The slowed processing speed that occurs with advanced age affects many cogni-
tive functions. For example, consider storing new information in memory: Older
adults generally acquire new information at a slower rate and thus typically need
more exposure to the to-be-stored material; they also need more practice in retriev-
ing the information after they have stored it. For these reasons, elderly people may
be impaired when carrying out tasks that require rapidly recalling and using stored
information (Fillit et al., 2002; Salthouse, 2001).
A not her cog n it ive f u nct ion t h at of ten decl i ne s w it h a ge i s at tent ion.
Attention involves selecting some information for more careful analysis: what a
person pays attention to gets processed more fully than what he or she does not
pay attention to. In part because processing slows down with aging, the ability
to switch attention sequentially among multiple tasks (known as multitasking) is
likely to decline as people age (Parasuraman et al., 1989). Thus, older adults may
have a harder time performing tasks such as scanning e-mail while talking on
the phone.
This man may remember that the cabbage
he’s holding is called bok choi. But if he
doesn’t, he shouldn’t worry about it. It isn’t
unusual for an older person to be unable
to recall the name of a common object
sometimes, but be able to recognize the name
if someone else says it. This and other normal
aging-related cognitive changes do not usually
impair daily functioning.
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Elderly people t ypically have problems using working memory ( De Beni &
Palladino, 2004; Li, Lindenberger, & Sikström, 2001). Working memory requires
keeping information activated (so that you are aware of it) while operating on it
in a specific way; for example, holding the steps of a recipe in mind while cook-
ing and progressing from one step to the next requires working memory. Work-
ing memor y relies on executive functions that are implemented in the frontal
lobes, which don’t operate as effectively in elderly people as they do in younger
people.
Psychological Disorders and Cognition
Most older adults don’t have a psychological disorder; in fact, older adults have
the lowest prevalence of psychological disorders and of significant psychological
distress of any age group (Centers for Disease Control and Prevention, 2012 ;
Karlin et al., 2008). But when an older person does have a psychological dis-
order, its symptoms can impair cognitive functioning. Thus, before assuming
that an older person’s deteriorated cognitive functioning is a result of a neuro-
cognitive disorder, the clinician must first determine whether the deterioration
could result from another sort of psychological disorder. For instance, Mrs. B.
had a histor y of depression and described herself as having a “hot temper” even
as a young adult. Mrs. B.’s daughter described her mother “as always somewhat
self-centered and suspicious of the motives of others, but this had worsened no-
ticeably in recent years, to the point where she had been isolated within her
own home,” which led to the move to the nursing home (La Rue & Watson,
1998, p. 6).
The neuropsychologist must determine whether Mrs. B.’s memory problems
might reflect a psychological disorder—such as depression, an anxiety disorder, or
schizophrenia.
Depression
Older adults are less likely than their younger counterparts to be diagnosed with
depression. When they are depressed, however, the symptoms often differ from those
of younger adults: Older depressed adults have more anxiety, agitation, and memory
problems (Segal, 2003). Thus, cognitive func-
tioning is affected by depression both directly
(memory problems) and indirectly (anxiety and
agitation affect attention, concentration, and
other mental processes; see Table 15.1).
In addition, a mental health clinician must
deter m ine whether symptoms of depression
in an older person could be caused by a neu-
rocog n it ive d i sorder : S ome s y m pt om s of
depression, such as fatigue, may be caused by
brain changes associated with a neurocognitive
disorder ( Puente, 2003). Mrs. B. had a history of
depression and was taking antidepressant medi-
cation. However, the neuropsychologist who
assessed Mrs. B.’s cognitive functioning deter-
mined that the difficulties she was having were
not a result of depression (La Rue & Watson,
1998). Mr. Rosen, in Case 15.1, had cognitive
problems that may or may not have been related
to his depression.
TABLE 15.1 • Common Cognitive Deficits in Late-Life Depression
Information Processing Speed
• Slow to respond or initiate behavior; incomplete grasp of complex information
(because of a lag in processing)
Attention and Concentration
• Absentmindedness for daily activities, events, and appointments; tasks left incomplete;
decreased attentiveness for reading or conversation
Executive Function
• Difficulty with calculating, sequencing, multitasking, and novel problem solving;
inflexible behavior or thinking; perseverative or ruminative thinking; decline in
organization and planning; indecisiveness, decreased initiation of behavior
Memory
• Forgetfulness and absentmindedness, but should improve with prompts, cues, or
memory aids
Source: Potter & Steffens, 2007. For more information see the Permissions section.
Neurocognitive Disorders 481
CASE 15.1 • FROM TH E OUTSIDE: Normal Aging or Something More?
Maurice Rosen was 69 when he made an appointment for a neurological evaluation. He
had recently noticed that his memory was slipping and he had problems with concentra-
tion that were beginning to interfere with his work as a self-employed tax accountant.
He complained of slowness and losing his train of thought. Recent changes in the tax
laws were hard for him to learn, and his wife said he was becoming more withdrawn and
reluctant to initiate activities. However, he was still able to take care of his personal fi-
nances and accompany his wife on visits to friends. Although mildly depressed about his
disabilities, he denied other symptoms of depression, such as disturbed sleep or appetite,
feelings of guilt, or suicidal ideation.
Mr. Rosen has a long history of treatment for episodes of depression, beginning in his
20s. He has taken a number of different antidepressants and once had a course of electro-
convulsive therapy. As recently as 6 months before this evaluation, he had been taking an
antidepressant.
(Spitzer et al., 2002, p. 70)
Anxiety Disorders
Like depression, anxiet y disorders are less common among older adults than
among younger adults. The anxiety disorder most prevalent among older adults is
generalized anxiety disorder ( Segal, 2003). About 5% of older adults have general-
ized anxiety disorder, most often along with depression; in about half the
cases, the anxiety disorder only emerged when the person became older
(Flint, 2005). The fears and worries that accompany generalized anxiety
disorder can impair cognitive functioning, in part because the person may
become preoccupied with fears and worries and have difficulty paying atten-
tion and concentrating.
Schizophrenia
About 15% of people with schizophrenia are older than 44 when they have
their first psychotic episode (Cohen et al., 2000). Schizophrenia can involve
both positive symptoms, such as delusions and hallucinations, and negative
symptoms, such as an absence of initiative (avolition; see Chapter 12); these
symptoms can also occur with neurocognitive disorders.
Medical Factors That Can Affect Cognition
In some cases, impaired cognitive functioning is not a result of a neuro-
cognitive disorder but rather is caused by medical problems. We summarize
some of these problems in the following sections.
Diseases and Illnesses
Various physical diseases and illnesses can affect cognition— directly or
indirectly. Some medical illnesses, such as encephalitis (a viral infection
of the brain) and brain tumors, directly affect the brain and, in doing
so, affect cognition. The specific cognitive deficits that arise depend on
the particular features of the illness, such as the size and location of a
brain tumor.
Some chron ic d iseases or i l lnesses ind irectly af fect cog n ition by
creating pain, which can disr upt attention, concentration, and other mental
processes. For example, arthritis can cause chronic pain, and the aftermath of
surger y can cause acute pain. In addition, pain can interfere with sleep, which
Many physical diseases and illnesses can
affect cognitive functioning. One example is
pain—such as that caused by arthritis. In such
cases, the person would not be considered to
have a neurocognitive disorder.
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further impairs mental processes. These detrimental effects may be temporary, so
that cognitive functioning improves as the symptoms resolve or the pain recedes.
In other cases, however, the person may never return to his or her prior level of
functioning.
In still other cases, an older adult may appear to have impaired cognitive func-
tioning but actually has undiagnosed or uncorrected sensor y problems, such as
hearing loss or vision problems. If someone chronically mishears what is said, he
or she will seem “not with it” or “senile” when, in fact, the problem is simply
that the person thinks the topic of conversation is something other than what it
actually is.
Stroke
A stroke (so named because it was originally assumed to be a “stroke of God”)
is the interruption of normal blood flow to or within the brain (often because of
an obstruction—such as a blood clot—in a blood vessel). The result is that part
of the brain fails to receive oxygen and nutrients, and the neurons in that area
die. The cognitive, emotional, and behavioral consequences of a stroke depend
crucially on which specific group of neurons is affected; depending on their loca-
tion in the brain, different deficits are produced. The most common deficits are
discussed below.
Aphasia
Aphasia is a problem in using language. (The word aphasia literally means “an
absence of speech.”) Traditionally, there are two main types of aphasia, each named
after the neurologist who first characterized it in detail. Broca’s aphasia is character-
ized by problems producing speech. Patients with Broca’s aphasia speak haltingly, and
their speech can be very telegraphic—consisting of only the main words. In contrast,
Wernicke’s aphasia is characterized by problems with both comprehending
language and producing meaningful utterances. Although these patients may appear
to speak fluently, they often order words incorrectly and sometimes make up non-
sense words.
Agnosia
Patients who have agnosia have difficulty understanding what they perceive, al-
though neither their sensory abilities nor their knowledge about objects is impaired.
Many forms of agnosia can arise. For example, prosopagnosia is a particular type of
agnosia in which the person cannot recognize faces—often including his or her
own face in a mirror! Some forms of agnosia can lead to disorientation, which must
be distinguished from disorientation that occurs with dementia (to be discussed
shortly).
Apraxia
A nother medica l condition that can af fect cog nitive functioning is apraxia
(Kosslyn & Koenig, 1995), which involves problems in organizing and carrying
out voluntary movements even though the muscles themselves are not impaired.
The problem is in the brain, not in the muscles. Apraxia can take a variet y of
forms. For example, some patients have trouble sequencing movements (such as
the movements necessar y to light a candle, that is, taking out a match, striking
it, and holding the flame to the wick). Clinicians must distinguish between such
problems with voluntar y movements and the avolition (difficult y initiating or
following through with activities) that may accompany schizophrenia (noted in
Chapter 12).
A stroke is an interruption of normal blood
flow to the brain that causes neurons in
that part of the brain to die. The effect of a
stroke depends on its location in the brain
and the size of the brain area that it affects.
This image shows a colored MRI scan of the
brain of a woman who had a stroke, with
orange indicating dead brain tissue and green
indicating healthy tissue.
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Stroke
The interruption of normal blood flow to or
within the brain, which results in neuronal
death.
Aphasia
A neurological condition characterized by
problems in producing or comprehending
language.
Broca’s aphasia
A neurological condition characterized by
problems producing speech.
Wernicke’s aphasia
A neurological condition characterized by
problems comprehending language and
producing meaningful utterances.
Apraxia
A neurological condition characterized by
problems in organizing and carrying out
voluntary movements even though the
muscles themselves are not impaired.
Neurocognitive Disorders 483
Head Injury
Cognitive disorders may arise from head injuries—which may re-
sult from a car accident, from a fall, or in a variety of other ways.
The specific cognitive deficits that develop depend on the exact
nature of the head injury. The same kinds of deficits that follow a
stroke can also occur after a head injury.
Substance-Induced Changes in Cognition
We saw in Chapter 9 that some people take substances (including
prescribed medications) to alter their level of awareness or their
emotional or cognitive state. But medications or exposure to toxic
substances can produce unintended changes in attention, memory,
judgment, or other cognitive functions, particularly when a per-
son takes a high dose. In fact, older people are more sensitive than
others to the effects of medications, and so a dose appropriate for a
younger adult is more likely to have negative effects or side effects
in an older adult (Mort & Aparasu, 2002). Even anesthesia for surgery can subse-
quently affect cognitive functioning (Thompson, 2003).
Delirium
Mrs. B.’s cognitive difficulties emerged gradually over time. Although she forgot
appointments, she never forgot—and was never confused about—who and where she
was. Moreover, she did not experience unusual or rapid changes in consciousness or
in the ability to focus her attention. If she had, these symptoms might have indicated
that she was delirious, as are many residents of nursing homes who are 85 years old or
older (American Psychiatric Association, 2013).
What Is Delirium?
Delirium is characterized by a disturbance in attention and awareness as well as
disruption of at least one other aspect of cognitive functioning (American Psychiatric
Association, 2013). These symptoms develop rapidly—over hours to days—and
fluctuate within a 24-hour period. The disturbance in attention is evidenced by
difficulty directing, focusing, sustaining, and shifting attention, as well as a decreased
awareness of the external environment; the person may appear “stoned” or seem
to be focusing on internally generated stimuli, such as mental images. A delirious
Thinking Like A Clinician
Evan is a first-year college student who lives with his grandmother because her home is
near his school. Before he started living with her, he had spent only a few days at a time
with her, usually on trips with his mother. Now that he’s spending more time with his
grandmother, he has noticed that she frequently tells him the same stories from her child-
hood. When she asks him to do an errand, she sometimes forgets the words of the objects
she wants him to bring home or the shop she wants him to visit. And sometimes when he
enters a room that she’s in, she seems momentarily confused about who he is and why
he’s there. Evan is concerned that there is something “not right” with his grandmother,
and is wondering whether he should suggest that she be evaluated by a doctor. Based on
what you’ve learned about normal versus abnormal changes with aging, what specific ad-
vice would you give to Evan to help him determine whether his grandmother’s cognitive
problems are likely to be those of normal aging (and so Evan need not urgently suggest that
she see her doctor)?
Head injury—which might arise from playing
football, soccer, or other sports, or from
accidents that damage the brain—can lead to
neurocognitive disorders.
©
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Delirium
A neurocognitive disorder characterized by a
relatively sudden disturbance in attention and
awareness as well as disruption of at least one
other aspect of cognitive functioning.
484 C H A P T E R 1 5
patient may have a hard time understanding a question, or may have trouble shifting
attention to a new question and remain focused on the previous one. Alternatively,
he or she may be distracted and unable to pay attention to any question. The DSM-5
diagnostic criteria are summarized in Table 15.2.
These attentional problems can make it difficult for a clinician to interview the
delirious patient; the clinician must infer the patient’s mental state from his or her
behavior and unusual responses and then seek information from family members or
friends. Case 15.2 describes one woman’s experience with delirium.
CASE 15.2 • FROM TH E OUTSIDE: Delirium
A 74-year-old African American woman, Ms. Richardson, was brought to a city hospital
emergency room by the police. She is unkempt, dirty, and foul-smelling. She does not look
at the interviewer and is apparently confused and unresponsive to most of his questions.
She knows her name and address, but not the day or the month. She is unable to describe
the events that led to her admission.
The police reported that they were called by neighbors because Ms. Richardson had
been wandering around the neighborhood and not taking care of herself. The medical
center mobile crisis unit went to her house twice but could not get in . . . they broke into
the apartment . . . and then found Ms. Richardson hiding in the corner, wearing nothing
but a bra. The apartment was filthy. . . .
[Ms. Richardson was diabetic, and her diabetes was out of control when she was
admitted to the hospital. They begin to stabilize her medically and decided to transfer
her the next day to a medical unit. Her mental state improved when the diabetes was
treated.]
(Spitzer et al., 2002, pp. 13–14)
When delirious, people may also be disoriented, not knowing where they are or
what the time, day, or year is; this was the case with Ms. Richardson in Case 15.2.
Less frequently, when delirious, people may not know who they are. In addition, they
may have difficulty speaking clearly, naming objects, or writing. The content of their
speech may resemble that of someone in a manic episode: pressured and nonsensical,
or flitting from topic to topic.
Delirious people may also experience perceptual alterations, including:
• misinterpretations (correctly perceiving sensor y stimuli but incorrectly inter-
preting what they are, such as cor rectly identif ying the smel l of smoke but
incorrectly attributing the smell to a roaring fire rather than to an extinguished
match);
• illusions (misperceiving an object, as in perceiving the form of a pair of pants crum-
pled on the floor as a dog); and
• hallucinations (seeing—or hearing—someone or something that isn’t actually there).
The perceptual disturbances are most frequently visual. Delirious people may
bel ieve that thei r percept ua l ex per iences a re rea l a nd behave accord i ng ly.
Hallucinations that are threatening may make them afraid, and they may respond
by attack ing others. Sometimes people in a delir ious state are injured while
responding to their altered perceptions, and their behavior can appear bizarre.
Because of the perceptual difficulties, such patients may not consent to appropri-
ate treatment.
Delirium is most common among the elderly and terminally ill, as well as
patients who have just had surgery; it is not yet known why delirium is more likely
among these groups, but neurological changes related to aging may make the elderly
more vulnerable to developing delirium. Table 15.3 provides additional information
about delirium.
TABLE 15.2 • DSM-5 General
Diagnostic Criteria for Delirium
A. A disturbance in attention (i.e., reduced
ability to direct, focus, sustain, and
shift attention) and awareness (reduced
orientation to the environment).
B. The disturbance develops over a short
period of time (usually hours to a few
days), represents a change from baseline
attention and awareness, and tends to
fluctuate in severity during the course of
a day.
C. An additional disturbance in cognition
(e.g., memory deficit, disorientation,
language, visuospatial ability, or
perception).
D. The disturbances in Criteria A and C
are not better explained by another
preexisting, established, or evolving
neurocognitive disorder and do not occur
in the context of a severely reduced level
of arousal, such as coma.
E. There is evidence from the history,
physical examination, or laboratory
findings that the disturbance is a direct
physiological consequence of another
medical condition, substance intoxication
or withdrawal (i.e., due to a drug of abuse
or to a medication), or exposure to a
toxin, or is due to multiple etiologies.
Reprinted with permission from the Diagnostic and
Statistical Manual of Mental Disorders, Fifth Edition,
(Copyright ©2013). American Psychiatric Association. All
Rights Reserved.
Neurocognitive Disorders 485
Symptoms that appear similar to delirium can occur with other disorders, which
may make it difficult to provide a definitive—or even a tentative—diagnosis. The
following symptoms may appear similar to those of delirium:
• Psychotic symptoms. In schizophrenia or a mood disorder with psychotic features,
the psychotic elements (i.e., delusions and hallucinations) are often consistent with
other symptoms of the disorder. In contrast, in delirium, the symptoms that appear
psychotic are not as consistent with the non-psychotic symptoms of schizophrenia
and mood disorders.
• Mood, anxiety, or dissociative symptoms. With mood, anxiety, or dissociative disorders,
the symptoms of fear, anxiety, or dissociation are relatively stable and tend not
to vary with cognitive symptoms. In contrast, with delirium, symptoms of fear,
anxiety, or dissociation tend to fluctuate along with the cognitive symptoms, and
attentional problems are prominent.
If a clinician has reason to suspect that the symptoms arise because of a medical
condition (such as untreated diabetes, infection, or substance use), delirium is a
tentative diagnosis, pending physical or laboratory tests.
TABLE 15.3 • Delirium Facts at a Glance
Prevalence
• Older adults are more likely than others to develop delirium.
• Between 14% and 24% of patients admitted to a hospital are delirious.
• Approximately 70–87% of people in intensive care may become delirious.
• Delirium occurs in up to 60% of nursing home residents.
• Up to 80% of terminally ill patients will become delirious at the end of life (Brown & Boyle,
2002).
Comorbidity
• Delirium may occur along with another neurocognitive disorder or as a result of a substance-
related disorder.
Onset
• When delirium arises after head trauma, symptoms often develop immediately.
Course
• Delirium typically resolves, and does so sooner, when the underlying problem is treated.
• Symptoms of delirium typically fluctuate over the course of the day.
• For most people, symptoms completely subside within a few hours or days; for others,
especially the elderly, symptoms may persist for months or longer.
• People who had relatively good health and cognitive functioning before their delirium began
are likely to make a better recovery than those with poor health and cognitive functioning.
• People with previous episodes of delirium are vulnerable to subsequent episodes.
Gender Differences
• Among elderly people, men are more likely than women to become delirious.
Cultural Differences
• Countries have different guidelines for diagnosing delirium, which can prohibit making
meaningful comparisons across countries (Leentjens & Diefenbacher, 2006).
Source: Unless otherwise noted, the source for information is American Psychiatric Association, 2013.
486 C H A P T E R 1 5
Understanding Delirium: A Side Effect?
Delirium can be a side effect of prescribed medication, substance use or exposure, or
can result from a medical condition.
Delirium Caused by Substance Use
Delirium can arise from the effects of a psychoactive substance such as alcohol or a
medication, or from withdrawal from such a substance. Intoxication and withdrawal
are considered to give rise to delirium only when the symptoms are severe enough
to require more than the usual clinical attention and treatment provided to someone
who used the substance in question. If the symptoms are not severe enough to reach
the level needed for a diagnosis of delirium, the appropriate diagnosis is a substance-
related disorder, either intoxication or withdrawal (see Chapter 9).
Delirium Caused by a General Medical Condition
Like a fever, delirium can arise for a variety of medical reasons:
• infection,
• dehydration,
• electrolyte imbalance (which can arise from an eating disorder; see Chapter 10),
• stroke,
• brain tumor,
• pneumonia,
• heart attack,
• head trauma, or
• surgery (arising from anesthesia).
Some of these causes, such as dehydration, can be fatal if not
treated (Brown & Boyle, 2002).
Clinicians determine the underlying cause of a person’s
delirium in several ways: from a physical examination, a
consultation with someone who knows the patient and may
know something about what led to the symptoms, results of
laboratory tests, and a review of the patient’s medical history.
Treating Delirium: Rectify the Cause
Treatment for delirium usually targets neurological factors— treating the underlying
medical condition or substance use that affects the brain and causes the delirium.
In most cases, as the medical condition improves or the substance intoxication or
withdrawal resolves, the delirium ends. In some cases, however, treatment for the
underlying medical problem—for example, administering antibiotics to treat bacte-
rial pneumonia—can take days to affect the delirium; in other cases, such as when
people are close to death, doctors may not be able to treat the underlying cause of the
delirium. For temporary relief, the patient may be given antipsychotic medication, usu-
ally haloperidol or risperidone (Leentjens & van der Mast, 2005). In fact, studies find
that giving haloperidol preventatively to elderly patients about to undergo surgery can
decrease the severity and duration of postoperative delirium ( Kalisvaart et al., 2005).
Treatment may also target psychological and social factors. Such interventions
for people with delirium include (Brown & Boyle, 2002):
• providing hearing aids or eyeglasses to eliminate sensory and perceptual impairments;
• teaching the person to focus on the here and now, by providing very visible clocks
and calendars or other devices and encouraging the person to use them;
Delirium can arise from a variety of
medical problems, including dehydration,
or after receiving anesthesia. Some surgery
patients—particularly elderly ones—
become temporarily delirious in response to
anesthesia.
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• creating an environment that optimizes stimulation, perhaps by providing adequate
lighting and reducing unnecessary noise;
• ensuring that the person is fed and warm;
• making the environment safe by removing objects with which the patient could
harm himself or herself or others; and
• educating the people who interact with the person (residential staff, friends, and
family members) about delirium.
Thinking Like A Clinician
Drew is on his college’s football team and had to have surgery on his knee. For the procedure,
he had general anesthesia. His mom was with him right after the surgery, and Drew was deliri-
ous and remained so for hours. What can you assume, and what should you not assume, about
Drew’s emotions and his cognitive functions? What might be a likely cause of his delirium?
What should be done, if anything, to help Drew?
Dementia (and Mild Versus Major
Neurocognitive Disorders)
Mrs. B. seemed to have memory problems. But memory was not the only aspect of
her cognitive functioning that had declined. During neuropsychological testing, “the
principal areas of difficulty on [certain] tests were in mental control, as evidenced
by tangential and repetitive speech; psychomotor slowing [in this case, slow move-
ments based on mental processes, not reflexes]; and reduced flexibility in thought and
action” (La Rue & Watson, 1998,p. 9). Some of these difficulties are characteristic of
dementia. Could Mrs. B. have dementia?
In this section we focus on dementia: what it is, what neurological factors give
rise to it, and what treatments are available for it.
What Is Dementia?
Although not a DSM-5 disorder, dementia is the general term for a set of neurocogni-
tive disorders characterized by deficits in learning new information or recalling infor-
mation already learned plus at least one of the following types of impaired cognition:
• Aphasia. In dementia, problems with using language often appear as overuse of the
words thing and it because of difficulty remembering the correct specific words.
• Apraxia. Problems with executing motor tasks (even though there isn’t anything
wrong with the appropriate muscles, limbs, or nerves). Such problems can lead to dif-
ficulties in dressing oneself and eating, at which point self-care becomes impossible.
• Agnosia. People with dementia may not recognize common objects—or friends,
family members, or even their own face.
• Executive function problems. These patients may also have difficulties in planning,
initiating, organizing, abstracting, and sequencing or even in recognizing that one
has memory problems. (These problems arise primarily in dementia that affects the
frontal lobes.) These deficits can make it impossible to meet the demands of daily
life. Mrs. B. had difficulties in tasks that required executive functions.
We discussed aphasia, apraxia, and agnosia earlier, in the context of effects of brain
damage on cognition. Unlike the effects caused by a stroke or a head injury, however,
dementia is not caused by an isolated incident, nor do the deficits emerge quickly.
Rather, they arise over a period of time, as brain functioning degrades; symptoms of
dementia often change over time, typically becoming progressively worse (referred
Dementia
A set of neurocognitive disorders characterized
by deficits in learning new information or
recalling information already learned plus at
least one other type of cognitive impairment.
488 C H A P T E R 1 5
to as a progressive dementia), but sometimes remaining static or in a minority of cases
even reversing course. Dementia can arise as a result of a medical disease, such as
Alzheimer’s and Parkinson’s diseases, but it is the dementia, not the medical disease it-
self, that is considered to be a neurocognitive disorder in DSM-5. In the United States,
one estimate is that caring for people with dementia costs as much as caring for those
with heart disease or cancer—up to $2.15 billion per year (Hurd et al., 2013). Most
people with dementia are over 65 years old when symptoms emerge, termed late onset.
When symptoms begin before age 65, the disorder is said to have early onset. Early on-
set, particularly before age 50, is rare and is usually hereditary (Ikeuchi et al., 2008).
Mild and Major Neurocognitive Disorders
In DSM-5, dementia is not a disorder; rather, people with dementia or other adult-
onset cognitive deficits (such as difficulties with language) are diagnosed with ei-
ther mild or major neurocognitive disorder (discussed below), depending on the person’s
symptoms and ability to function independently. Specifically, DSM-5 specifies six
cognitive domains in which def icits may occur for
these disorders:
• Complex attention—such as focusing and sustaining
attention,
• Executive functions—such as planning and decision
making,
• Learning and memory—such as learning new skills and
remembering them,
• Language—such as speaking or understanding,
• Perceptual-motor—such as hand–eye coordination,
• Social cognition—such as recognizing emotions in others.
Impaired cognitive functioning can lead many patients
to become easily overwhelmed or confused, causing
them to be agitated. The confusion or agitation may
then lead a patient to become violent, which can make
it difficult or potentially dangerous for the patient to re-
main living at home with family members—and hence
the patient may be moved to a residential care facility.
Depending on the specific cognitive processes that
are impaired, a patient with dementia may:
• behave inappropriately (for instance, tell unsuitable
jokes or be overly familiar with strangers);
• misperceive reality (for instance, think that a care-
taker is an intruder); or
• wander away while trying to get “home” (a place he
or she lived previously).
According to DSM-5, the hallmark of mild neu-
rocognitive disorder is evidence of a modest decline
from baseline in at least one of the six cognitive domains
above, but that decline is not enough to interfere with
daily functioning (see Table 15.4). In contrast, the hall-
mark of major neurocognitive disorder is evidence of
a substantial decline in at least one cognitive domain, and
impaired daily functioning that results from this decline
(see Table 15.5) ( American Psychiatric Association, 2013).
Mild neurocognitive disorder
A neurocognitive disorder characterized by
a modest decline from baseline in at least
one cognitive domain, but that decline is not
enough to interfere with daily functioning.
Major neurocognitive disorder
A neurocognitive disorder characterized by
evidence of a substantial decline in at least
one cognitive domain, and impaired daily
functioning.
TABLE 15.4 • DSM-5 Diagnostic Criteria for Mild
Neurocognitive Disorder
A. Evidence of modest cognitive decline from a previous level of performance in
one or more cognitive domains (complex attention, executive function, learning
and memory, language, perceptual motor, or social cognition) based on:
1. Concern of the individual, a knowledgeable informant, or the clinician that
there has been a mild decline in cognitive function; and
2. A modest impairment in cognitive performance, preferably documented
by standardized neuropsychological testing or, in its absence, another
quantified clinical assessment.
B. The cognitive deficits do not interfere with capacity for independence in
everyday activities (i.e., complex instrumental activities of daily living such
as paying bills or managing medications are preserved, but greater effort,
compensatory strategies, accommodation may be required).
C. The cognitive deficits do not occur exclusively in the context of a delirium.
D. The cognitive deficits are not better explained by another mental disorder
(e.g., major depressive disorder, schizophrenia).
Reprinted with permission from the Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition,
(Copyright ©2013). American Psychiatric Association. All Rights Reserved.
TABLE 15.5 • DSM-5 Diagnostic Criteria for Major
Neurocognitive Disorder
A. Evidence of significant cognitive decline from a previous level of performance in
one or more cognitive domains (complex attention, executive function, learning
and memory, language, perceptual-motor, or social cognition) based on:
1. Concern of the individual, a knowledgeable informant, or the clinician that
there has been a significant decline in cognitive function; and
2. A substantial impairment in cognitive performance, preferably documented
by standardized neuropsychological testing or, in its absence, another
quantified clinical assessment.
B. The cognitive deficits interfere with independence in everyday activities (i.e.,
at a minimum, requiring assistance with complex instrumental activities of
daily living such as paying bills or managing medications).
C. The cognitive deficits do not occur exclusively in the context of delirium.
D. The cognitive deficits are not better explained by another mental disorder
(e.g., major depressive disorder, schizophrenia).
Reprinted with permission from the Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition,
(Copyright ©2013). American Psychiatric Association. All Rights Reserved.
Neurocognitive Disorders 489
People whose cognitive functioning started out at a very high level may notice
deficits in functioning that are mild symptoms of dementia, but neuropsychological
testing is likely to show that the patient’s abilities are within the normal range for his
or her age. The early signs of dementia might otherwise go undiagnosed if current
abilities aren’t compared to previous abilities; with such early signs, the person might
be diagnosed with mild neurocognitive disorder ( American Psychiatric Association,
2013; Harvey, 2005a).
Dementia and Alzheimer’s Disease
T h e m o s t c o m m o n c a u s e o f d e m e n t i a i s
A l z h e i m e r ’s d i s e a s e ( a l s o c a l le d s i m pl y
Alzheimer’s), in which the aff licted person ini-
tially has problems with both memory and exec-
utive function. As the disease advances, memory
problems worsen, attention and language prob-
lem s emerge, a nd spat ia l abi l it ies m ay dete –
riorate; the patient may even develop psychotic
symptoms, such as hallucinations and delusions
(particularly persecutory delusions). In the final
stage, the patient’s memor y loss is complete—
he or she doesn’t recognize family members and
friends, can’t communicate, and is completely de-
pendent on others for care. In Case 15.3, Diana
Friel McGowin describes her experience with
dementia due to Alzheimer’s disease; additional
facts about dementia are provided in Table 15.6.
People with dementia can become confused
about where they live and become lost.
©
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Alzheimer’s disease
A medical condition in which the afflicted
person initially has problems with both
memory and executive function and which
leads to progressive dementia.
C U R R E N T C O N T R O V E R S Y
Mild and Major Neurocognitive
Disorders
A mong the new diagnoses in DSM-5 is the diagnosis of
mild neurocognitive disorder (see Table 15.6). This diagnosis is
controversial because only a “modest” cognitive decline is
needed (one or two standard deviations below what would
be expected for a given patient) —and unlike almost any
other diagnosis in DSM-5, the symptoms do not need to
cause distress or impair functioning. In fact, a requirement
for the diagnosis is that functioning is not impaired!
On the one hand, this new diagnosis can focus the at-
tention of researchers and clinicians on early signs of demen-
tia (Geda & Nedelska, 2012; Gutierrez et al., 1994). The new
diagnosis will make it easier for researchers to investigate
factors related to faster or slower decline, and clinicians may
able to intervene earlier with new medications that delay or
arrest further declines.
On the other hand, the new term can create confusion.
The medical term for the level of cognitive ability that is in
between normal functioning and dementia (or major neuro-
cognitive disorder, in DSM-5 lingo) is mild cognitive impairment.
This is the term neurologists use. So DSM-5 has created a dif-
ferent term, sowing confusion for mental health clinicians,
patients, and their families. Patients will receive two diagnoses
for the same condition (Siberski, 2013).
CRITICAL THINKING Given that neither distress nor impaired
functioning are criteria, do you think mild neurocognitive
disorder should be considered a “disorder”? Why or why not?
( James Foley, College of Wooster)
The diagnosis of mild neurocognitive disorder was introduced in DSM-5. The
inclusion of this diagnosis has been criticized as pathologizing normal aging, espe-
cially because daily functioning should not be impaired for this diagnosis. As we
discussed earlier, as people get older, some of their cognitive abilities modestly
decline relative to their baseline—without any significant problems in their daily life
( Frances, 2013; Greenberg, 2013).
490 C H A P T E R 1 5
CASE 15.3 • FROM TH E INSIDE: Dementia
Diana Friel McGowin was 45 years old when she became aware of memory problems. She got
lost on the way home because no landmarks looked familiar; she was unable to remember her
address or to recognize her cousin. After neuropsychological and neuroimaging tests, she was
diagnosed with early-onset Alzheimer’s disease (because the disorder emerged before age
65). In her memoir about the progressive nature of this disease, Living in the Labyrinth (1993),
McGowin describes sharing with her neurologist some of the symptoms she was having:
I showed him the burns on my wrists and arms sustained because I forgot to protect myself
when inserting or removing food from the oven. I told him of becoming lost in the neighbor-
hood grocery store where I had shopped for over twenty years. I showed him my scribbled notes
and sketched maps of how to travel to the bank, the post office, the grocery, and work. (p. 41)
She describes other memory problems as the disease progressed:
I sometimes lost my thread of thought in mid-sentence. Memories of childhood and long
ago events were quite clear, yet I could not remember if I ate that day. On more than one
occasion when my grandchildren were visiting, I forgot they were present and left them to
their own devices. Moreover, on occasions when I had picked them up to come play at my
house, the small children had to direct me home. (pp. 64–65)
Further into her memoir, she notes:
As my grip upon the present slips, more and more comfort is found within my memories
of the past. Childhood nostalgia is so keen I can actually smell the aroma of the small town
library where I spent so many childhood hours. (p. 109)
Painfully lonely, I still contrarily, deliberately, sit alone in my home. The radio and TV
are silent. I am suspended. Somewhere there is that ever-present reminder list of what I
am supposed to do today. But I cannot find it. (p. 112)
TABLE 15.6 • Dementia Facts at a Glance
Prevalence
• Approximately 5 million older Americans are estimated to have dementia (Alzheimer’s Association, 2007).
• In 2010, more than 35 million people worldwide were estimated to have dementia (Prince et al., 2013).
• Approximately 1–2% of 65-year-olds are diagnosed with dementia, but as many as 30% of 85-year-olds are so diagnosed.
Comorbidity
• Depression (Kales et al., 2005; Snow et al., 2005) and psychotic symptoms such as hallucinations and delusions (Tractenberg et al., 2003) com-
monly co-occur with dementia.
Onset
• Onset usually occurs late in life.
• Cognitive deterioration can be rapid or gradual, depending on the cause of the dementia.
• Impaired learning and recall are early signs of some types of dementia.
Course
• People with dementia may be unable to perform complex tasks in new situations but may still be able to perform simple ones in familiar surroundings.
• Some types of dementia, such as that caused by Alzheimer’s disease, get progressively worse; other types of dementia, such as that caused by HIV
infection, can get better with treatment of the underlying cause. Still other types remain relatively unchanging.
Gender Differences
• Dementia is slightly more common in males than in females.
Cultural Differences
• Some cultures and ethnic groups—such as African Americans, Asian Americans, and Hispanic Americans—may be more tolerant of impaired memory
and other cognitive dysfunctions that affect elderly people, in some cases viewing these changes as a normal part of aging. These family members
thus may wait longer before seeking medical assistance for an older person with dementia (Cox, 2007).
Source: Unless otherwise noted, the source for information is American Psychiatric Association, 2000, 2013.
Neurocognitive Disorders 491
In the early phases of a progressive dementia, when the person has relatively
little decline in executive function, he or she may become so depressed about the
diagnosis and its prognosis that he or she attempts suicide. Diana McGowin became
acutely aware of her symptoms during the early phase of the disease and worked hard
to try to compensate by making maps and lists. With some patients, mental health
clinicians may have difficulty determining whether the particular symptoms reflect
delirium, dementia, or both (see Table 15.7).
Understanding Dementia
Dementia is caused by a variety of neurological factors, and according to DSM-5,
each of these factors corresponds to the diagnosis of a specific mild or major neuro-
cognitive disorder. In what follows we review the most common types of dementia:
dementia due to Alzheimer’s disease, vascular dementia, and dementias that result
from other medical conditions.
Alzheimer’s Disease
Almost three quarters of dementia cases are caused by Alzheimer’s disease (Plassman
et al., 2007); in DSM-5, this form of dementia is referred to as neurocognitive disorder
due to Alzheimer’s disease. There is no routine lab test for diagnosing this disease at
present, and so this type of dementia is diagnosed by ruling out other possible causes.
Artist William Utermohlen learned in 1995 that
he had Alzheimer’s disease—which causes a
type of progressive dementia. He responded to
the news by painting self-portraits. Alzheimer’s
can specifically affect brain areas involved in
spatial abilities, which are crucial for painting. As
his dementia progressed, Utermohlen’s images
became less distinct and more abstract; these
three portraits were done in (left to right) 1998,
1999, and 2000. Although he recognized that his
paintings weren’t what he wanted, he said that
he “could not figure out how to correct them”
(Grady, 2006).
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TABLE 15.7 • Symptoms Unique and Common to Delirium and Dementia
Unique to delirium Unique to dementia Common to both delirium and dementia
• Delirium has a rapid onset.
• Symptoms (including changes in consciousness)
fluctuate within a 24-hour period.
• Hallucinations—frequently visual—are
present.
• Symptoms often gradually improve.
• The person is not alert and focused.
• Dementia has a gradual onset.
• Symptoms typically do not fluctuate within a
24-hour period.
• Hallucinations are often absent.
• Symptoms rarely improve.
• The person is consistently alert.
• Memory problems.
• Problems with other types of cognitive
functioning.
492 C H A P T E R 1 5
The Progression of Alzheimer’s Disease
The onset of Alzheimer’s disease is gradual, with symptoms becom-
ing more severe over time. Often, the early signs of dementia of the
Alzheimer’s type involve difficulty remembering recent events or
newly learned information. In the early stages of Alzheimer’s, the
memory problems are prominent (Petersen & O’Brien, 2006); it is
only as the disease progresses that other sorts of deficits in cognitive
processing emerge, such as aphasia, apraxia, agnosia, and deteriorated
spatial abilities. (Such patients may often become lost when walking
around their neighborhood.) Patients may also become irritable and
their personality may change—and such changes may become more
pronounced as cognitive functioning declines. In the final stage of the
disease, perceptual-motor problems arise, creating difficulties with walking, talking, and
self-care. Generally, these patients die about 8–10 years after the first symptoms emerge.
In some cases, people with dementia also have behavioral problems, such as those
a woman reported about her husband:
My husband used to be such an easy-going, calm person. Now, he suddenly lashes out
at me and uses awful language. Last week, he got angry when our daughter and her
family came over and we sat down to eat. I never know when it’s going to happen. He’s
changed so much—it scares me sometimes.
(National Institute on Aging, 2003, p. 47)
People with Alzheimer’s who behave in unusual or disturbed ways are more likely to
have greater declines in cognitive functioning and to need institutional care sooner
than patients whose behavior causes less concern (Scarmeas et al., 2007). As noted in
Table 15.8, slightly more females than males develop this form of dementia, and it
accounts for progressively more cases of dementia in older age groups.
Brain Abnormalities Associated With Alzheimer’s Disease:
Neurofibrillary Tangles and Amyloid Plaques
Two brain abnormalities are associated with Alzheimer’s disease: neurofibrillary tan-
gles and amyloid plaques. The internal support structure of a neuron includes micro-
tubules, which are tiny, hollow tubes that create tracks from the cell body to the
end of the axon; nutrients are distributed within the cell via these microtubules.
A protein, called tau, helps stabilize the structure of these tracks (see Figure 15.1).
TABLE 15.8 • Prevalence of Dementia Due to Alzheimer’s
From Age 65 On
Age
(in years)
Prevalence among
males
Prevalence among
females
65 0.6% 0.8%
85 11% 14%
90 21% 25%
95 36% 41%
As people age beyond 65 years old, they are
increasingly likely to develop Alzheimer’s
disease. About half the cases in each age group
have moderate to severe cognitive impairment
(American Psychiatric Association, 2000).
FI G U RE 15.1 • Neurofibrillary Tangles in
Alzheimer’s Disease Tau proteins stabilize the
structure of a neuron from the cell body through
the end of the axon. With Alzheimer’s disease, these
proteins become entangled, destroying the structure
of the neuron and disrupting its communication
with other neurons.
Source: National Institute on Aging
Healthy neuron
Microtubules
Stabilizing
tau proteins
Diseased neuron
Disintegrating
microtubules
Disintegrating
microtubule
Microtubule subunits
fall apart
Tangled clump
of tau proteins
Neurocognitive Disorders 493
With Alzheimer’s disease, the tau proteins become twisted together into neurofi-
brillary tangles, and these proteins no longer hold together the microtubules—
which thereby disrupts the neuron’s distribution system for nutrients. In addition,
the collapse of this support structure prevents normal communication with other
neurons. This process may also contribute to the death of neurons. In fact, people
with Alzheimer’s have smaller brains than usual (Henneman et al., 2009).
The brains of people with Alzheimer’s disease are abnormal in another way—they
have amyloid plaques, which are fragments of proteins (one type of which is called
amyloid) that accumulate on the outer surfaces of neurons, particularly neurons in the hip-
pocampus—the brain area predominately involved in storing new information in memory.
Researchers have not yet determined whether the neurofibrillary tangles and
plaques cause Alzheimer’s disease or are a byproduct of some other process that causes
the disease (National Institute on Aging, 2003; Schwitzer, 2012). However, neu-
rofibrillary tangles and amyloid plaques are generally discovered during autopsies,
and PET scanning that uses a particular chemical marker has been able to detect the
amyloid plaques and neurofibrillary tangles that distinguish Alzheimer’s disease from
other causes of memory problems in living patients (Ikonomovic et al., 2008; Small
et al., 2006; Snitz et al., 2013; Zhang et al., 2012).
Genetics
People who have a specific version of one gene, apo E, are more susceptible to late-
onset Alzheimer’s disease than people who don’t have this particular gene. However,
someone can have this version of the apo E gene and not develop Alzheimer’s; con-
versely, someone can develop Alzheimer’s and not have this version of the gene.
In contrast, early-onset Alzheimer’s is caused by the mutation of one of three
other genes, and two of these mutations lead to Alzheimer’s disease in 100% of cases.
However, the third type of mutation (a rare form called presenilin 2) does not always
cause the disease (Williamson-Catania, 2007), which suggests that other neurologi-
cal factors and/or psychosocial factors may play a role.
Vascular Dementia
Vascular refers to blood vessels, and vascular diseases refer to problems with blood ves-
sels, such as high blood pressure or high cholesterol. Vascular disease can reduce or
block blood supply to the brain, which in turn can cause vascular dementia (in
DSM-5, referred to as vascular neurocognitive disorder). Blood vessels can be involved
in dementia in two ways: (1) Plaque builds up on artery walls, making the arteries
narrower, which then diminishes blood flow to the brain, or (2) bits of
clotted blood block the inside of arteries, which then prevents blood from
reaching the brain. Such clots can cause a series of small strokes (sometimes
referred to as transient ischemic attacks or ministrokes), in which blood supply
to parts of the brain is temporarily blocked, leading to transient impaired
cognition or consciousness. When multiple ministrokes occur over time,
dementia can arise as brain areas involved in cognitive functioning become
impaired. This form of dementia can have a gradual onset. In contrast,
a single, large stroke inflicts more brain damage than a series of minis-
trokes; in such cases, vascular dementia has an abrupt onset. Note that be-
cause dementia involves deficits in memory and aphasia, apraxia, agnosia,
or problems with executive functions, not all strokes produce dementia:
Some strokes only produce very specific problems, such as aphasia or defi-
cits in executive functions, but the results of the stroke could still merit the
diagnosis of a mild or major neurocognitive disorder.
Symptoms of vascular dementia can wax and wane over a given 24-hour period,
but even the patient’s highest level of functioning is lower than it was before dementia
Neurofibrillary tangles
The mass created by tau proteins that become
twisted together and destroy microtubules,
leaving the neuron without a distribution
system for nutrients.
Amyloid plaques
Fragments of protein that accumulate on
the outside surfaces of neurons, particularly
neurons in the hippocampus.
Vascular dementia
A type of dementia caused by reduced or
blocked blood supply to the brain, which arises
from plaque buildup or blood clots.
A buildup of plaque in the arteries can lead to
a narrowing of the artery and decreased blood
supply to the brain, which in turn can cause
vascular dementia.
Plaque
Arterial
opening
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S
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n
ce
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494 C H A P T E R 1 5
set in (Puente, 2003). In addition, neuroimaging may reveal lesions (“dead” neurons)
in particular brain areas. People with vascular dementia may also have Alzheimer’s
disease, particularly if they are very old (Kalaria & Ballard, 1999). Vascular dementia
is more common in men than women.
The course of vascular dementia is variable, depending on the specific brain areas
affected; when symptoms become more severe, they worsen in a stepwise fashion,
with more deficits apparent after each instance of reduced blood supply to the brain.
Aggressive treatment of the underlying vascular disease (typically via medication)
may prevent additional strokes or reduced blood flow to brain areas.
Dementia Due to Other Medical Conditions
Dementia can also be caused by a variety of other medical conditions, includ-
ing Parkinson’s disease, late-stage HIV infection, and Huntington’s disease. With
these and certain other medical conditions, the onset can be gradual or sudden, the
course can range from acute to chronic, and the patient may also develop behavioral
disturbances.
Dementia Due to Parkinson’s Disease
Parkinson’s disease is characterized by a slow, progressive loss of motor function; typical
symptoms are trembling hands, a shuffling walk, and muscular rigidity. About 1 million
Americans have Parkinson’s disease, and approximately 50% of people with Parkinson’s
disease develop dementia due to this disease, in DSM-5 referred to as neurocognitive
disorder due to Parkinson’s disease. People who develop this type of dementia are usually
older (age of onset is about 65 years old) or are in a more advanced stage of the disease
(Papapetropoulos et al., 2005). The dementia generally involves problems in memory
and executive functions. Comorbid depression can cause additional cognitive deficits.
Parkinson’s disease causes damage to dopamine-releasing neurons in an area of
the brain known as the substantia nigra. As a consequence, the brains of these patients
do not have normal amounts of this neurotransmitter, which is critically involved in
motor functions as well as executive functions. Parkinson’s disease is thought to arise
from a combination of genetics and other neurological factors, such as brain damage
caused by exposure to pesticides and other toxins.
Dementia Due to Lewy Bodies
Another type of progressive dementia is dementia due to Lewy bodies, in DSM- 5 referred to
as neurocognitive disorder with Lewy bodies. Lewy bodies consist of a type of protein that, in some
people, builds up inside neurons that produce dopamine or acetylcholine and can eventu-
ally cause the neurons to die. The neurons most often affected are involved in memory
and motor control. (Neurons associated with other functions can also be affected.)
Clinicians may have diff icult y distinguishing this form of dementia from
Alzheimer’s, and autopsies have revealed that about 20% of people who were diag-
nosed with Alzheimer’s also had abnormal Lewy bodies (Rabin et al., 2006). How-
ever, although people who have dementia due to Lewy bodies have characteristics in
common with people who have Alzheimer’s, they have more severe disruptions of:
• visuospatial ability, and
• executive functions (Kaufer, 2002; Knopman et al., 2003; Walker & Stevens, 2002).
Moreover, people who have dementia due solely to Lewy bodies have three features
that are not shared by people who have dementia that arises from Alzheimer’s disease:
• the presence of (visual) hallucinations early in the course of the disorder,
• a tendency to retain the ability to name objects, and
• stiff movements early in the course of the disorder, which are similar to that of
people with Parkinson’s disease (rigid muscles, tremors, slowed movements, and a
shuffling style of walking).
Neurocognitive Disorders 495
Like patients with Alzheimer’s disease, patients with dementia due to Lewy bodies
progressively deteriorate until death, which on average occurs about 8–10 years after
diagnosis.
Dementia Due to HIV Infection
The human immunodeficiency virus (HIV) can destroy white matter and subcorti-
cal brain areas, which then gives rise to a type of dementia referred to in DSM-5 as
neurocognitive disorder due to HIV infection. The symptoms of this form of dementia include
impaired memory, concentration, and problem solving, as well as cognitive slowing.
Moreover, patients may exhibit signs of apathy, social withdrawal, delirium, delusions,
or hallucinations. They may develop tremors or repetitive movements or have problems
keeping their balance (McArthur et al., 2003; Price, 2003; Shor- Posner et al., 2000).
Antiretroviral medications that treat HIV infection slow—and in some cases may actu-
ally reverse—the brain damage, improving cognitive functioning (Sacktor et al., 2006).
Dementia Due to Huntington’s Disease
Huntington’s disease is a progressive disease that kills neurons and affects cog-
nition, emotion, and motor functions; it leads to dementia and eventually results
in death. Early symptoms of Huntington’s disease include bipolar-like mood swings
between mania and depression, irritability, and hallucinations or delusions; in DSM-5
it is referred to as neurocognitive disorder due to Huntington’s disease. Motor symptoms
include slow or restless movements, and the cognitive symptoms include memory
problems (which become severe as the disease progresses), impaired executive func-
tion, and poor judgment.
Huntington’s disease is inherited and is based on a single gene. If a parent has
Huntington’s disease, his or her children each have a 50% chance of developing it.
Genetic testing can assess whether the gene is present.
Dementia Due to Head Trauma
Head trauma can cause dementia or other impaired cognitive functioning, referred to
as neurocognitive disorder due to traumatic brain injury in DSM-5. The precise deficits and
their severity depend on which brain areas are affected and to what degree. A person
with this form of dementia may also behave unusually, such as being agitated. Such a
patient may have amnesia for events during and after the trauma, as well as other per-
sistent memory problems. In addition, he or she may have sensory or motor problems
and even personality changes (becoming increasingly aggressive or apathetic or suf-
fering severe mood swings) (American Psychiatric Association, 2000).
This form of dementia is most common among young males, who are more
likely than others to engage in risk-taking behaviors (such as reckless drinking) that
may lead to a single trauma to the head (such as a car accident); when the dementia is
caused by multiple traumas (as occurs with boxers), it may become worse over time
(American Psychiatric Association, 2013).
Substance/Medication-Induced Neurocognitive Disorder
When the cognitive def icits of dementia are caused by substance use but persist
beyond the period of intoxication or withdrawal, the clinician makes the DSM-5
diagnosis of substance/medication-induced neurocognitive disorder. A patient who receives
this diagnosis usually has a long history of substance use, and symptoms rarely occur
in patients younger than 20 years. The onset is slow, as is the progression of deficits;
the first symptoms arise while the person has a substance use disorder. If the person
is over age 50, the deficits often are not reversible and may even get worse when the
substance use is discontinued (American Psychiatric Association, 2013).
As we’ve noted, dementia may be caused by a number of medical illnesses or
conditions, and these causes are not mutually exclusive; a given person’s dementia may
have more than one cause. For example, someone may have both vascular dementia
Perhaps unique among the various types of
dementias, dementia due to HIV infection can
be reversed with antiretroviral medication for
HIV such as Truvada.
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Huntington’s disease
A progressive disease that kills neurons
and affects cognition, emotion, and motor
functions; it leads to dementia and eventually
results in death.
496 C H A P T E R 1 5
TABLE 15.9 • Key Facts About Different Types of Dementia
Dementia
due to . . .
Approximate percentage of
all dementia cases Prognosis/course Onset Gender difference
Alzheimer’s
disease
70% Poor Gradual, often after age
65; early onset is rare
Slightly more common among women
than men
Vascular
disease
15% (often comorbid with
Alzheimer’s type)
Cognitive loss may remain
stable or worsen in a
stepwise fashion.
Abrupt; earlier age of
onset than Alzheimer’s
More common among men
Lewy bodies
15% (can be comorbid with
Alzheimer’s type)
Poor Gradual; age of onset is
between 50 and 85
Slightly more common among men
than women
HIV infection
Less than 10% Poor unless treated with
antiretroviral medication
Gradual; depends on age
at which HIV infection
is acquired
Estimates of sex ratios vary, depending
in part on the sex difference in HIV
prevalence and the availability of
antiretroviral treatment at the time a
study is undertaken
Parkinson’s
disease
Less than 10%; often comorbid
with Alzheimer’s type and/or
vascular dementia; about 50%
of patients with Parkinson’s
disease develop dementia
Poor Gradual; typical age of
onset is in the 70s
More men than women develop
Parkinson’s disease, and so men are
more likely to develop this type of
dementia
Huntington’s
disease
Less than 10% Poor Gradual; onset usually
occurs in the 40s or 50s.
No sex difference
Head trauma
Unknown Depends on the specific
nature of the trauma
Usually abrupt, after the
head injury
Unknown, but most common among
young men
Substance-
induced
Unknown Variable, depends on the
specific substance and deficits
Gradual; in the 30s and
beyond
Unknown
Note: Most cases of dementia are caused by Alzheimer’s disease. However, dementia in a given person can arise from more than one cause, and the percentages in the
second column reflect these comorbidities; for this reason, the numbers add up to more than 100%.
and Alzheimer’s disease. When this occurs, the clinician diagnoses each type (cause)
separately. Table 15.9 summarizes key facts about the different types of dementia.
With a progressive dementia, such as occurs in Alzheimer’s disease, a person’s
diagnosis may change over time from a mild neurocognitive disorder to major neu-
rocognitive disorder; this changed diagnosis occurs after the disorder has advanced
and the person’s cognitive abilities are impaired to the point where he or she can’t
function effectively (e.g., can’t remember to pay bills or take medication). In other
cases, such as cognitive impairments that arise from head trauma, a person’s deficits
might remain relatively mild and stable, so that the person can functioning relatively
well in daily life, with perhaps some reduced ability relative to his or her pervious
baseline; in such cases, a mild neurocognitive disorder would not change to major
neurocognitive disorder.
Treating Dementia
With most types of dementia, such as the Alzheimer’s type and vascular dementia,
treatments cannot return cognitive functioning to normal (HIV-induced dementia
being the exception to the rule, as noted earlier), and instead consist of rehabilita-
tion. Given the high proportion of dementia that is caused by Alzheimer’s disease
(see Table 15.9), in the following sections we focus on treatment for that type of
dementia, unless otherwise noted.
Neurocognitive Disorders 497
Targeting Neurological Factors
Medications have been developed to delay the progression of cognitive difficulties
in people with Alzheimer’s disease. One class of drugs, cholinesterase inhibitors, such
as galantamine (Razadyne) or donepezil (Aricept), is used for mild to moderate cogni-
tive symptoms; these medications increase levels of acetylcholine (Lyle et al., 2008;
Poewe et al., 2006). Another type of drug, memantine (Namenda), affects levels of
glutamate (Tariot et al., 2004) and is used to treat moderate to severe Alzheimer’s
dementia (Kavirajan, 2009). Still other, experimental, medications are intravenous
immunoglobulin (Relkin et al., 2012) and EVP-6124 (Hilts et al., 2012). Although
each of these drugs may help some patients (Atri et al., 2008; Cummings et al., 2008;
Homma et al., 2008), they are new, and few carefully controlled studies of these
medications have been completed.
Antipsychotic medications are sometimes given for psychotic symptoms or behav-
ioral disturbances, but the side effects of both traditional and atypical antipsychotics cau-
tion against their long-term use (Ballard & Howard, 2006; Schneider et al., 2006b).
Patients with dementia due to Lewy bodies should not be given antipsychotic medication
for behavioral disturbances because this type of medication makes their symptoms worse.
Targeting Psychological Factors
The American Association for Geriatric Psychiatry (2006) recommends that the first
line of intervention for dementia should help patients maintain as high a quality of
life as is possible, given the symptoms. Such interventions focus on psychological and
social factors.
To target psychological factors, people in the early stages of dementia—and their
friends and relatives—may be taught strategies and given devices to compensate for mem-
ory loss. Such strategies include ways of organizing information so that it can later be re-
trieved from memory more readily. One such strategy is the use of mnemonics, which may
help people to remember simple information, such as where the car is parked at the mall.
For example, someone might repeatedly visualize the location of the car in the parking lot,
which will help him or her retain this information. In addition, structured and predictable
daily activities can reduce patients’ confusion (Gitlin et al., 2010; Spector et al., 2000).
Moreover, patients may be given a GPS tracking device to wear so that they
can be found relatively quickly and easily if they get lost (Rabin et al., 2006).
People who are in the early stages of progressive dementias are often
anxious and depressed (Porter et al., 2003; Ross et al., 1998). One type of
treatment that may alleviate these comorbid conditions is reality orientation
therapy (Giordano et al., 2010; Woods, 2004), which is designed to de-
crease a patient’s confusion by focusing on the here and now. For example,
the clinician may frequently repeat the patient’s name (“Good morning,
Mr. Rodrigues; how are you on this Monday morning, Mr. Rodrigues?”)
and remind the patient of the day and time; calendars and clocks are lo-
cated where the patient can see them easily. Patients whose cognitive func-
tioning is impaired to the point where they are in residential centers are
encouraged to join in activities rather than isolate themselves.
Another method that may decrease the depression and anxiety that
can accompany progressive cognitive decline is reminiscence therapy, which
stimulates the patients’ memories that are least affected by dementia—
those of their early lives. When providing this treatment, the therapist
focuses on patients’ life histories and asks patients to explore and share
their experiences with group members or with the therapist; patients may
feel relief at being able to remember some information, and their anxiety
decreases and their mood improves (Subramaniam & Woods, 2012).
People with dementia can wander off and
become confused about who they are and
where their home is. Some people with
dementia wear small GPS tracking devices, like
the one in this sneaker, so that if they wander
off they can be found relatively quickly and
easily.
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498 C H A P T E R 1 5
Caregivers—family members and paid caretakers—may be trained to treat be-
havioral disturbances, such as agitation and aggression that sometimes arise with de-
mentia. Such training may lead them to first be asked to identify the antecedents and
consequences of the problematic behavior ( Ayalon et al., 2006; Spira & Edelstein,
2006). Following this, they are advised how to modify those aspects of the environ-
ment or personal interactions. For instance, if a patient becomes aggressive only at
night after waking up to go to the bathroom, a night-light in his or her room may
help reduce any anxiety that arises because the patient is confused upon awakening.
Targeting Social Factors
One way to reduce the cognitive load of someone with dementia is to enlist others
to structure the patient’s environment so that memory is less important. For instance,
family members can place labels on the outside of cupboards and room doors at home
or at a residential facility; each label identifies what is on the other side of the door
(for example, “dishes,” “kitchen,” “Sally Johnson’s room”). In some rehabilitation
centers, the doors to bathrooms are painted a distinctive color, and arrows on the
walls or floors show the direction to a bathroom, so patients don’t need to rely as
much on memory to get around the facility (Wilson, 2004).
As cognitive and physical functioning decline, patients with dementia may re-
ceive services that target social factors—such as elder day care, which is a day treatment
program for older adults with cognitive or physical impairments. Such day treatment
both allows the patient to interact with other people and provides a respite for fam-
ily members who care for the patient. As the patient continues to decline, however,
he or she may require live-in caretakers or full-time care in a nursing home or other
residential facility.
Taking care of a family member who has Alzheimer’s disease is often extremely
stressful; for example, patients may need to be watched constantly and closely, for fear
that they may inadvertently harm themselves or other people. This stress increases
the caretaker’s risk of developing a psychological or medical disorder. In recent years,
clinicians who treat patients with dementia have also reached out to family members
who act as caretakers to provide education, support, and, when needed, treatment
to help these people develop less stressful ways of interacting with the patients. Such
interventions help family members (and, indirectly, the patients themselves) function
as well as possible under the circumstances.
Thinking Like A Clinician
Sixty-five-year-old Lucinda recently retired from her job as corporate vice-president of mar-
keting. Lucinda lives alone but frequently visits her son, his wife, and their young daughter.
She’s noticed lately that she loses umbrellas and often forgets things—such as where her
keys are, lunch dates with friends, and other appointments. She’s chalked up these problems
to her retirement and the resulting changes in her daily routines. At what point might losing
and forgetting things indicate a neurocognitive disorder? If you knew only that Lucinda had
dementia, what should and shouldn’t you assume about its cause(s) and her prognosis?
Diagnosing Mrs. B.’s Problems
Let’s reconsider the specific nature of Mrs. B.’s problems. The neuropsychologist re-
counted that Mrs. B. knew who and where she was and understood test instructions.
Results of tests of her ability to remember information both immediately after learn-
ing it and after a 30-minute delay were normal for her age, which indicated that she
probably did not have Alzheimer’s disease or another disease that involves significant
memory impairment. Instead, the neuropsychologist suggested that Mrs. B.’s problems
Neurocognitive Disorders 499
reflected a mild dementia (possibly a mild vascular neurocognitive disorder) combined
with depression and chronic pain. The neuropsychologist wrote in her report:
Feedback to Mrs. B. reinforced her belief that her current memory problems do not
suggest [Alzheimer’s disease]. She was asked about activities that she enjoys, and we ex-
plored ways of increasing her opportunities for these activities with her attendant (e.g.,
she has recently visited a senior day-care program and hopes to attend one or two days
a week). She was encouraged to give her current living situation a longer try, working
with her daughter and staff to improve the most bothersome aspects of the situation.
Written reports were provided to the daughter (who is Mrs. B.’s legal guardian) and
other medical professionals involved in her care. Feedback was also provided by tele-
phone to the daughter and the referring psychiatrist to answer questions about results
and to further discuss approaches to care. Recommendations included continuing psy-
chotherapy and antidepressant medication, negotiating brief written contracts between
Mrs. B. and staff members at the board-and-care home to clarify mutual expectations
in problem areas, and considering low-dose antipsychotic medication in the event that
aggressive and accusatory behaviors escalated despite behavioral intervention. Neither
returning home nor moving into the daughter’s home was recommended. . . .
For Mrs. B., things got worse before they got better. Her “fit” in the board-and-
care home continued to deteriorate, and after much discussion, she moved back to a
nursing home. For a time, she was taking multiple psychoactive medications and her
cognitive function deteriorated at a rapid rate [which might be considered a major
medication-induced neurocognitive disorder]. [She was taken off her medications] and
her [cognitive functioning] rebounded. A year later, after an intervening small stroke,
her memory function is slightly worse, but her mood is brighter, she communicates
well, and she has fewer complaints about staff and other residents than she did in the
board-and-care home.
(La Rue & Watson, 1998, p. 11)
SUMMING UP
Normal Versus Abnormal Aging and
Cognitive Functioning
• Most aspects of cognitive functioning re-
main stable during the normal course of
aging. However, fluid intelligence, pro-
cessing speed, recalling verbal informa-
tion on demand, maintaining attention,
and multitasking decline in older adults.
But these declines do not generally impair
daily functioning.
• The d isorder s that are most com mon
among older adults are depression and
generalized anxiety disorder. These disor-
ders can lead to impaired cognitive func-
tioning that may superf icially resemble
symptoms of a neurocognitive disorder.
• Bra in injur y, most com mon ly f rom a
stroke, can produce various cognitive def-
icits. Among the deficits that may follow a
stroke or a head injury are aphasia, agno-
sia, and apraxia.
• Legally prescribed medications or illegal
substances can alter awareness, emotional
states, and cognitive functioning.
Delirium
• According to DSM-5, delirium is char-
acter ized as a disturbance in attention
and awareness as well as changes in an-
other aspect of cog nitive functioning.
These sy mptom s develop rapid ly a nd
fluctuate over the course of a 24 -hour
period.
• Delirium most commonly occurs among
the elderly, the terminally ill, and patients
who have just had surgery.
• Delir ium can ar ise from substance in-
toxication or withdrawal; delirium can
also arise from a medical condition—such
as an infection or head trauma—or as a
result of anesthesia.
• Treatment for delirium that targets neu-
rological factors often addresses the un-
derlying physical cause, typically through
medication.
• Treatments that target psychological and
social factors include correcting sensory
impairments, helping patients increase
their awareness of the here and now, and
educating people who interact with the
delirious patient about the symptoms of
the disorder.
Dementia (and Mild Versus Major
Neurocognitive Disorders)
• Dementia is the umbrella term for a set of
cognitive disorders that involve deficits in
memory and aphasia, apraxia, agnosia, or
problems with executive functions.
• Dementia can give rise to hallucinations
and delusions.
• A l l t y pe s of dement i a a re cau sed by
neu rolog ica l f actor s. The most com-
mon t y pe of d ement i a — t h at due t o
A l zhei mer’s d isea se —is a prog ressive
disorder characterized by neurofibrillary
tangles and amyloid plaques in the brain.
Although symptoms may emerge before
age 65, the late-onset form is much more
common.
• Vascular dementia is caused by reduced or
blocked blood flow to the brain, usually
because of narrowed arteries or strokes.
500 C H A P T E R 1 5
• Other t ypes of dementia are caused by
medical conditions:
° Parkinson’s disease is a progressive dis-
order that affects motor functions.
° Lew y bodies build up inside certain
types of neurons and cause the neurons
to die, leading to progressive, irrevers-
ible dementia.
° HIV d isease can event ua l ly destroy
white matter and subcortical brain ar-
eas; however, in some cases this type of
dementia can be arrested and even re-
versed with antiretroviral medication.
° Huntington’s disease is a progressive
disease that involves death of neurons
in brain areas that are involved in cog-
nition, emotion, and motor control.
° Head trauma is caused by accidents or
incurred as part of an athletic sport.
° Substance use problems or medications
can lead to temporar y or persistent
dementia.
• Mild neurocognitive disorder is charac-
terized by evidence of a modest decline
in cognitive function from baseline but
people are able to function independently.
In contrast, major neurocognitive disor-
der is characterized by signif icant cog-
nitive decl ine and impaired abi l it y to
function independently.
• Treatments for dementia that target neu-
rolog ica l f actor s i nclude med icat ion s
that affect the levels of acetylcholine or
glutamate.
• Psychological and social interventions for
people with dementia are designed to im-
prove the patients’ quality of life. Methods
include the use of memor y aids, reality
orientation therapy, reminiscence therapy,
and restructuring of the environment.
Neurocognitive disorders (p. 477)
Crystallized intelligence (p. 479)
Fluid intelligence (p. 479)
Stroke (p. 483)
Aphasia (p. 483)
Broca’s aphasia (p. 483)
Wernicke’s aphasia (p. 483)
Apraxia (p. 483)
Delirium (p. 484)
Dementia (p. 488)
Mild neurocognitive disorder (p. 489)
Major neurocognitive disorder (p. 489)
Alzheimer’s disease (p. 490)
Neurofibrillary tangles (p. 494)
Amyloid plaques (p. 494)
Vascular dementia (p. 494)
Huntington’s disease (p. 496)
Key Terms
More Study Aids
For additional study aids related to this chapter, including
quizzes to make sure you’ve retained everything you’ve
learned and a Student Video Activity exploring the case
of a man who has lost both his short-term and long-term
memory, go to: www.worthpublishers.com/launchpad/
rkabpsych2e.
Photodisc
Neurocognitive Disorders 501
CHAPTER 16
Ethical and Legal Issues
t’s the early evening rush hour in New York City in January 1998.
People are waiting in a subway station for a train to take them
home, to meet friends, or to go out to dinner. Kendra Webdale,
a 32-year-old woman, is among the people waiting at the platform.
Andrew Goldstein, a 29-year-old man, comes up from behind her
and pushes her in front of an oncoming train as it enters the station.
He murdered her, as many witnesses later testified. This might seem
an open-and-shut criminal case, but it’s not. Goldstein had a 10-year
history of mental illness, had been in and out of psychiatric units and
hospitals, and had been diagnosed with paranoid schizophrenia.
If Goldstein wasn’t in his “right mind” when he pushed Webdale,
should he face a trial? And if found guilty, should he go to jail, or
perhaps be executed? Or should he be judged and treated as some-
one who is mentally ill—and if so, why? If the mentally ill commit
criminal acts, should they be dealt with differently than people who
are not mentally ill? Moreover, what if Goldstein had been seeing a
psychotherapist and had mentioned that he might do something like
this—should the therapist have reported his statement to the police?
Mental health clinicians are bound by a code of ethics and by state
and federal laws. What are the relevant ethical guidelines and laws
that affect how mental health clinicians treat their patients? These are
the types of questions that address the relationships among the law,
ethics, and the reality of mental illness and its treatment.
Ethical Issues
An Ethical Principle: The Role of Confidentiality
Informed Consent to Participate in Research on
Mental Illness: Can Patients Truly Be Informed?
Criminal Actions and Insanity
While Committing the Crime: Sane or Insane?
The Insanity Defense: Current Issues
After Committing the Crime: Competent to
Stand Trial?
Dangerousness: Legal Consequences
Evaluating Dangerousness
Actual Dangerousness
Confidentiality and the Dangerous Patient:
Duty to Warn and Duty to Protect
Maintaining Safety: Confining the Dangerously
Mentally Ill Patient
Legal Issues Related to Treatment
Right to Treatment
Right to Refuse Treatment
Competence to Refuse Treatment
Mental Health and Drug Courts
The Wheels of Justice: Follow-up on
Andrew Goldstein
503
In thIs chapter, we examine the legal and ethical issues that
can affect mental health professionals and their patients, paying par-
ticular attention to criminal actions by people who are mentally
ill—the circumstances under which they are considered insane, what
happens to them when they are dangerous to themselves or others,
and whether and when they receive treatment.
Yagi Studio/Taxi Japan/Getty Images. Photo for illustrative purposes only;
any individual depicted is a model.
Ethical Issues
Various mental health professionals had contact with Andrew Goldstein during the
years that led up to his pushing Kendra Webdale to her death. Any mental health
professional may at times have to balance ethical and legal obligations to a patient
against the safety of others. Suppose Goldstein had confided to a mental health pro-
fessional that he sometimes had impulses to hurt people—impulses that he felt he
might not be able to control. How should the clinician treat such information? If
Goldstein gave specifics about when, where, or with whom he was likely to become
violent, would that affect how the clinician should treat such information? What is
the clinician ethically bound to do in such instances? We address these questions in
the following sections.
An Ethical Principle: The Role of Confidentiality
Different types of mental health professionals assess and provide treatment for psy-
chological problems. Each profession has its own code of ethics, although all of the
codes have some guidelines in common. (Websites containing the specific codes of
ethics for the different types of mental health professionals are listed in Table 16.1.)
The most important common feature is the ethical requirement to maintain
confidentiality—not to disclose information about a patient (even whether some-
one is a patient) to others unless legally mandated to do so. The ethical principles
and code of conduct of the American Psychological Association requires that mental
health records remain confidential. In addition, the clinician must inform patients
about the limits of confidentiality—that is, under what circumstances confidentiality
may be broken.
Andrew Goldstein (left) killed Kendra Webdale
(right) by pushing her off a subway station
platform into an oncoming train. Goldstein
had a history of mental illness and had been
diagnosed with paranoid schizophrenia.
How do we determine whether he should be
treated as a person suffering from a disease or
as a cold-blooded murderer? AP
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TABLE 16.1 • Websites for the Ethical Codes of Various Mental Health Professions
Mental health profession URL of website presenting ethical code
Psychologist www.apa.org/ethics
Psychiatrist www.psychiatry.org/practice/ethics/resources-standards
Social worker www.socialworkers.org/pubs/code/code.asp
Psychiatric nurse
http://nursingworld.org/MainMenuCategories/EthicsStandards/
CodeofEthicsforNurses/Code-of-Ethics
List of specific types of
mental health clinicians
http://kspope.com/ethcodes/index.php
Confidentiality
The ethical requirement not to disclose
information about a patient (even whether
someone is a patient) to others unless legally
compelled to do so.
504 C H A P T E R 1 6
Ambiguities Regarding Confidentiality
The principle of confidentiality appears to be straightforward, but some clini-
cal situations are thorny and difficult to resolve. When a therapist is treating a
couple, for instance, the therapist is bound by confidentiality, but each person
in the couple is not; this means that each partner may tell other people about
what transpires in therapy sessions. Similarly, in group therapy, although the
therapist is bound by confidentiality, each member is not (although group
members are asked not to talk about anything they hear from other members).
However, when a patient is a minor (under 18 years of age), the clinician may
inform the parents about information that the child has told the clinician. The
clinician usually discusses the limits of confidentiality with a child old enough
to understand them—or at least discusses possible circumstances in which the
clinician may need to share information with parents or others.
In addition, the use of digital technology in therapy can lead to concerns about
confidentiality (Klein, 2011; Van Allen & Roberts, 2011). For instance, the visits with
a mental health clinician may also be part of a patient’s electronic medical records
( Steinfeld & Keys, 2011), which may be seen by other health providers. In addition, if
a patient contacts his or her therapist via e-mail, even if the therapist’s e-mail server is
secure, the patient’s e-mail server may not be (and if the patient e-mails from work, the
e-mails may remain the “property” of the employer). In such cases, despite the thera-
pist’s best efforts to ensure confidentiality, their correspondence may not remain pri-
vate. Similarly, when therapy is performed remotely—via the telephone, e-mail, or as
a videoconference—the therapist cannot ensure confidentiality because at the patient’s
locale, other people might be able to listen in or access the communication.
Limits of Confidentiality: HIPAA in Action
Congress passed the Health Insurance Portability and Accountability Act in 2002
(HIPAA; U.S. Department of Health and Human Services, 2002), and in doing so
widened the set of circumstances under which conf idential information could be
shared with other individuals and organizations participating in the care or moni-
toring of a patient in order to improve patient care. No longer was the patient’s per-
mission to share information with other health providers legally required. However,
according to HIPAA, patients must provide specific written consent before clinicians
can share separate notes from their psychotherapy sessions. Without such consent, the
mental health clinician can share only limited information—such as the dates of treat-
ment, the patient’s diagnosis and prognosis, and the medications prescribed—with
other people or organizations involved in the treatment or monitoring of the patient.
Thus, through HIPAA, patients lost some control over the distribution of their
health records (Appelbaum, 2002). The circumstances under which health care
information can be shared without a patient’s consent (or even without the patient’s
being told about it) now include the following (U.S. Department of Health and
Human Services, 2002):
1. During litigation. The opposing lawyer in a lawsuit can request health information
from a provider and must only state that he or she made reasonable attempts to
notify the patient about the request for information. During litigation, lawyers
can even request the medical records of witnesses!
2. When the person is a police suspect. Police officers can request health information
about a suspect without having a warrant or being under any judicial oversight.
3. Marketing efforts by health providers (and their business associates) to patients. For
instance, if a community health center were initiating a therapy group for people
with depression, the center would be able to send a brochure about the group to
patients currently receiving treatment at the facility.
A mental health clinician is bound by
confidentiality, but each member of a couple
participating in couples therapy is not.
D
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Ethical and Legal Issues 505
4. Research. When investigators have approval for a study that uses patients’ medical
records, the investigators may have access to those records without the patients’
explicit permission.
However, unless information is shared specifically to facilitate treatment, the law
specifies that the provider should disclose only the minimum necessary information.
Legal Restrictions on Confidentiality
States usually have laws to protect confidentiality. However, most states have excep-
tions to those rules. Typically, confidentiality can be violated in certain situations:
• when a patient gives the clinician permission to violate confidentiality, for example
by explicitly giving permission to a therapist to speak to the patient’s spouse;
• when a clinician has reasonable cause to suspect abuse of children, of elderly people,
or of disabled people. In such cases, the clinician usually must report the suspected
abuse to the appropriate authorities so that steps can be taken to protect those who
cannot otherwise protect themselves;
• when a clinician has reasonable cause to believe that a patient is likely to harm
himself or herself significantly or to attempt suicide. In this situation, the clinician
must take steps to protect the patient; and
• when a clinician has good reason to believe that a patient is likely to inflict signifi-
cant harm on a specified other person. In this case, the clinician must take steps to
protect that other person.
Thus, a clinician should not have violated Goldstein’s confidentiality if he spoke
in generalities about his violent urges. Even if Goldstein had said that he had violent
impulses that he couldn’t control when in subway stations or when around blond-
haired women, such a statement would probably not be viewed as posing a specific
enough danger to violate confidentiality. However, the clinician would have been
legally compelled to violate Goldstein’s confidentiality if he had specifically named
Kendra Webdale as someone he planned to harm.
Privileged Communication
Confidentiality is an ethical term. A related legal term, privileged communication,
refers to confidential information that is protected from being disclosed during
legal proceedings. Just as a priest cannot legally be compelled to reveal what was
said by a parishioner in the confessional, the Supreme Court has ruled that com-
munication between a patient and a therapist is privileged ( Jaffee v. Redmond, 1996;
Mosher & Swire, 2002). However, not all confidential information is privileged
and vice versa.
The person who shared information with the clinician is usually the one who
decides whether it can be revealed, but others can make this decision in certain
circumstances. For example, if a judge orders that a defendant must undergo a men-
tal health evaluation, as happened to Goldstein after he was taken into custody, the
communication between the mental health clinician(s) doing the evaluation and
the defendant may not be considered privileged in some courts, depending on the
jurisdiction (Meyer & Weaver, 2006; Myers, 1998). In such a circumstance, in or-
der to comply with the law and behave ethically, the mental health clinician should
explain to the defendant at the very beginning of the evaluation that anything said to
the clinician may be disclosed to the judge. Whenever the law regarding privileged
communication conflicts with the ethics of confidentiality, patients should be told of
the limits of confidentiality as soon as possible (Meyer & Weaver, 2006).
Another type of exception to the laws governing privileged communication
occurs when a patient (or former patient) initiates a civil lawsuit against another
party and raises the issue of personal injury with mental health consequences as part
The term confidentiality refers to the ethical
requirement not to disclose information
about a patient; in contrast, privileged
communication is a legal requirement that
refers to confidential information that should
not be disclosed during a legal proceeding.
There are some circumstances in which
mental health clinicians are legally obligated
to violate confidentiality, and thus the
communication is not privileged.
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Privileged communication
Confidential information that is protected
from being disclosed during legal proceedings.
506 C H A P T E R 1 6
of the suit. An example of this type of case would be one in which a woman sues her
employer for anguish that resulted from harassment at work. In these sorts of lawsuits
for personal injury, the mental health clinician is legally bound to testify if his or her
testimony is relevant to the case (Bartol & Bartol, 2004).
It is not always clear who owns a privileged communication about information
revealed during group therapy. In this situation, the therapist may not be compelled
to testify about what transpired, but group members may be. At present, judges
decide on a case-by-case basis whether a therapist must testify, depending on the spe-
cific circumstances (Meyer & Weaver, 2006).
Informed Consent to Participate in Research on Mental
Illness: Can Patients Truly Be Informed?
Can someone who is mentally ill give truly informed consent to participate in psy-
chological research pertaining to his or her disorder? People who have anxiety dis-
orders may be able to understand fully the research procedure and possible adverse
effects, but what about people with schizophrenia? Are such patients’ mental pro-
cesses impaired to the extent that their consent isn’t really informed? What about
people who are having a first episode of psychosis and agree to participate in a study
before the psychotic episode has abated?
The general rule of thumb for researchers is that potential participants must be
capable of understanding and reasoning about what they are consenting to (Meyer &
Weaver, 2006). Thus, the ability to understand and reason about the research pro-
cedure may be more important to informed consent than whether the person is psy-
chotic at the time of consent (Kovnick et al., 2003; Misra & Ganzini, 2004).
Researchers are developing ways to ensure that patients who may be cognitively
impaired by a psychological disorder adequately understand the benefits and risks of
their participating in research. For instance, Wirshing and colleagues (2005) developed
an educational video to increase awareness about informed consent among patients with
schizophrenia. Among other points, the video explained that participants can withdraw
from the study at any time. Researchers continue to develop and assess methods to ensure
that participants give truly informed consent to participate in research (Eyler et al., 2005).
Thinking Like A Clinician
Rina is taking medication and seeing a therapist for depression. During one therapy session,
she remarks, “Sometimes I think my family would be better off if I were dead.” Based on what
you have read, should Rina’s therapist violate confidentiality and take steps to prevent Rina
from hurting herself? Why or why not?
What if, instead, Rina had said about her multiply handicapped brother, “Sometimes I
think my family would be better off if he were dead”? Would your view of whether Rina’s
therapist should violate confidentiality change—why or why not? What would Rina need to
do or say to provide a clear indication that the therapist should violate confidentiality?
Criminal Actions and Insanity
After Andrew Goldstein pushed Kendra Webdale in front of the oncoming subway
train, other passengers detained him until the police arrived. When taken to the po-
lice station, he explained in a signed statement why he pushed her: “I felt a sensation
like something was entering me like a ghost or a spirit or something like that. . . .
When I have the sensation that something is entering me, I get the urge to push,
shove, or sidekick” (Rohde, 1999b).
Ethical and Legal Issues 507
Goldstein then said he “watched in ‘horror’” as the train ran over Webdale, after
which he is reported to have turned to the man next to him, “raised his arms in the
air and said, ‘I don’t know’” (Rohde, 1999b). When police came, he told them he
was a “ ‘psychotic patient’ who had suffered a ‘psychotic attack’ ” (Rohde, 1999b) and
asked to be taken to the hospital.
Goldstein was arraigned on the charge of second-degree murder and then,
perhaps because he seemed to be mentally ill or because of his long psychiatric his-
tory, he was taken to a hospital rather than to jail. As we shall see, if someone who al-
legedly committed a crime was mentally ill during or after the criminal act, jail may
not be the appropriate place for that person to be. Moreover, treatment—rather than
detention—may be an appropriate goal for such a defendant’s immediate future. In
what follows we review the legal and clinical issues that arise after a crime has been
committed by someone who is mentally ill.
As discussed in Chapter 1, the term insanity is a legal term and is not used in
DSM-5. The legal concept of insanity addresses the question of whether a person
was, at the time he or she committed a crime, criminally responsible—which involves
both action and intention: To be criminally responsible means that a defendant’s
crime was the product of both an action or attempted action (the alleged criminal
behavior) and his or her intention to perform that action (Greene et al., 2007; Meyer
& Weaver, 2006).
After a crime has been committed and a person has been arrested, the legal
system specif ies two distinct periods when the defendant could have been suf-
fering from a mental illness: (1) At the time he or she (allegedly) committed the act;
might the insanity defense be appropriate? (2) During the time of assessment, lead-
ing up to the trial; can the person adequately assist in his or her own defense? Is
the person competent to stand trial? We next discuss each of these circumstances
in turn.
While Committing the Crime: Sane or Insane?
In the United States, the legal definition of insanity corresponds to a “test” that is
used to determine whether a person is insane. The particular test used has changed
over time.
From the M’Naghten Test to the Durham Test
In England in 1841, a Scottish man named Daniel M’Naghten believed that the
British prime minister, Sir Robert Peel, was personally responsible for M’Naghten’s
woes. M’Naghten attempted to shoot Peel but missed him and killed Peel’s secretary.
During M’Naghten’s trial, witnesses testified that he was insane, and the jury found
him not guilty by reason of insanity (NGBI). This verdict did not sit well with many
citizens, including Queen Victoria, the reigning monarch at the time. In response,
the House of Lords narrowed the insanity defense by limiting the relevance of the
defendant’s mental state to the time the alleged crime was committed. In what came
to be known as the M’Naghten test (or rule), the question asked at a trial became
whether, at the time of committing the act, the defendant knew what he or she was doing
and, if so, knew that the act was wrong—and if he or she did not know this, it was
because of “a defect of reason, from disease of the mind.” With this narrower test, the
judges reversed the verdict and found M’Naghten guilty.
The M’Naghten test of insanity was adopted in the United States and continued
to be used until 1886, when the def inition of insanity was widened. The new
def inition, specif ied by the irresistible impulse test, focused on whether the
defendant knew that the criminal behavior was wrong but nonetheless performed it
because of an irresistible impulse.
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The earliest insanity defense case was that
of Daniel M’Naghten, a Scottish man whose
delusions about the British prime minister
led him, in 1841, to commit murder. After
M’Naghten was found not guilty by reason
of insanity, the House of Lords narrowed the
criteria for determining insanity; these criteria
came to be known as the M’Naghten test.
Criminally responsible
The determination that a defendant’s
crime was the product of both an action
or attempted action (the alleged criminal
behavior) and his or her intention to perform
that action.
M’Naghten test (or rule)
The legal test in which a person is considered
insane if, because of a “defect of reason, from
disease of the mind,” he or she did not know
what he or she was doing (at the time of
committing the act) and did not know that it
was wrong.
Irresistible impulse test
The legal test in which a person is considered
insane if he or she knew that his or her
criminal behavior was wrong but nonetheless
performed it because of an irresistible impulse.
508 C H A P T E R 1 6
In 1954, the Supreme Court r uled on a case, Durham v. U.S., and again
broadened the test for the insanity defense. The Durham test was designed to
determine whether the irresistible impulse was due to mental defect or disorder present
at the time of the alleged crime. The Durham ruling shifted the insanity defense so
that it hinged on evidence that the behavior did not arise entirely from free will.
The Durham ruling moved away from consideration about morality (knowing “right
from wrong”) and into the realm of science (having a mental impairment).
However, the Durham ruling had a major drawback: It left unclear what consti-
tuted a mental defect or disorder. For instance, it is possible that someone who was
drunk while committing a crime might be considered to have a mental defect. And
what about someone with antisocial personality disorder (or psychopathy)? Might
that disorder allow that person to use the insanity defense? Moreover, how could
the court decide whether the criminal behavior was caused by the disorder or defect
(Greene et al., 2007; Meyer & Weaver, 2006)? This drawback is so significant that
most states use other definitions of insanity; only New Hampshire still uses the Dur-
ham test (Wrightsman & Fulero, 2005).
The American Legal Institute Test
To address some of the thorny issues that arose from the Durham test, the American
Legal Institute (ALI) proposed two alternative criteria for insanity:
1. The person lacks a substantial capacity to appreciate that the behavior was wrong
(versus has no capacity); or
2. the person has a diminished ability to make his or her behavior conform to the
law, that is, an irresistible impulse.
The American Legal Institute (ALI) test consists of these criteria, which are
sometimes referred to as knowledge (cognition) and impulse (volition) criteria. The ALI test
broadened the test for insanity because it provided these two possible criteria (Greene
et al., 2007; Meyer & Weaver, 2006). The ALI test also specified that if an individual’s
only defect or disorder is criminal behavior, the insanity defense cannot be used. This
prevented people with antisocial personality disorder (or psychopathy) and people
whose only crime is using illegal substances from using these problems as the basis for
an insanity defense. The ALI test continues to be used by many states.
Insanity Defense Reform Acts
In federal courts, the insanity test changed again in 1984, as
a result of John Hinckley’s 1981 attempted assassination of
then-President Ronald Reagan and Hinckley’s subsequent
acquittal as not guilty by reason of insanity. Hinckley was a
young man with a history of mental illness; he reported that
he shot the president in order to impress actress Jodie Foster,
about whom he had obsessive delusions.
The jur y found Hinckley insane on the basis of the
impulse (volition) element of the ALI test. This means that
the jury decided that Hinckley knew it was wrong to shoot
the president but that he was not able to restrain himself.
He was sent to a psychiatric hospital, not prison. The fact
that Hinckley would serve no prison time greatly disturbed
some lawmakers, who, through the Insanity Defense Re-
form Acts of 1984 and 1988, proceeded to restrict the test
for insanity. The new test for insanity, used only in fed-
eral court, is most similar to the M’Naghten test—it asks
whether the individual, because of a severe mental defect or
Durham test
The legal test in which a person is considered
insane if an irresistible impulse to perform
criminal behavior was due to a mental defect
or disorder present at the time of the crime.
American Legal Institute (ALI) test
The legal test in which a defendant is
considered insane if he or she either lacks a
substantial capacity to appreciate that his or
her behavior was wrong or has a diminished
ability to make his or her behavior conform to
the law.
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John Hinckley developed an obsessive
preoccupation with actress Jodie Foster and
repeatedly tried to communicate with her
by phone and letter. After his attempts were
rebuffed, he developed the delusional belief that
assassinating President Ronald Reagan would
impress Foster and induce her to pay attention
to him. In 1981, he acted on that belief and shot
the president and three other people.
Ethical and Legal Issues 509
disorder, has a diminished capacity to understand right from wrong (cognition). In
an effort to make a plea of NGBI more difficult to enter, Congress also put an end
to the irresistible impulse element (volition) in federal courts. Defendants with intel-
lectual disability, psychotic disorders, or mood disorders may qualify for the insanity
defense under these new rules, depending on the circumstances of the crime and
the defendant’s state of mind at the time, but having a disorder in and of itself is not
enough for an insanity defense. Case 16.1 describes a woman who entered a plea of
insanity in a murder case. Table 16.2 provides an overview of the various tests of
insanity.
CASE 16.1 • FROM TH E OUTSIDE: The Insanity Defense
In 2001, Andrea Yates confessed to police that she drowned her five children, ages
6 months to 7 years old, in her bathtub. She reported that she believed Satan was inside
her, and she drowned them to try to save them from hell. Yates’s lawyers said that she had
been psychotic at the time of the murders and that she did not know that her actions were
wrong. (According to Texas state law, the key element of the insanity defense is knowing
that the actions were wrong at the time of the crime.) Her lawyers pointed to her history
of mental illness: two previous suicide attempts and four psychiatric hospitalizations for
schizophrenia and postpartum depression.
During her trial, an expert witness for the prosecution, psychiatrist Dr. Park Dietz,
agreed with previous witnesses that Yates had been psychotic at the time of the drown-
ings, but testified that she was still able to know right from wrong and therefore not insane
under Texas law. To support his position, Dr. Dietz brought up the television series Law and
Order, which he had been told Yates had watched. Dietz, who also served as a consul-
tant to the producers of that television series, testified that shortly before she drowned
her children, an episode of Law and Order aired that involved a woman with postpartum
depression who drowned her children in a bathtub and was declared insane. Prosecutors
used Dietz’s testimony about the television show to indicate that Yates knew her actions
were wrong (Greene et al., 2007).
It turns out, however, that no such episode had been aired; this error was dis-
covered af ter the jur y convicted Yates of murder but before they began deliberat-
ing about her punishment. Rather than declare a mistrial, the judge simply told the
jurors about the error. Yates was given a life sentence in prison. The appeals cour t
ruled that a mistrial had occurred, and Yates was retried. She was ultimately found
not guilty by reason of insanity and placed in a state mental hospital, where she will
remain until she is no longer considered a danger to others or herself.
(Ewing & McCann, 2006).
TABLE 16.2 • Tests for the Insanity Defense Used Over Time
Test Legal standard
M’Naghten (1843)
“Didn’t know what he or she was doing or didn’t
know it was wrong”
Irresistible impulse (1886) “Could not control conduct”
Durham (1954) “Criminal act was caused by mental illness”
American Legal Institute (ALI; 1962)
“Lacks substantial capacity to appreciate the
wrongfulness of the conduct or to control it”
[emphasis added]
Present federal law (1984 and 1988)
“Lacks capacity to appreciate the wrongfulness of
his or her conduct”
Source: Meyer & Weaver, 2006, p. 123, which was adapted in part from Morris, 1986.
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Andrea Yates, who was tried for murdering her
five children, said she drowned them in order
to save them from hell. Her lawyers used the
insanity defense.
510 C H A P T E R 1 6
The Insanity Defense: Current Issues
Use of the insanity defense is rare (only 1% of cases, according to one study), and suc-
cessful use of the defense is exceptionally rare—only one quarter of the time it is used,
or 0.25% of cases (Steadman et al., 1993). Despite its rarity, the federal requirements
for the insanity defense have narrowed over time. However, the courts have yet to
resolve two issues about how this defense can be applied:
• whether the person knew the act was wrong (a moral question) versus illegal (a legal
question); and
• whether the person knew in the abstract that the act was wrong versus knew that
the specific behavior was wrong in a particular circumstance. For instance, someone
can know that killing people is wrong but, because of a mental illness, believe
that killing a particular person for a specific reason is justified: “He was the devil,
tempting me, so I had to kill him.”
Let’s examine how these issues about the insanity defense apply to Andrew
Goldstein, who pleaded not guilty by reason of insanity. At the trial, an eyewitness
to the murder, Ms. Lorenzino, who was standing nearby on the platform, testified
that she:
entered the subway station . . . just behind Mr. Goldstein and immediately noticed
that he was acting strangely. “I saw a man walking in front of me walking oddly,”
Ms. Lorenzino said. She said Mr. Goldstein would take a few “baby steps” on his “tip
toes” and then stumble. Mr. Goldstein then started walking normally, then paced furi-
ously back and forth on the southern end of the platform. He mumbled to himself and
eyed Ms. Lorenzino and Ms. Webdale, who was reading a magazine about six feet away
from Ms. Lorenzino, each time he passed them. . . .
As the wait for a train dragged on, Mr. Goldstein walked up to Ms. Lorenzino
and stood beside her, she said. “I felt very uncomfortable that he was standing next to
me. . . . I said, ‘What are you looking at?’ Then he backed off as if he was frustrated.”
Mr. Goldstein paced for a few more minutes, Ms. Lorenzino said, looked down the
track as if checking for a train and then walked down the platform to Ms. Webdale.
“Do you have the time? ” he asked her. Ms. Webdale glanced at her watch and an-
swered, “a little after five,” Ms. Lorenzino said. Mr. Goldstein then positioned himself
against the wall behind Ms. Webdale, who returned to her magazine, Ms. Lorenzino
said.
When the train sped into the station, she said, Mr. Goldstein “darted” off the wall
and violently pushed Ms. Webdale. Ms. Lorenzino said she was struck by how well-
planned the push seemed. It gave Ms. Webdale no time to escape. “It was perfect,” she
said, referring to the timing. Ms. Webdale’s body never hit the rails, she said, “she just
flew right under the train.”
Police Off icer Raymond McLoughlin, who also testif ied . . . said he arrived
at the station to find people shouting, “He’s right here! He’s right here!” He found
Mr. Goldstein, who made no effort to escape, sitting on the platform with his legs
crossed, surrounded by 20 enraged people who were berating him, he said.
(Rohde, 1999c)
After the murder, during Goldstein’s confession, the prosecutor tried to understand
whether Goldstein understood what he was doing—that is, whether his
mental illness caused him to lack a “substantial capacity” to know or appreciate “the
nature and consequence” of the attack or know that it was wrong. On the video-
tape, [the prosecutor] pointedly asks Mr. Goldstein if he thinks it was wrong to push
Ms. Webdale. Mr. Goldstein nods and then appears confused. The prosecutor asks him
if he understands. Mr. Goldstein says no, and then [the prosecutor] asks him again if he
thinks the attack was wrong. “I wasn’t thinking about anything when I pushed her,”
Mr. Goldstein said. “It’s like an attack. You don’t really think. . . . It’s like whoosh,
whoosh,” he added, referring to what he repeatedly described during the confession as
Ethical and Legal Issues 511
the sensation of a “spirit” or “ghost” entering his body that gave him an overwhelm-
ing desire to push, kick or shove. Mr. Goldstein says that he pushed Ms. Webdale
only “slightly,” but then seems confused again. He blurts out that “I didn’t push her
thinking she would end up on tracks,” and that he did not know in what direction he
was pushing Ms. Webdale.
Mr. Goldstein then says, “I wouldn’t push anyone onto the tracks.”
“Because you know it’s wrong?” [the prosecutor] asks.
“Yes,” Mr. Goldstein replies.
(Rohde, 1999a)
The prosecutor continues to try to clarify whether Goldstein understood that what
he had done to Webdale was wrong:
“But you knew,” says the interrogator, “that if you pushed her off the platform, she
might get . . .”
“Killed, yeah,” Mr. Goldstein says.
“And you also knew that if you did that, it would be the wrong thing to do?”
“Yeah, definitely,” Mr. Goldstein says. “I would never do something like that.”
“Well, you did.”
“I know, but the thing is I would never do it on purpose.”
Assessing Insanity for the Insanity Defense
How does a jury go about determining whether a defendant was insane at the
time a crime was committed? The members of a jur y rely on testimony about
the defendant’s mental state during the time leading up to the crime. Such testi-
mony may come from friends and family members or from witnesses. In Gold-
stein’s case, witnesses testif ied that he was acting strangely before pushing Ms.
Webdale in front of the train. Jurors may hear about a defendant’s histor y of
mental illness prior to the crime (as occurred for both Goldstein and Hinckley).
Expert witnesses who are mental health clinicians may give testimony or submit
reports.
How do mental health clinicians determine whether a defendant was insane at the
time a crime was committed? They may interview the defendant in jail and admin-
ister and interpret psychological tests (see Chapter 3). However, such after-the-fact
assessments of the defendant’s mental state should take into account events that oc-
curred after the crime and before the clinician’s evaluation. Specifically, the defen-
dant’s mental state may be affected by his or her experiences in jail, medications he
or she may be taking, decision to plead NGBI, reactions to the crime, coaching from
the defendant’s lawyer or other inmates, and even responses to various assessment
methods (Meyer & Weaver, 2006).
Past psychiatric history doesn’t necessarily indicate a person’s mental state at
the time he or she committed a crime, but a history of mental illness can provide
a context for evaluating the person at the time when the crime was committed. In
Goldstein’s case, symptoms of schizophrenia arose when he was 16 years old, and
he was committed to a state psychiatric facility when he was in college. Follow-
ing this stay, he had a lengthy history of mostly brief hospital stays, each one last-
ing only until he was “stabilized” (not actively psychotic); he was then released to
outpatient treatment. However, because of a lack of state funds for mental health
care, Goldstein’s outpatient treatment usually consisted of almost no treatment. For
most of the time he was ill, he did not have close supervision or monitoring and
did not reliably take his medication (Kleinfield & Roane, 1999). He would eventu-
ally deteriorate to the point where he needed to be hospitalized, was stabilized and
released again, and then the cycle would be repeated—a process often referred to as
a “revolving door.”
512 C H A P T E R 1 6
States’ Rights: Doing Away with the Insanity Defense
Some states have abolished the insanity defense, replacing it with another type of
defense that recognizes that a defendant did not have “free will” while committing a
crime (Meyer & Weaver, 2006). Two alternative options are:
• Diminished capacity, whereby a person, due to mental illness or defect, was less able
to understand that the criminal behavior was wrong or to formulate a specific
intention. With this defense, the person is still considered guilty but receives a
lesser sentence, is convicted of a lesser crime, or receives a modified form of pun-
ishment. This defense contains variations on the two elements of the ALI test of
insanity.
• Guilty but mentally ill, whereby a convicted defendant is found to be “responsible”
for the crime but often sent to a psychiatric facility and, if his or her mental state
improves over time, may also serve time in prison; alternatively, the defendant
may be sent to a prison immediately, where he or she may or may not receive
psychiatric care. Note that with “guilty but mentally ill,” the person isn’t acquit-
ted (that is, found not guilty of a crime), and there is no guarantee that mental
health services will be provided (Meyer & Weaver, 2006; Ogundipe & Shankar,
2013). In fact, in many states, prisoners who have been found guilty but mentally
ill receive no more psychological treatment than do other prisoners (Wrightsman
& Fulero, 2005).
C U R R E N T C O N T R O V E R S Y
Criminal Behavior: Does Abnormal
Neural Functioning Make It More
Excusable?
With advances in medical technology and neuroimaging, a
question of particular relevance to the justice system, clinical
psychology, and neuroscience has emerged (Yang et al., 2008):
Should individuals with abnormal neural functioning be held
less responsible for their criminal behavior than people with
normally functioning brains?
On one hand, neuropsychological evidence suggests that
disruptions in brain structure and function may be associated
w ith cr im ina l behav ior. For example, ind iv idua ls who
commit impulsive murders generally have reduced activity
in the prefrontal cortex (Raine et al., 1998). The prefrontal
cortex, along with other areas of the frontal lobe, is impor-
tant for impulse control and plays a key role in regulating
social behavior (Beer et al., 2006). Disruptions in the func-
tions of these brain areas have been observed in individuals
with antisocial personality disorder (see Chapter 13; Volkow
et al., 1995; Raine et al., 1997). In one case, for example, a
man’s tumor in part of the frontal lobe is believed to have
led to his criminal sexual behavior, which included reduced
sexual impulse control and pedophilia. He claimed that be-
fore his tumor he’d never engaged in such behavior; when
the tumor was removed, the aberrant sexual behavior stopped,
but it resurfaced when the tumor regrew less than a year later
(Burns & Swerdlow, 2003).
On the other hand, caution is needed when considering
the relationship between brain structure and behavior. First,
even seemingly simple behaviors are remarkably complex
from a neurological and cognitive standpoint; as such, it is
often diff icult and even irresponsible to claim that abnor-
mality of any single brain structure is the “cause” of abnor-
mal behavior. Also, although the findings from some studies
of individuals with antisocial personality disorder suggest
an association between structure and function, association
(that is, correlation) is not causation. This point is particu-
larly striking when we consider that although we usually
think that brain structure and function drive behavior, our
behavior can impact brain structure and function as well. For
example, drug abuse can produce harmful changes in neuro-
chemistry and brain structure (Rosenbloom et al., 2003), just
as cognitive and behavioral interventions can enhance neu-
ral function and lead to positive changes in brain structure
(Olesen et al., 2003).
CRITICAL THINKING If it turns out that criminal behavior can
be caused by disrupted neural functioning, how do you think
society should deal with criminals who have abnormal brains?
Should they be considered not guilty by reason of insanity?
(Meghana Karnik-Henry, Green Mountain College)
Ethical and Legal Issues 513
With the Insanity Defense, Do People Really “Get Away
with Murder”?
After the Hinckley trial, some people perceived the insanity defense as a way to
“get away with murder.” But as noted earlier, this perception isn’t very accurate.
Consider a landmark study of 9,000 felony cases across eight states from 1976
to 1987 (Steadman et al., 1993). Among those cases, only one quarter of 1% of
defendants were acquitted (that is, found not guilty of the crime). And of this
0.25% , only 7% —2 cases—were acquitted by a jur y rather than a judge. This
indicates that the defense of not guilty by reason of insanity was not very success-
ful. Researchers have also compared the average time spent in jail by defendants
who were found guilty (5 years) versus the average time spent in a mental hospital
by those who were found NGBI (4.7 years) and concluded that when the insan-
ity defense is used successfully, people do not “get away with murder” (Meyer &
Weaver, 2006).
After Committing the Crime: Competent to Stand Trial?
Whereas the insanity defense refers to a defendant’s mental state at the time the
crime was committed, his or her competency to stand trial is based on an
evaluation of mental state during the time leading up to the trial. That is, does a
mental defect or disorder prevent the defendant from participating in his or her own
defense? Competency to stand trial usually entails being able to:
• understand the proceedings that will take place,
• understand the facts in the case and the legal options available,
• consult with his or her “lawyer with a reasonable degree of rational understanding”
(Dusky v. United States, 1960), and
• assist the lawyer in building the defense.
With this a l l-or-nothing standard, Goldstein was found competent to stand
trial.
The same all-or-nothing standard is used to determine whether a defendant is
competent to plead guilty as well as competent to waive the right to an attorney (Godinez v.
Moran, 1993; Perlin, 2000a). If a person is found not competent to stand trial, he or
she would also be considered to be not competent to plead guilty or to waive the
right to an attorney. Someone who is found not competent is referred for mental
health treatment (Dusky v. United States, 1960). Case 16.2 examines the issue of com-
petency to stand trial and waive counsel.
CASE 16.2 • FROM TH E OUTSIDE: Competent to Stand Trial and
Waive Counsel
On December 7, 1993, Colin Ferguson intentionally killed 6 people and injured 19 others on a
New York commuter train. After his arrest, Ferguson was diagnosed with paranoid personality
disorder. Because he was assessed as rational and not delusional, he was deemed competent
to stand trial; he fired his attorney when the attorney stated that he would propose an
insanity defense. Ferguson then chose to represent himself but did not use the insanity
defense. The legal system allowed a mentally ill man to be his own legal counsel, although
he did not defend himself adequately. Those following the trial witnessed an intelligent but
clearly mentally ill man state that he would call as a witness an exorcist who would testify
that a microchip—supposedly planted by the governor of New York—had been lasered out
of Ferguson’s head by a remote control device (McQuiston, 1995; Perlin, 2000a). That witness
was never called to the stand.
Ferguson was convicted on 6 counts of murder and 19 counts of attempted murder.
Competency to stand trial
The determination that a defendant’s mental
state during the time leading up to the trial
enables him or her to participate in his or her
own defense.
514 C H A P T E R 1 6
When defendants are found not competent to stand trial, they sometimes are
medicated to reduce the symptoms of their mental illness and make them able to
stand trial. Occasionally, defendants do not want to take the medication but are
given it against their will, perhaps by injection. However, the Supreme Court ruled
that mentally ill patients accused of nonviolent crimes could not be forced to take
medication in order to become competent to stand trial (Sell v. United States, 2003).
If it appears unlikely that a person will become competent to stand trial, he or she
may be civilly committed to a psychiatric facility if deemed a danger to self or
others.
Jon has been arrested for disturbing the peace and destroying private property; at 2 A.M. last
night, he was yelling and kicking over trash cans on Main Street, and he broke several store
windows. His rant went on for 25 minutes, until the police arrived. Jon initially resisted arrest
and then cooperated. It seemed to the police that Jon was behaving as if he were having a
manic episode, and, in fact, he had a history of bipolar disorder. How might mental health
clinicians and the legal system go about determining whether Jon was “insane” at the time
of the crime? What information would you want to know in order to determine whether he
was insane? What if, rather than a history of bipolar disorder, Jon had a history of alcohol
use disorder and was drunk the night of the crime. Would that change your opinions? Why
or why not?
Thinking Like A Clinician
Dangerousness: Legal
Consequences
Andrew Goldstein’s attack on Kendra Webdale wasn’t the first time he had engaged
in dangerous behavior, and his dangerous behavior wasn’t a secret:
In the two years before Kendra Webdale was instantly killed on the tracks, Andrew
Goldstein attacked at least 13 other people. The hospital staff members who kept
treating and discharging Goldstein knew that he repeatedly attacked strangers in public
places.
He was hospitalized after assaulting a psychiatrist at a Queens clinic. [The clinic
note from November 14, 1997, reads]: “Suddenly, without any warning, patient springs
up and attacks one of [the] doctors, pushing her into a door and then onto the floor.
He was hospitalized after threatening a woman, [again] after attacking two strangers
at a Burger King [and yet again] after fighting with an apartment mate.” [A note from
March 2, 1998, says]: “Broke down roommate’s door because he could not control the
impulse.” And particularly chilling, six months before Kendra Webdale’s death, he was
hospitalized for striking another woman he did not know on a New York subway.
(Winerip, 1999a)
Goldstein’s histor y indicates that he had become dangerous. Dangerousness,
a legal term, refers to someone’s potential to harm self or others. Determining
whether someone is dangerous, in this sense, rests on assessing threats of violence
to self or to others, or establishing an inability to care for oneself. Dangerousness
can be broken down into four components regarding the potential harm (Brooks,
1974; Perlin, 2000c):
1. severity (how much harm might the person inflict?),
2. imminence (how soon might the potential harm occur?),
3. frequency (how often is the person likely to be dangerous?), and
4. probability (how likely is the person to be dangerous?)
A
P
P
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o
to
/G
e
o
rg
e
Fr
ey
, P
o
o
l
In 2002, while suffering from delusions, Brian
David Mitchell kidnapped young Elizabeth
Smart. He was apprehended 9 months later
(Smart was found alive and returned to her
parents) and continued to have delusions. In
2009, he had yet to be found competent to
stand trial. A judge had ruled against forcing
Mitchell to take medication in order to be
competent to stand trial because the judge did
not believe that the treatment would succeed
(Carlisle, 2009). In 2010, he was found guilty.
Dangerousness
The legal term that refers to someone’s
potential to harm self or others.
Ethical and Legal Issues 515
Evaluating Dangerousness
Clinicians are sometimes asked to evaluate how dangerous a patient may be— specifically,
the severity, imminence, and likelihood of potential harm (McSherry & Keyzer, 2011;
Meyer & Weaver, 2006). Such evaluations are either/or in nature—the individual is
either deemed not to be dangerous (or at least not dangerous enough to violate confi-
dentiality) or deemed to be dangerous, in which case, confidentiality is broken or the
patient remains in a psychiatric facility in order to protect the individual from self-harm
or to protect others (Otto, 2000; Quattrocchi & Schopp, 2005). Prior to each discharge
from a hospital or psychiatric unit, Goldstein had to be evaluated for dangerousness; he
was then discharged because he was deemed not dangerous, or not dangerous enough.
Researchers set out to determine the risk factors that could best identify which
patients discharged from psychiatric facilities would subsequently act violently.
A summary of the findings appears in Table 16.3.
Confining people who are deemed to be dangerous involves taking away their
liberty—their freedom—and is not done lightly. Loitering or yelling at “voices”
should not be considered legally dangerous. Rather, the legal system allows a person
to be incarcerated or hospitalized, or to continue to be incarcerated or hospitalized,
in only two types of situations:
1. when the person has not yet committed a violent crime but is perceived to be at
imminent risk to do so, or
2. when the person has already served a prison term or received mandated treat-
ment in a psychiatric hospital and is about to be released but is perceived to be at
imminent risk of behaving violently.
To prevent such people from harming themselves or others, the law provides that
they can be confined as long as they continue to pose a significant danger.
Actual Dangerousness
Although we have focused on the relationship between some forms of mental illness
and violence, as occurred with Goldstein, most mentally ill people are not violent.
Mentally ill people who engage in criminal acts receive a lot of media attention,
which may give the impression that the mentally ill commit more crimes than they
really do (Pescosolido et al., 1999). In fact, criminal behavior among the mentally ill
population is no more common than it is in the general population (Fazel
& Grann, 2006). Indeed, when mentally ill people are in jail or prison, it
is usually for minor nonviolent offenses related either to trying to survive
(e.g., stealing food) or to substance abuse—the mental illness usually is not a
direct cause of the incarceration (Hiday & Wales, 2003).
However, two sets of circumstances related to mental illness do increase
dangerousness: (1) when the mental illness involves psychosis, and the per-
son may be a danger to self as well as others (Fazel & Grann, 2006; Wallace
et al., 2004)—particularly when delusions lead the mentally ill person to
be angry (Coid et al., 2013), and especially (2) when serious mental illness
is combined with substance abuse (Howsepian, 2011; Maden et al., 2004).
The relationship between various major mental illnesses, substance use dis-
orders, and violence is shown in Figure 16.1.
Confidentiality and the Dangerous Patient:
Duty to Warn and Duty to Protect
In the 1960s, University of California college student Prosenjit Poddar liked fel-
low student Tatiana Tarasoff. However, his interest in her was greater than was
hers in him. He became depressed by her rejection and began treatment with a
TABLE 16.3 • Major Risk Factors for a
Patient to Act Violently
Patient’s Prior Arrests
• More serious crimes
• Greater frequency of crimes
Patient Experienced Child Abuse
• Experienced more serious abuse
• Experienced greater frequency of abuse
Patient’s Father . . .
• Used drugs
• Was absent during patient’s childhood
Patient’s Demographics
• Younger
• Male
• Unemployed
Patient’s Diagnosis
• Antisocial personality disorder
Other Clinical Information About
Patient
• Has substance abuse problems
• Has problems controlling anger
• Has violent fantasies
• Has had loss of consciousness
• Has been brought to the attention of
mental health professionals involuntarily,
through the legal system
Source: Monahan et al., 2001. For more information see
the Permissions section.
A
d
a
m
S
y
lv
e
st
e
r/
P
h
o
to
R
e
se
a
rc
h
e
rs
, I
n
c.
Although some people with mental illness may
create a public nuisance, like this man yelling at
voices that only he can hear, such public displays
are not dangerous and should not, in and of
themselves, lead to hospitalization (Perlin, 2000c).
516 C H A P T E R 1 6
psychologist. During the course of his treatment, his therapist became concerned
that Mr. Poddar might hurt or kill Ms. Tarasoff. (Poddar had purchased a gun
for that purpose.) The therapist informed campus police that Poddar might harm
Tarasoff. The police briefly restrained him, but they determined that he was ratio-
nal and not a threat to Tarasoff. Ms. Tarasoff was out of the country at the time, and
neither she nor her parents were alerted to the potential danger. Two months later,
Poddar killed Tarasoff.
Her parents sued the psychologist, saying that Tarasoff should have been pro-
tected either by warning her or by having Poddar committed to a psychiatric fa-
cility. In what has become known as the Tarasoff rule, the Supreme Court of
California (and later courts in other states) ruled that psychologists have a duty
to protect potential victims who are in imminent danger (Tarasoff v. Regents of the
University of California, 1974, 1976). This rule has been extended to other mental
health clinicians.
Mental health professionals who decide that a patient is about to harm a specific
person can choose to do any of the following (Quattrocchi & Schopp, 2005):
• warn the intended victim or someone else who can warn the victim,
• notify law enforcement agencies, or
• take other reasonable steps to prevent harm (depending on the situation), such as
having the patient voluntarily or involuntarily committed to a psychiatric facility
for an extended evaluation (that is, have the patient confined).
The Tarasoff rule effectively extended a clinician’s duty to warn of imminent harm
to a duty to protect (Werth et al., 2009). The clinician must violate confidentiality in
order to take reasonable care to protect an identifiable—or reasonably foreseeable—
victim (Brady v. Hopper, 1983; Cairl v. State, 1982; Egley, 1991; Emerich v. Philadelphia
Center for Human Development, 1998; Schopp, 1991; Thompson v. County of Alameda,
1980). Note, however, that potential danger to property is not sufficient to compel
clinicians to violate confidentiality (Meyer & Weaver, 2006).
0
10
20
30
40
50
P
re
va
le
n
ce
o
f
vi
o
le
n
ce
(
p
er
ce
n
ta
g
e)
No major
psychological
disorder
Schizophrenia,
bipolar disorder,
or major
depressive
disorder
Substance
use
disorders
only
Major
psychological
disorder and
substance abuse
FI G U RE 16.1 • Lifetime Prevalence of Violent Behavior Substance use disorders
(with or without a comorbid major psychological disorder) are associated with a much higher
rate of violent behaviors (such as the use of a weapon in a fight or coming to blows with another
person) than is observed in the general population (Swanson, 1994).
Source: Monahan et al., 1994. For more information see the Permissions section.
Tarasoff rule
A ruling by the Supreme Court of California
(and later other courts) that psychologists
have a duty to protect potential victims who
are in imminent danger.
Ethical and Legal Issues 517
Maintaining Safety: Confining the Dangerously
Mentally Ill Patient
A dangerously mentally ill person can be confined via criminal commitment or civil
commitment.
Criminal Commitment
Criminal commitment is the involuntary commitment to a mental health facility
of a person charged with a crime. This can happen before trial or after trial:
• If the defendant hasn’t yet had a trial, the time at the mental health facility is used to
evaluate whether he or she is competent to proceed with the legal process (for
instance, is the defendant competent to stand trial?) and
provide treatment so that the defendant can become competent to participate in
the legal proceedings.
• If the defendant has had a trial and was acquitted due to insanity (Meyer & Weaver, 2006).
Based on a 1972 ruling ( Jackson v. Indiana, 1972), it is illegal to confine someone
indefinitely under a criminal commitment. Thus, a defendant found not competent
to stand trial cannot remain in a mental health facility for life. But the law is unclear
as to exactly how long is long enough. Judges have discretion about how long they
can commit a defendant to a mental health facility to determine whether treatment
may lead to competence to stand trial. Such treatment may last several years. If the
defendant does not become competent, he or she may not remain committed for the
original reason—to receive treatment in order to become competent. In this case,
the process of deciding whether he or she should be released from the mental health
facility proceeds just as it does for anyone who hasn’t been criminally charged. If the
individual is deemed to be dangerous, however, he or she may be civilly committed.
Civil Commitment
When an individual hasn’t committed a crime but is deemed to be at significant risk
of harming himself or herself, or of harming a specific other person, the judicial
system can confine that individual in a mental health facility, which is referred to as a
civil commitment. This is the more common type of commitment.
There are two types of civil commitment: (1) inpatient commitment to a 24-hour
inpatient facility, and (2) outpatient commitment to some type of monitoring and/
or treatment program (Meyer & Weaver, 2006). Civil commitment grows out of the
idea that the government can act as a caregiver, functioning as a “parent” to people
who are not able to care for themselves; this legal concept is called parens patriae.
Civil commitments can conflict with individual rights, so guidelines have been
created to protect patients’ rights by establishing the circumstances necessary for an
involuntary commitment, the duration of such a commitment—and who decides
when it ends—as well as the right to refuse a specific type of treatment or treatment
in general (Meyer & Weaver, 2006). It may seem that civil commitments are always
forced or coerced, but that is not so. Some civil commitments are voluntary (that is,
the patient agrees to the hospitalization); however, some “voluntary” hospitalizations
may occur only after substantial coercion (Meyer & Weaver, 2006).
Many people who are civilly committed belong to a subset of the mentally ill
population—those who are overrepresented in the revolving door after their release
that leads to jails or hospitals. This revolving door evolved because lawmakers and
clinicians wanted a more humane approach to dealing with the mentally ill, by treat-
ing them in the least restrictive setting—before their condition deteriorates to the
point where they harm themselves or others (Hiday, 2003).
Criminal commitment
The involuntary commitment to a mental
health facility of a person charged with a
crime.
Civil commitment
The involuntary commitment to a mental
health facility of a person deemed to be at
significant risk of harming himself or herself or
a specific other person.
518 C H A P T E R 1 6
Mandated Outpatient Commitment
Mandated outpatient commitment developed in the 1960s and 1970s, along with
increasing deinstitutionalization of patients from mental hospitals; the goal was to
develop less restrictive alternatives to inpatient care (Hiday, 2003). Such outpatient
commitment may consist of legally mandated treatment that includes some type of
psychotherapy, medication, or periodic monitoring of the patient by a mental health
clinician. The hope is that mandated outpatient commitment will preempt the
“revolving door” cycle that occurs for many patients who have been committed:
(1) getting discharged from inpatient care, (2) stopping their medication, (3) becom-
ing dangerous, and (4) ending up back in the hospital through a criminal or civil
commitment or landing in jail.
Researchers have investigated whether mandated outpatient commitment is
effective: Are the patient and the public safer than if the patient was allowed to obtain
voluntary treatment after discharge from inpatient care? Does mandated outpatient
treatment result in less frequent hospitalizations or incarcerations for the patient?
To address these questions, one study compared involuntarily hospitalized patients
who either were invited to use psychosocial treatment and services voluntarily upon
discharge or who were court-ordered to obtain outpatient treatment for 6 months—
and made frequent use of services (between 3 and 10 visits/month) (Hiday, 2003;
Swartz et al., 2001). The results indicated that those who received mandated outpa-
tient treatment:
• went back into the hospital less frequently and for shorter periods of time,
• were less violent,
• were less likely to be victims of crime themselves, and
• were more likely to take their medication or obtain other treatment, even after the
mandated treatment period ended.
Other studies have found similar benef its of mandated outpatient commitment
(Hough & O’Brien, 2005). That said, it is also clear that mandated outpatient com-
mitment is not effective without adequate funding for increased therapeutic services
(Perlin, 2003; Rand Corporation, 2001). In what follows we examine what happens
without adequate funding.
The Reality of Treatment for the Chronically Mentally Ill
Andrew Goldstein generally wanted to be hospitalized and repeatedly tried to make
that happen:
He signed himself in voluntarily for all 13 of his hospitalizations. His problem was
what happened after discharge. The social workers assigned to plan his release knew
he shouldn’t have been living on his own, and so did Goldstein, but everywhere they
looked they were turned down. They found waiting lists for long-term care at state
hospitals, waiting lists for supervised housing at state-financed group homes, waiting
lists for a state-financed intensive-case manager, who would have visited Goldstein
daily at his apartment to make sure he was coping and taking his meds.
More than once he requested long-term hospitalization at Creedmoor, the state hospi-
tal nearby. In 1997, he walked into the Creedmoor lobby, asking to be admitted. “I want
to be hospitalized,” he said. “I need a placement.” But in a cost-cutting drive, New York
[had] been pushing hard to reduce its patient census and to shut state hospitals. Goldstein
was instead referred to an emergency room, where he stayed overnight and was released.
Again, in July 1998, Goldstein cooperated with psychiatrists, this time during
a month-long stay at Brookdale Hospital, in hopes of getting long-term care at
Creedmoor. Brookdale psychiatrists had a well-documented case. In a month’s time,
Goldstein committed three violent acts: punching the young woman on the subway;
attacking a Brookdale therapist, a psychiatrist, a social worker and a ward aide; striking
a Brookdale nurse in the face. This time, Creedmoor officials agreed in principle to
Ethical and Legal Issues 519
take him, but explained that there was a waiting list, that they were under orders to
give priority to mental patients from prison and that they did not know when they
would have an opening. Days later, Goldstein was discharged from Brookdale.
(Winerip, 1999a)
Not only was Goldstein underserved by the mental health system, but so was the
public at large. When appropriate services were available to him, Goldstein made
good use of them. He spent a year in a residential setting on the grounds of the state
hospital—he did well, was cooperative and friendly, and regularly took his medi-
cations. But personnel at state hospitals are under pressure to move patients to less
expensive programs, even if the patients aren’t ready. Goldstein was considered too
low-functioning to qualify for a program that provided less supervision, but he was
discharged from the residential program nonetheless—to a home where he received
almost no support. A year before the murder he tried, without success, to return to a
supervised group but no spaces were available (Winerip, 1999a).
Goldstein’s history with the mental health system in New York is not unique.
People with severe mental illness generally don’t receive the care they need (which
is also in society’s interest for them to receive) unless their families are wealthy
and willing to pay for needed ser vices—long-term hospitalization, super vised
housing, or intensive daytime supervision. Even when a defendant is deemed to be
mentally ill and ordered to be transferred to a psychiatric facility, space may not
be available in such a facility; the options then are to hold the defendant in jail or
to release him or her and provide a less intensive form of mental health treatment
(Goodnough, 2006).
As discussed in Chapter 12, deinstitutionalization is a reasonable option for those
who can benefit from newer, more effective treatments, and providing treatment in
the least restrictive alternative setting is also a good idea. However, such community-
based forms of care are not adequately funded, which forces facilities to prioritize
and provide treatment only to the sickest, leaving everyone else to make their own
way. Thus, most people with severe mental illness lack adequate supervision, care,
or housing. They may be living on their own in tiny rented rooms, on the street, in
homeless shelters that are not equipped to handle mentally ill people, or they may be
in jail. The law may mandate treatment for severely mentally ill individuals, but that
doesn’t mean they receive it.
After the murder of Kendra Webdale, New York State passed Kendra’s law,
allowing family members, roommates, and mental health clinicians to request court-
mandated outpatient treatment for a mentally ill person who refuses treatment; a
judge makes the final decision about mandating treatment. The unfortunate irony is
that Goldstein sought further treatment. In his case, the real culprit may have been
the lack of resources to provide the type of support and services that he and others
like him—such as David Tarloff, described in Case 16.3—need.
CASE 16.3 • FROM THE OUTSIDE: A Failed Mandated Outpatient Treatment
On February 12, 2008, David Tarloff murdered psychologist Kathryn Faughey and injured
psychiatrist Kent Shinbach in a delusional plan to steal money to fly to Hawaii with his
elderly mother. Tarloff, who had been a patient of Shinbach, was hospitalized over a
dozen times since 1991, when he was diagnosed with paranoid schizophrenia. In the year
leading up to the murders, Tarloff received psychiatric care three times after violent or
threatening behavior; he was stabilized on medication and released, despite his family’s
request for continued inpatient treatment. After release each time, he stopped taking his
medication. His family even made use of Kendra’s law, so that Tarloff was supposed to
receive mandated outpatient treatment, but he avoided the periodic outpatient visits. He
was released from a psychiatric unit 10 days before he murdered Faughey.
(Konigsberg & Farmer, 2008).
Ja
m
e
s
K
ei
vo
m
/N
Y
D
a
il
y
N
e
w
s
A
rc
h
iv
e
vi
a
G
e
tt
y
I
m
ag
e
s
Eight months after David Tarloff committed
murder, the judge hearing the case declared
Tarloff unfit to stand trial. Tarloff was sent to a
psychiatric facility (Eligon, 2008). His 2013 trial
was declared a mistrial because the jury was
deadlocked about whether he was not guilty
by reason of insanity (Buettner & Goodman,
2013). In prison, he awaits a new trial.
520 C H A P T E R 1 6
Sexual Predator Laws
People who are repeat sexual offenders—often referred to as sexual predators—are
clearly dangerous. How do they fit into the legal concept of dangerousness? Are they
to be treated as mentally ill? How do the criminal justice and mental health systems
view such individuals?
The answers to these questions have evolved over time. Before the 1930s, a sexual
offense was viewed as a criminal offense: The perpetrator was seen as able to control
the behavior although he or she didn’t do so. In the 1930s, sexual offenses were
viewed as related to mental illness (sexual psychopaths), and treatment programs for
those who committed such offenses proliferated. Unfortunately, the treatments were
not effective. By the 1980s, sexual offenses were again seen as crimes for which prison
sentences were appropriate consequences. In the 1990s, after highly publicized cases
of sexual mutilation and murder of children, some states passed additional laws to deal
with sexually violent predators, who were seen as having no or poor ability to control
their impulses. Rather than emphasizing treatment (which had not been effective),
the new laws called for incarcerating these individuals as a preventative measure.
In 1997, the Supreme Court upheld the constitutionality of state laws regard-
ing sexual predators (Kansas v. Hendricks, 1997); these laws are based on the concept
of parens patriae, under which the government, as “parent,” has the power to protect
the public from threats, as well as the duty to care for those who cannot take care
of themselves (Perlin, 2000c). These laws were intended to prevent sex offenders
from committing similar offences, in some cases by ensuring that offenders do not
reenter society while there is a significant risk that they will reoffend. At the end of
a prison term, if a sexual predator was deemed likely to reoffend and was suffering
from a mental abnormality or personality disorder, that person could be committed
to a psychiatric hospital indefinitely (Tucker & Brakel, 2012; Winick, 2003). In 2010,
the Supreme Court extended such civil commitments to sexually violent predators in
federal custody (United States v. Comstock, 2010).
However, some people viewed such laws as too restrictive, and in 2002, the
Supreme Court ruled that in order to commit a sexual offender indefinitely after a
jail or prison sentence has been served, it must be demonstrated that the person has
difficulty controlling the behavior (Kansas v. Crane, 2002; the Supreme Court did
not say how to demonstrate this, other than pointing to the individual’s past history).
In prison, treatment is voluntary, whereas with commitment it is mandatory.
Thinking Like A Clinician
Tyrone was diagnosed with schizoaffective disorder when he was 25; his mother couldn’t su-
pervise and take care of him to the extent that he needed. Cutbacks in mental health services
in his community meant that he couldn’t receive adequate services outside of a hospital. By
age 30, he was living on the streets or in jail for petty crimes such as stealing food from a
grocery store, and he’d been treated for brief periods in a psychiatric facility. Based on what
you have read, do you think Tyrone is dangerous—why or why not? Suppose, during psy-
chotic episodes, he darts across busy streets—causing car accidents as drivers quickly brake
to avoid hitting him. Would he legally be considered dangerous then—why or why not? What
would be the advantages and disadvantages to him, and to society, of committing him to
inpatient treatment? To outpatient treatment?
Legal Issues Related to Treatment
In the 1960s and 1970s, the courts decided several landmark cases regarding the
rights of the mentally ill. These cases addressed the right to treatment and the right
to refuse treatment.
Ethical and Legal Issues 521
Right to Treatment
In 1966, the Supreme Court ruled that people who are forced to receive treatment
through civil commitment should be given the least restrictive alternative treatment
available (Lake v. Cameron). That is, they should have the type of treatment that in-
fringes the least on their individual liberties. If a person doesn’t need the 24-hour
monitoring and care of an inpatient unit, that person should be treated in a less re-
strictive environment (such as in a residential setting and with outpatient treatment).
One year after this ruling, the Supreme Court ruled that civil commitment
must entail more than warehousing or conf ining people; the Court ruled that
appropriate treatment must also be provided, while recognizing that treatment
might not necessarily be successful (Rouse v. Cameron, 1967). In subsequent cases
during the 1970s, courts in various jurisdictions outlined specific minimal criteria
for such treatment—including the minimum staffing ratio (number of patients per
care provider) and number of hours per week of treatment, as well as the need for
each patient to have an individualized treatment plan (Wyatt v. Stickney, 1971). The
specifics of these requirements differ from jurisdiction to jurisdiction.
The Supreme Court also ruled that civil commitment may not be used simply to
confine people against their will indefinitely (except as previously noted with some
sexual predators). When patients no longer meet the criteria for commitment (that
is, they are no longer dangerous) and can survive independently or with help from
willing family members, then they must be discharged (O’Connor v. Donaldson, 1975).
The reasoning behind this ruling is that the purpose of the confinement is treatment,
and so when inpatient treatment is no longer required, the person should be released.
Right to Refuse Treatment
A federal district court in New Jersey set another standard when it ruled that a civilly
committed patient has the right to refuse treatment (Rennie v. Klein, 1978). Generally,
this ruling has been applied to a patient’s right to refuse to take medications, most
frequently traditional antipsychotics that carry the risk of a serious side effect called
tardive dyskinesia (see Chapter 12) (Perlin, 2000b). However, the court did not estab-
lish the right to refuse treatment in all situations. As long as there has been a fair and
adequate hearing of the issues involved for a given patient, his or her refusal can be
overridden after weighing certain factors (Meyer & Weaver, 2006):
• the patient is physically threatening to others (which may include patients and staff
members),
• the proposed treatment carries only a small risk of irreversible side effects,
• there are no less restrictive treatment alternatives available, and
• the patient has significantly diminished capacity to decide rationally about particu-
lar treatments
Competence to Refuse Treatment
One of the acceptable circumstances for overriding a committed patient’s refusal of
a treatment is that he or she does not have the capacity to decide rationally about
treatment. Being competent to refuse treatment is different from being competent to
stand trial, although both competencies involve some of the same mental processes
and abilities. Does being mentally ill imply that a person cannot make rational deci-
sions? One study that investigated the general question of competence to refuse treat-
ment (Appelbaum & Grisso, 1995; Grisso & Appelbaum, 1995) found that about half
of patients with schizophrenia performed reasonably well on several tasks assessing
522 C H A P T E R 1 6
their ability to make decisions. Not surprisingly, the more severe the symptoms the
less well they performed on the tasks. An even greater proportion of patients hospi-
talized for depression—about 75% —performed adequately on the tasks that assess
decision making. Unlike the patients with more severe symptoms of schizophrenia,
patients with more severe depression were generally competent to make decisions.
Thus, having a severe mental illness did not routinely make these patients “not com-
petent to refuse treatment.” (Note though that while some individuals who receive
outpatient commitment may be competent to refuse treatment, the law may not al-
low them to refuse.)
Mental Health and Drug Courts
Federal, state, and local court dockets are filled with cases awaiting a hearing or trial.
In order to hasten the speed with which cases are resolved, municipalities have insti-
tuted specialized courts, such as divorce courts, to address particular types of prob-
lems. Two such special courts are particularly relevant to the mentally ill: drug courts
and mental health courts.
Drug courts were developed in Miami in 1989 for first-time drug abusers—
those whose substance abuse was viewed as the underlying motivation for their crime
( Miethe et al., 2000). Soon after arrest, these people were offered an alternative to
jail: They could attend a drug treatment program, submit to random and frequent
drug testing by urinalysis, and meet with the drug court judge regularly. If they did
not show up for a court hearing, a bench warrant would be issued within hours and
they could be sent to jail.
The overall goal of drug courts is to help defendants reintegrate into society.
Thus, drug courts not only promote intensive treatment for drug abuse and relapse
prevention—they also encourage education and employment. Drug court programs
do not simply aim to decrease substance abuse; they recognize the complex nature of
the factors that contribute to such abuse.
Relapse rates are between 4% and 20% for those entering a program and even
lower (less than 4%) for those who complete one. Many com-
munities have extended drug court programs to include peo-
ple who were previously jailed for substance abuse– related
crimes, with equivalent success (Drug Court Clearinghouse
and Technical Assistance Project, 1998).
The success of drug courts led to the development of
mental health courts, which began in Florida and now exist
in most states, but not necessarily in most districts (Coun-
cil of State Governments, 2005). Mental health courts seek
to treat, rather than incarcerate, mentally ill people who are
charged with a misdemeanor. When mentally ill people re-
ceive treatment, they are subsequently less likely to become
violent or to reoffend (Dirks-Lindhorst & Linhorst, 2012;
Hiday & Ray, 2010).
Thinking Like A Clinician
Ella is in the throes of a psychotic episode and is in the hospital. At times, she feels bugs
crawling under her skin, and so she viciously scratches herself until she bleeds. At other times,
she thinks she has superpowers and can fly—if there were an open window, she’d jump out of
it. Her psychiatrist has prescribed an antipsychotic medication, but she won’t take it: “I don’t
like the way it makes me feel.” Based on what you have read, do you think Ella has the right to
refuse treatment? Why or why not?
Drug courts recognize that maintaining
abstinence can depend on a complex interplay
of factors, such as educational opportunities
and employment.
Jo
h
n
S
u
n
d
lo
f/
A
la
m
y
Ethical and Legal Issues 523
The Wheels of Justice: Follow-up
on Andrew Goldstein
The jury that heard Andrew Goldstein’s case was deadlocked—some jurors voted
to convict and some voted him not guilty by reason of insanity. The deadlocked
jury meant that another trial was necessary. This time, with Goldstein’s permis-
sion, his lawyers took him off his medication several weeks before he was to testify
so that jurors could see the extent of his mental illness. However, his mental state
at the time of trial could not be used to determine his mental state at the time he
committed the crime. This strategy was very controversial, and the judge allowed
it, provided that Goldstein be asked daily whether he wanted to receive medica-
tion and that he be given medication forcibly if he appeared to become not com-
petent to stand trial (Rohde, 2000). Goldstein hit his social worker within several
weeks of stopping his medication, which meant that he resumed taking it and did
not take the stand. The jury found Goldstein guilty, although they acknowledged
that he was mentally ill. They decided that he knew what he was doing when he
threw Kendra Webdale onto the tracks, and that he knew it was wrong.
After his trial, Goldstein was sent to prison, where he was evaluated to deter-
mine whether he needed to be admitted to a psychiatric hospital to become stable.
If so, once stable, he would be returned to prison. In such cases, hospitalizations are
brief, only long enough to get the defendant well enough to return to prison. In
2006, 8 years after the murder, Goldstein’s conviction was overturned because of a
technical misstep during the second trial. In a third trial, Goldstein’s lawyers entered
a plea of guilty, with the understanding that he would serve 23 years in prison, fol-
lowed by 5 years of psychiatric oversight and supervision after his release.
SUMMING UP
Ethical Issues
• Each type of mental health professional
works under his or her discipline’s ethical
code; all disciplines include in their ethical
code the principle of confidentiality, which
applies to information that patients share
with mental health professionals.
• Because of HIPA A, the lim its of con-
f identialit y have been redef ined. Now
limited information about a patient may
be shared with the patient’s other health
providers in order to facilitate treatment.
• Although laws protect confidentiality, confi-
dentiality may be violated against a patient’s
wishes when a clinician has reasonable cause
to: (1) suspect abuse of children, the elderly,
or the disabled, or (2) believe that a patient
is likely to do significant harm to himself or
herself or a specified other person.
• T he leg a l cou nter pa r t of t he et h ica l
principle of confidentiality is privileged
communication—the protection of confi-
dential information from disclosure dur-
ing legal proceedings.
Criminal Actions and Insanity
• Var ious tests have been used to deter-
mine whether a defendant is insane. The
f irst was the M’Naghten test in 1843,
followed by the irresistible impulse test.
After almost 70 years came the Durham
test. Many states presently use the Ameri-
can Legal Institute (ALI) test, which re-
quires either impaired knowledge that the
behavior was wrong (cognition) or im-
paired capacity to resist the impulse to act
illegally (volition). The Insanity Defense
Reform Acts of the 1980s did away with
the volition element to determine insanity
in federal courts.
• To assess insanity, a jury may rely on tes-
timony about the defendant’s mental state
during the time leading up to the crime,
the defendant’s history of mental illness
prior to the crime, and testimony or re-
ports from expert witnesses about the de-
fendant’s mental state or mental illness.
• Menta l hea lth cl in icians may a ssess a
defendant’s san it y through inter v iews
with the person, psychological tests and
questionnaires, and interviews with fam-
ily members and friends. However, such
measures may be affected by the defen-
dant’s exper iences in jail, medications
he or she may be taking, the decision to
plead not guilty by reason of insanity, re-
actions to the crime, coaching from the
defendant’s lawyer or other inmates, and
the way the defendant responds to vari-
ous assessment methods. But none of this
information necessarily indicates the de-
fendant’s mental state at the time of the
crime.
• Research indicates that acquittal on the
basis of the insanity defense is extremely
rare, particularly when the decision is
made by a jury rather than a judge.
• Competency to stand trial addresses the
defendant’s mental state before the trial
and whether the defendant is competent
to participate in his or her own defense;
someone who is not competent to stand
trial would also be deemed not competent
to plead g ui lt y and not competent to
waive the right to an attorney.
524 C H A P T E R 1 6
Dangerousness: Legal Consequences
• Dangerousness has four components re-
lated to the potential harm the person
may inf lict: sever it y, im m inence, fre-
quency, and probability.
• Mental health clinicians have a legal duty
to warn and to protect specified potential
victims who are judged to be in imminent
danger of being harmed by a patient. A
clinician may warn the intended victim,
notify law enforcement agencies, and/or
take other reasonable steps, such as having
the patient confined to a psychiatric facil-
ity. Clinicians may violate confidentiality
to fulfill these duties.
• Cr im inal com m itment may occur be-
fore a defendant’s tr ial to evaluate his
or her competence for upcoming legal
proceedings or to obtain treatment for the
defendant so that he or she can become
competent to take part in legal proceed-
ings. When criminal commitment occurs
after a trial, it is because the defendant
was acquitted for the reason of insanity.
• Civil commitments occur before a crime
has been committed, in order to prevent
harm to the patient or others deemed to
be at signif icant risk of harm. Patients
may be committed to inpatient or outpa-
tient facilities.
Legal Issues Related to Treatment
• The Supreme Court has ruled that peo-
ple who are civil ly com m itted should
be given the least restrictive alternative
treatment available. Civil commitments
may not be used solely to confine people
against their will indefinitely.
• Patients usual ly have a r ight to refuse
treatment, such as medication. However,
patients who have physically threatened
other people may be forced to take medi-
cation or receive other treatment, as long
as there has been a fair and adequate hear-
ing of the issues involved.
• Defendants may be sent to drug courts if
their drug use was the underlying motiva-
tion for the crime; such courts have been
successful in decreasing rates of relapse
and reoffending.
• Mental health courts can mandate treat-
ment for mental ly il l defendants; such
programs have been found to decrease
violence and subsequent offences.
Confidentiality (p. 504)
Privileged communication (p. 506)
Criminally responsible (p. 508)
M’Naghten test (or rule) (p. 508)
Irresistible impulse test (p. 508)
Durham test (p. 509)
American Legal Institute test (ALI test) (p. 509)
Competency to stand trial (p. 514)
Dangerousness (p. 515)
Tarasoff rule (p. 517)
Criminal commitment (p. 518)
Civil commitment (p. 518)
Key Terms
More Study Aids
For additional study aids related to this
chapter, including quizzes to make sure
you’ve retained everything you’ve learned
and a Student Video Activity exploring the
ethical and legal dilemmas involved in the
case of a man diagnosed with schizophrenia
who is also convicted of murder, go to:
www.worthpublishers.com/launchpad/
rkabpsych2e.
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Ethical and Legal Issues 525
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° A °
Abnormal psychology The subfield of
psychology that addresses the causes and
progression of psychological disorders; also
referred to as psychopathology.
Abstinence violation effect The result of
violating a self-imposed rule about food
restriction, which leads to feeling out of
control with food, which then leads to
overeating.
Action potential The wave of chemical
activity that moves from the cell body down
the axon when a neuron fires.
Active phase The phase of a psychological
disorder (such as schizophrenia) in which
the person exhibits symptoms that meet the
criteria for the disorder.
Acute stress disorder A traumatic stress disorder
that involves (a) intrusive re-experiencing of the
traumatic event, (b) avoidance of stimuli related
to the event, (c) negative changes in thought and
mood, (d) dissociation, and (e) hyperarousal and
reactivity, with these symptoms lasting for less
than a month.
Affect An emotion that is associated with a
particular idea or behavior, similar to an attitude.
Age cohort A group of people born in a
particular range of years.
Agoraphobia An anxiety disorder
characterized by persistent avoidance of
situations that might trigger panic symptoms
or from which help would be difficult to
obtain.
Allegiance effect A pattern in which studies
conducted by investigators who prefer a
particular theoretical orientation tend to obtain
data that supports that particular orientation.
Alzheimer’s disease A medical condition
in which the afflicted person initially has
problems with both memory and executive
function and which leads to progressive
dementia.
American Legal Institute (ALI) test The legal
test in which a defendant is considered insane
if he or she either lacks a substantial capacity to
appreciate that his or her behavior was wrong
or has a diminished ability to make his or her
behavior conform to the law.
Amnesia Memory loss, which in dissociative
disorders is usually temporary but, in rare cases,
may be permanent.
Amyloid plaques Fragments of protein that
accumulate on the outside surfaces of neurons,
particularly neurons in the hippocampus.
Anhedonia A difficulty or inability to
experience pleasure.
Anorexia nervosa An eating disorder
characterized by significantly low body weight
along with an intense fear of gaining weight or
using various methods to prevent weight gain.
Antabuse A medication for treating alcohol
use disorder that induces violent nausea and
vomiting when it is mixed with alcohol.
Antisocial personality disorder A personality
disorder diagnosed in adulthood characterized
by a persistent disregard for the rights of
others.
Anxiety A sense of agitation or nervousness,
which is often focused on an upcoming
possible danger.
Anxiety disorder A category of psychological
disorders in which the primary symptoms
involve fear, extreme anxiety, intense arousal,
and/or extreme attempts to avoid stimuli that
lead to fear and anxiety.
Aphasia A neurological condition
characterized by problems in producing or
comprehending language.
Applied behavior analysis A technique used
to modify maladaptive behaviors by reinforcing
new behaviors through shaping.
Apraxia A neurological condition characterized
by problems in organizing and carrying out
voluntary movements even though the muscles
themselves are not impaired.
Asylums Institutions to house and care for
people who are afflicted with mental illness.
Attention-deficit/hyperactivity
disorder (ADHD) A disorder that typically
arises in childhood and is characterized by
inattention, hyperactivity, and/or impulsivity.
Attrition The reduction in the number of
participants during a research study.
Atypical antipsychotics A relatively new
class of antipsychotic medications that affects
dopamine and serotonin activity; also referred
to as second-generation antipsychotics.
Autism spectrum disorder (ASD) A
neurodevelopmental disorder characterized
by deficits in communication and social
interaction skills, as well as stereotyped
behaviors and narrow interests.
Avoidant personality disorder A personality
disorder characterized by extreme shyness
that usually stems from feeling inadequate and
being overly sensitive to negative evaluation.
Avolition A negative symptom of
schizophrenia marked by difficulty initiating or
following through with activities.
° B °
Behavior therapy The form of treatment
that rests on the ideas that: (1) maladaptive
behaviors stem from previous learning, and
(2) new learning can allow patients to develop
more adaptive behaviors, which in turn can
change cognitions and emotions.
Behavioral genetics The field that investigates
the degree to which the variability of
characteristics in a population arises from
genetic versus environmental factors.
Behaviorism An approach to psychology that
focuses on understanding directly observable
behaviors in order to understand mental illness
and other psychological phenomena.
Bias A tendency that distorts data.
Binge eating Eating much more food at one
time than most people would eat in the same
period of time or context.
Binge eating disorder An eating disorder
characterized by binge eating without
subsequent purging.
Biofeedback A technique in which a person
is trained to bring normally involuntary or
unconscious bodily activity, such as heart rate
or muscle tension, under voluntary control.
Biological marker A neurological, bodily, or
behavioral characteristic that distinguishes
people with a psychological disorder (or a
first-degree relative with the disorder) from
those without the disorder.
Biopsychosocial approach The view that
a psychological disorder arises from the
combined influences of three types of
factors—biological, psychological, and social.
Bipolar disorders Mood disorders in which
a person’s mood is often persistently and
abnormally upbeat or shifts inappropriately
from upbeat to markedly down.
Body dysmorphic disorder A disorder
characterized by excessive preoccupation with
a perceived defect or defects in appearance
and repetitive behaviors to hide the perceived
defect.
Borderline personality disorder A personality
disorder characterized by volatile emotions, an
unstable self-image, and impulsive behavior in
relationships.
Brain circuits Sets of connected neurons that
work together to accomplish a basic process.
Brain systems Sets of brain circuits that work
together to accomplish a complex function.
Brief psychotic disorder A psychotic disorder
characterized by the sudden onset of positive or
disorganized symptoms that last between 1 day
and 1 month and are followed by full recovery.
Broca’s aphasia A neurological condition
characterized by problems producing speech.
Bulimia nervosa An eating disorder
characterized by binge eating along with
vomiting or other behaviors to compensate for
the large number of calories ingested.
° C °
Case studies (in studies of psychopathology)
A research method that focuses in detail on
one individual and the factors that underlie
that person’s psychological disorder or
disorders.
Catatonia A condition in which a person
does not respond to the environment or
remains in an odd posture or position, with
rigid muscles, for hours.
Cerebral cortex The outer layer of cells on the
surface of the brain.
Civil commitment The involuntary commitment
to a mental health facility of a person deemed to
be at significant risk of harming himself or herself
or a specific other person.
G-1
GLOSSARY
G-2 Glossary
Classical conditioning A type of learning
that occurs when two stimuli are paired so
that a neutral stimulus becomes associated
with another stimulus that elicits a reflexive
behavior; also referred to as Pavlovian
conditioning.
Clinical assessment The process of obtaining
relevant information and making a judgment
about mental illness based on the information.
Clinical interview A meeting between
clinician and patient during which the
clinician asks questions related to the patient’s
symptoms and functioning.
Clinical psychologist A mental health
professional who has a doctoral degree that
requires several years of related coursework
and several years of treating patients while
receiving supervision from experienced
clinicians.
Cluster A personality disorders Personality
disorders characterized by odd or eccentric
behaviors that have elements related to those
of schizophrenia.
Cluster B personality disorders Personality
disorders characterized by emotional, dramatic,
or erratic behaviors that involve problems with
emotional regulation.
Cluster C personality disorders Personality
disorders characterized by anxious or fearful
behaviors.
Cognitive-behavior therapy (CBT) The form
of treatment that combines methods from
cognitive and behavior therapies.
Cognitive distortions Dysfunctional,
maladaptive thoughts that are not accurate
reflections of reality and contribute to
psychological disorders.
Cognitive therapy The form of treatment
that rests on the ideas that: (1) mental
contents influence feelings and behavior;
(2) irrational thoughts and incorrect beliefs
lead to psychological problems; and (3)
correcting such thoughts and beliefs will
therefore lead to better mood and more
adaptive behavior.
Common factors Helpful aspects of therapy
that are shared by virtually all types of
psychotherapy.
Common liabilities model The model that
explains how neurological, psychological, and
social factors make a person vulnerable to a
variety of problematic behaviors, including
substance use disorders; also called problem
behavior theory.
Community care Programs that allow mental
health care providers to visit patients in their
homes at any time of the day or night; also
known as assertive community treatment.
Comorbidity The presence of more than one
disorder at the same time in a given patient.
Competency to stand trial The mental state
during the time leading up to the trial enables
him or her to participate in his or her own
defense.
Complex inheritance The transmission of
traits that are expressed along a continuum by
the interaction of sets of genes.
Compulsions Repetitive behaviors or mental
acts that a person feels driven to carry out and
that usually must be performed according to
rigid “rules” or correspond thematically to an
obsession.
Computerized axial tomography (CT) A
neuroimaging technique that uses X-rays to
build a three-dimensional image (CT or CAT
scan) of the brain.
Concordance rate The probability that both
twins will have a characteristic or disorder,
given that one of them has it.
Conditioned emotional responses Emotions
and emotion-related behaviors that are
classically conditioned.
Conditioned response (CR) A response that
comes to be elicited by the previously neutral
stimulus that has become a conditioned
stimulus.
Conditioned stimulus (CS) A neutral stimulus
that, when paired with an unconditioned
stimulus, comes to elicit the reflexive behavior.
Conduct disorder A disorder that typically
arises in childhood and is characterized by
the violation of the basic rights of others or
of societal norms that are appropriate to the
person’s age.
Confidentiality The ethical requirement not
to disclose information about a patient (even
whether someone is a patient) to others unless
legally compelled to do so.
Confounding variables Factors that might
inadvertently affect the variables of interest in
an experiment.
Contingency management A procedure
for modifying behavior by changing the
conditions that led to, or are produced by, it.
Control group A group of participants in
an experiment for which the independent
variable is not manipulated, but which
is otherwise treated identically to the
experimental group.
Conversion disorder A somatic symptom
disorder that involves sensory or motor
symptoms that are incompatible with known
neurological and medical conditions.
Correlation The relationship between the
measurements of two variables in which
a change in the value of one variable is
associated with a change in the value of the
other variable.
Correlation coefficient A number that
quantifies the strength of the correlation
between two variables; the correlation
coefficient is most typically symbolized by r.
Counseling psychologist A mental health
professional who has either a Ph.D. degree
from a psychology program that focuses on
counseling or an Ed.D. degree from a school
of education.
Criminal commitment The involuntary
commitment to a mental health facility of a
person charged with a crime.
Criminally responsible The determination
that a defendant’s crime was the product of
both an action or attempted action (the alleged
criminal behavior) and his or her intention to
perform that action.
Crystallized intelligence A type of intelligence
that relies on using knowledge to reason
in familiar ways; such knowledge has
“crystallized” from previous experience.
Culture The shared norms and values of
a society that are explicitly and implicitly
conveyed to its members by example and
through the use of reward and punishment.
Cyclothymic disorder A mood disorder
characterized by chronic, fluctuating mood
disturbance with numerous periods of
hypomanic symptoms alternating with
depressive symptoms, each of which does
not meet the criteria for its respective mood
episodes.
° D °
Dangerousness The legal term that refers to
someone’s potential to harm self or others.
Data Methodical observations, which include
numerical measurements of phenomena.
Defense mechanisms Unconscious processes
that work to transform psychological conflict
in order to prevent unacceptable thoughts and
feelings from reaching consciousness.
Delayed ejaculation A sexual dysfunction
characterized by a man’s delay or absence of
orgasm.
Delirium A neurocognitive disorder
characterized by a relatively sudden
disturbance in attention and awareness as well
as disruption of at least one other aspect of
cognitive functioning.
Delirium tremens (DTs) The symptoms of
alcohol withdrawal that include uncontrollable
shaking, confusion, convulsions, visual
hallucinations, and fever.
Delusional disorder A psychotic disorder
characterized by the presence of delusions that
have persisted for more than 1 month.
Delusions Persistent false beliefs that are held
despite evidence that the beliefs are incorrect
or exaggerate reality.
Dementia A set of neurocognitive disorders
characterized by deficits in learning new
information or recalling information already
learned plus at least one other type of cognitive
impairment.
Dependent personality disorder A personality
disorder characterized by submissive and clingy
behaviors, based on fear of separation.
Dependent variable A variable that is
measured and that may change its values as
a result of manipulating the independent
variable.
Glossary G -3
Depersonalization A dissociative symptom in
which the perception or experience of self—
either one’s body or one’s mental processes—
is altered to the point that the person feels like
an observer, as though seeing oneself from the
“outside.”
Depersonalization-derealization disorder
A dissociative disorder, the primary symptom
of which is a persistent feeling of being
detached from one’s mental processes, body, or
surroundings.
Derealization A dissociative symptom in
which the external world is perceived or
experienced as strange or unreal.
Detoxification Medically supervised
discontinuation of substances for those with
substance use disorders; also referred to as detox.
Diagnosis The identification of the nature of
a disorder.
Diagnostic bias A systematic error in
diagnosis.
Dialectical behavior therapy (DBT) A form
of treatment that includes elements of CBT as
well as an emphasis on validating the patient’s
experience, a Zen Buddhist approach, and a
dialectics component.
Diathesis–stress model A model that
rests on the idea that a psychological
disorder is triggered when a person with a
predisposition—a diathesis—for the particular
disorder experiences an environmental event
that causes significant stress.
Disruptive mood dysregulation disorder
(DMDD) A depressive disorder in children
characterized by persistent irritability and
frequent episodes of out-of-control behavior.
Dissociation The separation of mental
processes—such as perception, memory, and
self-awareness—that are normally integrated.
Dissociative amnesia A dissociative disorder
in which the sufferer has significantly impaired
memory for important experiences or personal
information that cannot be explained by
ordinary forgetfulness.
Dissociative disorders A category of
psychological disorders in which consciousness,
memory, emotion, perception, body
representation, motor control, or identity are
dissociated to the point where the symptoms
are pervasive, cause significant distress, and
interfere with daily functioning.
Dissociative identity disorder (DID)
A dissociative disorder characterized by the
presence of two or more distinct personality
states, or an experience of possession trance,
which gives rise to a discontinuity in the
person’s sense of self and agency.
Dizygotic twins Twins who developed from
two fertilized eggs and so have the same
overlap in genes (50%) as do siblings not
conceived at the same time; also referred to as
fraternal twins.
Dopamine reward system The system of
neurons, primarily in the nucleus accumbens
and ventral tegmental area, that relies on
dopamine and gives rise to pleasant feelings.
Dose–response relationship The association
between more treatment (a higher dose) and
greater improvement (a better response).
Double-blind design A research design
in which neither the participant nor the
investigator’s assistant knows the group to
which specific participants have been assigned
or the predicted results of the study.
Drug cues The stimuli associated with drug
use that come to elicit conditioned responses
through their repeated pairings with use of
the drug.
Durham test The legal test in which a person
is considered insane if an irresistible impulse
to perform criminal behavior was due to a
mental defect or disorder present at the time
of the crime.
Dyslexia A learning disorder characterized
by difficulty with reading accuracy, speed, or
comprehension that interferes with academic
achievement or activities of daily functioning
that involve reading.
° E °
Eating disorder A category of psychological
disorders characterized by abnormal eating and
a preoccupation with body image.
Ego According to Freud, the psychic structure
that is charged with mediating between the id’s
demands for immediate gratification and the
superego’s high standards of morality, as well as
the constraints of external reality.
Electroconvulsive therapy (ECT) A procedure
that sends electrical pulses into the brain to
cause a controlled brain seizure, in an effort to
reduce or eliminate the symptoms of certain
psychological disorders.
Emotion A short-lived experience evoked by
a stimulus that produces a mental response,
a typical behavior, and a positive or negative
subjective feeling.
Epidemiology The type of correlational
research that investigates the rate of
occurrence, the possible causes and risk factors,
and the course of diseases or disorders.
Erectile disorder A sexual dysfunction
characterized by a man’s persistent difficulty
obtaining or maintaining an adequate erection
until the end of sexual activity, or a decrease
in erectile rigidity; sometimes referred to as
impotence.
Etiology The factors that lead a person to
develop a psychological disorder.
Executive functions Mental processes
involved in planning, organizing, problem
solving, abstract thinking, and exercising good
judgment.
Exhibitionistic disorder A paraphilic
disorder in which sexual fantasies, urges, or
behaviors involve exposing one’s genitals to an
unsuspecting person.
Expansive mood A mood that involves
unceasing, indiscriminate enthusiasm for
interpersonal or sexual interactions or for
projects.
Experimenter expectancy effect The
investigator’s intentionally or unintentionally
treating participants in ways that encourage
particular types of responses.
Experiments Research studies in which
investigators intentionally manipulate
one variable at a time, and measure the
consequences of such manipulation on one or
more other variables.
Exposure A behavioral technique that involves
repeated contact with a feared or arousing
stimulus in a controlled setting, bringing about
habituation.
Exposure with response prevention
A behavioral technique in which a patient is
carefully prevented from engaging in his or her
usual maladaptive response after being exposed
to a stimulus that usually elicits the response.
External validity A characteristic of a study
that indicates that the results generalize from
the sample to the population from which it
was drawn and from the conditions used in the
study to relevant conditions outside the study.
° F °
Factitious disorder A psychological disorder
marked by the false reporting or inducing of
medical or psychological symptoms in order to
receive attention.
Family therapy A treatment that involves an
entire family or some portion of a family.
Female orgasmic disorder A sexual
dysfunction characterized by a woman’s
normal sexual excitement not leading to
orgasm or to her having diminished intensity
of sensations of orgasm.
Female sexual interest/arousal disorder
A sexual dysfunction characterized by a
woman’s persistent or recurrent lack of or
reduced sexual interest or arousal; formerly
referred to as frigidity.
Fetishistic disorder A paraphilic disorder in
which the person repeatedly uses nonliving
objects or nongenital body parts to achieve
or maintain sexual arousal and such an arousal
pattern causes significant distress or impairs
functioning.
Fight-or-flight response The automatic
neurological and bodily response to a
perceived threat; also called the stress response.
Flat affect A lack of, or considerably
diminished, emotional expression, such as
occurs when someone speaks robotically and
shows little facial expression.
Flight of ideas Thoughts that race faster than
they can be said.
Fluid intelligence A type of intelligence that
relies on the ability to create novel strategies to
solve new problems, without relying solely on
familiar approaches.
G-4 Glossary
Frotteuristic disorder A paraphilic disorder
in which recurrent, intense, sexually arousing
fantasies, sexual urges, or behaviors involve
touching or rubbing against a nonconsenting
person.
Functional magnetic resonance imaging
(fMRI) A neuroimaging technique that
uses MRI to obtain images of brain functioning,
which reveal the extent to which different brain
areas are activated during particular tasks.
° G °
Gateway hypothesis The proposal that use
can become a use disorder when “entry” drugs
serve as a gateway to (or the first stage in a
progression to) use of “harder” drugs.
Gender dysphoria A psychological disorder
characterized by an incongruence between
a person’s assigned gender at birth and the
subjective experience of his or her gender, and
that incongruence causes distress.
Gender identity The subjective sense of being
male or female (or having the sense of a more
fluid identity, outside the binary categories
of male and female), as these categories are
defined by a person’s culture.
Gender role The outward behaviors, attitudes,
and traits that a culture deems masculine or
feminine.
Generalized anxiety disorder (GAD) An
anxiety disorder characterized by
uncontrollable worry and anxiety about a
number of events or activities, which are not
solely the result of another disorder.
Genes Segments of DNA that control the
production of particular proteins and other
substances.
Genito-pelvic pain/penetration disorder
A sexual dysfunction in women characterized
by pain, fear, or anxiety related to the vaginal
penetration of intercourse.
Genotype The sum of an organism’s genes.
° H °
Habituation The process by which the
emotional response to a stimulus that elicits
fear or anxiety is reduced by exposing the
patient to the stimulus repeatedly.
Hallucinations Sensations that are so vivid
that the perceived objects or events seem real,
although they are not. Hallucinations can
occur in any of the five senses.
Heritability An estimate of how much of
the variation in a characteristic within a
population (in a specific environment) can be
attributed to genetics.
High expressed emotion (high EE) A
family interaction style characterized by
hostility, unnecessary criticism, or emotional
overinvolvement.
Histrionic personality disorder A personality
disorder characterized by attention-seeking
behaviors and exaggerated and dramatic
displays of emotion.
Hoarding disorder An obsessive-compulsive-
related disorder characterized by persistent
difficulty throwing away or otherwise parting
with possessions—to the point that the
possessions impair daily life, regardless of the
value of those possessions.
Hormones Chemicals that are released directly
into the bloodstream that activate or alter the
activity of neurons.
Huntington’s disease A progressive disease
that kills neurons and affects cognition,
emotion, and motor functions; it leads to
dementia and eventually results in death.
Hypervigilance A heightened search for
threats.
Hypothesis A preliminary idea that is
proposed to answer a question about a set of
observations.
Hysteria An emotional condition marked by
extreme excitability and bodily symptoms for
which there is no medical explanation.
° I °
Id According to Freud, the seat of sexual
and aggressive drives, as well as of the desire
for immediate gratification of physical and
psychological needs.
Identity problem A dissociative symptom in
which a person is not sure who he or she is or
may assume a new identity.
Illness anxiety disorder A somatic symptom
disorder marked by a preoccupation with a fear
or belief of having a serious disease in the face
of either no or minor medical symptoms and
excessive behaviors related to this belief.
Inappropriate affect An expression of
emotion that is not appropriate to what a
person is saying or to the situation.
Inclusion The placement of students with
disabilities in a regular classroom, with
guidelines for any accommodations that the
regular classroom teacher or special education
teacher should make.
Independent variable A variable that a
researcher manipulates.
Intellectual disability A neurodevelopmental
disorder characterized by cognitive abilities
that are significantly below normal, along with
impaired adaptive functioning in daily life;
also called intellectual developmental disorder and
previously referred to as mental retardation.
Internal validity A characteristic of a study
that indicates that it measures what it purports
to measure because it has controlled for
confounds.
Interoceptive exposure A behavioral therapy
method in which patients intentionally elicit
the bodily sensations associated with panic so
that they can habituate to those sensations and
not respond with fear.
Interpersonal therapy (IPT) The form of
treatment that is intended to improve the
patient’s skills in relationships so that they
become more satisfying.
In vivo exposure A behavioral therapy
method that consists of direct exposure to
a feared or avoided situation or stimulus.
Irresistible impulse test The legal test in
which a person is considered insane if he or
she knew that his or her criminal behavior
was wrong but nonetheless performed it
because of an irresistible impulse.
° L °
Labile affect Affect that changes inappropriately
rapidly.
Learned helplessness The state of “giving up”
that arises when an animal or person is in an
aversive situation where it seems that no action
can be effective.
Lithium The oldest mood stabilizer.
Longitudinal studies (in studies of
psychopathology) Research studies that are
designed to determine whether a given variable
is a risk factor by using data collected from the
same participants at various points in time.
° M °
Magnetic resonance imaging (MRI)
A neuroimaging technique that creates
especially sharp images of the brain by
measuring the magnetic properties of atoms in
the brain.
Major depressive disorder (MDD) A mood
disorder marked by five or more symptoms
of an MDE lasting more than 2 weeks.
Major depressive episode (MDE) A mood
episode characterized by severe depression that
lasts at least 2 weeks.
Major neurocognitive disorder A
neurocognitive disorder characterized by
evidence of a substantial decline in at least
one cognitive domain, and impaired daily
functioning.
Male hypoactive sexual desire disorder
A sexual dysfunction characterized by a
persistent or recurrent lack of erotic or sexual
fantasies or an absence of desire for sexual
activity.
Malingering Intentional false reporting
of symptoms or exaggeration of existing
symptoms, either for material gain or to avoid
unwanted events.
Manic episode A period of at least 1 week
characterized by abnormally increased energy
or activity and abnormal and persistent
euphoria or expansive mood or irritability.
Maudsley approach A family treatment for
anorexia nervosa that focuses on supporting
parents as they determine how to lead their
child to eat appropriately.
Mental contents The specific material that is
stored in the mind and operated on by mental
processes.
Mental processes The internal operations that
underlie cognitive and emotional functions
(such as perception, memory, and guilt feelings)
and most human behavior.
Glossary G -5
Meta-analysis A research method that
statistically combines the results of a number
of studies that address the same question to
determine the overall effect.
Mild neurocognitive disorder A
neurocognitive disorder characterized by a
modest decline from baseline in at least one
cognitive domain, but that decline is not
enough to interfere with daily functioning.
Monoamine oxidase inhibitors (MAOIs)
Antidepressant medications that increase the
amount of monoamine neurotransmitter in
synapses.
Monozygotic twins Twins who have basically
the same genetic makeup because they began
life as a single fertilized egg (zygote), which
then divided into two embryos; also referred to
as identical twins.
Mood A persistent emotion that is not
attached to a stimulus; it exists in the
background and influences mental processes,
mental contents, and behavior.
Mood disorders Psychological disorders
characterized by prolonged and marked
disturbances in mood that affect how people feel,
what they believe and expect, how they think
and talk, and how they interact with others.
Mood stabilizer A category of medication
that minimizes mood swings.
Moral treatment Treatment of the mentally
ill that involved providing an environment in
which people with mental illness were treated
with kindness and respect and functioned as
part of a community.
Motivational enhancement therapy A form
of treatment specifically designed to boost
a patient’s motivation to decrease or stop
substance use by highlighting discrepancies
between stated personal goals related to
substance use and current behavior; also
referred to as motivational interviewing.
M’Naghten test (or rule) The legal test in
which a person is considered insane if, because
of a “defect of reason, from disease of the
mind,” he or she did not know what he or she
was doing (at the time of committing the act)
and did not know that it was wrong.
° N °
Narcissistic personality disorder A personality
disorder characterized by an inflated sense
of self-importance, an excessive desire to be
admired, and a lack of empathy.
Negative punishment The type of
punishment that takes place when a behavior is
followed by the removal of a pleasant or desired
event or circumstance, which decreases the
probability of that behavior’s recurrence.
Negative reinforcement The type of
reinforcement that occurs when an aversive
or uncomfortable stimulus is removed after a
behavior, which makes that behavior more
likely to be produced again in the future.
Negative symptoms Symptoms of
schizophrenia that are characterized by the
absence or reduction of normal mental
processes, mental contents, or behaviors.
Neurocognitive disorders A category of
psychological disorders in which the primary
symptom is significantly reduced cognitive
abilities, relative to a prior level of functioning;
also referred to as cognitive disorders.
Neurofibrillary tangles The mass created by
tau proteins that become twisted together
and destroy microtubules, leaving the neuron
without a distribution system for nutrients.
Neurons Brain cells that process information
related to physical, mental, and emotional
functioning.
Neuropsychological testing The employment
of assessment techniques that use behavioral
responses to test items in order to draw
inferences about brain functioning.
Neuropsychosocial approach The view that a
psychological disorder arises from the combined
influences of neurological, psychological, and
social factors—which affect and are affected by
one another through feedback loops.
Neurosis According to psychoanalytic theory,
a pattern of thoughts, feelings, or behaviors
that expresses an unresolved conflict between
the ego and the id or between the ego and the
superego.
Neurotransmitters Chemicals that are
released by the terminal buttons and cross
the synaptic cleft.
° O °
Objectification theory The theory that girls
learn to consider their bodies as objects and
commodities.
Observational learning The process of
learning through watching what happens to
others; also referred to as modeling.
Obsessions Intrusive and unwanted thoughts,
urges, or images that persist or recur and
usually cause distress or anxiety.
Obsessive-compulsive disorder (OCD)
A disorder characterized by one or more
obsessions or compulsions.
Obsessive-compulsive personality disorder
A personality disorder characterized by
preoccupations with perfectionism, orderliness,
and self-control, as well as low levels of
flexibility and efficiency.
Operant conditioning A type of learning
in which the likelihood that a behavior will
be repeated depends on the consequences
associated with the behavior.
Oppositional defiant disorder A disorder that
typically arises in childhood or adolescence
and is characterized angry or irritable mood,
defiance or argumentative behavior, or
vindictiveness.
° P °
Panic An extreme sense (or fear) of imminent
doom, together with an extreme stress
response.
Panic attack A specific period of intense
fear or discomfort, accompanied by physical
symptoms, such as a pounding heart, shortness
of breath, shakiness, and sweating, or cognitive
symptoms, such as a fear of losing control.
Panic disorder An anxiety disorder
characterized by frequent, unexpected panic
attacks, along with fear of further attacks and
possible restrictions of behavior in order to
prevent such attacks.
Paranoid personality disorder A personality
disorder characterized by persistent and
pervasive mistrust and suspiciousness,
accompanied by a bias to interpret other
people’s motives as hostile.
Paraphilia An intense and persistent sexual
interest that is different than the usual fondling
or genital stimulation with “normal physically
mature consenting human partners.”
Paraphilic disorder A category of disorders
characterized by paraphilias that lead to distress,
impaired functioning, or harm—or risk of
harm—to the person or to others.
Partial cases Cases in which patients have
symptoms that meet only some of the
necessary criteria but not enough symptoms to
meet all the necessary criteria for the diagnosis
of a disorder.
Pedophilic disorder A paraphilic disorder in
which recurrent sexually arousing fantasies,
sexual urges, or behaviors involve a child who
has not yet gone through puberty.
Persistent depressive disorder (dysthymia)
A depressive disorder that involves as few as two
symptoms of a major depressive episode but in
which the symptoms persist for at least 2 years.
Personality Enduring characteristics that lead
a person to behave in relatively predictable
ways across a range of situations.
Personality disorders A category of
psychological disorders characterized by an
enduring pattern of inflexible and maladaptive
thoughts, emotional responses, interpersonal
functioning, and impulse control problems that
arise across a range of situations and lead to
distress or dysfunction.
Phenotype The sum of an organism’s
observable traits.
Phobia An exaggerated fear of an object or a
situation, together with an extreme avoidance
of the object or situation.
Phototherapy Treatment for depression that
uses full-spectrum lights; also called light-box
therapy.
Placebo effect A positive effect of a medically
inert substance or procedure.
Polysubstance abuse A behavior pattern of
abusing more than one substance.
Population The complete set of possible
relevant participants.
Positive punishment The type of punishment
that takes place when a behavior is followed by
an undesirable consequence, which makes the
behavior less likely to recur.
G-6 Glossary
Positive reinforcement The type of
reinforcement that occurs when a desired
reinforcer is received after a behavior, which
makes the behavior more likely to occur again
in the future.
Positive symptoms Symptoms of
schizophrenia that are characterized by the
presence of abnormal or distorted mental
processes, mental contents, or behaviors.
Positron emission tomography (PET)
A neuroimaging technique that measures
blood flow (or energy consumption) in the
brain and requires introducing a very small
amount of a radioactive substance into the
bloodstream.
Posttraumatic stress disorder (PTSD)
A traumatic stress disorder that involves
persistent (a) intrusive re-experiencing
of the traumatic event, (b) avoidance of
stimuli related to the event, (c) negative
changes in thoughts and mood, and (d)
hyperarousal and reactivity that persist for
at least a month.
Predictions Hypotheses that should be
confirmed if a theory is correct.
Premature (early) ejaculation A sexual
dysfunction characterized by ejaculation that
occurs within a minute of vaginal penetration
and before the man wishes it, usually
before, immediately during, or shortly after
penetration.
Premorbid Referring to the period of time
prior to a patient’s illness.
Prevalence The number of people who have
a disorder in a given period of time.
Privileged communication Confidential
information that is protected from being
disclosed during legal proceedings.
Prodromal phase The phase that is between
the onset of symptoms and the time when the
minimum criteria for a disorder are met.
Prodrome Early symptoms of a disorder.
Prognosis The likely course and outcome of
a disorder.
Projective test A tool for personality
assessment in which the patient is presented
with ambiguous stimuli (such as inkblots or
stick figures) and is asked to make sense of and
explain them.
Psychiatric nurse A mental health professional
who has an M.S.N. degree, plus a C.S.
certificate in psychiatric nursing.
Psychiatrist A mental health professional
who has an M.D. degree and has completed a
residency that focuses on mental disorders.
Psychoactive substance A chemical that alters
mental ability, mood, or behavior.
Psychoanalytic theory The theory that
thoughts, feelings, and behaviors are a result of
conscious and unconscious forces continually
interacting in the mind.
Psychoeducation The process of educating
patients about research findings and therapy
procedures relevant to their situation.
Psychological disorder A pattern of thoughts,
feelings, or behaviors that causes significant
personal distress, significant impairment in daily
life, and/or significant risk of harm, any of
which is unusual for the context and culture in
which it arises.
Psychopathy A set of emotional and
interpersonal characteristics marked by a lack
of empathy, an unmerited feeling of high self-
worth, and a refusal to accept responsibility for
one’s actions.
Psychosexual stages According to Freud, the
sequence of five distinct stages of development
(oral, anal, phallic, latency, and genital) through
which children proceed from infancy to
adulthood; each stage has a key task that
must be completed successfully for healthy
psychological development.
Psychosis An impaired ability to perceive
reality to the extent that normal functioning
is difficult or not possible. The two types of
psychotic symptoms are hallucinations and
delusions.
Punishment The process by which an event
or object that is the consequence of a behavior
decreases the likelihood that the behavior will
occur again.
Purging Attempting to reduce calories that
have already been consumed by vomiting or
using diuretics, laxatives, or enemas.
° R °
Random assignment Assigning participants to
each group in a study using a procedure that
relies on chance.
Randomized clinical trial (RCT) A research
design that has at least two groups—a
treatment group and a control group (usually
a placebo control)—to which participants are
randomly assigned.
Rapid cycling (of moods) Having four or
more episodes that meet the criteria for any
type of mood episode within 1 year.
Reactivity A behavior change that occurs
when one becomes aware of being observed.
Receptors Specialized sites on dendrites
and cell bodies that respond only to specific
molecules.
Reinforcement The process by which the
consequence of a behavior increases the
likelihood of the behavior’s recurrence.
Reliable A property of classification systems
(or measures) that consistently produce the
same results.
Relief craving The desire for the temporary
emotional relief that can arise from using a
substance.
Replication The process of repeating a study
using the same data collection methods
under identical or nearly identical conditions
to obtain data that should have the same
characteristics as those from the original study.
Response bias The tendency to respond in a
particular way, regardless of what is being asked
by the question.
Restrained eating Restricting intake of
specific foods or overall number of calories.
Reuptake The process of moving leftover
neurotransmitter molecules in the synapse back
into the sending neuron.
Reward craving The desire for the gratifying
effects of using a substance.
° S °
Sample The small portion of a population that
is examined in a study.
Sampling bias The distortion that
occurs when the participants in an
experiment have not been drawn
randomly from the relevant population
under investigation.
Schizoaffective disorder A psychotic
disorder characterized by the presence of
both schizophrenia and a depressive or manic
episode.
Schizoid personality disorder A personality
disorder characterized by a restricted range of
emotions in social interactions and few—
if any—close relationships.
Schizophrenia A psychological disorder
characterized by psychotic symptoms that
significantly affect emotions, behavior, and
mental processes and mental contents.
Schizophreniform disorder A psychotic
disorder characterized by symptoms that
meet all the criteria for schizophrenia except
that the symptoms have been present for
only 1–6 months, and daily functioning may
or may not have declined over that period
of time.
Schizotypal personality disorder
A personality disorder characterized
by eccentric thoughts, perceptions, and
behaviors, in addition to having very few
close relationships.
Scientific method The process of gathering
and interpreting facts that generally consists
of collecting initial observations, identifying
a question, developing a hypothesis that
might answer the question, collecting
relevant data, developing a theory, and
testing the theory.
Selective serotonin reuptake inhibitors (SSRIs)
Medications that slow the reuptake of
serotonin from synapses.
Sensate focus exercises A behavioral
technique that is assigned as homework in
sex therapy, in which a person or couple
seeks to increase awareness of pleasurable
sensations that do not involve genital touching,
intercourse, or orgasm.
Separation anxiety disorder A disorder
that typically arises in childhood and is
characterized by excessive anxiety about
separation from home or from someone to
whom the person is strongly attached.
Sex reassignment surgery A procedure in
which a person’s genitals (and breasts) are
surgically altered to appear like those of the
other sex.
Glossary G -7
Sexual dysfunctions Sexual disorders that
are characterized by problems in the sexual
response cycle.
Sexual masochism disorder A paraphilic
disorder in which the person repeatedly
becomes sexually aroused by fantasies,
urges, or behaviors related to being hurt—
specifically, being humiliated or made
to suffer in other ways—and this arousal
pattern causes significant distress or impairs
functioning.
Sexual response cycle The four stages of
sexual response—excitement, plateau, orgasm,
and resolution—outlined by Masters and
Johnson.
Sexual sadism disorder A paraphilic disorder
in which recurrent sexually arousing fantasies,
urges, and behaviors inflict, or would inflict,
physical or psychological suffering on a
nonconsenting person.
Single-participant experiments Experiments
with only a single participant.
Social anxiety disorder An anxiety disorder
characterized by intense fear of public
humiliation or embarrassment; also called social
phobia.
Social causation hypothesis The hypothesis
that the daily stressors of urban life, especially
as experienced by people in a lower
socioeconomic class, trigger mental illness in
those who are vulnerable.
Social desirability A bias toward answering
questions in a way that respondents think
makes them appear socially desirable, even if
the responses are not true.
Social selection hypothesis The hypothesis
that people who are mentally ill “drift” to a
lower socioeconomic level because of their
impairments; also referred to as social drift.
Social support The comfort and assistance
that an individual receives through interactions
with others.
Social worker A mental health professional
who has an M.S.W. degree and may have had
training to provide psychotherapy to help
individuals and families.
Somatic symptom disorder (SSD) A somatic
symptom disorder characterized by at least one
somatic symptom that is distressing or disrupts
daily life, about which the person has excessive
thoughts, feelings, or behaviors.
Somatic symptom disorders A category
of psychological disorders characterized by
symptoms about physical well-being along
with cognitive distortions about bodily
symptoms and their meaning; the focus on
these bodily symptoms causes significant
distress or impaired functioning.
Specific factors The characteristics of a
particular treatment or technique that lead it to
have unique benefits, above and beyond those
conferred by common factors.
Specific learning disorder A
neurodevelopmental disorder characterized
by skills well below average in reading,
writing, or math, based on the expected level
of performance for the person’s age, general
intelligence, cultural group, gender, and
education level.
Specific phobia An anxiety disorder
characterized by excessive or unreasonable
anxiety about or fear related to a specific
situation or object.
Stages of change A series of five stages that
characterizes how ready a person is to change
problematic behaviors: precontemplation,
contemplation, preparation, action, and
maintenance.
Statistically significant The condition in
which the value of a statistical test is greater
than what would be expected by chance alone.
Stereotyped behaviors Repetitive behaviors—
such as body rocking—that do not serve a
function; also referred to as stereotypies.
Stimulus generalization The process whereby
responses come to be elicited by stimuli that
are similar to the conditioned stimulus.
Stroke The interruption of normal blood
flow to or within the brain, which results in
neuronal death.
Substance intoxication The reversible
dysfunctional effects on thoughts, feelings,
and behavior that arise from the use of a
psychoactive substance.
Substance use disorders Psychological
disorders that are characterized by loss of
control over urges to use a psychoactive
substance, even though such use may impair
functioning or cause distress.
Subthreshold cases Cases in which patients
have symptoms that fit all the necessary
criteria, but at levels lower than required for
the diagnosis of a disorder.
Suicidal ideation Thoughts of suicide.
Superego According to Freud, the seat of the
conscience, which works to impose morality.
Synapse The place where the tip of the axon of
one neuron sends signals to another neuron.
° T °
Tarasoff rule A ruling by the Supreme Court
of California (and later other courts) that
psychologists have a duty to protect potential
victims who are in imminent danger.
Tardive dyskinesia An enduring side effect
of traditional antipsychotic medications that
produces involuntary lip smacking and odd
facial contortions as well as other movement-
related symptoms.
Temperament The aspects of personality that
reflect a person’s typical emotional state and
emotional reactivity (including the speed and
strength of reactions to stimuli).
Teratogens Substances or other stimuli that
are harmful to a fetus.
Theory A principle or set of principles that
explains a set of data.
Theory of mind A theory about other people’s
mental states (their beliefs, desires, and feelings)
that allows a person to predict how other
people will react in a given situation.
Tolerance The biological response that
arises from repeated use of a substance such
that more of it is required to obtain the
same effect.
Transcranial magnetic stimulation (TMS) A
procedure that sends sequences of short,
strong magnetic pulses into the brain via a
coil placed on the scalp, which is used to
reduce or eliminate the symptoms of certain
psychological disorders.
Transvestic disorder A paraphilic disorder
in which the person cross-dresses for sexual
arousal and experiences distress or impaired
functioning because of the cross-dressing.
Tricyclic antidepressants (TCAs) Older
antidepressants named after the three rings of
atoms in their molecular structure.
° U °
Unconditioned response (UCR) A behavior
that is reflexively elicited by a stimulus.
Unconditioned stimulus (UCS) A stimulus that
reflexively elicits a behavior.
° V °
Valid A property of classification systems (or
measures) that actually characterize what they
are supposed to characterize.
Vascular dementia A type of dementia caused
by reduced or blocked blood supply to the
brain, which arises from plaque buildup or
blood clots.
Voyeuristic disorder A paraphilic disorder
in which sexual fantasies, urges, or behaviors
involve observing someone who is in the
process of undressing, is nude, or is engaged
in sexual activity, when the person being
observed has neither consented to nor is aware
of being observed.
° W °
Wernicke’s aphasia A neurological condition
characterized by problems comprehending
language and producing meaningful utterances.
Withdrawal The set of symptoms that arises
when a regular substance user decreases or
stops intake of an abused substance.
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CHAPTER 1
Figure 1.3: The Diathesis-Stress Model.
American Psychological Association. Copyright
© 1991 American Psychological Association.
CHAPTER 2
Table 2.3: Cognitive Distortions, adapted from
Feeling Good: The New Mood Therapy, by
David Burns, 1980. Adaptation of Table 3-1:
Definitions of Cognitive Distortions (abridged
from ten to six) from Feeling Good: The New Mood
Therapy by David D. Burns, M.D. Copyright
© 1980 by David D. Burns, M.D. Reprinted by
permission of HarperCollins Publishers.
CHAPTER 3
Table 3.1: The 22 Categories of Mental
Disorders in DSM-5. From the Diagnostic and
Statistical Manual of Mental Disorders.
Table 3.4: Table: MMPI-2 Scales. Sample
of MMPI-2 Scales. Excerpted from the
MMPI®-2 (Minnesota Multiphasic Personality
Inventory®-2) Manual for Administration,
Scoring, and Interpretation, Revised Edition.
Copyright © 2001 by the Regents of the
University of Minnesota. Items excerpted from
the MMPI®-2 Booklet of Abbreviated Items.
Copyright © 2005 by the Regents of the
University of Minnesota. Used by permission
of the University of Minnesota Press. All rights
reserved. “MMPI” and “Minnesota Multiphasic
Personality Inventory” are trademarks owned
by the Regents of the University of Minnesota.
Figure 3.3: Figure: Rates of Serious Mental Illness
Across Countries. From WHO World Mental
Health Survey Consortium. Copyright © 2004
American Medical Association. All rights reserved.
CHAPTER 4
Table 4.2: Information Provided for Obtaining
Informed Consent. Copyright © American
Psychological Association.
Table 4.4: Ethical Guidelines for Research
on Experimental Treatments. Copyright ©
American Psychological Association.
CHAPTER 5
Excerpts from An Unquiet Mind by Kay
Redfield Jamison, Copyright © 1995 by Kay
Redfield Jamison. Used by permission of Alfred
A. Knopf, a division of Random House, Inc.
CHAPTER 6
Excerpt from The Earl Campbell Story, by Earl
Campbell and John Ruane, published by ECW
Press Ltd., 1999, 9781550223910. Reprinted
by permission.
Figure 6.5: Heritablities of Specific Phobias,
by K.S. Kendler, L.M. Karkowski, and C.A.
Prescott, from “Fears and Phobias: Reliability
and Heritability.” Psychological Medicine, 29,
539–553, 1999. Copyright © 1999 Cambridge
University Press. Reprinted with the
permission of Cambridge University Press.
Table 6.8: Table: Interoceptive Exposure
Exercises for Treatment of Panic Disorder,
from CCC/Guilford Publications, Inc. Clinical
Handbook of Psychological Disorders: A Step-
by-step Treatment Manual by Barlow, David H.
Reproduced with permission of GUILFORD
PUBLICATIONS, INCORPORATED in the
format Book via Copyright Clearance Center.
Table 6.3: DSM-5 Criteria for a Panic Attack.
American Psychiatric Association. Reprinted
with permission from The Diagnostic and
Statistical Manual of Mental Disorders,
Fifth Edition (Copyright 2013) American
Psychiatric Association.
CHAPTER 9
Table 9.1: The Twelve Steps of Alcoholics
Anonymous. The Twelve Steps are reprinted
with permission of Alcoholics Anonymous
World Services, Inc. (“AAWS”) Permission to
reprint the Twelve Steps does not mean that
AAWS has reviewed or approved the contents
of this publication, or that AAWS necessarily
agrees with the views expressed herein. A.A. is
a program of recovery from alcoholism only-
use of the Twelve Steps in connection with
programs and activities which are patterned
after A.A., but which address other problems,
or in any other non-A.A. context, does not
imply otherwise.
Figure 9.6: Figure from BSCS. (2003).
Understanding Alcohol: Investigations into
Biology & Behavior. NIH publication
No. 04-4991. Copyright © 2003 by BSCS. All
rights reserved. Used with permission.
CHAPTER 10
Excerpts from pp. 6, 27, 40, 44, 102, 195-6, 284
(518 words) from WASTED: A MEMOIR OF
ANOREXIA AND BULIMIA by MARYA
HORNBACHER. Copyright © 1998 by
Marya Hornbacher Beard. Reprinted by
permission of HarperCollins Publishers.
CHAPTER 13
Excerpt from Get Me Out of Here: My Recovery
from Borderline Personality Disorder by Reiland,
Rachel. Reproduced with permission of
Hazelden in the format republish in a book via
Copyright Clearance Center.
CHAPTER 15
Excerpts from Excerpts from “Psychological
Assessment of Older Adults” by Asenath
La Rue and Jennifer Watson from Professional
Psychology: Research and Practice, 29, 5-14,
1998. Copyright © 1998 by the American
Psychological Association. Adapted with
permission. The use of this information does
not imply endorsement by the publisher.
CHAPTER 16
Excerpt from “Jury hears a confession in killing”
by D. Rohde, The New York Times, October 16,
1999, © 1999. The New York Times. All rights
reserved. Used by permission and protected
by the Copyright Laws of the United States.
The printing, copying, redistribution, or
retransmission of the Material without express
written permission is prohibited.
Excerpt from “Witness tearfully describes fatal
subway shoving” by D. Rohde, The New York
Times, October 9, 1999, © 1999. The New York
Times. All rights reserved. Used by permission and
protected by the Copyright Laws of the United
States. The printing, copying, redistribution, or
retransmission of the Material without express
written permission is prohibited.
Tables of Diagnostic Criteria for Disorders
throughout this book are reprinted with
permission from the Diagnostic and Statistical
Manual of Mental Disorders, Fifth Edition,
(Copyright ©2013). American Psychiatric
Association. All Rights Reserved.
PERMISSIONS AND ATTRIBUTIONS
P-1
° A °
Abbott, C., 44, 383
Abbott, P., 277
Abel, G. G., 338
Aberg, K. A., 384
Abrams, K., 345
Abramson, L. Y., 116, 125, 127
Achenbach, T. M., 48, 101
Adamec, R., 214
Adams, G., 8
Adams, H. E., 349, 352, 424, 425
Adams, S., 111
Addolorato, G., 309
Aderka, I. M., 181
Adityanjee, R., 236
Adler, D. A., 119
Adler, L., 466
Adson, D. E., 319
Agerbo, E., 143
Aghajanian, G. K., 383
Agras, W. S., 320, 321
Agrawal, A., 261
Ahern, D. K., 252
Ahmetzanov, M. V., 48
Ainsworth, M. D. S., 21, 126
Akins, C. K., 346
Alba, J., 62
Albertini, R. S., 201
Aldao, A., 47
Alden, L. E., 180
Alegría, M., 299, 303
Allen, J. G., 228
Allen, J. J., 235
Allen, L. A., 252
Allen, N. B., 126
Allen, W., 356
Allison, P. D., 38
Alloy, L. B., 46, 124, 127, 142
Allsop, D. J., 280
Althof, S. E., 350, 361
Altindag, A., 167
Altshuler, L., 140, 142
Amador, X. F., 385
Ambrogne, J. A., 285
Andersen, A. E., 314
Andersen, B. L., 355
Anderson, I. M., 130
Andreasen, N. C., 381, 383
Andrews, J., 381
Andrews, J. A., 269
Andrews-Hanna, J. R., 480
Angell, M., 22
Angst, J., 120, 127
Anna O., 223–227, 239, 240, 241,
243, 246, 248, 252, 253
Annas, P., 184
Ansbacher, H. L., 17
Ansbacher, R. R ., 17
Ansher, L. S., 320
Antony, M. M., 44, 176, 180, 184,
185, 187, 312
Anzalone, D. A., 261
Aparasu, R. R., 484
Apfelbaum, B., 351, 356
Appelbaum, P. S., 505, 522
Apple, R. F., 321
Arana, G. W., 122, 130, 142, 144,
205, 217, 286, 287
Arnau, R., 217
Arnstein, A. F., 469
Arseneault, L. A, 54
Asmundson, G. J. G., 169
Ataoglu, A., 252
Athwal, B. S., 247
Atladóttir, H. O., 452
Atlantis, E., 353
Atri, A., 498
Austin, A. M., 292
Auyeung, B., 332
Avery, D. H., 132
Ayalon, L., 499
Ayondrinde, O., 54
Aziz, A., 82
° B °
Bacaltchuk, J., 319
Bach, A. K., 356
Baddeley, A., 369
Baer, J. C., 52
Baghurst, T., 317
Bagøien, G., 289
Bailer, U. F., 310
Bailey, A. L., 453
Baker, D., 230, 231, 232
Balash, Y., 472
Baldwin, D. S., 162
Ballard, C., 495, 498
Balon, R., 354
Bancroft, J., 359
Bandelow, B., 409
Bandura, A., 45, 408
Baranek, G. T., 454
Baranowsky, A. B., 218
Barbaree, H. E., 346, 421
Barbaresi, W. J., 466
Barbarich, N. C., 319
Barbee, J. G., 120
Barber, N., 317
Barch, D. M., 369
Barkley, R. A., 462, 468, 472, 473
Barlett, D. L., 195, 196, 204, 206, 218
Barlow, D. H., 44, 157, 158, 159,
160, 164, 170, 173, 180, 184,
185, 187, 215, 217
Barnard, P. J., 133
Baron-Cohen, S., 455
Barrett, P. M., 179
Barroclough, C., 395
Barsky, A. J., 240, 243, 250, 251,
252
Bartholomew, R. E., 8, 225
Bartoi, M. G., 355, 356
Bartol, A. M., 507
Bartol, C. R., 507
Bartolucci, G., 145
Barzee, W., 374
Bass, C., 240, 243, 248, 252
Basson, R., 354
Batelaan, N. M., 171
Bateman, A., 425
Bates, J. E., 332
Battle, C. L., 51
Baucom, D. H., 359, 360
Baumeister, R. F., 312, 313
Baxter, L. R., 203, 207
Beale, E., 3–10, 21, 22, 23, 29, 30,
41, 42, 43, 45, 47, 49, 50, 51,
52, 56
Beale, E. B., 3–10, 20, 21, 22, 23,
29, 30, 41, 42, 43, 44, 47, 49, 50,
51, 52, 56
Beale, P., 9
Bean, N. M., 268
Beasley, C. M., Jr., 130
Beatty, M. J., 178
Beck, A. T., 20, 46, 124, 133, 150,
171, 174, 179, 386, 387, 395, 408,
410, 416, 417, 427, 431, 438, 439
Beck, J. G., 169, 360
Becker, A. E., 314, 315, 355
Becker, J. V., 355
Beckham, D., 203
Becoña, E., 269
Beer, J. S., 513
Beevers, C. G., 129
Begg, M. D., 381
Beidel, D. C., 204
Bell, C. J., 169
Bell, S. M., 21
Bellgrove, M. A., 32
Ben-Tovim, D. L., 303
Ben-Zeev, D., 63
Bender, D. S., 437
Bender, L., 74
Benjamin, L. S., 410
Bennedetti, F., 105
Berenbaum, H., 416
Bergin, A. E., 107
Berglund, P., 8
Berglund, P. A., 50
Berman, J., 359
Berman, J. R., 356
Berman, L. A., 356
Bernstein, J., 463
Berrios, G. E., 232
Bertelsen, A., 385
Berthier, M. L., 203
Beutler, L. E., 65, 68, 111
Bhatia, T., 373
Bhugra, D., 54
Bhui, K., 54
Bibb, J. L., 158
Biederman, J., 178
Bieleu, H., 150
Bienvenu, O. J., 179
Bienvenue, O. J., 42
Bierer, L. M., 51
Bifulco, A., 127
Bilefsky, D., 345
Binks, C. A., 427, 428
Bird, H. R., 466
Bissell, K., 315
Bjornsson, A. S., 201
Black, D. W., 203, 421
Black, M. C., 208
Blackburn, S., 312
Blair, R. J. R., 463
Blais, M. A., 417
Blanchard, J. J., 366, 371
Blanchard, R., 208, 331
Bland, R. C., 146
Blanks, B., 458
Blin, O., 203
Bliss, E. L., 235
Blumberg, S. J., 452
Boaz, M., 470
Bobes, J., 394, 395
Bock, M. A., 455
Boddy, J., 225
Bohart, A. C., 106
Boldrini, M., 150
Bölte, S., 454
Bolton, P., 134
Bond, G. R., 396
Bondy, A. S., 449
Borch-Jacobsen, M., 235
Bordo, S., 317
Borges, G., 147
Borkovec, T. D., 160, 161
Bourgeois, J. A., 247
Boutilier, L. R., 426
Bouton, M. E., 157, 165, 170, 171
Bowen, M., 135, 322
Bower, G. H., 47
N-1
NAME INDEX
Name Index N -2
Bowers, K. S., 228
Bowers, W. A., 320, 376, 377
Bowlby, J., 126, 408, 421
Bowman, E. S., 123, 246
Boyd, J. D., 239
Boylan, J., 342
Boyle, C. A., 457
Boyle, M. F., 486, 487
Boysen, G. A., 236, 237
Bradford, J. M., 344
Bradford, J. M. W., 345
Bradley, B. P., 48
Bradley, S. J., 331, 332
Brady, K., 217, 262
Brady, K. T., 264
Brakel, S. J., 521
Brambilla, P., 130
Brandon, T., 330
Brannigan, G. G., 74
Branson, R., 458
Braun, J., 469
Brauser, D., 68
Breiter, H. C., 202–203
Bremner, J. D., 230, 236
Breslau, J., 8, 208
Breslau, N., 215
Bressan, R. A., 35
Bretherton, L., 408
Breuer, J., 223, 224, 225, 226, 227,
239, 240, 246, 253
Brewer, D. D., 270
Brewer, K. R., 45
Briere, J., 208
Brodey, D., 315
Broekman, B. F. P., 214
Broeske, P. H., 220
Bromberg, W., 12
Bromberger, J. T., 126
Brook, J. S., 313
Brook, U., 470
Brooks, A., 515
Brooks, S., 45
Brown, A. S., 381
Brown, G. K., 148
Brown, H. D., 46
Brown, I., 127
Brown, P. H., 220
Brown, R. J., 243, 247
Brown, S. A., 158, 159, 284
Brown, T. A., 164, 170
Brown, T. M., 486, 487
Brozgold, A. Z., 387
Brückl, T. M., 190
Brunelin, J., 367, 394
Bryant, B., 214
Bryant, R. A., 211, 215, 217, 218
Buchsbaum, M. S., 35, 416
Buckley, P. F., 376 385
Buettner, R., 520
Buhlmann, U., 45, 202
Bulik, C. M., 305, 310, 317
Burgess, S., 144
Burke, J. D., Jr., 198
Burns, D. D., 46
Burns, J. M., 513
Burri, A., 356
Bush, G., 472
Bustillo, J., 383, 393, 397
Butala, A., 345
Butcher, J. N., 79
Butler, J. N., 239
Butler, R. N., 355
Butzlaff, R. L., 51, 388
° C °
Cachelin, F. M., 309, 314
Caddell, K. M., 214
Caldwell, C., 379
Calkins, M. E., 414
Calogero, R. M., 316
Calvocoressi, L., 204
Camilleri, J. A., 339
Campbell, E., 155–156, 157, 158,
159, 165, 166, 167, 168, 171,
173, 174, 175, 191
Campbell, P., 205
Cannon, T. D., 370
Cantor, C., 241, 246, 250
Cantor-Graae, E., 389
Cao, F., 458
Caparulo, B. K., 452
Caplan, P. J., 68
Caputo, A. A., 462
Cardeña, E., 229
Carey, M. P., 351, 359
Carlisle, N., 515
Carmelli, D., 276
Carroll, K. M., 264, 289, 290
Cartwright, S., 9
Caseras, X., 124
Cash, T. F., 314
Caspi, A., 409, 420, 462
Cassady, J. D., 246
Cassano, G. B., 138
Cassin, S. E., 299
Castellanos, F. X., 468
Catanzaro, S. J., 268
Cattell, R. B., 479
Celani, D., 248
Chacko, A., 473
Chakrabarti, S., 390
Chakraborty, A., 54
Chamberlain, P., 461
Chambers, J., 183, 185
Chambless, D. L., 158, 170, 435
Chapple, B., 379
Charcot, J.-M., 15
Chartier, M. J., 177
Chase, D., 277
Chawarska, K., 453
Chelminski, I., 159
Cheung, V. Y., 38
Chilcoat, H. D., 215
Chiu, W. T, 8
Christophersen, E. R., 459, 464,
466
Cicchetti, D., 48, 51
Cicero, T. J., 275
Cipriani, A., 130
Claes, S. J., 36
Clark, C. M., 371
Clark, D. A., 206
Clark, D. M., 174, 181
Clark, L. A., 158, 404, 405
Clarke, A. R., 472
Clarke, J. C., 185
Clarkin, J. F., 106, 428
Clayton, R. R., 261
Cleary, P. D., 243
Clifton, A., 405
Cloitre, M., 101
Cloninger, C. R., 49, 407, 420
Cloos, J., 172
Cobb, H. C., 70
Cochran, C. K., 178
Cochran, S. D., 54
Coelho, C. M., 186
Cohen, A., 390
Cohen, C. I., 482
Cohen, D. J., 452
Cohen, P., 127, 233, 313, 408
Cohen-Kettenis, P. T., 334
Coid, J. W., 516
Cole, S. W., 39
Coles, M. E., 201
Collett, B. R., 469
Colloca, L., 105
Colman, I., 461
Coltheart, M., 416
Combris, M., 367
Combs, D., 387
Combs, D. R., 82
Compton, S. N., 53
Compton, W. M., 283, 419
Conger, R. D., 53
Conklin, G. H., 150
Conti, R., 422
Conway, K. P., 262, 419
Conwell, Y., 148
Cooke, D., 419
Coolidge, F. L., 332
Cooper, M. L., 127
Cooper, S., 314
Cooper, Z., 305, 307, 311
Copeland, W. E., 54, 208, 214
Coplan, J. D., 171
Corbitt, E. M., 419, 432
Corchs, F., 213
Cornblatt, B., 370, 385
Cornblatt, B. A., 69
Correa, H., 150
Correll, C. U., 69
Corrigan, P. W., 64
Cosoff, S. J., 376
Cossey, C., 334
Costanzo, P. R., 416
Costello, E. J., 53, 123, 462
Cottler, L. B., 266
Cottraux, J., 205
Cottrauz, J., 162
Coughlin, J. W., 323
Coupland, N. J., 178
Courchesne, E., 453
Coursey, R. D., 397
Cox, C. B., 491
Coyne, J., 128
Coyne, J. C., 126
Crago, M., 315
Craig, T. K., 243
Craig, T. K. J., 243
Craighead, W. E., 406
Craske, M. G., 159, 161, 166, 173,
187
Crawford, H. J., 239
Crawford, T. N., 408
Crick, F., 36
Crippa, J. A., 35
Critchfield, K. L., 410
Critchley, H. D., 48
Crits-Christoph, P., 291
Cronk, N. J., 191
Crow, S., 302
Crow, S. J., 319, 320, 321
Crowe, R., 169
Crowe, S., 158
Crowell, S. E., 468
Crowther, J. H., 303
Csernansky, J. G., 393
Csipke, E., 302
Cuijpers, P., 134
Cummings, J. L., 498
Curran, G. M., 284
Curtis, G. C., 183
Cyranowski, J., 127
N -3 Name Index
° D °
D’Amico, E. J., 284
D’Ippoliti, D., 287
D’Silva, K., 422
Dackis, C. A., 269
Dahl, A. A., 179
Daley, D. C., 276
Dalgard, O. S., 127
Dare, C., 321
Darracot-Cankovic, R., 281
Dassori, A. M., 377
Dauncey, K., 390
Davey, G., 42
Davidson, J. R. T., 162, 181
Davidson, K., 428
Davidson, R., 48, 49
Davidson, R. T., 217
Davis, C., 317
Davis, J. H., 9
Davis, K. L., 409, 416
Davis, R. D., 430
Dawson, G., 453, 454
Dawson, M., 451
De Bellis, M. D., 281
De Beni, R., 481
De Hert, M., 373
De Leo, D., 147, 150
De Los Reyes, A., 101
de Silva, P., 383
de Zwaan, M., 320
Deb, S., 448
Decker, S. L., 74
Degun-Mather, M., 227
Del Casale, A., 177
Delinsky, S. S., 303
DeLisi, L. E., 380
Dell’Osso, L., 101
Delwiche, L., 452
Demenescu, L. R., 48
Demopoulos, S., 469
Dempsey, P., 458
Dennerstein, L., 350
Dennis, W., 448
DeRubeis, R. J., 110
des Ports, V., 455
Descarte, R., 12
Deshpande, S. W., 156
Deuschle, M., 123
Deutsch, M., 344
DeVane, C. L., 169
Devereux, M., 358
DeYoung, N. J., 407
Di Ceglie, D., 332, 334
Dickey, C. C., 374
Dickinson, D., 371, 397
DiDomenico, L., 314
Dietz, P., 510
Difenbacher, A., 486
Diforio, D., 383
Dikel, T. N., 22, 208
DiLillo, D., 356
Dillard, J. P., 126
DiMauro, J., 172
Dimeff, L., 427
Dingemans, A. E., 299
Dinnel, D. L., 177, 179
Dirks-Lindhorst, P. A., 523
Dishion, T. J., 270
Dix, D., 14
Dixon, L., 395
Docter, R. F., 342
Dodge, K. A., 462, 472
Doerfel-Bausen, D., 54
Dolan, A., 203
Dolan, M., 420
Dolan, S. L., 108
Dolan-Sewel, R., 309
Dolan-Sewell, R., 406, 417
Domjan, M., 42, 344
Donegan, N. H., 425
Dong, W. K., 448
Donley, M. P., 177
Donnellan, M. B., 53
Donovan, J., 261
Dorcus, R. M., 16
Dowd, E. T., 52
Downey, G., 128
Dragan, W. L., 49
Draijer, N., 236
Driessen, M., 424
Drotar, D., 97
Drummond, K. D., 329
Druss, B. G., 119
Duberstein, P. R., 148
Duffy, M., 218
Durham, R. C., 162
Durston, S., 468
Dye, H., 448
Dzokoto, V. A., 8
° E °
Eakin, A., 9
Earle, M., 232
Easton, C. J., 262
Eaton, W. W., 53, 82
Ecker, C., 450
Eckert, E. D., 302
Edelson, M. G., 452
Edelstein, B. A., 499
Edgerton, R. B., 390
Eger, E. L., II, 35
Egley, L. C., 517
Ehlers, A., 214
Eisen, J. L., 438
Eisler, I., 321
Eisman, E. J., 84
El-Bassel, N., 287
El-Islam, M. F., 391
Eligon, J., 520
Elkin, I., 108, 109
Ellickson, P. L., 261
Elliott, D., 208
Elliott, G. C., 52
Elliott, R., 106
Ellison, J. M., 186
Elllis, A., 20
Emery, G., 179
Emmelkamp, P. M. G., 132, 186,
438
Emmons, S., 367
Engel, G. L., 25
Enriquez, C., 443, 444, 459
Enriquez, J., 443, 444, 455, 459,
467
Enriquez, L., 443, 444, 459
Enriquez, P., 443, 444, 459
Enriquez, R., 443, 444, 449, 450,
451, 455
Eplov, L., 350
Epstein, C. M., 132
Epstein, D. H., 269
Epstein, J. N., 472
Erickson, W. D., 340
Erikson, K., 63, 68
Erlenmeyer-Kimling, L., 370, 384
Ernst, A. M., 281
Escobar, J. I., 55
Essau, C. A., 120
Etheridge, R. M., 289
Evans, G., 150
Evans, S., 163
Everitt, B. J., 267
Ewing, C. P., 510
Eyler, L. T., 507
Eysenck, H. J., 420
° F °
Fabre, L. F., 353
Fagot, B., 462
Fahy, T. A., 239
Fairburn, C., 303
Fairburn, C. G., 305, 307, 311, 313,
320, 321
Falco, M., 262
Fallon, B. A., 251
Fals-Stewart, W., 263
Fan, A. P., 53
Faraone, S. V., 37, 469
Faravelli, C., 434
Farberow, N. L., 150
Farmer, A., 146, 240, 520
Farmer, R. F., 408, 417, 421, 431,
438
Farrow, T. F. D., 371
Faughey, K., 520
Fauman, M. A., 370
Fava, G. A., 145, 250
Fava. G. A., 133
Fay, C., 201
Fazel, S., 52
Federoff, I. C., 180
Feinstein, S., 251
Feldman, H. A., 350
Fenton, W. S., 371, 379
Ferguson, C. J., 316
Fergusson, D. M., 270
Fibiger, H. C., 267
Fichter, M. M., 299
Fiedler, N., 96
Field, A. E., 314
Field, S., 235
Field, T., 126
Figiel, G. S., 132
File, S. E., 184
Fillit, H. M., 480
Finch, A. E., 110
Finch, E., 277
Fink, M., 131
Finzi-Dottan, R., 52
Fiorentine, R., 111, 292
First, M. B., 78, 118, 328, 338
Fischer, D. J., 189
Fisher, C., 139
Fisher, S. E., 458
Fitzgibbon, M. L., 304
Flaherty, J., 111
Flint, A. J., 482
Fluent, T. E., 189
Foa, E. B., 45, 102, 205, 211, 218
Foley, D. L., 126, 190
Foley, J., 121, 190, 249, 375, 446,
490
Fonagy, P., 108, 127, 177, 425
Fontenelle, L. F., 204
Foote, B., 229
Forbush, K., 312
Forgas, J. P., 47
Forman, E. M., 109
Forty, L., 119
Fossati, A., 415
Fountain, C., 452
Fowler, R. D., 207
Fox, N. A., 49
Fraley, R. C., 25, 49
Name Index N – 4
Frances, A., 66, 69, 70, 122, 141,
249, 307, 328, 338, 375, 490
Francks, C., 458
Franco-Paredes, K., 312
Frank, E., 134, 142, 145, 321
Frank, G. K., 309, 310
Frank, R. G., 6
Frankel, F., 473
Franklin, M. E., 205
Franko, D. L., 315
Fredrickson, B. L., 316
Freedman, R., 382
Freels, S. A., 54
Freeman, H., 37, 53, 278, 390
Freeman, L., 223, 253
Freeman, W., 470
Freidman, R. F., 457
Frese, F., 386
Freud, A., 16
Freud, S., 14–17, 223, 224, 225,
226, 240, 246
Frezza, M., 272
Friborg, O., 433
Frick, P. J., 459, 462, 463, 464, 472,
473
Fridman, C., 142
Friedl, M., 236
Friedman, J. M., 355
Friedrich, M. J., 144
Frink, H. W., 15
Frischolz, E. J., 235
Frith, C. D., 388, 453
Frost, L. A., 449
Frueh, B. C., 422
Frühauf, S., 360
Fulero, S. M., 509, 513
Fuller, R., 286
Funahashi, T., 379
Furmark, T., 181
Furstenberg, F. F., Jr., 38
Furukawa, T. A., 181
Fyer, A. J., 178
° G °
Gaab, N., 459
Gacono, C. B., 419, 421
Gagne, G. G., 131
Gaher, R. M., 277
Galassi, F., 174
Galen, 12
Gallers, J., 209
Gammon, K., 315
Ganzini, L., 507
Gara, M. A., 63
Garber, J., 120
Garety, P. A., 386
Garfield, S. L., 111
Garfinkel, P. E., 311
Garnefski, N., 126
Garner, D., 314, 315
Garner, D. M., 312, 320
Gaser, C., 73
Gauvain, M., 344, 345, 462
Gavin, J., 302
Geda, Y. E., 490
Gee, T., 238
Geller, J., 313
Genain, Henry, 365, 374
Genain, Hester, 365, 369, 370, 380,
388, 397
Genain, I., 365, 368, 370, 377, 397
Genain, Maud, 365, 374, 397
Genain, Myra, 365, 370, 379, 388
Genain, N., 365, 370, 377, 380, 397
Gentile, K., 315
George, L. K., 355
George, M. S., 132
Gerguson, C., 514
Gerlernter, J., 44
Ghaderi, A., 320
Ghaemi, N., 69
Ghaemi, S. N., 143
Gianoulakis, C., 275
Gibb, B. E., 124
Gibbon, M., 436
Giele, C. L., 204
Giesbrecht, T., 236
Gijs, L., 345
Gilbert, L. A., 45
Gilbertson, M. W., 213
Gillespie, N. A., 49, 251
Gilmer, W. S., 126
Gimpel, G. A., 469
Ginsberg, G. L., 157
Ginsberg, G. S., 167
Giordano, M., 498
Girgus, J., 127
Girvin, H., 288
Gitin, N. M., 186
Gitlin, M., 394, 498
Giuffrida, A., 35
Giulino, L, 96
Gizer, I. R., 469
Gleaves, D. H., 236, 305
Glenn, C. R., 422
Godart, N. T., 299, 303
Goddard, A. W., 35
Godemann, F., 170
Goff, B. S. N., 218
Goisman, R. M., 167
Golan, O., 455
Goldapple, K., 135
Golden, R. N., 119
Goldsmith, S. K., 151
Goldstein, A., 503, 504, 506, 507,
508, 511, 512, 515, 516, 519,
520, 524
Goldstein, A. J., 170
Goldstein, D. S., 31
Goodman, D. J., 520
Goodnough, A., 520
Goodwin, F. K., 142, 143
Goodwin, J., 11
Goodwin, R., 376
Gooren, L., 345
Gooren, L. J. G., 334
Gordon, C. M., 359
Gordon, J. R., 289
Gorman, J. M., 169, 178, 385
Gortner, E. T., 132
Gorwood, P., 160
Gotlib, I. H., 116, 124, 179
Gottesman, I. I., 30, 38, 378, 379,
384, 385, 388
Grabe, H. J., 214
Grabe, S., 315
Grady, D., 492
Graff, G., 271
Graham, K. G., 21
Graham, K. S., 280
Grann, M., 516
Grant, B. F., 263, 406, 419, 434,
436, 438
Grant, J. E., 201
Grant, P. M., 395
Gray, J. A., 420
Graybar, S. R., 426
Graziottin, A., 350
Green, A. R., 266
Green, J. G., 51
Green, J. P., 229
Green, M. F., 369, 370, 379, 381,
392, 393
Green, P., 376
Green, R., 332
Greenberg, G., 66, 68, 69, 490
Greene, E., 508, 509, 510
Greene, R. L., 80
Greenfield, S. F., 272, 277
Greenough, W. T., 448
Greenwood, T. A., 30
Gregory, R. J., 428
Greig, T. C., 387
Grigorenko, E. L., 458
Grilo, C. M., 321, 404, 415, 424,
434, 438
Grimes, K., 382
Grisso, T., 522
Grocholewski, A., 202
Gropalis, M., 252
Gruber, A. J., 201
Gruber, K. J., 262
Grucza, R. A., 305, 306
Guan, L., 469
Guarnaccia, P. J., 167, 179
Gude, T., 438
Guller, Y., 381
Gunderson, J. G., 416, 417, 423,
424, 436
Gunewardene, A., 315
Gunnar, M. R., 51
Gur, R. E., 369 380
Guralnick, O., 231
Guthrie, R. M., 215
Gutierrez, M. J., 145
Gutierrez, R., 490
Gyulai, L., 32
° H °
Haber, J., 71
Hackett, G. I., 353
Haedt, A., 322
Haeffel, G. J., 126
Hafner, R. J., 376
Hahn, C. G., 144
Halbreich, U., 127
Hall, G. C. N., 111
Halligan, P. W., 247, 248
Hallmayer, J., 384, 453
Hallowell, E. M., 465, 466
Halmi, K. A., 300, 317
Hamburg, P., 355
Hames, J. L., 126
Hamilton, M. D., 269
Hammer, M. R., 51
Hanewinkel, R., 270
Hanks, D. L., 167
Hanna, G. L., 189
Hanrahan, F., 162
Hansen, N. B., 109, 110
Hansenne, M., 425
Hanson, R. K., 346
Hare, R. D., 419, 422
Harford, T., 406
Hargreaves, I., 334
Harrison, G., 257, 263, 284
Harrison, K., 316
Harrow, M., 376
Hart, S. D., 422
Hartley, H., 353
Hartmann, H., 17
Harvey, A. G., 211, 217
Harvey, P. D., 480, 490
Hasin, D. S., 406, 419, 434, 436,
438
N -5 Name Index
Haskett, M. E., 52
Hasler, G., 30, 117, 123, 128
Havey, J. M., 466
Hawke, J. L., 458
Hawkins, J., 269
Hayden, D., 22
Haydon, P. G., 34
Heard, H. L., 424
Heath, A. C., 260
Heatherton, T. F., 312, 313
Hefner, V., 316
Heil, P., 340
Heilbrun, K., 346
Heim, A. K., 425
Heiman, J. R., 353, 360
Heimberg, R. G., 178, 179, 181
Heinrichs, M., 214
Heinz, A., 383
Hellström, K., 186
Helverskov, J. L., 322
Henderson, C., 126
Henggeler, S. W., 473
Henneman, W. J. P., 494
Hennen, J., 344
Henning, K. R., 422
Herba, C. M., 52
Herholz, K., 309, 310
Herman, C. P., 311, 313, 315
Herman, J., 218
Hermelin, B., 451
Hernandez, D. V., 63
Hertz-Picciotto, I., 452
Herzberger, S., 469
Hesslinger, B., 468
Hettema, J. M., 38, 160, 289
Hewit, J. L., 373
Hidalgo, R. B., 217
Hiday, V. A., 516, 518, 519, 523
Higgins, S. T., 289
Hilgard, E. R., 228, 229
Hill, E. M., 81
Hiller, W., 243, 250
Hillhouse, M. P., 111
Hilts, D., 498
Hilty, D., 241
Himle, J. A., 215
Hinckley, J., 509
Hinshaw, S. P., 472
Hinton, D., 167
Hippocrates, 11–12
Hirschfield, R. M., 133
Hoechstetter, K., 247
Hoek, H. W., 299, 303
Hoff, A., 384
Hoff, A. L., 370
Hoffman, L. W., 38
Hoffman, R. E., 381
Hofmann, S. G., 177
Hogue, A., 292
Holder-Perkins, V., 242, 243, 253
Hollander, E., 310
Hollier, L. M., 38
Hollifield, M., 242
Hollon, S. D., 133
Holtzheimer, P. E., III, 132
Holzman, P. S., 382
Homma, A., 498
Hong, L. E., 382
Honig, A., 143, 145
Hoogduin, K. A. L., 248
Hooley, J. M., 51, 388
Hopper, K., 378
Hopwood, C. J., 406
Horan, W. P., 371
Horesh, N., 170
Hornbacher, M., 297, 298, 301,
307, 308–309, 312, 314, 316,
322, 324
Horne, O., 302
Horney, K., 17
Horowitz, J. L., 120
Horowitz, L. M., 430
Horwath, E., 183, 198
Hough, W. G., 519
Hovey, J. D, 134
Howard, R., 498
Howsepian, A. A., 516
Hoy, H., 345
Hrabosky, J. I., 298
Hsieh, D. K., 77, 101
Hu, S., 160
Huang, Y. Y., 161
Hubbard, R. L., 292
Hudson, C. G., 390
Hudson, J., 179
Hudson, J. I., 297, 299, 303, 305,
306
Hugdahl, K., 31
Hughes, C. C., 150
Hughes, H., 195–196, 200, 203,
204, 206, 207, 208, 212, 218, 220
Hui, C. H., 55
Hui, L. K., 169
Hull, C. L., 19
Humphreys, K., 292
Hunt, I. M., 379
Hunter, E. C. M., 230, 232, 238
Huntjens, R. J. C., 234
Hurd, M. D., 489
Hurt, R. D., 262
Hutchison, K. E., 128
Huttonlocher, P. R., 381
Hybels, C. F., 126
Hyde, J. S., 127, 128, 315
Hyman, S. E., 39, 42, 69, 264, 269,
286
Hyman, S. M., 21
° I °
Iacono, W. G., 382
Igartua, K. J., 148
Ikeuchi, T., 489
Ikonomovic, M. D., 494
Ilgen, M. A., 128
Inaba, A., 126
Inan, S., 32
Insel, T., 66, 203
Insel, T. R., 309
Ireland, T., 268
Ironson, G. I., 217
Isometsä, E. T., 148
Ivarsson, T., 148
° J °
Jablensky, A., 67
Jackson, M., 200
Jacobi, C., 309
Jacobsen, L. K., 215
Jakupcak, M., 215
Jamison, K. R., 115–116, 119, 133,
136, 137, 138, 142, 143, 146
Jamison, R. N., 244
Janet, P., 228
Jang, K. L., 178, 235, 421
Jansen, A., 45
Jansen, K. L., 281
Janssen, I., 387
Jarvis, E., 389
Javeline, D., 102
Jaycox, L. H., 54
Jenike, M. A., 203
Jensen, J., 453
Jensen, P. S., 472
Jessor, R., 261
Jewel, 458
Jimerson, D. C., 310
Joan of Arc, 12
Joe, G. W., 289
Johns, L. C., 387
Johnson, C. L., 299
Johnson, C. P., 454
Johnson, J. G., 53, 233, 313, 404,
406, 408
Johnson, S. D., 271
Johnson, S. L., 143
Johnson, V., 347, 355, 356
Johnston, C., 469
Joiner, T., 128
Joiner, T. E., 126
Joiner, T. E., Jr., 158
Jones, H. E., 145
Jones, S., 289
Joormann, J., 179
Jose, P. E., 127
Joseph, R., 228
Joseph, S., 214
Jourdan, A., 106
Joyce, P. R., 438
Judd, L. L., 140
Jung, C. G., 17
Just, N., 124
° K °
Kagan, J., 178
Kagan, R. M., 421
Kahan, D., 313
Kahn, E., 18
Kahn, L., 127
Kahn, R. S., 376
Kaka, M. P., 344
Kalaria, R. N., 495
Kales, H. C., 491
Kalisvaart, K. J., 487
Kalivas, P. W., 35, 267
Kalodner, C., 323
Kaltiala-Heino, R., 128
Kameya, Y., 353
Kandel, D., 39, 261
Kandel, D. B., 261
Kandel, E., 213
Kandel, E. R., 33, 34, 36, 161
Kaniasty, K. Z., 215
Kaplan, A., 63, 199
Kaplan, H. S., 347, 356
Kaplan, L. J., 344
Kaplan, M. S., 355
Kapur, N., 280, 383
Kar, N., 8
Karkowski, L. M., 142, 184
Karlin, B. E., 481
Karlsson, R., 111
Karnik-Henry, M., 513
Karu, T., 52
Kasch, K. L., 124
Kasen, S., 313
Kasper, S., 172
Katerndahl, D., 52
Katz, P. S., 118
Kaufer, D. I., 495
Kaufmann, A. S., 79
Kavanagh, D. J., 388
Kavirajan, H., 498
Kawane, S. D., 156
Kaye, W. H., 309, 310
Name Index N – 6
Kazdin, A. E., 48, 473
Kazdin, A. E., 101, 105, 472
Keane, T. M., 214, 215, 217
Keck, P. E., Jr., 144
Keefe, R. S. E., 369
Keel, P. K., 68, 299, 303, 314, 315,
322
Keery, H., 314
Kehrer, C. A., 427
Keith, S., 377
Keller, M. B., 167
Keller, W. R., 383
Kelley, M. L., 263
Kelly, T. M., 425
Kelsey, J. E., 34, 35, 36
Kelsoe, J. R., 30
Keltikangas-Järvinen, L., 49
Kemp, S., 12
Kendall, P. C., 105, 107, 108, 109,
190
Kendell, R., 67
Kendler, K. S., 25, 38, 69, 118, 123,
142, 160, 169, 184, 242, 270,
276, 284, 384
Kennedy, N., 140
Kennedy, S. H., 122
Kent, J. M., 178
Kernberg, O., 422
Kernberg, O. F., 17
Kerns, K. A., 468
Keski-Rahkonen, A., 299
Kessing, L. V., 143
Kessler, R. C., 6, 8, 50, 69, 119, 120,
147, 306, 466
Keuneman, R., 394
Keyes, J. A., 505
Keyes, K. M., 270
Keys, A., 300, 301
Keyzer, P., 516
Kieseppä, T., 142
Kihlstrom, J. F., 104, 229, 233, 235,
238, 247
Kilen, J. D., 286
Kiliç, B. G., 468
Killaspy, H., 396
Kilpatrick, D. G., 214, 269
Kim, J.-H., 315
Kim, M., 370
Kinder, B. N., 355, 356
King, B. H., 251
King, D. W., 209, 215
Kinsley, C. H., 32–33, 34, 35
Kirk, S. A., 77, 101
Kirmayer, L. J., 240, 252, 253
Kirsch, I., 277
Kirsch, L., 105, 111, 229
Kirschenbaum, H., 106
Klee, H., 265
Klein, C. A., 505
Klein, D. A., 300
Klein, D. N., 134
Klein, E., 132
Kleinfield, N. R., 512
Kleinman, A., 81
Kleinplatz, P. J., 343, 354
Klerman, G. L., 134, 321
Klonsky, E. D., 422, 423
Kluft, R. P., 238, 239
Klump, K. L., 314
Knapp, C., 274, 299, 300
Knightley, K., 458
Knopman, D. S., 495
Knutelska, M., 230, 232
Koenig, O., 483
Koenigsberg, H. W., 417, 427
Kohn, R., 55
Kohut, H., 17
Köksal, F., 344
Kolur, U. S., 142
Kong, L. L ., 234
Konigsberg, E., 520
Koob, G. F., 267
Kosslyn, S. M., 31, 46, 235, 239,
344, 483
Kotler, L., 313
Kouri, E. M., 280
Kovnick, J. A., 507
Kowalski, S. D., 109
Kozlowska, K., 248
Kraaij, V., 126
Kransny, L., 455
Krasnoperova, E., 124
Kratochvil, C. J., 47, 472, 473
Kremen, W. S., 370
Kress, V. E., 63, 68
Krueger, R. F., 39
Kruijver, F. P., 332
Krupnick, J. L., 109
Krystal, J. H., 265, 281
Kulhara, P., 390
Kulkarni, J., 384
Kundert, D. K., 450
Kunen, S., 63
Kunstche, E., 282
Kupfer, D. J., 66
Kushner, M. G., 214
° L °
La Rue, A., 477, 478, 481, 488, 500
Labott, S. M., 234
Laffaye, C., 290
Lahey, B. B., 466
Lahti, M., 408
Lam, A. G., 111
Lam, K., 127
Lam, R. W., 131, 144
Lamb, K., 118
Lambert, K., 32–33, 34, 35
Lambert, M. J., 105, 106, 107, 108,
109, 110
Lambrou, C., 199, 201
Landen, M., 334
Lane, S. D., 280
Lang, M., 383
Lang, P. J., 49
Lang, R. A., 338
Langdon, R., 416
Langenbucher, J. W., 260
Langevin, R., 338, 346
Langton, C. M., 346
Lanphear, B. P., 447
Large, M., 376
Larson, C. L., 30
Larson, K., 466
Laumann, E., 351, 352
Laumann, E. O., 355, 356
Laurent, J., 268
Lauriello, J., 393
Lawson, C., 35, 169
Lazarus, R. S., 11
Le Couteur, A., 453
Le Grange, D., 321
Le Moal, M., 267
Leccese, A. P., 265
Ledger, H., 262
Ledley, D. R., 178
LeDoux, J. E., 42, 141, 184, 425
Lee, A. M., 315
Lee, C., 217
Lee, D. O., 96
Lee, P., 390
Lee, S., 177, 315
Lee, S. H., 179
Lee, Y. H., 424
Leenaars, A. A., 148
Leentjens, A. F., 486, 487
Leff, J., 395
LeGris, J., 424
Lehman, A. F., 395
Lehrer, P. M., 163
Leiblum, S. R., 355
Leighton, A. H., 150
Lelewer, N., 456
Lemche, E., 231
Lennon, J., 257, 258, 271, 278, 279,
284, 285
Lennon, S. J., 315
Lenox, R. H., 144
Lenzenweger, M. F., 406, 416
Leone, P., 267
Leung, K. S., 266
Lev-Ran, S., 262
Levin, A., 209
Levin, R. J., 347, 349
Levine, M. P., 316
Levine, S. Z., 377
Levitan, C., 381
Levitt, E. E., 341
Levy, D., 382
Levy, K. N., 106
Levy, T. M., 421
Lewinsohn, P. M., 120, 126, 132
Lewis, D. A., 383
Lewis, D. O., 234, 236
Lewis, M. L., 355
Lewis, P. A., 48
Lewis-Fernández, R., 247
Lewontin, R. C., 37
Leyman, L., 124
Li, S.-C., 178, 481
Lichtenstein, P., 184
Lieb, R., 427
Lieberman, J. A., 73, 394
Liebowitz, M. R., 160
Lilienfeld, S. O., 80, 233, 235, 237,
310
Lin, E. H. B., 71
Lindblom, K. M., 82
Linde, K., 131
Linde, P., 83, 111
Lindenberger, U., 178, 481
Linehan, M. M., 148, 408, 409, 424,
425, 426, 427, 428
Lingford-Hughes, A., 262
Linhorst, D. M., 523
Lipsitz, J. D., 183
Littell, J. H., 288
Little Albert, 41, 42, 91, 185
Litz, B. T., 218
Livesley, W. J., 178, 405, 406, 413,
423
Lock, J., 321
Locke, J., 13
Locker, D., 187
Loewenstein, R. J., 233, 239
Logan, J., 261
Loney, B. R., 462, 463
Looper, K. J., 240, 252, 253
Lopez, A. D., 8, 376
Lopez, S. R., 51
LoPiccolo, J., 355, 359
Lorenz, J., 247
Louis, M., 109
Lowe, M. R., 305
Luborksy, L., 108, 109
N -7 Name Index
Luby, J. L., 120
Lucka, I., 299
Lundberg, P., 389
Lundgren, J. D., 321
Lundh, L., 178
Lutz, W., 109
Lyketsos, C. G., 35
Lykken, D. T., 420
Lykouras, L., 178
Lyle, S., 498
Lynch, W. C., 315
Lynn, S. J., 105, 111, 229, 234, 236,
237, 277
Lyon, H. M., 142
Lyons, M. J., 23, 126, 215
Lyons-Ruth, K., 420
° M °
M’Naughten, D., 508
MacCabe, J. H., 377
MacKay, D. G., 48
Mackie, S., 468
MacLaren, C., 20
Maden, A., 516
Magee, W. J., 167
Maidhof, C., 111
Mailis-Gagnon, A., 247, 248
Main, M., 21
Makela, K., 277
Malatesta, V. J., 327, 349, 352
Maldonado, J. R., 243, 245, 246,
252, 253
Malik, M. L., 65, 68
Malkoff-Schwartz, S., 143
Mancebo, M. C., 438
Mangelli, L., 250
Maramba, G. G., 111
Marcus, S. M., 127
Marder, S. R., 393
Marek, G. J., 383
Marengo, J. T., 368
Maric, N., 377
Marino, C., 458
Maris, R. W., 148
Markowitz, J. C., 428, 436
Marlatt, G. A., 289
Marques, L., 306
Marsella, A., 215
Marshall, C. R., 457
Marshall, R. D., 230
Marshall, W. L., 346
Marten, P. A., 160
Martens, W. H. J., 418, 421
Martin, D., 4, 5
Martin, N. C., 469
Martin-Santos, R., 268, 269, 271
Martinez, C., 130
Martinez, C. D., 52
Martorano, J. T., 252
Mascolo, M., 300, 303
Maslach, C., 82
Maslow, A., 18
Masters, W., 347, 355, 356
Mataix-Cols, D., 196
Mather, C., 8
Mathew, S. J., 178
Mathews, M., 391
Matson, J. L., 448
Matsunaga, H., 198
Maughan, B., 409
Maurer, K., 377
Mausner-Dorsch, H., 82
Maxfield, L., 217
Mayou, R., 240, 247, 250, 252
Mayou, R. A., 214
Mays, V. M., 54
Maysles, A., 4, 5, 41, 47, 51
Maysles, D., 4, 41, 47, 51
McAnulty, R. D., 338, 340, 343
McArthur, J. C., 496
McCae, M. P., 317
McCandliss, B., 458
McCann, J. T., 510
McCarter, R. H. G., 186
McCartney, K., 40
McCartney, P., 257, 258, 270
McClure, J. N., 169
McCook, A., 94
McDermott, E., 383
McElroy, S. L., 144, 310
McElwain, J., 454
McEvoy, J. P., 393
McEwen, B. S., 213
McFarlane, W. R., 375
McGee, C. L., 447
McGlashan, T. H., 371, 379, 381,
415, 417
McGorry, P. D., 375
McGowin, D. F., 490, 491, 492
McGrath, J. J., 119, 377, 387
McGuffin, P., 142
McHugh, P., 239
McHugh, P. R., 67
McInerney, R. J., 468
McIntosh, J. L., 146
McIntosh, V. V. W., 320
McKay, D., 415
McKee, L., 49
McKenna, K., 9
McKenzie, K., 54
McKetin, R., 265
McLeod, D. S., 214
McLoughlin, D. M., 131
McMullin, R. E., 182
McNally, R. J., 170, 213
McNamara, B., 394
McNeil, T. F., 382
McPartland, J., 454
McQuiston, J. T., 514
McRae, A. L., 287
McSherry, B., 516
McWilliams, S., 395
Meana, J. J., 35, 36
Meares, R., 146
Medford, N., 231
Medici Skaggs, N., 270
Mednick, S. A., 391, 420
Meehl, P., 63
Meehl, P. E., 23
Mehler, P. S., 300
Mehta, M. M., 275
Meier, M. H., 280
Melartin, T. K., 118
Menard, W., 201
Mennin, D. S., 161
Menzies, R. G., 183, 185
Merckelbach, H., 235
Merikangas, K. R., 140
Merskey, H., 228, 234, 236
Metalsky, G. I., 48
Metalsky, G. L., 125
Meuret, A. E., 166
Meyer, B., 438
Meyer, G. J., 75, 77
Meyer, R. G., 506, 507, 508, 509,
510, 512, 513, 514, 516, 517,
518, 522
Meyer, U., 382
Mezey, G., 215
Micallef, J., 203
Michael, N., 142
Middleton, K. L., 208
Midence, K., 334
Miethe, T. D., 523
Miklowitz, D. J., 51, 143, 145
Mikulincer, M., 44
Milak, M. S., 122
Milich, R., 469
Miller, A. B., 416
Miller, F. G., 105
Miller, I., 143
Miller, J. J., 163
Miller, L. S., 416
Miller, M., 458
Miller, W. R., 44, 289
Millet, B., 198, 204
Millon, T., 409, 430
Mills, T. C., 54, 126
Milner, P., 267
Minde, K., 21
Mineka, S., 44, 48, 128, 158, 179,
185
Miniño, A. M., 147
Minshew, N. J., 453
Minuchin, S., 135, 322
Mirsky, A. F., 370, 377, 380, 388,
394, 397
Misra, S., 507
Mitchell, A. J., 133
Mitchell, B. D., 374, 515
Mitchell, J., 275
Mitchell, J. E., 319
Mitendorfer-Rutz, E., 53
Miura, Y., 51
Modell, J. G., 203
Moffitt, T. E., 159, 462
Mogg, K., 48, 101, 124
Moghaddam, B., 383
Moldin, S. O., 384
Monahan, J., 379, 516, 517
Mond, J. M., 300
Monroe, S. M., 23
Montano, C. B, 118
Montgomery, S. A., 144
Moore, C., 451
Moore, G. A., 49
Moore, T. H. M., 376
Moos, B. S., 81
Moos, R. H., 81, 292
Moose, B., 292
Moradi, B., 316
Moran, P., 419
Morey, L. C., 405, 438
Morey, R. A., 32
Morgan, C., 80
Moritz, S., 386
Morris, A. S., 462, 463, 472
Morris, N., 510
Morrow, J., 124, 127
Mort, J. R., 484
Mortensen, P. B., 377, 390
Mortweet, S. L., 459, 464, 466
Moscicki, E., 147
Moser, C., 340, 343, 358
Mosher, P. W., 506
Mottron, L., 451
Movius, H. L., II, 235
Mowrer, O. H., 170, 179, 214
Moynihan, R., 354
Mrug, S., 470
Mueser, K. T., 396
Muhle, R., 453
Mulas, F., 468
Muller, J., 204
Name Index N – 8
Muller, N., 35
Mullins-Sweatt, S. N., 406
Mulvany, F., 53
Mulvey, E. P., 379
Mundo, E., 35, 142, 203
Muñoz, L., 462, 464, 472, 473
Munroe, R. L., 344, 345
Murias, M. A., 453
Murnen, S. K., 316
Murphy, M., 243
Murray, C. J. L., 8, 376
Murray, H., 80
Myers, J. E. B., 506
° N °
Nanke, A., 243
Napolis, D., 373
Nash, J., 367
Nathan, P. E., 108
Naughton, A. M., 51
Nazareth, I., 353
Neale, M. C., 38, 178
Nedelska, Z., 490
Neighbors, H. W., 139
Nelson-Gray, R. O., 408, 417, 421,
431, 438
Nemeroff, C., 35, 123, 128
Nemeroff, C. J., 314
Nestler, E. J., 39
Neuman, R. J., 469
Neumeister, A., 123
New, A. S., 425
Newmann, C., 382
Newmark-Sztainer, D., 311
Newton, T. F., 286
Neziroglu, F., 415
Nicdao, E. G., 299, 303
Nicholas, M., 480
Nichols, M., 360
Nicoll, R. A., 35
Nicolle, R. A., 281
Nigg, J. T., 49, 470
Nobre, P., 356
Nobre, P. J., 355
Nock, M. K., 147, 462
Nolan, S. A., 128
Nolen-Hoeksema, S., 46, 101, 124,
127, 128
Nomura, M., 49
Norasakkunkit, V., 179
Norcross, J. C., 70
Nordling, N., 341
Norman, P., 257
Norris, F. H., 215
Noyes, R., Jr., 252
Nurnberger, J. I., 123
Nurnberger, J. I., Jr., 276
Nutt, D., 35, 160, 169, 262
Nutt, D. J., 169
Nuttbrock, L., 330
° O °
O’Brien, C. P., 258, 269, 286
O’Brien, J., 493
O’Brien, K. P., 519
O’Connor, R. C., 148
O’Leary, T. A., 164
O’Malley, P. G., 252
O’Neill, M. L., 422
Ofovwe, C. E., 466
Ogden, C. A., 315
Ogles, B. M., 105, 106, 107, 108
Ogloff, J. R. P., 419, 421, 422
Ogrodniczuk, J. S., 410
Ogundipe, T., 513
Oh, D. S., 179
Ohlsson, H., 270
Öhman, A., 183
Okubo, Y., 383
Oldham, J. M., 406, 411
Olds, J., 267
Olesen, P. J., 513
Olino, T. M., 158
Olivardia, R., 317
Olson, I. R., 381
Olver, M., 422
Onasis, J. K., 4, 8
Oniszcenko, W., 49
Onken, L. S., 290
Oquendo, M. A., 148
Orlans, M., 421
Orr, S. P., 213
Osborne, C., 344
Osmond, M., 120
Öst, L., 178, 182, 186
Ostacher, M. J., 144
Ott, S. L., 370
Otto, M. W., 110, 158, 201, 516
Ousley, L., 315
Overmier, J. B., 44, 125
Owen, M. J., 385
Oxnam, R. B., 234
Ozcan, M. E., 139
Ozkan, M., 167
Ozonoff, S., 452, 453
° P °
Packman, W. L., 147
Packnett, E. R., 211
Pagnin, D., 131
Paisner, D., 454
Palladino, P., 481
Pallister, E., 311
Palmer, R. H., 276
Paniagua, F. A., 411
Pantelis, C., 33, 381
Papadimitriou, G. N., 139
Papapetropoulos, S., 495
Papp, L. A., 169
Pappenheim, B., 253
Parasuraman, R., 480
Pardini, D. A., 462, 463
Paris, J., 407, 408, 409, 424, 425
Park, I., 420
Parker, G., 127
Parker, L., 183
Parner, E. T., 452
Parpura, V., 34
Passman, L., 299
Patel, V., 127
Patkar, A. A., 130
Pauli, P., 185
Pauls, D. L., 203
Pavlov, I., 19, 42
Pelham, W. E., 466
Pelc, K., 469, 470
Penders, T. M., 266
Pengilly, J. W., 52
Penn, D. L., 387
Penn, S., 445
Perez, M., 315
Perilla, J. L., 215
Perkins, B. R., 217
Perlin, M. L., 514, 516, 519, 521,
522
Perlis, R. H., 144
Perroud, N., 427
Pescosolido, B. A., 516
Peter, M., 423
Petersen, R. C., 493
Peterson, C., 125
Peterson, C. B., 305
Petry, N., 289
Pettit, G. S., 462, 472
Pfäfflin, F., 345
Pfammatter, M., 395
Pfeiffer, M., 445
Phan, K. L., 177
Phillips, A. G., 267
Phillips, K. A., 200, 201, 202, 317
Phillips, M., 240
Phillips, M. L., 142
Pickles, A., 190
Pigott, T. A., 157, 203
Pike, K. M., 315, 320, 322
Pillmann, F., 373
Pilowsky, D. J., 52
Pincus, A. L., 438
Pine, D. S., 31
Pinel, P., 13
Piñeros, M., 246
Pinkerman, J. E., 80
Pinto-Gouveia, J., 355
Piper, A., 228, 234, 236
Piper, W. E., 410
Pissiota, A., 74
Pithers, W. D., 346
Pitman, R. K., 213
Pitts, F. M., 169
Plassman, B. L., 492
Pliszka, S. R., 472
Plomin, R., 23, 36, 37, 40
Pluess, M., 160
Poddar, P., 516, 517
Poewe, W., 498
Polanczyk, G., 466
Polivy, J., 311, 313, 315
Polkinghorn, C., 162
Pollak, S. D., 51
Pollock, V. E., 421
Pomery, C., 304
Poortinga, Y. H., 79
Pope, H. G., 201, 280, 317
Pope, H. G., Jr., 227, 229
Porter, R., 11, 13, 14
Porter, V. R., 498
Potter, G. G., 481
Poulet, E., 394
Poulton, R., 185
Poustka, F., 454
Power, K. G., 217
Prazeres, A. M., 205
Prescott, C. A., 160, 184
Pressman, L. J., 470
Pretzer, J. L., 408, 439
Price, R. W., 496
Prichard, Z. M., 420
Pridmore, S., 420
Prince, M., 491
Prince, V., 342
Prins, A., 213
Prochaska, J. O., 288, 289
Propper, C., 49
Puente, A. E., 481, 495
Pull, C. B., 186
Putnam, F. W., 236, 238, 239
° Q °
Quattrocchi, M. R., 516, 517
Quinn, O. W., 370, 380, 397
Quinn, P. O., 466
Quinsey, V. L., 339
Quinta Gomes, A. L., 356
Quinton, D., 409
N -9 Name Index
° R °
Rabin, L. A., 495, 498
Rachman, S. J., 174
Raimo, E. B., 230
Raine, A., 414, 415, 416, 417, 420,
421, 513
Rakoff, D., 9
Ramaekers, J. G., 280
Ramafedi, G., 148
Ramanathan, S., 53
Ramírez-Esparza, N., 234
Ramos, B. M. C., 282
Ramus, F., 457
Rao, V., 35
Rapee, R. M., 44, 179
Rapoport, J. L., 380
Rasmussen, P. R., 434
Ratey, J. J., 465
Rauch, S. L., 203
Rauh, H., 54
Ray, B., 523
Raymond, N. C., 340
Rayner, R., 41, 91
Reagan, R., 509
Rebec, G. V., 264
Rector, N. A., 386, 387, 395
Regier, D. A., 198, 262, 264, 376
Reich, J., 438
Reid, G., 271
Reid, W. J., 421
Reifman, A., 151
Reiland, R., 401–403, 406, 407,
408, 411, 417, 418, 423, 425, 427,
429, 431, 432, 436, 437, 440
Reinberg, A., 64
Reinders, A. A., 235
Reiss, S., 170
Relkin, N., 498
Remen, A. L., 428
Rende, R., 23
Renner, L. M., 51
Resinger, E., 172
Rettew, D. C., 49
Retz, W., 468
Reynolds, C. A., 414
Rhode, P., 119, 120
Ricciardelli, L. A., 317
Riccio, C. A., 468
Rice, F., 123
Rice, M. E., 421, 422
Richter, M. A., 35, 203
Rickman, R. L., 170
Rieber, R. W., 235
Rief, W., 243
Ries, R. K., 291
Rifkin, A., 233
Riley, E. A., 328
Riley, E. P., 447
Riskind, J. H., 46, 185
Rivas-Vazquez, R. A., 180
Roane, K. R., 512
Robbins, I., 215
Robbins, T. W., 267
Roberson-Nay, R., 191
Roberts, A. L., 330
Roberts, J. E., 204
Roberts, M. C., 505
Roberts, T., 316
Robins, C. J., 425, 427, 428
Robinson, D., 394
Robinson, J., 277
Robinson, L. A., 116
Robinson, T., 345
Rodewald, F., 225
Roelofs, K., 248
Roesler, A., 344
Rogan, R. G., 51
Rogers, C., 18
Rogers, S. J., 454
Rohde, D., 507, 508, 511, 524
Rohde, L. A., 466
Rohde, P., 120
Roisman, G. L., 49
Rollnick, S., 289
Romach, M. K., 276
Romero, M. P., 147
Room, R., 277
Rorschach, H., 80
Rosa, A. R., 144
Rosario-Campos, M. C., 205
Rosen, B. R., 202–203
Rosen, J., 310
Rosen, J. B., 177
Rosen, R. C., 352
Rosenbaum, B., 393
Rosenbaum, J. F., 122, 130, 142,
144, 180, 205, 217, 286, 287
Rosenberg, H., 285
Rosenberg, R. S., 66
Rosenbloom, M., 73, 513
Rosenfarb, I. S., 51, 389
Rosenthal, D., 365, 374, 377, 394
Rosenthal, R., 98
Rospenda, K., 54
Ross, C. A., 234, 236
Ross, L. K., 498
Ross, L. T., 81
Ross, R., 122, 141
Roth, A., 108, 177
Rothbaum, B. O., 186
Rothman, E., 63
Rouanzoin, C. C., 217
Roy, A., 246
Ruane, J., 156, 157, 165, 166, 167,
168, 173, 174, 191
Rubia, K., 468
Ruffolo, J. S., 201
Ruini, C., 250
Ruiz-Sancho, A. M., 410
Rund, B. R., 370
Ruscio, A. M., 159
Rush, A. J., 120
Rush, B., 14
Russell, C. J., 315
Russell, M., 276
Russell, T. A., 388
Rutherford, M. D., 454
Rutter, M., 54, 409
Ryan, C. F., 281
Rybakowski, F., 49
° S °
Saatcioglu, O., 292
Saba, G., 394
Sachdev, P. S., 8
Sachs-Ericssson, N., 126
Sacktor, N., 496
Sadock, B. J., 341
Sadock, V. A., 341
Safren, S. A., 472
Saha, S., 378
Saladin, M. E., 285
Salekin, R., 422
Salkovskis, P. M., 186, 205, 251
Salloum, I., 276
Salmán, E., 167
Salo, R., 265
Salthouse, T. A., 479, 480
Sánchez, H. G., 148, 149
Sanderson, W. C., 158
Sands, J. R., 376
Sanfilipo, M., 381
Sansone, L. A., 299
Sansone, R. A., 299
Santa Ana, E. J., 285
Santangelo, S. L., 453
Santisteban, D. A., 134
Sar, V., 230
Sarbin, T. R., 237
Sareen, J., 419
Sarró, R., 12, 13
Sartor, C. E., 214
Satcher, D., 151
Sattler, J. M., 452
Saudino, K. J., 49
Sava, F. A., 133
Saxena, S., 203
Sayette, M. A., 269
Scarmeas, N., 493
Scarpa, A., 52
Scarr, S., 40
Schafe, G. E., 42
Schena, M., 39
Schmahl, C. G., 424
Schmaling, K. B.. 63
Schmidt, N. B., 170
Schmitt, D. P., 408
Schneider, F. R., 49, 420
Schneider, L. S., 498
Schneider, M., 468
Schneider-Axmann, T., 73, 387
Schnurr, P. P., 217, 218
Schoevers, R. A., 159
Schopp, R. F., 516, 517
Schore, A. N., 421
Schulenberg, J., 273
Schulte-Körne, G., 458
Schultze-Lutter, F., 375
Schwartz, J. M., 207
Schwarz, M., 35
Schwarz, N., 102
Schweighardt, R., 278
Schwitzer, G., 494
Scott, D. J., 105
Scott, J., 142, 145
Seedat, S., 217, 225
Seeman, M., 373
Seeman, M. V., 37
Segal, Z. V., 340, 481, 482
Segraves, R. T., 355
Segrin, C., 116, 126
Segui, J., 230
Seidman, L. J., 381
Seidman, S. N., 111
Seivewright, H., 419
Seligman, M. E., 44, 125
Sellers, E. M., 267, 269, 276, 287
Selten, J., 389
Semkovska, M., 131
Senior, R., 314
Sereny, G., 286
Sergi, M. J., 385
Serin, R. C., 421
Serra, M., 453
Seto, M. C., 421
Shabsigh, R., 350
Shadish, W. R., 109, 292
Shaffer, G. W., 11, 16
Shah, N., 323
Shalev, A. Y., 214, 218
Shaley, A. Y., 211
Shankar, C., 513
Shapira, B., 131
Name Index N -10
Shapiro, F., 217
Shattuck, P. T., 452
Shaver, P. R., 25, 408
Shaw, H., 315, 323
Shaw-Zirt, B., 469
Shawcross, C. R., 131
Shaywitz, B. A., 457, 458, 459
Shea, M. T., 109, 434
Shear, K., 190
Shedler, J., 406
Sheehy, G., 3, 6, 7, 9, 10
Sheets, E., 406
Sheperd, G. M., 34
Sher, K. J., 260
Sherman, M. D., 218
Shi, Z., 421
Shiah, L., 341
Shifren, J. L., 353
Shin, L. M., 213
Shinbach, K., 520
Shindel, A. W., 340
Shooka, A., 204
Shor-Posner, G., 50
Siberski, J., 490
Siegel, S., 282
Sierra, M., 231, 232, 238
Siever, L. J., 41, 409, 425
Sigman, M., 452
Sigmon, S. T., 127
Sikström, S., 178, 481
Silber, T. J., 304
Silk, T. J., 453
Silver, E., 52
Silverman, K., 289
Silverman, W. K., 167
Silvershorn, P., 459
Silverstein, J. L., 355
Silverstein, M. L., 420
Simeon, D., 224, 230, 231, 232, 238
Simkins, S., 146
Simoni-Wastila, L., 262
Simons, A. D., 23
Simons, D., 340
Simons, R. L., 54
Simos, P. G., 459
Simpson, D. D., 292
Simpson, M. E., 150
Sinha, R., 262
Siqueland, L., 191
Siris, S. G., 379
Skeels, H., 448
Skeem, J. L., 379
Skinner, B. F., 19, 42
Skinstad, A. H., 108
Skodol, A. E., 404, 405, 406, 411,
413, 416, 417, 418, 425, 431,
434, 435, 439
Slack, K. S., 51
Slavich, G. M., 39, 100
Slavney, P. R., 67
Slomkowski, C., 469
Slomski, A., 266
Slotema, C. W., 132
Small, G. W., 494
Smart, E., 515
Smeets, G., 251
Smith, A., 420
Smith, D. B., 218
Smith, E. E., 31, 344
Smith, L., 26
Smith, L. C., 353
Smith, T. C., 209
Smith, Y. L. S., 334
Smolak, L., 311, 316
Smoller, J. W., 203
Snitz, B. E., 494
Snow, A. C., 305
Snowden, L. R., 378
Snyder, L. B., 277
Sobell, L. C., 285
Sobell, M. B., 285
Solanto, M. V., 470
Soloff, P. H., 409, 425
Solomon, D. A., 120
Solomon, J., 21
Somers, J. M, 157, 167, 169
Sonuga-Barke, E. J. S., 472
Soomro, G. M., 205
Soto, O. R., 373
Sourander, A., 54
South, S. C., 39, 407
Sowell, E. R., 468
Spanier, C., 321
Spanos, N. P., 235, 237
Sparén, P., 300
Spector, A., 498
Spector, I. P., 351
Spiegel, D., 224, 226, 229, 230, 239,
243, 245, 246, 252, 253
Spiegel, H., 248
Spielberg, S., 373
Spielberger, C. D., 170
Spielmans, G. L., 133
Spira, A. P., 499
Spiro, C. S., 367
Spitz, B., 263, 278
Spitzer, R. L., 280, 339, 340, 342,
343, 351, 352, 368, 436, 482, 485
Spoor, S. T. P., 311
Squire, L. R., 32, 213
Staba, D., 139
Stafford, J., 234
Staines, G. L., 262
Stanton, M. D., 292
Staples, J., 356
Starr, R., 257, 271, 284
Steadman, H. J., 511, 514
Steele, J. B., 195, 196, 204, 206,
218
Stefens, D. C., 481
Stein, A., 314
Stein, D. J., 160, 180, 209, 217
Stein, M. B., 44, 169, 178
Steiner, B. W., 334
Steinfeld, B. I., 50
Steinhausen, H., 299
Steketee, G., 197
Stephens, J. H., 148
Stermac, L. E., 340
Stevens, J., 466
Stevens, M. C., 468
Stevens, T., 495
Stevenson, J., 469
Stewart, J., 269
Stewart, S., 271, 277
Stewart, W. F., 119
Stice, E., 316, 323
Stinson, F. S., 183, 406
Stitzer, M., 289
Stock, W. E., 359
Stolley, M. R., 304
Stone, A. L., 266
Stone, J., 246, 247
Strain, E. C., 287
Strakowski, S. M., 63, 69, 70
Straube, T., 184
Striegel-Moore, R. H., 309, 311,
314, 315
Strober, M., 310, 314
Stuart, G. L., 262
Stuart, S., 252
Styron, W., 117
Subramaniam, P., 498
Sue, S., 111
Suh, J. J., 286
Sullivan, H. S., 17
Sullivan, T., 353
Sulpy, D., 278
Sundgot-Borgen, J., 315
Sundquist, A., 395
Sundquist, K., 276, 284
Surguladze, S. A., 45
Swaab, D. F., 32
Swanson, J. M., 268, 469, 517
Swartz, M. S., 376, 519
Sweeney, P. D., 469
Swerdlow, R. H., 513
Swica, Y., 236
Swift, A., 21
Swinson, R. P., 176, 312
Swire, P. P., 506
Szapocznik, J., 292
° T °
Tager-Flusberg, H., 454
Takeshita, J., 389
Tallman, K., 106
Tan, H. M., 353
Tandon, R., 378
Tang, T. Z., 110
Tanielian, T., 54
Tanofsky-Kraff, M., 321
Tantleft-Dunn, S., 314, 321
Tarasoff, T., 516, 517
Tareen, A., 82
Tariot, P. N., 498
Tarloff, D., 520
Tarrier, N., 217, 394, 395
Tarullo, A. R., 51
Taylor, C. T., 180, 438
Taylor, J. Y., 299, 303, 315
Taylor, M. F., 262
Taylor, S., 174, 180, 217, 218, 252
Teasdale, B., 52
Teasdale, J. D., 101, 133
Tebartz van Elst, L., 424
Teicher, M. H., 409
Temple, E., 459
Tengström, A., 379
Tennant, C., 126
Tennen, H., 469
ter Kuile, M., 360
Thase, M. E., 133
Thom, A., 187
Thomas, G. V., 404
Thompson, J. K., 299, 311, 314,
316
Thompson, J. M., 142
Thompson, P. M., 265
Thompson, S. B. N., 484
Thomsen, P. H., 203
Thorn, B. L., 45
Thorndike, E. L., 19
Tidley, J. W., 376
Tiefer, L., 354, 356
Tienari, P., 384, 385, 391, 416
Tillfors, M., 74, 435
Timko, C., 292
Tolin, D. F., 211
Tomarken, A. J., 185
Tomkins, D. M., 267, 269, 287
Torey, E. F., 369, 370, 376, 377
N -11 Name Index
Torgersen, S., 404, 416, 434, 436
Torgersen, S. G., 169
Torrens, M., 268, 269, 271
Torrey, E. F., 396
Tost, H., 344
Toth, S. L., 48, 51
Towbin, K. E., 450
Tozzi, F., 305
Tractenberg, R. E., 491
Trestman, R. L., 416
Triandis, H. C., 55
Trierweiler, S. J., 63
Trimarchi, C. L., 450
Trimble, J. E., 263
Trull, T. J., 405, 406, 424
Tsatsanis, K., 453
Tsoi, W. F., 390
Tsuang, M. T., 375
Tsuchiya, K. J., 143
Tucker, D., 521
Tucker, J. A., 290
Turetsky, B. I., 366
Turkington, D., 395
Turnbull, J. D., 316
Turner, S. M., 204
Tuthill, R. W., 470
Twenge, J. M., 50, 170
Tye, C., 453
Tyrer, P., 414
Tyson, A. S., 150
° U °
Unwin, G. L., 448
Urban, K., 6
Utermohlen, W., 492
V
Vajk, F. C., 127
Valcour, F., 345
Valera, E. M., 468
Van Allen, J., 505
van Balkom, A. J. L. M., 180
Van Bergen, A., 237
van den Heuvel, O. A., 45, 169
van der Kloet, D., 236
Van der Linden, G. J. H., 180
van der Mast, R. C., 487
van Duijl, M., 236
van Elst, L. T., 383
van Erp, T. G. M., 382
Van Gerwen, L. J., 186
van Goozen, S. H. M., 334
van Hoeken, D., 299, 303
van Os, J., 381
van Reekum, R., 424
Van Thiel, D. H., 272
van Zuiden, M., 215
Vance, A., 468
Vansteenwegen, D., 186
Veale, D., 201
Vehmanen, L., 142
Veling, W., 389
Verduin, T. L., 190
Verheul, R., 268, 406
Verkes, R. J., 266
Vidal, C. N., 33
Viding, E., 463
Vieweg, R., 131
Vijayakumar, L., 150
Villaseñor, Y., 63
Viney, W., 14
Vita, A., 100, 381
Vogel, M., 383
Voglmaier, M. M., 416
Voineskos, A. M., 371
Volkow, N. D., 35, 265, 267, 268,
469, 471
Völlum, B., 420
Von Holle, A., 299
von Ranson, K. M., 299
von Zerssen, D., 390
Vuchinich, R. E., 290
° W °
Waber, R. L., 105
Wade, D., 375
Wade, D. T., 248
Wadsworth, S. J., 458
Wagner, P. S., 367
Wahlbeck, K., 381
Waitzkink, H., 63
Wakefield, J. C., 64, 118
Walach, H., 111
Waldeck, T. L., 416
Waldman, I. D., 469
Wales, H. W., 516
Walker, E., 381
Walker, E. F., 382, 383, 385
Walker, L. S., 244
Walker, M., 142
Walker, Z., 495
Wallace, C., 516
Wallach, H. R., 234
Waller, G., 311
Waller, N. G., 408
Wallien, M. S., 332
Walling, M. K., 243
Walls, B., 59
Walls, J., 59–62, 72, 81, 84
Walls, L., 59
Walls, M., 59, 62
Walls, R., 59–62, 65, 72, 84
Walls, R. M., 59–62, 64, 65, 72, 84
Walsh, A. E., 317
Walsh, B. T., 111, 300, 303, 319,
320
Walsh, T., 315
Walters, E. E., 242
Wampold, B. E., 106, 107, 108
Wang, P. S., 71
Wann, D. L., 45
Waslick, B. D., 120
Wasserman, E. M., 132
Watanabe, Y., 382
Waters, M., 147
Watkins, P. C., 101
Watson, A. C., 64
Watson, D., 158
Watson, J., 36, 477, 478, 481, 488,
500
Watson, J. B., 19, 41, 91
Watson, J. C., 53
Watts-English, T., 51
Weaver, C. M., 506, 507, 508, 509,
510, 512, 513, 514, 516, 517,
518, 522
Webb, S. J., 454
Webdale, K., 507, 515, 520
Wegner, D. M., 205
Weiler, S. J., 355
Weinberg, I., 424
Weinberger, J., 75
Weinstein, N. D., 261
Weiser, M., 376
Weisman, A. G., 391
Weiss, L. A., 453
Weissman, M. M., 52, 120, 146,
198, 204, 321
Weisz, J. R., 48
Welkenhuyusen-Gybels, J., 102
Weltzen, T. E., 317
Wender, P. H., 53
Wentz, P., 62
Wenzel, A., 178, 428
Wenzlaff, R. M., 129
Werch, C. E., 261
Werstiuk, E. S., 123
Werth, J. L., Jr., 517
Wertz, J. M., 269
West, S. G., 105
Westen, D., 75, 406, 425
Westenberg, H. G. M., 160
Whitaker, R., 14
White, H. R., 261
White, J. M., 281
White, K., 197
White, K. H., 170
White, M. A., 306
White, R. W., 12
Whitlock, J. L., 424
Whittinger, N. S., 464
Wiborg, I. M., 179
Wickramaratne, P., 52
Wickramaratne, P. J., 120
Wicks, S., 384
Widiger, T. A., 405, 406, 419, 423,
424
Widom, C. S., 125, 268
Wilfley, D. E., 321
Wilk, C. M., 369
Williams, D. L., 453
Williams, D. R., 54
Williams, N. M., 303
Williams, T., 151
Williams-Morris, R., 54
Williamson-Catania, J., 494
Wilson, B A., 499
Wilson, G. T., 320
Wilson, J. S., 416
Wilson, K. R., 438
Wilson, L., 71
Wilson, R. I., 35, 281
Wilson, W., 281
Windle, M., 151, 261
Windle, R. C., 261
Winerip, M., 515, 520
Winick, B. J., 521
Wintemute, G. J., 147
Wisco, B. E., 101
Wise, T., 344
Wise, T. N., 242, 243, 253
Wisner, K. L., 119
Witztum, E., 344
Wolk, S., 120
Wong, K. E., 390
Wong, S. C. P., 422
Wood, J. M., 80
Woods, B., 498
Woods, S. W., 393
Woodward, J., 235
Woodward, T. S., 386
Woody, E. Z., 228
Wool, C., 251
Woolfolk, R. L., 163
Woolley, H., 314
Wright, L., 3, 7, 21, 52
Wright, M. O., 21
Wright, S., 265
Wrightsman, L. S., 509, 513
Wu, K. D., 438
Wuerker, A. K., 388
Wynne, L. C., 384
° X °
Xiao, Z., 236
Name Index N -12
° Y °
Yanaguchi, K., 261
Yang, L. H., 51
Yates, A., 510
Yates, P. M., 340
Yen, S., Sr., 416
Yildiz, A., 144
Yip, P. S. F., 146
Yoon, T., 381
Young, D. M., 127
Yovel, L., 48
Yurgelin-Todd, D., 280
° Z °
Zabinski, M. F., 323
Zalsman, G., 150
Zammit, S., 376
Zanarini, M. C., 404, 417, 424
Zeeck, A., 303
Zhang, A. Y., 378, 383
Zhang, L., 494
Zhou, P., 315
Ziegler, F. J., 246
Zimering, R. T., 214
Zimmerman, M., 159
Zinbarg, R., 44, 179
Zipfel, S., 298, 299
Zisook, S., 118
Zlotnick, C., 134
Zornberg, G. L., 382
Zorumski, C. F., 34
Zubieta, J.-K., 142
Zucker, K. J., 329, 331, 332, 333
Zuckerman, M., 420
° A °
ABAB design, single-participant
studies and, 97
Abnormal brain structures,
neuroimaging techniques and,
73, 73f
Abnormal communications,
neurons and, 36
Abnormal psychomotor behavior,
368
Absent fathers, separation anxiety
disorder and, 191
Abstinence-focused treatments,
substance use disorders and,
284–285
Abstinence reinforcement,
substance use disorders and, 289
Abstinence violation effect, 311
Acculturation, 55
Acetylcholine, 35t
Acquiescence, questionnaires and,
102
Action potential, 34
Active interaction, genes and, 40
Active phase, schizophrenia and, 37
Acute stress disorder, 208, 211–212,
212t
Adaptive functioning, intellectual
disability and, 444–445
Adderall, 264
Adolescent-onset type, conduct
disorder and, 462
Adoption studies, 38–39
Adrenaline (epinephrine), 35t
Affect, 47, 403
Aging. See also Cognitive
functioning
anxiety disorders and, 482
attention and, 480
cognitive functioning and,
479–481
depression and, 119, 481, 481t
intelligence and, 479–480
memory and, 480
processing speed and, 480
schizophrenia and, 482
sexual dysfunctions and, 355
working memory and, 481
Agnosia, 483, 488
Agoraphobia
anxiety sensitivity and, 170
behavioral methods and, 173
brain systems and, 169
catastrophic thinking and, 170
cognitive explanations and, 170
cognitive methods and, 173–174
DSM-5 diagnostic criteria for, 168t
facts at a glance and, 169t
feedback loops and, 171, 172f,
174, 175f
genetics and, 169
learning theory and, 170
nature of, 167–168
neural communication and, 169
neurological factors and, 169
psychological factors and, 170
safe people and, 171
social factors and, 170–171
targeting neurological factors
and, 171–172
targeting psychological factors
and, 172–174
targeting social factors and, 174
Alcohol intake, 272–274
alcohol use disorder and,
273–274
binge drinking and, 273
blackouts and, 274
blood alcohol concentration and,
272–273, 272f
cravings and, 273
loss of control and, 273
physical dependence and, 273
tolerance and, 273
Alcohol use disorder
abstinence-only position
regarding, 285
biological by-products of,
275–276, 275f
as coping strategy, 276–277
cultural differences and, 277
delirium tremens and, 275
gender and, 277
genetics and, 275
hangovers and, 275–276
twelve-step facilitation and,
290–291, 290t
Alcoholics Anonymous, 290–291,
290t, 291
All-or-nothing thinking, 46t
Allegiance effect, 109
Alogia, 369
Alphabetic principle, treating
dyslexia and, 458–459
Alprazolam (Xanax), 171, 274
Altered appearance, gender
dysphoria and, 333–334
Alternative female sexual response
cycle, 354f
Alzheimer’s disease, 490–494
amyloid plaques and, 494
brain abnormalities and,
493–494
genetics and, 494
neurofibrillary tangles and,
493–494, 493f
prevalence of, 493t
progression of, 493
targeting neurological factors
and, 498
targeting psychological factors
and, 498–499
targeting social factors and, 500
American Foundation for Suicide
Prevention, 151t
American Legal Institute (ALI)
test, 509
Americans with Disabilities Act, 449
Amitriptyline (Elavil), 130
Amnesia. See Dissociative amnesia
Amobarbital (Amytal), 274
Amok, 227
Amphetamine psychosis, 265
Amphetamines, 264–265
Amygdala
bipolar disorders and, 141
borderline personality disorder
and, 424–425
central role of, 32
depressants and, 275
social anxiety disorder and, 178
specific phobia and, 184
Amyloid plaques, 494
Analgesics, 278–279
Ancient views of psychopathology,
10–14
ancient Greeks and Romans,
11–12
asylums and, 13
Chinese Qi, 11
eighteenth and nineteenth
centuries, 12–14
imbalance of substances within
body, 11–12
mental treatment and, 13
Middle Ages and Renaissance, 12
moral treatment and, 13–14
supernatural forces and, 11
Angelman syndrome, 447t
Anhedonia, 116, 369
Animal type of phobia, 182
Anorexia nervosa, 298–302. See also
Eating disorders
binge eating/purging type and,
300
body image distortions and, 298,
299f
cognitive-behavior therapy and,
320
dehydration and, 301
distinction from bulimia, 305
DSM-5 diagnostic criteria and,
298–300, 299t
facts at a glance and, 299t
intense fear and, 298
medical effects of, 301
muscle wasting and, 301
obsessive-compulsive disorder
and, 300
psychological effects and,
301–302
restricting type and, 300
social effects and, 301–302
starvation and, 301–302
very low body weight and, 298
Anticonvulsants, 144
Antidepressants, 130–131
Antiepileptic medications, bipolar
disorders and, 144
Antipsychotic medications
dementia and, 498
schizophrenia and, 393–394
Antisocial personality disorder,
418–422
criminality and, 419–420, 420t
DSM-5 diagnostic criteria and,
418t
facts at a glance and, 419t
feedback loops and, 421
neurological factors and, 420
psychological factors and, 420
psychopathy and, 419
social factors and, 421
treatment of, 421–422
Anxiety disorders
cognitive psychology and, 20
comorbidity and, 157–158
delirium and, 486
depression and, 120, 158, 158f
fight-or-flight response and,
156–157
gender and, 157
generalized anxiety disorder,
158–165
illness anxiety disorder, 250
nature of, 156
older adults and, 482
panic and, 157
panic disorder and agoraphobia,
165–175
phobias and, 157
posttraumatic stress disorder and,
214
schizophrenia and, 376
separation anxiety disorder,
188–191
social anxiety disorder, 175–181
specific phobias, 182–187
Anxious-ambivalent attachment,
126
Aphasia, 483, 488
Appearance
clinical interviews and, 75
excessive concern with, 311
Applied behavior analysis, autism
spectrum disorder and, 454
Approach emotions, 49
Apraxia, 483, 488
Archetype, 17
Aripiprazole (Abilify), 144
Aromatherapy, 109
Arousal patterns, paraphiliac
disorders and, 336, 337t
Arthritis, 482–483
Asociality, 369, 371
Asperger’s disorder, 450
S-1
SUBJECT INDEX
Subject Index S -2
Assertive community treatment,
schizophrenia and, 396
Assessment. See also Clinical
interviews
abnormal brain structures and, 73
brain function and, 73–74
clinical interview and, 75–78
cognitive assessment, 78–79
community factors and, 82
computerized axial tomography
(CT) and, 73
cultural factors and, 82–83, 83f
family functioning and, 81
functional magnetic resonance
imaging (MRI) and, 74
as interactive process, 83–84
magnetic resonance imaging
(MRI) and, 73
neurological and other biological
factors and, 72–73
neuropsychological testing and,
74
personality assessment, 79–80
positron emission tomography
(PET) and, 74
social factors and, 81–83
tests of psychological functioning,
78–80
X-rays and, 73
Asylums, 13, 13f
Ataque de nervios, 167
Atenolol, 286
Atomoxetine (Strattera), 472
Attachment difficulties, child
maltreatment and, 52
Attachment style, 21, 21f, 126–127,
408
Attention, mental processes and,
45, 480
Attention biases, depressive
disorders and, 124
Attention-deficit/hyperactivity
disorder (ADHD), 464–473
blame and credit and, 469
brain systems and, 467–468
changes over time, 466–467
changing parent’s behavior and,
472
contingency management and,
473
DSM-5 diagnostic criteria and,
465t
facial expression recognition and,
468–469
facts at a glance and, 466t
feedback loops and, 469–471,
471f, 473, 473f
forms of, 465–466
gender and, 465
genetics and, 468
group settings and, 466–467
hyperactive/impulsive form of,
466
inattentive form of, 466
medication and, 471
multisystemic therapy and, 473
neural communication and,
467–468
neurological factors and,
467–470
parent management training
and, 472
psychological factors and,
468–469
reinforcement in relationships
and, 472–473
self-esteem and, 468–469
social factors and, 469
targeting neurological factors
and, 471
targeting psychological factors
and, 471–472
targeting social factors and,
472–473
treating disruptive behavior and,
471–472
Attention difficulties
delirium and, 484–485
schizophrenia and, 369, 385–386
Attenuated psychosis syndrome,
375
Attributional style, depressive
disorders and, 124–125
Attributions
emotions and, 48
schizophrenia and, 386–387
Atypical antipsychotics,
schizophrenia and, 393–394
Auditory hallucinations, 7, 387
Autism spectrum disorder, 449–455
applied behavior analysis and,
454–455
brain systems and, 453
childhood milestones and, 451
cognitive deficits and, 453–454
communication problems and,
454
DSM-5 diagnostic criteria and,
450t
facilitating communication and,
455
facts at a glance and, 452t
genetics and, 453
intelligence tests and, 451
neurological factors and, 453
psychological factors and,
453–454
recognizing facial expressions
and, 453
social factors and, 454
social skills and, 455
symptoms of, 450–451
targeting neurological factors
and, 454
targeting psychological factors
and, 454–455
targeting social factors and, 455
theory of mind and, 454
unique skills and, 451
Autonomic nervous system (ANS),
31
Aversive self-awareness, 312–313
Avoidant attachment, 21, 126
Avoidant personality disorder
distinguishing from other
disorders, 434–435
DSM-5 diagnostic criteria and,
433t
facts at a glance and, 434t
social phobia and, 435
Avolition, 369
Axons, 34
° B °
Barbiturate use disorder, 274
Basal ganglia, obsessive-compulsive
disorder and, 203
Baseline assessments, 107
Bath salts, 266
Beck, Aaron, 20
Bed nucleus of the stria terminalis,
332
Behavior therapy, depression and,
132–133
Behavioral activation, 132
Behavioral consequences,
personality disorders and, 408
Behavioral genetics, 37
Behavioral symptoms
clinical interviews and, 76
depression and, 116–117
emotions and, 47–48
personality disorders and, 403
Behavioral therapy methods
generalized anxiety disorder and,
162–163
obsessive-compulsive disorder
and, 206
panic disorder and agoraphobia
and, 173
specific phobias and, 186
Behaviorism, 19–20, 19f
Bender Visual-Motor Gestalt
Test-II, 74
Benzedrine, 264
Benzodiazepines, 186, 274–275
Bereavement exclusion, depression
and, 118
Beta-blockers, social anxiety
disorder and, 180
Bias, experimental, 92
Binge drinking, 273
Binge eating disorder, 305–307
as an escape, 312–313, 312f
anorexia nervosa and, 300
bulimia nervosa and, 305
DSM-5 diagnostic criteria and,
305t
facts at a glance and, 306t
as valid diagnosis, 307
Biofeedback, generalized anxiety
disorder and, 162
Biological factors
alcohol use disorder and,
275–276, 275f
eating disorders and, 319–320
gender dysphoria and, 333–334
paraphilic disorders and, 345
psychological disorders and, 22
schizophrenia and, 382
sexual dysfunctions and, 358–359
Biopsychosocial approaches, 23–25
Bipolar disorders, 136–145
brain systems and, 141
cognitive deficits and, 142
cyclothymic disorder and,
140–141, 140t
diagnostic criteria for, 139t
dissociative identity disorder
and, 234
expansive mood and, 137
facts at a glance and, 140t
feedback loops and, 143, 145
flight of ideas and, 139
genetics and, 142
hypomanic episodes and, 139
manic episodes and, 136–139,
137t
mood episodes and, 136–139
neural communication and, 142
neurological factors and, 141–142
pleasurable activities pursuit and,
139
psychological factors and, 142
rapid cycling and, 139
social factors and, 143
stress and, 143
targeting neurological factors
and, 144
targeting psychological factors
and, 144
targeting social factors and, 145
types of, 139–141
Blackouts, alcohol use disorder and,
273–274
Blood alcohol concentration,
272–273, 272f
Blood-injection-injury type of
phobia, 182
Bodily complaints, somatic
symptom disorders and, 240, 240t
Bodily signals, misinterpretation
of, 243
Body dysmorphic disorder, 199–202
catastrophic thinking and, 202
cognitive biases and, 202
common preoccupations and,
200
S -3 Subject Index
compulsions and, 200
defect perceptions and, 200
DSM-5 diagnostic criteria and,
200t
facts at a glance and, 201t
Body image distortions, anorexia
nervosa and, 298, 299f
Body weight, anorexia nervosa
and, 298
Borderline personality disorder,
422–429
brain systems and, 424–425
cognitive-behavior therapy and,
427
comorbid depression and, 423
dialectical behavior therapy and,
428
DSM-5 diagnostic criteria and,
422t
emotional stimuli and, 423
emphasizing patient’s experience
and, 427
facts at a glance and, 424t
feedback loops and, 426–427,
426f, 428–429, 429f
genetics and, 425
interpersonal therapy and, 428
invalidation and, 425–426
medication and, 427
neural communication and, 425
neurological factors and, 424–425
parasuicidal behavior and, 423
psychological factors and, 425
self-destructive behaviors and, 425
social factors and, 425–426
targeting neurological factors
and, 427
targeting psychological factors
and, 427–428
targeting social factors and, 428
Zen Buddhist approach to, 427
Brain activation, conversion
disorder and, 248f
Brain circuits, 33
Brain function, clinical assessment
and, 73–74
Brain lobes, 31–32, 31f
Brain stimulation
depressive disorders and, 131–132
schizophrenia and, 394
Brain structure and function, 30–36
action potential and, 34
Alzheimer’s disease and,
493–494
axon, dendrites, and glial cells, 34
brain circuits and, 33
brain lobes, 31–32, 31f
brain systems and, 33
cell body and, 33
central nervous system and, 31
chemical signals and, 34–36
cortex and, 32
neurons and, 32–33, 33f
peripheral nervous system and,
31
subcortical brain areas and, 32, 32f
Brain systems
attention-deficit/hyperactivity
disorder and, 467–468
autism spectrum disorder and,
453
bipolar disorders and, 141
depressants and alcohol use and,
275
depressive disorders and, 122
eating disorders and, 309–310
gender dysphoria and, 332
generalized anxiety disorder and,
160
obsessive-compulsive disorder
and, 202–203
panic disorder and agoraphobia
and, 168–169
posttraumatic stress disorder and,
213
schizophrenia and, 380–382
social anxiety disorder and,
177–178
specific learning disorder and,
457–458
specific phobias and, 184
stimulant abuse and, 267–268
Brain trauma, dissociative amnesia
and, 228
Brain tumors, 482
Breathing retraining
generalized anxiety disorder and,
162
panic disorder and agoraphobia
and, 173
posttraumatic stress disorder and,
219
Brief psychotic disorders, 373, 375t
Broca’s aphasia, 483
Bulimia nervosa, 302–305. See also
Eating disorders
cognitive-behavior therapy and,
320
distinction from anorexia, 305
distinction from binge eating
disorder, 305
DSM-5 diagnostic criteria and,
302–303, 303t
facts at a glance and, 303t
frequent vomiting and, 304
laxative use and, 304
medical effects of, 304
purging and, 304
Bullying, 54
Buprenorphine (Subutex), 287
Bupropion (Zyban), 286
Burnout, 82
Buspirone (Buspar), 161
° C °
Cannabinoids, 281
Cannabis use disorder, 280
Carbamazepine (Tegretol), 144
Caregiver training, dementia and,
499
Case studies, 96–97, 98t
Castration, 345
Catastrophic thinking
body dysmorphic disorder and,
202
illness anxiety disorder and, 251
panic disorder and agoraphobia
and, 170
somatic symptom disorder and,
243
Catatonia, 368
Causation, correlational research
and, 94
Cell body, 33
Cell migration, 381–382
Central nervous system (CNS), 31
Cerebellum, attention-deficit/
hyperactivity disorder and, 467
Cerebral cortex, 32
Chemical castration, 345
Chemical receptors, 35
Chemical signals, 34–36
abnormal communications and,
36
chemical receptors and, 35
neurotransmitters and, 34–35, 35t
reuptake and, 36
synapse and, 34, 35f
Childhood maltreatment, 51–52
altered bodily and neurological
response to stress and, 51
attachment difficulties and, 52
bullying and, 54
depression and, 120
emotional abuse and, 231
facial expression responses and,
51
learned behaviors and, 51
molestation and, 337t, 339–340
physical or sexual abuse and, 229,
355–356
social isolation and, 52
Childhood-onset type, conduct
disorder and, 462–463
Chinese Qi, 11
Cholinesterase inhibitors, 498
Citalopram (Celexa), 205
Civil commitment, mentally ill
patient and, 518
Classical conditioning, 41–42
conditioned responses and, 42
conditioned stimulus and, 41
fear and, 42f
feedback loops and, 44
paraphilic disorders and, 344
social anxiety disorder and, 179
specific phobias and, 185
stimulant abuse and, 268–269
stimulus generalization and, 42
unconditioned response and, 41
unconditioned stimulus and, 41
Classification systems, diagnosis
and, 64
Claustrophobia, 187, 187t
Client-centered therapy, 18
Clinical interviews, 75–78
appearance and, 75
behavior and, 76
factitious disorder and, 77
malingering and, 77
mental processes and, 76
mental status exam and, 77–78
movements and, 76
observation and, 75–76
patient’s self-report, 76–77
reporting bias and, 77
researching psychological factors
and, 101
semistructured interviews, 75,
77–78
speech and, 76
structured interviews, 75
unstructured interviews, 75
Clinical neuropsychologists, 70
Clinical psychologists, 70
Clomipramine (Anafranil), 171
Clonazepam (Klonopin), 171, 274
Clonidine (Catapres), 287
Cloninger, C. Robert, 49–50, 50t
Club drugs, 280–281
Cluster A personality disorders, 405
Cluster B personality disorders, 405
Cluster C personality disorders, 405
Cocaine use, 264, 264t, 267, 267f
Cognitive assessment, 78–79
Cognitive-behavior therapy
anorexia and, 320
anxiety disorders and, 181
attention-deficit/hyperactivity
disorder and, 472
borderline personality disorder
and, 427
bulimia and, 320
depression and, 133
generalized anxiety syndrome
and, 163
histrionic personality disorder
and, 431
mood disorders and, 133
narcissistic personality disorder
and, 432
obsessive-compulsive disorder
and, 206
odd/eccentric personality disorders
and, 417
Body dysmorphic disorder
(continued)
Subject Index S – 4
panic disorder and agoraphobia
and, 173–174
paraphilic disorders and, 346
personality disorders and,
409–410
posttraumatic stress disorder and,
218
schizophrenia and, 394
sexual dysfunctions and, 359
specific phobias and, 186–187
substance use disorders and,
289–290
Cognitive biases
body dysmorphic disorder and,
202
social anxiety disorder and,
178–179
Cognitive deficits
asociality and, 371
attention deficits, 369
autism spectrum disorder and,
453–454
bipolar disorders and, 142
depersonalization-derealization
disorder and, 231
depression and, 124
enduring over time, 370
executive functioning deficits,
370
loosening of association and, 371
obsessive-compulsive disorder
and, 204
panic disorder and agoraphobia
and, 170
schizophrenia and, 369–370,
385–386
working memory deficits,
369–370
Cognitive distortions of reality,
46, 46t
Cognitive functioning. See also
Delirium; Dementia
agnosia and, 483
anxiety disorders and, 482
aphasia and, 483
apraxia and, 483
attention and, 480
delirium and, 484–488
dementia and, 488–499
depression and, 481, 481t
diseases and illnesses and,
482–483
head injury and, 484
intelligence and, 479–480
medical factors affecting,
482–484
memory and, 480
normal aging and, 479–481
processing speed and, 480
psychological disorders and
cognition, 481–482
schizophrenia and, 482
stroke and, 483, 483f
substance-induced changes in,
484
working memory and, 481
Cognitive psychology, 20–21
Cognitive restructuring
generalized anxiety syndrome
and, 163
mood disorders and, 133
obsessive-compulsive disorder
and, 206
panic disorder and agoraphobia
and, 173–174
social anxiety disorder and,
180–181
Cognitive vulnerabilities, 46
Collectivist cultures, 54–55
Common liabilities model,
substance use disorders and, 261
Communication difficulties
autism spectrum disorder and,
454, 455
intellectual disability and, 449
Community-based care,
schizophrenia and, 396
Community factors, clinical
assessment and, 82
Comorbidity
agoraphobia and, 169t
anorexia nervosa and, 299t
antisocial personality disorder
and, 419t
anxiety disorders and, 157–158
attention-deficit/hyperactivity
disorder and, 466t
autism spectrum disorder and,
452t
avoidant personality disorder
and, 434t
binge eating disorder and, 306t
body dysmorphic disorder and,
201t
borderline personality disorder
and, 424t
bulimia nervosa and, 303t
clinical diagnosis and assessment
and, 66
conduct disorder and, 462t
conversion disorder and, 246t
delirium and, 486t
dementia and, 491t
dependent personality disorder
and, 436t
depersonalization-derealization
disorder and, 230t
dissociative amnesia and, 227t
dissociative identity disorder and,
233t
gender dysphoria and, 331t
histrionic personality disorder
and, 430t
intellectual disability and, 446t
narcissistic personality disorder
and, 432t
obsessive-compulsive disorder
and, 198t
obsessive-compulsive personality
disorder and, 437t
oppositional defiant disorder
and, 464t
panic disorder and, 167t
paranoid personality disorder
and, 412t
personality disorders and, 406, 406t
posttraumatic stress disorder and,
211t, 214–215
schizoid personality disorder and,
413t
schizophrenia and, 376–377, 395
schizotypal personality disorder
and, 415t
separation anxiety disorder and,
190t
sexual dysfunctions and, 353t
social anxiety disorder and, 177t
somatic symptom disorder and,
242t
specific learning disorder and, 457t
specific phobias and, 183t
substance use disorders and, 262
Competence to refuse treatment,
522–523
Competency to stand trial, 514–515
Complex attention disorders, 489
Complex inheritance, 37
Compulsions, 196
Compulsive gambling, 99
Computerized axial tomography
(CT), 73
Concordance rate, 169
Conditional emotional responses, 42
Conditioned arousal, paraphilic
disorders and, 344
Conditioned response, 42
Conditioned stimulus, 41
Conduct disorder, 460–463
adolescent-onset type, 462
antisocial personality disorder
and, 418
callous and unemotional traits
and, 463
childhood-onset type, 462–463
differences from oppositional
defiant disorder and, 464
DSM-5 diagnostic criteria and,
460t
facts at a glance and, 462t
levels of intensity and, 461
neither callous nor unemotional,
462
school problems and, 461
substance abuse and, 461
Confidentiality, 504–507
ambiguities regarding, 505
digital technology in therapy
and, 505
informed consent and mental
illness, 507
legal restrictions on, 506
limits of, 505–506
patient dangerousness and,
516–517
privileged communications and,
506–507
Confounding variables, 91
Congenital hypothyroidism, 447t
Conscious, psychoanalytic theory
and, 15
Contamination obsession, 198t
Contingency management
attention-deficit/hyperactivity
disorder and, 473
substance use disorders and, 289
Control delusions, 367
Control groups, 91–92
Conversion disorder, 244–248.
See also Somatic symptom
disorders
brain activation and, 248f
cognitive-behavior therapy for,
252t
criticisms of diagnostic criteria
and, 247
DSM-5 diagnostic criteria and,
245t
facts at a glance and, 246t
glove anesthesia and, 245f
malingering and, 247
military combat and, 248
motor symptoms and, 245
nature of, 245–247
neurological factors and, 247
psychological factors and,
247–248
seizures and, 245
self-hypnosis and, 247–248
sensory symptoms and, 245
social factors and, 248
stress response and, 248
symptoms and, 245
Coping illusion, generalized
anxiety disorder and, 161
Coping strategies
alcohol use disorder and,
276–277
dissociative disorders and, 238
somatic symptom disorder and,
243
Correlational coefficient, 94
Correlational research, 93–96, 98t
causation and, 94
correlational coefficient and, 94
epidemiology and, 95
five values of correlation, 95f
longitudinal studies and, 95–96
measurement and, 94
negative relationship and, 94
S -5 Subject Index
positive relationship and, 94
risk factors and, 95–96
statistical significance and,
94–95
using correlational methods,
95–96
Cortisol, schizophrenia and, 383
Counseling psychologists, 70
COX-2 inhibitors, 383
Crack, 264, 264t
Cravings, alcohol use disorder and,
273–274
Criminal acts and insanity, 507–515.
See also Insanity defense
American Legal Institute test
and, 509
competency to stand trial,
514–515
criminal responsibility and, 508
dangerousness and, 515–521
Durham test and, 509
insanity defense, 510t, 511–514
Insanity Defense Reform Acts,
509–510
irresistible impulse test and, 508
M’Naghten test and, 508
Criminal commitment, mentally ill
patient and, 518
Criminal responsibility, 508
Criminality, antisocial personality
disorder and, 419–420, 420t
Crisis intervention, suicide and, 151
Cross-dressing, 342
Cross-gender identification, 329
Crystallized intelligence, 479
Cultural differences
acculturation, 55
agoraphobia and, 169t
alcohol use disorder and, 277
anorexia nervosa and, 299t
attention-deficit/hyperactivity
disorder and, 466t
binge eating disorder and, 306t
bipolar disorders and, 140t
body dysmorphic disorder and,
201t
borderline personality disorder
and, 424t
bulimia nervosa and, 303t
clinical assessment and, 82–83,
83f
collectivist cultures, 54–55
conversion disorder and, 246t
delirium and, 486t
dementia and, 491t
depressive disorders and, 127
dissociative amnesia and, 227t
dissociative identity disorder and,
233t
eating disorders and, 314–315
evaluating symptoms and,
103–104
gender dysphoria and, 331t
generalized anxiety disorder and,
160t
individualist cultures, 55
intellectual disability and, 446t
maladaptive cognitive distortions
and, 47
obsessive-compulsive disorder
and, 198t, 204–205
oppositional defiant disorder
and, 464t
panic disorder and, 166–167,
167t
posttraumatic stress disorder and,
211t, 215
psychological disorders and, 7–10
schizophrenia and, 377, 378t,
390–391
separation anxiety disorder and,
190t
sexual dysfunctions and, 353t
social anxiety disorder and, 177t,
179
somatic symptom disorder and,
242t, 243
specific learning disorder and,
457t
specific phobias and, 183t, 185
substance use disorders and, 263
suicide and, 147t, 150
unhealthy functioning and,
54–55
Cultural Formulation Interview,
82–83
Culturally sanctioned placebo
effects, 111
Cyclothymic disorder, 140–141,
141t
Cyprotercone acetate (Androcur),
345
° D °
Dangerousness, 515–521
actual dangerousness, 516
civil commitment and, 518
components of, 515
confidentiality and, 516–517
criminal commitment and, 518
deinstitutionalization and, 520
evaluating, 516
Kendra’s law and, 520
lifetime prevalence of violent
behavior and, 517f
major risk factors and, 516t
mandated outpatient commitment
and, 519
sexual predator laws and, 521
Tarasoff rule and, 517
treatment realities and, 519–520
Data, scientific method and, 88
Debriefing, 99
Defect perceptions, body
dysmorphic disorder and, 200
Defense mechanisms, 16–17, 17t
Deficit subtype, schizophrenia and,
371
Dehydration, anorexia nervosa and,
301
Deinstitutionalization, 396, 520
Delayed ejaculation, 348t, 351
Delirium, 484–488
attentional problems and,
484–485
dementia compared, 492t
disorientation and, 485
DSM-5 clinical criteria and, 484t
facts at a glance and, 486t
general medical conditions and,
487
mood, anxiety, or dissociative
symptoms and, 486
perceptual alterations and, 485
psychotic symptoms and, 486
substance use and, 487
treatment of, 487–488
Delirium tremens, 275
Delusional beliefs, schizophrenia
and, 367, 386–387
Delusional disorder, 373–374, 375t
Dementia
Alzheimer’s disease and, 490–494
delirium compared, 492t
early onset, 489
facts at a glance and, 491t
head trauma and, 496
HIV infection and, 496
Huntington’s disease and, 496
impaired cognition and, 488–489
key facts about, 497t
late onset, 489
Lewy bodies and, 495–496
mild and major neurocognitive
disorders and, 489–490, 489t
monitoring whereabouts and, 498
Parkinson’s disease and, 495
progressive dementia, 489
substance/medication-induced
neurocognitive disorder and,
496–497
targeting neurological factors
and, 498
targeting psychological factors
and, 498–499
targeting social factors and, 499
vascular dementia, 494–495
Demonic possession, 12
Dendrites, 34
Dependent personality disorder,
435–436
DSM-5 diagnostic criteria and,
435t
facts at a glance and, 436t
Dependent variables, 90–91
Depersonalization-derealization
disorder, 229–231
childhood emotional abuse and,
231
cognitive deficits and, 231
DSM-5 diagnostic criteria and,
229t
facts at a glance and, 230t
feedback loops and, 232
nature of, 229–231
neurological factors and, 231
psychological factors and, 231
social factors and, 231
Depressant use disorders
alcohol and, 272–274
brain systems and, 275
neural communication and, 275
neurological factors and, 275–276
psychological factors and, 276–277
sedative-hypnotic drugs, 274–275
social factors and, 277
Depressive disorders, 116–135. See
also Major depressive disorder;
Major depressive episode
anxiety and, 158, 158f
attention biases and, 124
behavior therapy and, 132–133
borderline personality disorder
and, 423
brain stimulation and, 131–132
brain systems and, 122
children and adolescents and, 120
cognitive-behavior therapy and,
133
cognitive therapy and, 133
culture and, 127
disruptive mood dysregulation
disorder, 121
dysfunctional thoughts and, 124
eating disorders and, 313
feedback loops and, 128–129,
129f, 136, 136f
gender and, 127–128
generalized anxiety disorder and,
159
genetics and, 123–124
interpersonal therapy and, 134
late-life depression, 481, 481t
learned helplessness and, 125
major depressive disorder,
118–122
major depressive episode,
116–118
medications and, 130–131
neural communication and, 122
neurological factors and, 122–124
persistent depressive disorder,
120–122
psychological factors and, 124–125
rumination and attributional
style and, 124–125
Correlational research (continued)
Subject Index S – 6
schizophrenia and, 372, 372t
social exclusion and, 126
social factors and, 126–129
social interactions and, 126–127
social selection and, 53
stress-related hormones and, 123
stressful life events and, 126
suicide and, 150
systems therapy and, 134–135
targeting neurological factors
and, 130–132
targeting psychological factors
and, 132–133
targeting social factors and,
133–135
Derealization, 224
Detoxification, substance use
disorders and, 285–286
Dexedrine, 264
Diagnosis, 61–71
classification systems and, 64
clinical psychologists and, 70
counseling psychologists and, 70
Diagnostic and Statistical Manual of
Mental Disorders (DSM), 65–70
diagnostic bias, 63–64
general practitioners and, 71
mental health professionals with
master’s degrees and, 71
psychiatric nurses and, 71
psychiatrists and, 71
reasons to categorize, 62–63
stigmatizing labels and, 63–64
Diagnostic and Statistical Manual of
Mental Disorders (DSM), 65–70
comorbidity and, 66, 69
criticisms regarding, 69–70
different symptoms and disorder
diagnosis, 67–68
disorders as categories, not
continuous dimensions, 67, 67f
DSM-5, 66–70, 66t
duration criteria and, 68
ensuring payment and, 68
evolution of early versions of,
65–66
restrictive criteria and, 68
social factors and, 68–69
structured clinical interview for, 78
subjectivity in determining
clinical significance and, 66–67
Diagnostic bias, 63–64
Dialectical behavior therapy,
borderline personality disorder
and, 428
Diathesis-stress model, 23, 23f
Diazepam (Valium), 274
Dieting, 313
Digital technology, confidentiality
issues and, 505
Disconnected mental processes,
228–229
Discrimination, 54
Diseases, cognitive functioning and,
482–483
Disinhibited eating, 313
Disordered eating, 311–312
Disorganized attachment, 21
Disorganized speech, schizophrenia
and, 368
Disorientation, delirium and, 485
Disqualifying the positive, 46t
Disruptive behavior and attention
disorders, 459–473
attention-deficit/hyperactivity
disorder, 464–473
conduct disorder, 460–463
oppositional defiant disorder and,
463–464
Disruptive mood dysregulation
disorder, 121
Dissociation, 224
Dissociation theory, 228
Dissociative amnesia, 226–229
brain trauma and, 228
childhood physical or sexual
abuse and, 229
dissociative fugue and, 227
facts at a glance and, 227t
forms of, 226
generalized amnesia, 226
indirect effects and, 229
localized amnesia, 226
neurological factors and, 228
psychological factors and,
228–229
selective amnesia, 226
social factors and, 229
Dissociative anesthetics, 280–281
Dissociative disorders, 224–239
coping and integration and,
238–239
depersonalization and, 224
depersonalization-derealization
disorder, 229–231
derealization and, 224
dissociative amnesia, 224,
226–229
dissociative identity disorder,
232–238
DSM-5 diagnostic criteria and,
226t
feedback loops and, 239
hypnosis and, 239
identity problems and, 224
normal vs. abnormal dissociation,
225–226
symptoms of, 224–225
targeting neurological factors
and, 238
targeting psychological factors
and, 238–239
targeting social factors and,
238–239
Dissociative fugue, 227
Dissociative identity disorder,
232–238
bipolar disorders and, 234
criticisms of diagnostic criteria
for, 234
debate about, 237–238
DSM-5 diagnostic criteria and,
233t
facts at a glance and, 233t
faking symptoms and, 234
feedback loops and, 236–237
genetics and, 235
nature of, 232–233
neurological factors and, 234–235
personality states and, 234
posttraumatic model and, 236
psychological factors and, 235
self-hypnosis and, 235
social factors and, 235–236
sociocognitive model and, 237
Dissociative symptoms, delirium
and, 486
Distress, 4–5
Disulfiram (Antabuse), 286
Divalproex (Depakote), 144
Dix, Dorothea, 14, 14f
Dizygotic twins, 38
DNA, 36, 36f
Do-it-yourself (DIY) surgery, 201
Doctor shopping, 251
Domestic abuse, 218
Donepezil (Aricept), 498
Dopamine
attention-deficit/hyperactivity
disorder and, 468
major functions and, 35t
schizophrenia and, 383
stimulant abuse and, 267–268,
267f
Dose-response relationship,
109–110, 110f
Double-blind designs, 103
Doubt obsession, 198t
Down syndrome, 447t, 449
Dramatic/erratic personality
disorders, 417–432
antisocial personality disorder,
418–422
borderline personality disorder,
422–429
histrionic personality disorder,
429–431
narcissistic personality disorder,
431–432
Drapetomania, 9
Dropouts, research study, 105
Drug courts, 523
Drug cues, 269
Drug effect or placebo effect, 105
Drug use stages, 261
Duloxetine (Cymbalta), 131
Durham test, 509
Dusky v. United States, 1960, 514
Dysfunctional thoughts, depressive
disorders and, 124
Dyslexia, 456–459. See also Specific
learning disorder
Dysthymia, 121–122, 121t
° E °
Eating disorders
abstinence violation effect and,
311
anorexia nervosa, 298–302
binge eating disorder, 305–307
brain systems and, 309–310
bulimia nervosa, 302–305
cognitive-behavior therapy and,
320–321
cultural influences and, 314–315
depressive disorder and, 313
dieting and, 313
disinhibited eating and, 313
excessive concern with weight
and appearance, 311
family and peer role and, 314
family therapy and, 321–322
feedback loops and, 317–318,
318f, 323–324
gender and, 315, 316–317, 316f
genetics and, 310
intensity of treatment and, 319
interpersonal therapy and, 321
Maudsley approach and, 321–322
media role and, 315–316
medical hospitalization and, 319
medication and, 319–320
neural communication and, 310
nutritional focus and, 319
objectification theory and,
316–317, 316f
operant conditioning and,
311–312
other eating disorders, 307
partial cases and, 307
personality traits as risk factors,
312–313
prevention programs and, 323
psychiatric hospitalization and,
322–323
psychological factors and,
310–313, 313f
reinforcing disordered eating,
311–312
restrained eating and, 313
serotonin and, 310
social factors and, 313–317
subthreshold cases and, 307
systems therapy and, 322
targeting biological factors and,
319–320
S -7 Subject Index
targeting neurological factors
and, 319–320
targeting psychological factors
and, 320–321
targeting social factors and,
321–323
women’s body size over time,
315f
Economic factors, schizophrenia
and, 390
Ecstasy, 265–266
Ego, 15–16
Elder day care, dementia and, 499
Electroconvulsive therapy (ECT),
131, 394
Ellis, Albert, 20
Emotional dysregulation, borderline
personality disorder and, 425
Emotional expressions,
schizophrenia and, 387
Emotional reasoning, social anxiety
disorder and, 179
Emotional stimuli, borderline
personality disorder and, 423
Emotions and disorders, 47–50
affect and, 47
approach emotions, 49
behavior and, 47–48
externalizing problems and, 48
internalizing problems and, 48
mental contents and, 48
mental processes and, 48
mood and, 47
neurological bases of, 48–49
regulation of and psychological
disorders, 48
temperament and, 49–50, 50t
withdrawal emotions, 49
Encephalitis, 482
Endocrine system, hormones and, 36
Endogenous cannabinoids, 35t
Endogenous opioids, 275
Endorphin rush, binge eating and,
312
Environmental affects, genes and,
39–40
Epidemiology, 95
Erectile disorder, 348t, 350
Erotica, 344–345
Erotomanic delusions, 373
Escitalopram (Lexapro), 162
Estrogens, schizophrenia and,
383–384
Eszopidone (Lunesta), 275
Ethics, 504–507
confidentiality and, 504–507
debriefing and, 99
experimental treatments and,
112, 112t
informed consent and, 98, 98t
research and, 98–99
websites regarding, 504t
Ethnicity
diagnostic bias and, 63
patient and therapist relationships
and, 111
substance use disorders and, 261
Etiology, 29
Evidence-based practice, 109
Evocative interaction, genes and, 40
Excitement, sexual response cycle
and, 347
Executive function, schizophrenia
and, 370, 385–386
Exhibitionistic disorder, 337t, 338
Exogenous opioids, 278
Expansive mood, bipolar disorders
and, 137
Experiments, 90–93
bias and, 92
confounding variables and, 91
control conditions and, 92
control groups and, 91–92
counterbalancing and, 92
dependent variables and, 90–91
experimental design and, 98t
experimental treatments, 112,
112t
experimenter expectancy effects,
103
external validity and, 93
independent variables and, 90–91
internal validity and, 92
population and, 92
random assignment and, 92
sampling and, 92
sampling bias and, 92
Exposure
generalized anxiety disorder and,
162–163
obsessive-compulsive disorder
and, 206
panic disorder and agoraphobia
and, 173
posttraumatic stress disorder and,
217
social anxiety disorder and,
180–181
specific phobias and, 186
External attributional style, 125
External validity, experiments and, 93
Externalizing problems, 48
Eye movement desensitization and
reprocessing (EMDR), 217
° F °
Facial expressions
attention-deficit/hyperactivity
disorder and, 468
autism spectrum disorder and,
453
child maltreatment and, 51
Factitious disorder, 77, 240
Families, 50–52
child maltreatment and, 51–52
eating disorders and, 314
functioning and clinical
assessment, 81
gender dysphoria and, 334
interaction styles and, 51
parental psychological disorders,
52
stimulant use disorders and,
269–270
Family Environment Scale, 81
Family therapy and education
bipolar disorders and, 145
depression and, 134–135
eating disorders and, 321–322
obsessive-compulsive disorder
and, 206
personality disorders and, 410
posttraumatic stress disorder and,
218
schizophrenia and, 395
separation anxiety disorder and,
191
somatic symptom disorders and,
252–253
substance use disorders and,
292
Faulty estimations, specific phobias
and, 185
Fearful/anxious personality
disorders, 433–439
avoidant personality disorder,
433–435
cognitive and behavioral factors
and, 438
dependent personality disorder,
435–436
neurological factors and, 438
obsessive-compulsive personality
disorder, 436–438
social factors and, 438
treatment of, 438
understanding, 438–439
Feedback loops
antisocial personality disorder
and, 421
attention-deficit/hyperactivity
disorder and, 469–470, 469f,
473, 473f
bipolar disorders and, 143, 145
borderline personality disorder
and, 426–427, 426f, 428–429,
429f
classical and operant conditioning
and, 44
depersonalization-derealization
disorder and, 231
depressive disorders and,
128–129, 129f, 136, 136f
dissociative disorders and, 239
dissociative identity disorder and,
236–237
eating disorders and, 317–318,
318f, 323–324
generalized anxiety syndrome
and, 164–165
genes and environment and,
39–40
neuropsychosocial approach and,
25, 25f
obsessive-compulsive disorder
and, 205, 206–207
panic disorder and agoraphobia
and, 171, 172f, 174, 175f
personality disorders and,
408–409
posttraumatic stress disorder and,
215–216, 216f, 218–219, 219f
psychopathy and, 421
schizophrenia and, 391, 392f,
397–398, 398f
schizotypal personality disorder
and, 416
sexual dysfunctions and, 356–357,
356f, 360–361, 360f
social anxiety disorder and,
179–180
somatic symptom disorder (SSD)
and, 243–244, 244f
somatic symptom disorders and,
253
specific phobias and, 186, 187
substance use disorders and,
292–293
Female issues. See Gender
Female orgasmic disorder, 348t,
351
Female sexual interest/arousal
disorder, 348t, 350
Fetal alcohol syndrome, 447
Fetishistic disorder, 337t, 341–342
Fight Club, 237
Fight-or-flight response, 31,
156–157
Fixation, 16
Flat affect, 47, 369
Flight of ideas, bipolar disorders
and, 138
Fluid intelligence, 479
Fluoxetine (Prozac), 130, 205, 207,
320
Fluvoxamine (Luvox), 205
Folie à deux, 374
Follow-up assessments, 107, 109
Fragile X, 447t
Free association, 15
Freud, Sigmund, 14–17
defense mechanisms and, 16–17,
17t
evaluating contributions of,
17–18
humanist response and, 18
mental illness and, 16
psychoanalytic theory and,
15–16
Eating disorders (continued)
Subject Index S – 8
psychosexual stages and, 16
unconscious forces and, 14–15
Frontal lobe
attention-deficit/hyperactivity
disorder and, 467
autism spectrum disorder and,
453
borderline personality disorder
and, 424
eating disorders and, 309
functions of, 32
obsessive-compulsive disorder
and, 203
schizophrenia and, 381
Frotteuristic disorder, 337t, 339
Fugue, dissociative, 227
Functional magnetic resonance
imaging (fMRI), 74
Functional neurological symptom
disorder. See Conversion
disorder
° G °
Gabapentin (Neurontin), 144
Galantamine (Razadyne), 498
Gambling, 99
Gamma-amino butyric acid
(GABA), 35t, 184
Gateway hypothesis, substance use
disorders and, 261
Gender
agoraphobia and, 169t
alcohol use disorder and, 277
anorexia nervosa and, 299t
antisocial personality disorder
and, 419t
anxiety disorders and, 157
attention-deficit/hyperactivity
disorder and, 465, 466t
autism spectrum disorder and,
452t
avoidant personality disorder
and, 434t
binge eating disorder and, 306t
bipolar disorders and, 140t
blood alcohol concentrations
and, 272–273
body dysmorphic disorder and,
201t
borderline personality disorder
and, 424t
bulimia nervosa and, 303t
conduct disorder and, 462t
conversion disorder and, 246t
delirium and, 486t
dementia and, 491t
dependent personality disorder
and, 436t
depersonalization-derealization
disorder and, 230t
depressive disorders and,
127–128
dissociative amnesia and, 227t
dissociative identity disorder and,
233t
eating disorders and, 315,
316–317, 316f
gender identity, 328–329
generalized anxiety disorder and,
160t
histrionic personality disorder
and, 430t
intellectual disability and, 446t
major depressive disorder and,
120t
narcissistic personality disorder
and, 432t
obsessive-compulsive disorder
and, 198t
obsessive-compulsive personality
disorder and, 437t
oppositional defiant disorder
and, 464t
panic disorder and, 167t
paranoid personality disorder
and, 412t
patient and therapist relationship
and, 111
personality disorders and, 406t
posttraumatic stress disorder and,
211t
schizoid personality disorder and,
413t
schizophrenia and, 377, 378t
schizotypal personality disorder
and, 415t
separation anxiety disorder and,
190t
social anxiety disorder and, 177t
somatic symptom disorder and,
242t
specific learning disorder and,
457t
specific phobias and, 183t
suicide and, 147t
women’s body size over time, 315f
Gender dysphoria, 328–334
altered appearance and, 333–334
brain systems and, 332
DSM-5 diagnostic criteria in
adolescents and adults, 330t
DSM-5 diagnostic criteria in
children, 329t
facts at a glance and, 331t
family support and, 334
gender differences and, 331
gender identity and, 328–329
gender role and, 329
genetics and, 332
homosexuality and, 331
neural communication and, 332
neurological factors and, 332
physical attractiveness ratings
and, 333f
psychological factors and, 332
responses from others and, 330,
332–333
sex reassignment surgery and,
333–334
significant distress and, 330
social factors and, 332–333
targeting biological factors and,
333–334
targeting neurological factors
and, 333–334
targeting psychological factors
and, 334
targeting social factors and, 334
General paresis, 22
General practitioner (GP), 71
Generalized amnesia, 226
Generalized anxiety disorder
behavioral methods and, 162–163
biofeedback and, 162
brain systems and, 160
cognitive methods and, 163
depression and, 159
DSM-5 diagnostic criteria and,
159t
exposure technique and, 162–163
facts at a glance and, 160t
feedback loops and, 161, 164–165
genetics and, 160
habituation and, 162
hypervigilance and, 160
illusion of coping and, 161
nature of, 158–159
neural communication and, 160
neurological factors and, 160
psychoeducation and, 163
psychological factors and,
160–161
social factors and, 161
stressors and, 161
targeting neurological factors
and, 161–162
targeting psychological factors
and, 162–163
targeting social factors and, 163
worry exposure and, 164f
Genes, 36
Genetics, 36–40
active interaction and, 40
alcohol use disorder and, 275
Alzheimer’s disease and, 494
antisocial personality factors and,
420
attention-deficit/hyperactivity
disorder and, 468
autism spectrum disorder and,
453
behavioral genetics, 37
bipolar disorders and, 142
borderline personality disorder
and, 425
complex inheritance and, 37
depressive disorders and, 123–124
dissociative identity disorder
and, 235
DNA and, 36, 36f
eating disorders and, 310
environment and, 39–40
evocative interaction and, 40
gender dysphoria and, 332
generalized anxiety disorder and,
160
genotypes and, 36
heritability and, 37–38
intellectual disability and, 447,
447t
obsessive-compulsive disorder
and, 203
panic disorder and agoraphobia
and, 169
passive interaction and, 40
personality disorders and, 407
phenotypes and, 36
posttraumatic stress disorder and,
213–214
schizophrenia and, 384–385,
384t
schizotypal personality disorder
and, 416
separation anxiety disorder and,
191
social anxiety disorder and, 178
somatic symptom disorder and,
242
specific learning disorder and,
458
specific phobias and, 184, 184f
twin and adoption studies and,
38–39
Genito-pelvic pain/penetration
disorder, 348t, 352–353
Genotypes, 36
Glial cells, 34
Glove anesthesia, 245f
Glutamate
bipolar disorders and, 142
major functions and, 35t
schizophrenia and, 383
substance use disorders and, 281
Graded exposure, specific phobias
and, 186
Grandiose delusions, 6, 367, 373
Greeks, mental illness beliefs and,
11–12
Grief, depression and, 118
Grossly disorganized psychomotor
behavior, 368
Group therapy
gender dysphoria and, 334
panic disorder and agoraphobia
and, 174
personality disorders and, 410
schizophrenia and, 395–396
social anxiety disorder and, 181
substance use disorders and,
291–292
Guilt, 49
S -9 Subject Index
° H °
Habituation, 162
Hair-pulling disorder, 199
Hallucinations
delirium and, 485
schizophrenia and, 367
Hallucinogens, 279–280
LSD, 279
marijuana, 279–280
neurological factors and, 281
treatment for abuse of, 287
Hangovers, 275–276
Harm avoidance, 50t
Harm reduction treatments,
substance use disorders and,
284–285
Hashish, 279
Head trauma
cognitive functioning and, 484
dementia and, 496
Health Insurance Portability and
Accountability Act (HIPAA),
505–506
Heavy episodic drinking, 273
Helplessness, learned, 125
Heritability, 37–38. See also
Genetics
Heroin, 278–279, 281, 286–287
Heroin overdoses, 282
High expressed emotion, 51, 388
Hippocampus
borderline personality disorder
and, 424–425
dissociative amnesia and, 228
posttraumatic stress disorder and,
213
role of, 32
schizophrenia and, 381
Hippocrates, 11–12
Histrionic personality disorder,
429–431
distinguishing from other
disorders, 431
DSM-5 diagnostic criteria and,
430t
facts at a glance and, 430t
treatment of, 431
Hoarding disorder, 199
Homosexuality, 9, 148
Hopelessness depression, 125
Hormones
depression and, 127
endocrine system and, 36
stress-related, 123
Horney, Karen, 17
HPA axis, 123, 123f, 128
Human immunodeficiency virus
(HIV), 496
Humanistic psychology, 18
Huntington’s disease, 496
Hydrocodone (Vicodin), 278
Hydrophobia, 182
Hypersomnia, depression and, 117
Hypervigilance, generalized anxiety
disorder and, 160
Hypnosis, 15, 239
Hypochondriasis, 248–249
Hypomanic episodes, bipolar
disorder and, 139
Hypothalamus, 32
Hypotheses, 89
Hysteria, 223
° I °
Id, 15
Identity problems, 224
Illness
cognitive functioning and,
482–483
sexual dysfunctions and, 354–355
Illness anxiety disorder, 248–251.
See also Somatic symptom
disorders
anxiety disorders and, 250
catastrophic thinking and, 251
cognitive-behavior therapy and,
252t
DSM-5 diagnostic criteria and,
249t
hypochondriasis and, 248–249
memory bias and, 46
nature of, 249–250
neurological factors and, 251
obsessive-compulsive disorder
and, 250
psychological factors and, 251
shared features of, 250
social factors and, 251
Illusions, delirium and, 485
Imaginal exposure, 163
Imipramine therapy, 108
Immigrants, schizophrenia and,
389–390
Impairment in daily life, 5–6, 6f
Impotence, 350
In vivo exposure, 163
Inappropriate affect, 47
Inclusion, intellectual disability
and, 449
Incongruence, 18
Independent variables, 90–91
Individualist cultures, 55
Individualized education programs,
intellectual disability and, 449
Individuals with Disabilities
Education Act, 449
Informed consent, 98, 98t, 507
Initial observations, scientific
method and, 88
Inpatient treatment
schizophrenia and, 396
substance use disorders and, 291
Insanity defense
abnormal neural functioning
and, 513
assessing insanity and, 512
current issues and, 511–514
diminished capacity and, 513
guilty but mentally ill and, 513
perceptions regarding, 514
reform acts and, 509–510
states’ rights and, 513
Insanity Defense Reform Acts,
509–510
Insecure attachment style, 408
Institutional Review Board (IRB),
99
Intellectual disability, 444–449
adaptive functioning and,
444–445
communication deficits and, 449
DSM-5 diagnostic criteria and,
444t
facts at a glance and, 446t
genetics and, 447, 447t
mild intellectual disability, 445
moderate intellectual disability,
445
neurological factors and, 447
prevention and, 448
problem behaviors and, 448
profound intellectual disability,
445
psychological factors and, 448
severe intellectual disability, 445
social factors and, 448
special education and, 449
targeting neurological factors
and, 448
targeting psychological factors
and, 449
targeting social factors and, 449
teratogens and, 447
understimulation and, 448
Intelligence, 479–480
Intelligence quotient (IQ), 78
Internal attributional style, 125
Internal validity, experiments and,
92
Internalizing problems, 48
International Classification of
Diseases (ISD), 65
Interneurons, 33
Interoceptive exposure, panic
disorder and agoraphobia and,
173, 173f, 173t
Interpersonal and social rhythm
therapy (IPSRT), 145
Interpersonal therapy
borderline personality disorder
and, 428
depression and, 108, 134
eating disorders and, 321
Interviews. See Clinical interviews
Invalidation, borderline personality
disorder and, 425–426
Inventories, personality assessment
and, 79–80
Investigator-influenced biases, 103
Involuntary movements, 382
Irresistible impulse test, 508
° J °
Jealous delusions, 374
Jumping to conclusions, 46t
° K °
Kansas v. Crane, 2002, 521
Kansas v. Hendricks, 1997, 521
Kendra’s law, 520
Ketamine, 281
Koro, 8
Korsakoff ’s syndrome, 275
° L °
LAAM (levo-alpha-acetyl-
methadol), 287
Labile affect, 47
Lake v. Cameron, 1966, 522
Lamotrigine (Lamictal), 144
Lanugo hair, 301
Laxative use, bulimia nervosa and,
304
Lead exposure
attention-deficit/hyperactivity
disorder and, 469
intellectual disability and, 448
Learned behaviors, child
maltreatment and, 51
Learned helplessness, 44, 125
Learning disorder. See Specific
learning disorder
Learning theory, panic disorder and
agoraphobia and, 170
Legal issues. See Criminal acts and
insanity; Treatment legal issues
Lewy bodies, dementia and,
495–496
Limbic system, 32
Lithium, bipolar disorders and, 141,
144
Little Albert case, 41–42, 90–91
Localized amnesia, 226
Longitudinal studies, 95–96
Loosening of association, cognitive
deficits and, 371
Lorazepam (Ativan), 274
Losing control obsession, 198t
Loss of control, alcohol use disorder
and, 273–274
LSD, 279
Subject Index S -10
° M °
Magnetic resonance imaging
(MRI), 73
Mainlining, 279
Mainstreaming, intellectual
disability and, 449
Major depressive disorder (MDD),
118–122
aging and, 119
anxiety disorders and, 120
children and adolescents and, 120
dysthymia and, 121–122, 121t
facts at a glance and, 120t
peripartum onset and, 119–120
persistent depressive disorder and,
120–122, 121t
phototherapy and, 119
psychotic features and, 120
recurrent depression and, 119
seasonal affective disorder and,
119
single episode and, 119
Major depressive episode (MDE),
116–118
anhedonia and, 116
behavioral and physical
symptoms and, 116–117
bereavement exclusion and, 118
cognitive symptoms and,
117–118
DSM-5 diagnostic criteria and,
117t
grief and, 118
hypersomnia and, 117
mood symptoms of, 116
premorbid level of functioning
and, 118
prodrome and, 118
psychomotor agitation and, 116
psychomotor retardation and,
117
Major neurocognitive disorders,
489–490, 489t
Male hypoactive sexual desire
disorder, 348t, 349
Malingering
clinical diagnosis and assessment
and, 77
conversion disorder and, 247
dissociative identity disorder
and, 234
Mandated outpatient commitment
and, mentally ill patient and, 519
Manic episodes
bipolar disorders and, 136–138,
137t
schizophrenia and, 372
Manual-based treatment, 108
Marijuana, 279–280
Marriage and family therapists, 71
Maslow, Abraham, 18
Masochism, 337t, 341
Maternal illness, brain
abnormalities and, 381–382
Maternal malnourishment, brain
abnormalities and, 381
Mathematics, specific learning
disorder and, 456
Maudsley approach, 321–322
MDMA (methylenedioxy-
methamphetamine), 265–266
Media influences, eating disorders
and, 315–316
Medication
attention-deficit/hyperactivity
disorder and, 471
bipolar disorders and, 143–144
borderline personality disorder
and, 427
delirium and, 487
depressive disorders and, 130–131
dissociative disorders and, 238
eating disorders and, 319–320
generalized anxiety disorder and,
161–162
obsessive-compulsive disorder
and, 205
panic disorder and agoraphobia
and, 171–172
paraphilic disorders and, 345
posttraumatic stress disorder and,
217
schizophrenia and, 393–394
sexual dysfunctions and,
358–359, 358t
social anxiety disorder and, 180
specific phobias and, 186
substance use disorders and,
286–287, 287t
Meditation, generalized anxiety
syndrome and, 163
Medroxyprogesterone acetate
(Depo-Provera), 345
Melancholy, 11
Memantine (Namenda), 498
Memory, 45–46, 480
Memory difficulties, schizophrenia
and, 385–386
Mental contents
cognitive distortions and, 46–47
emotions and, 48
psychodynamic theory and, 18
Mental filter, 46t
Mental health, treatment issues and,
521–523
Mental illness according to Freud,
16
Mental processes, 45–46
attention and, 45
clinical interviews and, 76
emotions and, 48
memory and, 45–46
perception and, 45
psychodynamic theory and, 18
researching psychological factors
and, 101
schizophrenia and, 385–386
Mental retardation. See Intellectual
disability
Mental status exam, 77–78
Mental treatment, ancient views
on, 13
Meta-analysis, 97–98, 98t
Methadone, 286–287
Methamphetamine, 265, 265t, 267,
268f
Methylphenidate (Ritalin,
Concerta, Focalin), 471
Middle ages, forces of evil in, 12
Mild intellectual disability, 445
Mild neurocognitive disorders,
489–490, 489t
Military combat. See also
Posttraumatic stress disorder
conversion disorder and, 248
preexisting anxiety sensitivity
and, 170
suicides and, 151
Ministrokes, 494
Minnesota Multiphasic Personality
Inventory (MMPI), 79–80, 79t, 80f
Mirtazapine (Remeron), 180
Misinterpretations, delirium and,
485
M’Naghten test (or rule), 508
Mnemonics, dementia and, 498
Modeling, specific phobias and, 185
Moderate intellectual disability, 445
Monoamine oxidase inhibitors
(MAOIs), 130
Monozygotic twins, 38
Mood, 47
Mood disorders. See also Bipolar
disorders; Depressive disorders
bipolar disorders, 136–145
delirium and, 486
depressive disorders, 116–135
differential diagnosis and, 141f
incidence of, 115–116
schizophrenia and, 376
suicide and, 146–151
types of, 116, 116t
Mood stabilizers, bipolar disorders
and, 144
Mood symptoms, depression and,
116
Moral treatment, ancient views on,
13–14
Motivational enhancement therapy,
substance use disorders and, 289
Motor neurons, 33
Motor symptoms, conversion
disorder and, 245
Movements, clinical interviews
and, 76
Multiple personality disorder. See
Dissociative identity disorder
Multisystemic therapy, attention-
deficit/hyperactivity disorder
and, 473
Multitasking, 480
Muscle relaxation training,
generalized anxiety disorder
and, 162
Muscle wasting, anorexia nervosa
and, 301
° N °
Naloxone (Suboxone), 287
Naltrexone (reVia and Vivitrol),
286, 287
Narcissistic personality disorder
DSM-5 diagnostic criteria and,
431t
facts at a glance and, 432t
treatment of, 432
Narcotic analgesics, 278–279
Narcotics Anonymous, 291
National Alliance for the Mentally
Ill, 64
National Suicide Prevention
Lifeline, 151t
Natural environment type of
phobia, 182
Needle exchange programs,
285–286
Nefazodone (Serzone), 180
Negative attributional style, 125
Negative punishment, 43–44
Negative reinforcement, 43
Negative symptoms, schizophrenia
and, 369
Neodissociation theory, 228–229
Neologisms, 368
Neural communication
attention-deficit/hyperactivity
disorder and, 467–468
bipolar disorders and, 142
borderline personality disorder
and, 425
depressant use disorders and, 275
depressive disorders and, 122
eating disorders and, 310
gender dysphoria and, 332
generalized anxiety disorder and,
160
obsessive-compulsive disorder
and, 202–203
panic disorder and agoraphobia
and, 169
posttraumatic stress disorder and,
213–214
schizophrenia and, 383–384
social anxiety disorder and,
177–178
specific phobias and, 184
stimulant abuse and, 267–268
S -11 Subject Index
Neurocognitive disorders. See
Cognitive functioning
Neurofibrillary tangles, 493–494,
493f
Neuroimaging studies, eating
disorders and, 309–310
Neurological bases, emotions and,
48–49
Neurological factors, 29–40
antisocial personality disorder
and, 420
attention-deficit/hyperactivity
disorder and, 467–468, 471
autism spectrum disorder and,
453–454
bipolar disorders and, 141–144
borderline personality disorder
and, 424–425, 427
brain structure and brain
function, 30–36
conversion disorder and, 247
dementia and, 498
depersonalization-derealization
disorder and, 231
depressant use disorders and,
275–276
depressive disorders and,
122–124, 130–132
dissociative amnesia and, 228
dissociative anesthetics and, 281
dissociative disorders and, 238
dissociative identity disorder and,
234–235
eating disorders and, 319–320
etiology and, 29
gender dysphoria and, 332,
333–334
generalized anxiety disorder and,
160, 161–162
genetics of psychopathology,
36–40
hallucinogens and, 281
illness anxiety disorder and, 251
intellectual disability and, 447,
448
obsessive-compulsive disorder
and, 202–203, 205
opioids and, 281
panic disorder and agoraphobia
and, 168–169, 171–172
paraphilic disorders and, 344, 345
personality disorders and, 409
posttraumatic stress disorder and,
213–214, 217
psychopathy and, 420
research and, 100
researching treatments targeting,
104–105
schizophrenia and, 380–385,
393–394
schizotypal personality disorder
and, 416
sexual dysfunctions and,
354–355, 358–359
social anxiety disorder and,
177–178, 180
somatic symptom disorder and,
242
specific learning disorder and,
457–458
specific phobias and, 184, 186
stimulant use disorders and, 268t
substance use disorders and,
285–287
suicide and, 149–150
Neurological functioning
assessment, 72–73
Neurons, 32–33, 33f, 36
Neuropsychological testing, 74
Neuropsychosocial approach,
psychopathology and, 25, 25f
Neurosis, 16
Neurotransmitters, 34–35, 35t
Nonbenzodiazepines, 275
Nonconsenting people, paraphilic
disorders and, 336–340
Nondeficit subtype, schizophrenia
and, 371
Nonhuman objects, paraphilic
disorders and, 341–342
Noradrenaline (norepinephrine),
35t
Noradrenergic and specific
serotonergic antidepressants
(NaSSAs), 131, 180
Norepinephrine
bipolar disorders and, 141
depersonalization-derealization
disorder and, 231
Novelty seeking, 50t
Nutritional focus, eating disorders
and, 319
° O °
Objectification theory, eating
disorders and, 316–317, 316f
Observation, clinical assessment
and, 75–76
Observational learning, 45, 243
Obsessional thinking, obsessive-
compulsive disorder and, 204
Obsessions, 196
Obsessive-compulsive disorder
(OCD), 196–207
anorexia nervosa and, 300
behavioral methods and, 206
body dysmorphic disorder and,
199–202, 200t
brain systems and, 202–203
case studies and, 96
cognitive explanations and, 204
cognitive methods and, 206
cognitive restructuring and, 206
common types of, 198t
compulsions and, 196
cultural differences and, 204–205
DSM-5 diagnostic criteria and,
197t
exposure with response
prevention and, 206
facts at a glance and, 198t
family therapy and, 206
feedback loops and, 205,
206–207
genetics and, 203
hair-pulling disorder and, 199
hoarding disorder and, 199
illness anxiety disorder and, 250
nature of, 196–199
neural communication and,
202–203
neural loop underlying, 202f
neurological factors and, 202–203
obsessional thinking and, 204
obsessions and, 196
operant conditioning and, 203
psychological factors and,
203–204
skin-picking disorder and, 199
social factors and, 204–205
stress and, 204
targeting neurological factors
and, 205
targeting psychological factors
and, 205–206
targeting social factors and, 206
Obsessive-compulsive personality
disorder, 436–438
distinguishing from OCD, 438
DSM-5 diagnostic criteria and,
437t
facts at a glance and, 437t
relationships and, 438
workaholics and, 438
Occipital lobe, 31
O’Connor v. Donaldson, 1975, 522
Odd/eccentric personality
disorders
paranoid personality disorder,
411–412
schizoid personality disorder,
413–414
schizotypal personality disorder,
414–416
treatment of, 417
Olanzapine (Zyprexa), 144
Operant conditioning, 42–44
eating disorders and, 311–312
feedback loops and, 44
learned helplessness and, 44
negative punishment and, 43–44
negative reinforcement and, 43
observational learning and, 45
obsessive-compulsive disorder
and, 203
positive punishment and, 43
positive reinforcement and, 43
punishment and, 43–44
reinforcement and, 42–43
social anxiety disorder and, 179
specific phobias and, 185
stimulant abuse and, 268–269
types of, 44t
Opioid use disorder, 278–279
medications treating, 286–287
neurological factors and, 281
Oppositional defiant disorder,
463–464
differences from conduct disorder,
464
DSM-5 classification criteria
and, 463t
facts at a glance and, 464t
Order obsession, 198t
Orgasm, 347
Orgasmic disorders, 350–352
Other abused substances, 278–284
dissociative anesthetics, 280–281
feedback loops and, 282–284,
283f
hallucinogens, 279–280
neurological factors and,
281–282
opioids, 278–279
psychological factors and, 282
social factors and, 282
Outcome assessments, 107
Overgeneralization, 46t
Overprotective family members,
separation anxiety disorder and,
191
Oxycodone (OxyContin), 278
Oxygen deprivation, brain
abnormalities and, 382
° P °
Panic, anxiety disorders and, 157
Panic attacks, 91, 165, 165t
Panic disorder, 165–175
anxiety sensitivity and, 170
behavioral methods and, 173
brain systems and, 168–169
catastrophic thinking and, 170
cognitive explanations and, 170
cognitive methods and, 173–174
cultural aspects and, 166–167
DSM-5 diagnostic criteria and,
166t
facts at a glance and, 167t
feedback loops and, 171, 172f,
174, 175f
genetics and, 169
learning theory and, 170
nature of, 166–167
neural communication and, 169
neurological factors and, 169
panic attacks and, 165, 165t
psychological factors and,
169–170
Subject Index S -12
social factors and, 170–171
targeting neurological factors
and, 171–172
targeting psychological factors
and, 172–174
targeting social factors and, 174
Paralytic dementia, 22
Paranoia, 7
Paranoid delusions, 6
Paranoid personality disorder,
411–412
DSM-5 diagnostic criteria and,
411t
facts at a glance and, 412t
Paraphilic disorders, 335–346
arousal patterns and, 336, 337t
assessment of, 343
classification criticisms and, 343
classification of, 335–336
cognitive-behavior therapy and,
346
conditioned arousal and, 344
criminal behaviors and, 338
DSM-5 diagnostic criteria and,
337t
erotica and, 344–345
exhibitionistic disorder, 338
fetishistic disorder, 341–342
frotteuristic disorder, 339
medication and, 345
neurological factors and, 344
nonconsenting people and,
336–340
nonhuman objects and, 341–342
pedophilic disorder, 339–400
prevalence and, 336
psychological factors and, 344
sexual masochism disorder, 341
sexual sadism disorder, 340
social factors and, 344–345
targeting biological factors and,
345
targeting neurological factors
and, 345
targeting psychological factors
and, 346
targeting social factors and, 346
transvestic disorder, 342–343,
342t
voyeuristic disorder, 338
Parasuicidal behavior, 148, 423
Parasympathetic nervous system, 31
Parent management training,
attention-deficit/hyperactivity
disorder and, 472
Parental behavior, attention-deficit/
hyperactivity disorder and, 472
Parental psychological disorders, 52
Parietal lobe, 31
Parkinson’s disease, 495
Paroxetine (Paxil), 130, 162, 180,
205, 217
Partial cases, eating disorders and,
307
Passive interaction, genes and, 40
Pastoral counseling, 71
Patient violence. See Dangerousness
Patient’s self report, 76–77
Pavlov, Ivan, 19
Pavlovian conditioning, 19–20
Pediatric autoimmune
neuropsychiatric disorder
associated with streptococcal
infection (PANDAS), 96
Pedophilic disorder, 337t, 339–340
Peer relationships, stimulant use
disorders and, 269–270
Peer roles, eating disorders and, 314
Penile plethysmograph, 343
Pentobarbital (Nembutal), 274
Perceived norms, stimulant use
disorders and, 270
Perception, 45
Perceptional distortions, specific
phobias and, 185
Perceptual alterations, delirium
and, 485
Perceptual-motor disorders, 489
Perceptual reasoning tests, 78
Perfectionism, eating disorders and,
423
Peripartum depression, 119–120,
134
Peripheral nervous system (PNS), 31
Persecutory delusions, 6, 367, 373
Persistence, 50t
Persistent depressive disorder,
120–122, 121t
Personality assessment, 79–80
inventories and, 79–80
projective tests and, 80
Personality characteristics, 403
Personality disorders
affect and, 403
antisocial personality disorder,
418–422
assessment of, 404–405
avoidant personality disorder,
433–435
behavior and, 403
behavioral consequences and,
408
borderline personality disorder,
422–429
cognition and, 403
cognitive-behavior therapy and,
409–410
dependent personality disorder,
433–435
diagnostic criteria criticisms and,
405–406
dramatic/erratic personality
disorders, 417–432
DSM-5 general diagnostic
criteria and, 402t
DSM-5 personality clusters, 405
facts at a glance and, 406
fearful/anxious personality
disorders, 433–439
feedback loops and, 408–409
genes and temperament and, 407
histrionic personality disorder,
429–431
insecure attachment and, 408
narcissistic personality disorder,
431–432
neurological factors and, 407
obsessive-compulsive personality
disorder, 436–438
odd/eccentric personality
disorders, 410–417
paranoid personality disorder,
411–412
psychodynamic therapy and,
409–410
psychological factors and, 408
schizoid personality disorder,
413–414
schizotypal personality disorder,
414–416
social factors and, 408
stability and, 404, 404f
targeting neurological factors
and, 409
targeting psychological factors
and, 409–410
targeting social factors and, 410
temperamental characteristics
and, 408
Personality states. See Dissociative
identity disorder
Personality traits, eating disorders
and, 312–313
Personalization, 46t
Phencyclidine (PCP), 280
Phenelzine (Nardil), 130
Phenotypes, 36
Phenylketonuria (PKU), 447t, 448
Phobias. See Specific phobias
Phonological practice, dyslexia
and, 458
Phosphodiesterase type 5 inhibitors
(PDE-5 inhibitors), 358
Phototherapy, 119
Physical dependence, alcohol use
disorder and, 273–274
Physical symptoms, depression and,
116–117
Pibloktoq, 227
Picture Exchange Communication
System, 449
Pinel, Phillipe, 13
Placebo control groups, 107
Placebo effects, 105, 111
Plateau, sexual response cycle and,
347
Pleasure chemicals, 275
Polysubstance abuse, 262
Population, experiments and, 92
Positive punishment, 43
Positive reinforcement, 43
Positive symptoms, schizophrenia
and, 366–368
Positron emission tomography
(PET), 74
Possession trance, 225
Postpartum depression, 119–120
Posttraumatic Diagnostic Scale, 102
Posttraumatic model, dissociative
identity disorder and, 236
Posttraumatic stress disorder
(PTSD), 208, 209–211, 213–219
behavioral methods and, 217–218
brain systems and, 213
breathing retraining and, 218
cognitive behavior training and,
218
comorbidity and, 214–215
conditioning and, 214–215
culture and, 215
DSM-5 diagnostic criteria and,
210t
exposure and, 217
eye movement desensitization
and reprocessing and, 217
facts at a glance and, 211t
family education and, 218
feedback loops and, 215–216,
216f, 218–219, 219f
genetics and, 213–214
neural communication and,
213–214
neurological factors and, 213–214
psychological factors and,
214–215
relaxation and, 218
safety and, 218
social factors and, 215
social support and, 215
socioeconomic factors and, 215
subtype of, 209
support and, 218
symptoms and, 209
targeting neurological factors
and, 217
targeting psychological factors
and, 217–218
targeting social factors and, 218
trauma history and, 214–215
Prader-Willi syndrome, 447t
Preconscious, psychoanalytic
theory and, 15
Predictions, scientific method and,
89
Prejudice, depression and, 126
Premature (early) ejaculation, 348t,
351
S -13 Subject Index
Premorbid functioning, depression
and, 118
Preoccupations, body dysmorphic
disorder and, 200
Prevalence, 64
Prevention programs, eating
disorders and, 323
Privileged communication,
506–507
Problem behaviors, intellectual
disability and, 448
Problem solving, generalized
anxiety syndrome and, 163
Processing speed, cognitive
functioning and, 480
Processing speed tests, 78
Prodromal phase, schizophrenia
and, 377
Prodrome, 118
Profound intellectual disability, 445
Prognosis, 64
Projection, 17t
Projective tests, personality
assessment and, 80
Propranolol (Inderal), 180
Prosopagnosia, 483
Pruning, 381
Psychiatric hospitalization
eating disorders and, 322–323
substance use disorders and, 291
Psychiatric nurses, 71
Psychiatrists, 71
Psychoanalytic theory, 15–18
beyond Freud, 17
conscious and, 15
ego and, 15–16
evaluating contributions and,
17–18
humanist response to, 18
iceberg metaphor and, 16, 16f
id and, 15
preconscious and, 15
superego and, 15
unconscious and, 15
Psychodynamic theory, 17–18
Psychodynamic therapy
histrionic personality disorder
and, 431
narcissistic personality disorder
and, 432
personality disorders and,
409–410
Psychological anesthesia, 247
Psychological disorders
ancient views of psychopathology,
10–14
behaviorism and, 19–20
biological explanations and, 22
cognition and, 481–482
cognitive psychology and, 20–21
context and culture and, 7–10
criteria for determining, 4–10, 4f
distress and, 4–5
facts at a glance and, 8t
impairment in daily life and,
5–6, 6f
modern synthesis of explanations,
23–25
neurological factors and, 29–40
psychoanalytic theory and, 15–18
psychological factors and, 41–50
risk of harm and, 6–7
scientific accounts of, 19–25
social factors and, 50–55
social forces and, 21–22
transition to scientific accounts
of, 14–18
Psychological effects, starvation
and, 301–302
Psychological factor research
clinical interviews and, 101
mental processes biases and, 101
questionnaires and, 101–102
research challenges and, 101–102
Psychological factors, 41–50
attention-deficit/ hyperactivity
disorder and, 468–469,
471–472
autism spectrum disorder and,
453–454
behavior and learning, 41–44
bipolar disorders and, 142, 144
borderline personality disorder
and, 425, 427–428
classical conditioning and, 41–42
cognitive distortions and, 46, 46t
conversion disorder and, 247–248
dementia and, 498–499
depersonalization-derealization
disorder and, 231
depressant use disorders and,
276–277
depressive disorders and, 124–125,
132–133
dissociative amnesia and, 228–229
dissociative disorders and,
238–239
dissociative identity disorder
and, 235
eating disorders and, 310–313,
313f, 320–321
emotions and, 47–50
gender dysphoria and, 332, 334
generalized anxiety disorder and,
160–161, 162–163
illness anxiety disorder and, 251
intellectual disability and, 448, 449
mental contents and, 46–47
mental processes and, 45–46
observational learning and, 45
obsessive-compulsive disorder
and, 203–204, 205
operant conditioning and, 42–44
other abused substances and, 282
panic disorder and agoraphobia
and, 169–170, 172–174
paraphilic disorders and, 344, 346
personality disorders and, 408,
409–410
posttraumatic stress disorder and,
214–215, 217–218
researching treatments targeting,
105–110
schizophrenia and, 394–395
schizotypal personality disorder
and, 416
sexual dysfunctions and, 355–356,
359–360
social anxiety disorder and,
178–179, 180–181
specific learning disorder and, 458
specific phobias and, 185,
186–187
stimulant use disorders and,
268–269, 269t
substance use disorders and,
287–291
suicide and, 150
Psychomotor agitation, depression
and, 116
Psychomotor retardation,
depression and, 117
Psychopathology
ancient views of, 10–12
biopsychosocial approaches and,
23–25
diathesis-stress model and, 23, 23f
neuropsychosocial approaches
and, 25, 25f
Psychopathy
emphasis of, 419
feedback loops and, 421
neurological factors and, 420
psychological factors and, 420
social factors and, 421
treatment of, 421–422
Psychosexual stages, 16
Psychosis, defined, 6
Psychotic disorders, 372–375
brief psychotic disorders,
373, 375t
delusional disorder, 373–374, 375t
schizoaffective disorder, 373, 375t
schizophreniform disorder,
372–373, 375t
Public speaking anxiety, 46
Punishment, 43–44
Purging
anorexia nervosa and, 300
bulimia nervosa and, 304
Pyromania, 204
° Q °
Qi, 11
Quasi-experimental design, 93, 98t
Question identification, scientific
method and, 88
Questionnaires
acquiescence and, 102
researching psychological factors
and, 101–102
response bias and, 102
social desirability bias and, 102
° R °
Random assignment, experiments
and, 92
Randomized clinical trials, 108–109
Rape, 340
Rapid cycling, bipolar disorders
and, 139
Rationalization, 17t
Reaction formation, 17t
Reactive interaction, genes and, 40
Reactivity, research participants
and, 103
Reading, specific learning disorder
and, 456
Reality orientation therapy,
dementia and, 498
Reciprocal gene-environment
model, 38
Recurrent depression, 119
Referential delusions, 367
Reinforcement, 42–43
Relapse prevention training,
paraphilic disorders and, 346
Relaxation training
panic disorder and agoraphobia
and, 173
posttraumatic stress disorder and,
218
Reliability, classification systems
and, 64
Relief craving, stimulant abuse and,
268
Reminiscence therapy, dementia
and, 498
Renaissance, forces of evil in, 12
Rennie v. Klein, 1978, 522
Replication, data, 88
Reporting bias, clinical interviews
and, 77
Repression, as defense mechanism,
17t
Research methods
case studies, 96–97
correlational research, 93–96
cultural differences and, 103–104
ethical guidelines and, 98–99
experiments and, 90–93
meta-analysis, 97–98
quasi-experimental design, 93
researching neurological factors,
100
researching psychological factors,
101–102
researching social factors,
102–104, 110–111
Subject Index S -14
researching treatment, 104–112
scientific method and, 88–90
scientific research types, 90–98
Residential settings, schizophrenia
and, 397
Residential treatment, substance
use disorders and, 291
Resistant/anxious attachment, 21
Resolution, sexual response cycle
and, 347
Response bias, questionnaires and,
102
Responses from others, gender
dysphoria and, 330, 332–333
Restrained eating, 313
Restricting type, anorexia nervosa
and, 300
Restructuring, 20
Rett’s disorder, 447t
Reuptake, 36
Reward craving, stimulant abuse
and, 268
Reward dependence, 50t
Rey Osterrieth Test, 74
Right to refuse treatment, 522
Right to treatment, 522
Risk factors, correlational research
and, 95–96
Risk of harm, psychological
disorders and, 6–7
Risperdal (risperidone), 393
Ritalin, 265
Rogers, Carl, 18
Romans, mental illness beliefs and,
11–12
Rorschach test, 80, 80f
Rouse v. Cameron, 1967, 522
Rumination, depressive disorders
and, 124–125
Rush, Benjamin, 14
° S °
Sadism, 337t, 340
Safe person, agoraphobia and,
171–172
Safety, posttraumatic stress disorder
and, 218
Sample, experiments and, 92
Sampling bias, 92
Schizoaffective disorder, 373, 375t
Schizoid personality disorder,
413–414, 413t, 415
Schizophrenia
abnormal hippocampus and, 381
active phase and, 377
attention deficits and, 369
attention difficulties and,
385–386
atypical antipsychotics and,
393–394
avolition and, 369
beliefs and attributions and,
386–387
biological markers and, 382
brain abnormality causes,
381–382
brain stimulation and, 394
brain systems and, 380–382
catatonia and, 368
cognitive-behavior therapy and,
394
cognitive deficits and, 369–371
cognitive difficulties and,
385–386
community-based care and, 396
comorbid substance abuse and,
395
comorbidity and, 376–377
course of, 377, 377t
cultural differences and, 377,
378t
cultural factors and, 390–391
deficit/nondeficit subtypes and,
371
delusions and, 367
depression and, 372, 372t
diagnostic criteria limitations
and, 370–371
differentiation with other disorders,
371–372
discontinuing medication and,
394
disorganized speech and, 368
dopamine and, 383
DSM-5 diagnostic criteria and,
366t
economic factors and, 390
emotional expression and, 387
estrogen and, 383–384
executive functions and, 370,
385–386
facts at a glance and, 378t
family education and therapy
and, 395
feedback loops and, 391, 392f,
397–398, 398f
flat affect and, 369
frontal lobe and, 32, 381
gender and, 377, 378t
genetics and, 384–385, 384t
grossly disorganized psychomotor
behavior and, 368
group therapy and, 395–396
hallucinations and, 367
highly expressed emotion and,
51, 388
immigrants and, 389–390
impaired temporal lobe and
thalamus and, 381
inpatient treatment and, 396
interactions among brain areas
and, 381
involuntary movements and, 382
mania and, 372
medication and, 393–394
memory difficulties and, 385–386
mental processes and, 385–386
minimizing hospitalization and,
396
negative symptoms and, 369
neural communication and,
383–384
neuroimaging and, 73, 73f
neurological factors and, 380–385
older adults and, 482
other psychotic disorders and,
372–375
positive symptoms and, 366–368
prevalence and, 376, 376f
prodromal phase and, 377
prognosis and, 379, 379t
psychological factors and,
385–387
psychotic symptoms and,
371–372
residential setting and, 397
sensory gating and, 382
serotonin and glutamate and, 383
smooth pursuit eye movements
and, 382, 382f
social causation hypothesis and,
390
social factors and, 387–391
social selection hypothesis and,
390
social skills training and, 395–396
stress and cortisol and, 383
stressful environments and,
388–389
substance-related disorders and,
372
suicide and, 379
targeting neurological factors
and, 393–394
targeting psychological factors
and, 394–395
targeting social factors and,
395–397
theory of mind and, 388
traditional antipsychotics and,
393
treatment steps, 392–393
understanding social world and,
388
violence and, 379
vocational rehabilitation and, 397
working memory deficits and,
369–370
Schizophreniform disorder, 372–373,
375t
Schizotypal personality disorder,
374–375, 414–416
DSM-5 criteria and, 414t
facts at a glance and, 415t
feedback loops and, 416
neurological factors and, 416
psychological factors and, 416
schizoid personality disorder
compared, 415
social factors and, 416
symptoms of, 414–415
Scientific method, 88–90
collecting initial observations
and, 88
data replication and, 88
hypotheses and, 89
predictions and, 89
question identification and, 88
steps of, 90f
theory development and, 89
theory testing and, 89
Seasonal affective disorder, 93, 119
Seasonal relationship, suicides and,
146
Secobarbital (Seconal), 274
Secure attachment, 21, 126, 408
Sedative-hypnotic drugs, 274–275
barbiturates, 274
benzodiazepines, 274–275
Seizures, conversion disorder and,
245
Selective amnesia, 226
Selective serotonin reuptake
inhibitors (SSRIs), 130–131,
162, 180, 205, 213, 217, 252,
319–320, 344
Self-destructive behaviors,
borderline personality disorder
and, 425
Self-esteem
attention-deficit/hyperactivity
disorder and, 468–469
eating disorders and, 313
Self-help groups, substance use
disorders and, 291–292
Self-hypnosis, 235, 247–248
Self-injurious behaviors, intellectual
disability and, 448
Self-monitoring, generalized
anxiety syndrome and, 163
Seligman, Martin, 44
Sell v. United States, 2003, 515
Semistructured interviews, 75, 77–78
Sensate focus exercises, 359
Sensory deficits, conversion
disorder and, 247
Sensory gating, 382
Sensory neurons, 33
Separation anxiety disorder,
188–191
adults with, 189
development differences and, 190
DSM-5 diagnostic criteria and,
188t
facts at a glance and, 190t
genetics and, 1981
nature of, 188–189
overprotective family members
and, 191
understanding and treating, 191
S -15 Subject Index
Seroquel (Quetiapine), 393
Serotonin
bipolar disorders and, 141
borderline personality disorder
and, 425
eating disorders and, 310
major functions of, 35t
obsessive-compulsive disorder
and, 203
posttraumatic stress disorder and,
213
schizophrenia and, 383
Serotonin/norepinephrine reuptake
inhibitors (SNRIs), 131, 162,
180
Sertraline (Zoloft), 130, 180, 205,
217
Severe intellectual disability, 445
Sex offender classification, 345
Sex reassignment surgery, 329,
333–334
Sex therapy, 360
Sexual abuse, 355–356
Sexual arousal disorders, 349–352
Sexual desire disorders, 349–352
Sexual dysfunctions, 346–362
aging and, 355
alternative female sexual response
cycle, 354f
biological factors and, 354–355
childhood sexual abuse and,
355–356
cognitive behavior therapy and,
359
delayed ejaculation, 351
diagnostic criteria criticisms and,
354
disease and illness and, 354–355
DSM-5 diagnostic criteria and,
348–349, 348t
erectile disorder, 350
facts at a glance and, 353t
feedback loops and, 356–357,
356f, 360–361, 360f
female orgasmic disorder, 351
female sexual interest/arousal
disorder, 350
genito-pelvic pain/penetration
disorder, 352–353
male hypoactive sexual desire
disorder, 349
medications for, 358–359, 358t
medications interfering with
response, 355
neurological factors and,
354–355
normal sexual response cycle
and, 347, 347f
orgasmic disorders, 350–352
predisposing events and, 355t
premature (early) ejaculation, 351
psychological factors and,
355–356
sensate focus exercises and, 359
sex therapy techniques and, 360
sexual arousal disorders, 349–352
sexual desire disorders, 349–352
sexual pain disorder, 352
social factors and, 356
targeting biological factors and,
358–359
targeting neurological factors
and, 358–359
targeting psychological factors
and, 359–360
targeting social factors and, 360
Sexual harassment, workplace, 54
Sexual masochism disorder, 337t,
341
Sexual pain disorder, 352
Sexual predator laws, 521
Sexual response cycle, 347, 347f
Sexual sadism disorder, 337t, 340
Shared delusions, 374
Sheltered employment,
schizophrenia and, 397
Single-participant experiments,
97, 98t
Situational type of phobia, 183
Skin-picking disorder, 199
Skin popping, 279
Skinner, B. F., 19, 42
Smooth pursuit eye movements,
382, 382f
Social anxiety, 45
Social anxiety disorder, 175–181
brain systems and, 177–178
classical conditioning and, 179
cognitive biases and distortions
and, 178–179
DSM-5 diagnostic criteria and,
176t
facts at a glance and, 177t
feedback loops and, 179–180,
181
genetics and, 178
key features of, 176
nature of, 176
neural communication and,
177–178
neurological factors and, 177–178
operant conditioning and, 179
psychological factors and,
178–179
social factors and, 179
targeting neurological factors
and, 180
targeting psychological factors
and, 180–181
targeting social factors and, 181
Social causation hypothesis,
schizophrenia and, 390
Social cognition disorders, 489
Social desirability bias,
questionnaires and, 102
Social drift, 390
Social effects, starvation and,
301–302
Social environment, clinical
assessment and, 82
Social exclusion, depression and,
126
Social factor research
cultural differences and, 103–104
double-blind design and, 103
experimental expectancy effects
and, 103
investigator-influenced biases
and, 103
reactivity and, 103
research challenges and, 102–104
Social factors
antisocial personality disorder
and, 421
assessment of, 81–83
attention-deficit/hyperactivity
disorder and, 469, 472–473
autism spectrum disorder and,
454, 455
bipolar disorders and, 142–143,
144–145
borderline personality disorder
and, 425–426, 428
bullying and, 54
child maltreatment and, 51–52
community support and, 52
conversion disorder and, 248
dementia and, 499
depersonaliztion-derealization
disorder and, 231
depressant use disorders and, 277
depressive disorders and,
126–129, 133–135
discrimination and, 54
dissociative amnesia and, 229
dissociative disorders and,
238–239
dissociative identity disorder and,
235–236
eating disorders and, 313–317,
321–323
family interaction and relapse, 51
family matters and, 50–52
gender dysphoria and, 334
generalized anxiety disorder and,
161
generalized anxiety syndrome
and, 163
illness anxiety disorder and, 251
indirect effects and, 229
intellectual disability and, 448,
449
obsessive-compulsive disorder
and, 204–205, 206
other abused substances and, 282
panic disorder and agoraphobia
and, 170–171, 174
paraphilic disorders and, 346
parental psychological disorders
and, 52
personality disorders and, 408,
410
posttraumatic stress disorder and,
215, 218
psychological disorders and,
21–22
psychopathy and, 421
researching treatments targeting,
110–111
schizophrenia and, 387–391,
395–397
schizotypal personality disorder
and, 416
sexual dysfunctions and, 356, 360
social anxiety disorder and, 179,
181
socioeconomic status and, 53–54
somatic symptom disorders and,
243, 252–253
specific learning disorder and,
458
specific phobias and, 185, 187
stimulant use disorders and,
269–271, 270, 271t
substance use disorders and,
291–292
suicide and, 150
war and, 54
Social phobia. See Social anxiety
disorder
Social selection
psychological disorders and, 53
schizophrenia and, 390
Social skills
autism spectrum disorder and,
455
schizophrenia and, 395–396
Social workers, psychotherapy and,
71
Sociocognitive model, dissociative
identity disorder and, 237
Sociocultural factors, stimulant use
disorders and, 271
Socioeconomic factors,
posttraumatic stress disorder
and, 215
Socioeconomic status, 53–54
Somatic delusions, 6, 374
Somatic symptom disorder (SSD),
241–244
cognitive-behavior therapy and,
252t
cultural differences and, 243
DSM-5 diagnostic criteria and,
241t
facts at a glance and, 242t
feedback loops and, 243–244,
244f
genetics and, 242
misinterpreting bodily signals
and coping and, 243
nature of, 241
Subject Index S -16
neurological factors and, 242
observational learning and, 243
psychological factors and, 243
social factors and, 243
Somatic symptom disorders,
240–253
bodily preoccupation and, 240
cognitive-behavior therapy and,
252, 252t
common bodily complaints and,
240, 240t
common features and, 240
conversion disorder, 244–248
factitious disorder and, 240
family education and, 252–253
feedback loops and, 253
history of, 240
illness anxiety disorder and,
248–251
social support and, 252–253
somatic symptom disorder (SSD)
and, 241–244
symptom amplification and, 240
targeting neurological factors
and, 251–252
targeting psychological factors
and, 252
targeting social factors and,
252–253
Special education, intellectual
disability and, 449
Specific learning disorder, 455–459
brain systems and, 457–458
DSM-5 diagnostic criteria and,
456t
dyslexia and, 456
facts at a glance and, 457t
genetics and, 458
mathematics and, 456
neurological factors and,
457–458
psychological factors and, 458
reading and, 456
shaping motivation and, 458
social factors and, 458
treating dyslexia and, 458–459
written expression and, 456
Specific phobias, 182–187
animal type of, 182
behavioral methods and, 186
blood-injection-injury type of,
182
brain systems and, 184
classical conditioning and, 185
cognitive methods and, 186–187
culture and, 185
DSM-5 diagnostic criteria and,
182t
exposure and, 186
facts at a glance and, 183t
faulty estimations and, 185
feedback loops and, 186, 187
genetics and, 184, 184f
modeling and, 185
natural environment type of, 182
nature of, 182–183
neural communication and, 184
neurological factors and, 184
operant conditioning and, 185
psychological factors and, 185
situational type of, 183
social factors and, 185
stimuli and, 183
targeting neurological factors
and, 186
targeting psychological factors
and, 186–187
targeting social factors and, 187
virtual reality simulations and,
186
Speech observations, clinical
interviews and, 76
St. John’s wort, 131, 252
Stages of change, substance use
disorders and, 288–289
Starvation, psychological and social
effects of, 301–302
Statistical significance, correlational
research and, 94–95
Stereotyped behaviors, intellectual
disability and, 448
StigmaBusters, 64
Stimulant use disorders, 263–271
amphetamines, 264–265
bath salts, 266
brain systems and, 267–268
classical conditioning and,
268–269
cocaine and crack, 264, 264t,
267, 267f
dopamine reward system and,
267–268, 267f
drug cues and, 269
family relations and peers and,
269–270
MDMA (ecstasy), 265–266
medications modifying, 286
methamphetamine, 265, 267,
268f
neural communication and,
267–268
neurological factors contributing
to, 268t
norms and perceived norms and,
270
operant conditioning and,
268–269
psychological factors and,
268–269, 269t
relief craving and, 268
reward craving and, 268
Ritalin, 265
social factors and, 269–271, 271t
sociocultural factors and, 271
Stimulus generalization, 42
Stress
bipolar disorders and, 142–143
child maltreatment and, 51
conversion disorder and, 248
depression and, 123, 126
generalized anxiety disorder and,
161
military action and, 54
obsessive-compulsive disorder
and, 204
schizophrenia and, 383, 388–389
stress response, 31
Stroke, 483, 483f
Structured Clinical Interview for
DSM, 78
Structured interviews, 75
Subcortical brain area, 32, 32f
Sublimation, as defense mechanism,
17t
Substance imbalance within body,
11–12
Substance-induced cognition
changes, 484
Substance intoxication, 258, 258t
Substance/medication-induced
neurocognitive disorder, 496–497
Substance use disorders
abstinence-focused treatments
and, 284–285
as category or a continuum, 260
cognitive-behavior therapy and,
289–290
common liabilities model and,
261
comorbidity and, 262
culture and context and, 263
delirium and, 487
depressants and, 271–277
detoxification and, 285–286
dissociative anesthetics and,
280–281
drug use stages, 261f
DSM-5 diagnostic criteria and,
258–259, 259t
family therapy and, 292
feedback loops and, 292–293
gateway hypothesis and, 261
group-based treatment and,
291–292
hallucinogens and, 279–280
harm reduction treatments and,
284–285
medications and, 286–287, 287t
motivation to stop and, 288–289
motivational enhancement therapy
and, 289
opioids and, 278–279
other abused substances and,
278–284
polysubstance abuse and, 262
prevalence and costs and,
262–263
residential treatment and, 291
schizophrenia and, 372, 376
self-help groups and, 291–292
stages of change and, 288–289
stimulant use disorders, 263–271
substance use vs. intoxication,
258, 258t
suicide and, 148
targeting neurological factors
and, 285–287
targeting psychological factors
and, 287–291
targeting social factors and,
291–292
tolerance and withdrawal and,
259–260, 260f
treatment goals and, 284–285
twelve-step facilitation and,
290–291, 290t
use becoming problem and, 261
Substantia nigra, 495
Subthreshold cases, eating disorders
and, 307
Suicide, 146–151
attempting, 6–7, 147–148
crisis intervention and, 151
facts at a glance and, 147t
feedback loops and, 150–151
homosexuality and, 148
ideation and, 146
incidence rates and, 146
long-term prevention and, 151,
151t
military and, 151
neurological factors and,
149–150
planning of, 147
psychological factors and, 150
risk and protective factors,
148–149, 149t
schizophrenia and, 379
seasonal relationship and, 146
social factors and, 150
substance abuse and, 148
suicidal ideation, 146
warning signs and, 147
Suicide Prevention Resource
Center, 151t
Superego, 15
Supernatural forces, 11
Supported employment programs,
schizophrenia and, 397
Surgical castration, 345
Surgical treatment, body
dysmorphic disorder and, 201
Sybil, 235
Sympathetic nervous system, 31
Symptom amplification, somatic
symptom disorder and, 243
Synapse, 34, 35f
Synaptic cleft, 34
Syphilis, 22, 22f
S -17 Subject Index
Systems therapy
depression and, 134–135
eating disorders and, 322
° T °
Taijin kyofusho, 179
Tarasoff rule, 517
Tardive dyskinesia, 393, 522
Teenage depression, 120
Temperament
genetics and, 407
personality disorders and, 408
Temporal lobes
eating disorders and, 309
role of, 31–32
schizophrenia and, 381
Teratogens, intellectual disability
and, 447
Tetrahydrocannabinol (THC), 279
Thalamus, schizophrenia and, 381
Thematic Apperception Test (TAT),
80, 81f
Theory development, scientific
method and, 89
Theory of mind
autism spectrum disorder and,
454
schizophrenia and, 388
Theory testing, scientific method
and, 89
Thorazine (Chlorpromazine), 393
Thought insertion, 367
Tolerance
alcohol use disorder and,
273–274
substance use disorders and,
259–260, 260f
Transcranial magnetic stimulation
(TMS), 132, 394
Transgender, 329
Transient ischemic attacks, 494
Transsexuals, 329
Transvetic disorder, 337t, 342–343,
342t
Trauma history, posttraumatic stress
disorder and, 214–215
Trauma-related disorders, 207–219
acute stress disorder, 211–212,
212t
examples of, 208
nature of, 208–209
persistent symptoms and,
207–208
posttraumatic stress disorder,
209–211, 213–219
types of, 208–209
Traumatic brain injury, dementia
and, 496
Treatment, 104–112
allegiance effect and, 109
attrition and, 105
baseline assessments and, 107
common factors and, 106
comparing therapy or no
treatment, 107–108
culturally sanctioned placebo
effects, 111
dose-response relationship and,
109–110, 110f
dropouts and, 105
drug effect or placebo effect, 105
evidence-based practice and, 109
experimental treatments, 112,
112t
follow-up assessments and, 107,
109
gender and ethnicity and, 11
manual-based treatment, 108
neurological factors and, 104–105
outcome assessments and, 107
placebo control groups and, 107
psychological factors and,
105–110
randomized clinical trials and,
108–109
social factors and, 110–111
specific factors and, 106
treatment-related variables, 106t
wait-list control groups and, 107,
107f
Treatment legal issues, 521–523
competence to refuse treatment,
522–523
mental health and drug courts,
523
right to refuse treatment, 522
right to treatment, 522
Treatment of Depression
Collaborative Research Program
study (TDCRP), 108
Trephination, 11
Treponema pallidum, 22
Triazolam (Halcion), 274
Tricyclic antidepressants (TCAs), 130
Truvada, 496
Twin studies, 38–39
° U °
Unconditioned response, 41
Unconditioned stimulus, 41
Unconscious, psychoanalytic
theory and, 15
Understimulation, intellectual
disability and, 448
United States v. Comstock, 2010, 521
Unstructured interviews, 75
° V °
Validity, classification systems and,
64
Vascular dementia, 494–495
Venlafaxine (Effexor), 131, 162, 180
Verbal comprehension tests, 78
Viagra (Sildenafil citrate), 358
Violent behavior, patient. See
Dangerousness
Virtual reality exposure, 163
Virtual reality simulations, specific
phobias and, 186
Vocational rehabilitation,
schizophrenia and, 397
Voyeuristic disorder, 337t, 338
° W °
Wait-list control groups, 107, 107f
War, extreme and prolonged stress
and, 54
Wechsler Adult Intelligence Scale,
78
Wechsler Intelligence Scale for
Children, 78
Weight, excessive concern with,
311
Wernicke’s aphasia, 483
Wind overload, 166
Witches, 12
Withdrawal, substance use disorders
and, 259–260, 260f
Withdrawal emotions, 49
Word salad, 368
Working memory deficits,
schizophrenia and, 369–370
Working memory tests, 78
Worry exposure, 164f
Written expression, specific
learning disorder and, 456
Wyatt v. Stickney, 1971, 522
° X °
X-ray images, clinical assessment
and, 73
° Y °
Yuit Eskimos, suicides and, 150
° Z °
Zaleplon (Sonata), 275
Zeigarnik effect, 344
Zen Buddhist approach, borderline
personality disorder and, 427
Zolpidem (Ambien), 275
Zyprexa (Olanzapine), 393
Cover
Title Page: Abnormal Psychology 2nd Edition
Copyright
Dedication
About the Authors
List of Chapters
Contents
Preface
Acknowledgments
Half Title: Abnormal Psychology
Chapter 1: The History of Abnormal Psychology
The Three Criteria for Determining Psychological Disorders
Distress
Impairment in Daily Life
Risk of Harm
Context and Culture
Views of Psychological Disorders Before Science
Ancient Views of Psychopathology
Supernatural Forces
Imbalance of Substances Within the Body
Forces of Evil in the Middle Ages and the Renaissance
Rationality and Reason in the 18th and 19th Centuries
Asylums
Pinel and Mental Treatment
Moral Treatment
The Transition to Scientific Accounts of Pyschological Disorders
Freud and the Importance of Unconscious Forces
Psychoanalytic Theory
Psychosexual Stages
Mental Illness, According to Freud
Defense Mechanisms
Psychoanalytic Theory Beyond Freud
Evaluating the Contributions of Freud and His Followers
The Humanist Response
Scientific Accounts of Psychological Disorders
Behaviorism
The Cognitive Contribution
Social Forces
Biological Explanations
The Modern Synthesis of Explanations of Psychopathology
The Diathesis–Stress Model
The Biopsychosocial and Neuropsychosocial Approaches
Chapter 2: Understanding Psychological Disorders: The Neuropsychosocial Approach
Neurological Factors in Psychological Disorders
Brain Structure and Brain Function
A Quick Tour of the Nervous System
Neurons
Chemical Signals
Hormones and the Endocrine System
The Genetics of Psychopatholgoy
Behavioral Genetics
Feedback Loops in Understanding Genes and the Environment
The Environment Affects the Genes
The Genes Affect the Environment
Psychological Factors in Psychological Disorders
Behavior and Learning
Classical Conditioning
Operant Conditioning
Feedback Loops in Understanding Classical Conditioning and Operant Conditioning
Observational Learning
Mental Processess and Mental Contents
Mental Processes
Mental contents
Emotion
Emotions and Behavior
Emotions, Mental Processes, and Mental Contents
Emotional Regulation and Psychological Disorders
Neurological Bases of Emotion
Temperament
Social Factors In Psychological Disorders
Family Matters
Family Interactions Style and Relapse
Child Maltreatment
Parental Psychological Disorders
Community Support
Social Stressors
Socioeconomic Status
Discrimination, Bullying, and War
Culture
A Neuropsychosocial Last Word on the Beales
Chapter 3: Clinical Diagnosis and Assessment
Diagnosing Psychological Disorders
Why Diagnose?
A Cautionary Note About Diagnosis
Reliability and Validity in Classification Systems
The Diagnostic and Statistical Manual of Mental Disorders
The Evolution of DSM
The Evolution of DSM-5
The People Who Diagnose Psychological Disorders
Clinical Psychologists and Counseling Psychologists
Psychiatrists, Psychiatric Nurses, and General Practitioners
Mental Health Professionals with Master’s Degrees
Assessing Psychological Disorders
Assessing Neurological and Other Biological Factors
Assessing Abnormal Brain Structures with X-Rays, CT Scans, and MRIs
Assessing Brain Function with PET Scans and fMRI
Neuropsychological Assessment
Assessing Psychological Factors
Clinical Interview
Test of psychological Functioning
Assessing Social Factors
Family Functioning
Community
Culture
Assessment as an Interactive Process
Diagnosing and Assessing Rose Mary and Rex Walls?
Chapter 4: Research Methods
Using the Scientific Method to Understand Abnormality
The Scientific Method
Collect Initial Observations
Identify a Question
Develop and Test a Hypothesis
Develop a Theory
Test the Theory
Types of Scientific Research
Conducting Research with Experiments
Quasi-Experimental Design
Correlational Research
Case Studies
Meta-Analysis
Ethical Guidelines for Research
Research Challenges in Understanding Abnormality
Challenges in Researching Neurological Factors
Challenges in Researching Psychological Factors
Biases in Mental Processes That Affect Assessment
Research Challenges with Clinical Interviews
Research Challenges with Questionnaires
Challenges in Researching Social Factors
Investigator-Influenced Biases
Cultural Differences in Evaluating Symptoms
Researching Treatment
Researching Treatments That Target Neurological Factors
Drug Effect or Placebo Effect?
Dropouts
Researching Treatments That Target Psychological Factors
Common Factors and Specific Factors
Is Therapy Better Than No Treatment?
Is One Type of Therapy Generally More Effective Than Another?
The Therapy Dose–Response Relationships
Researching Treatments That Target Social Factors
Gender and Ethnicity of Patient and Therapist
Culturally Sanctioned Placebo Effects
Ethical Research on Experimental Treatments
Chapter 5: Mood Disorders and Suicide
Despressive Disorders
Major Depressive Episode
Affect: The Mood symptoms of Depression
Behavioral and Physical Symptoms of Depression
Cognitive Symptoms of Depression
Major Depressive Disorder
Depression in Children and Adolescents
Persistent Depressive Disorder
Current Controversy: Disruptive Mood Dysregulation Disorder: Overlabeling of Tantrums?
Understanding Depressive Disorders
Neurological Factors
Psychological Factors
Social Factors
Feedback Loops in Understanding Depressive Disorders
Treating Depressive Disorders
Targeting Neurological Factors
Targeting Psychological Factors
Targeting Social Factors
Feedback Loops in Treating Depressive Disorders
Bipolar Disorders
Mood Episodes for Bipolar Disorders
Manic Episode
Hypomanic Episode
The Two Types of Bipolar Disorder
Cyclothymic Disorder
Understanding Bipolar Disorders
Neurological Factors
Psychological Factors: Thoughts and Attributions
Social Factors: Social and Environmental Stressors
Feedback Loops in Understanding Bipolar Disorders
Treating Bipolar Disorders
Targeting Neurological Factors: Medication
Targeting Psychological Factors: Thoughts, Moods, and Relapse Prevention
Targeting Social Factors: Interacting with Others
Feedback Loops in Treating Bipolar Disorder
Suicide
Suicidal Thoughts and Suicide Risks
Thinking About, Planning, and Attempting Suicide
Risk and Protective Factors for Suicide
Understanding Suicide
Neurological Factors
Psychological Factors: Hopelessness and Impulsivity
Social Factors: Alienation and Cultural Stress
Feeback Loops in Understanding Suicide
Preventing Suicide
Crisis Intervention
Long-Term Prevention
Chapter 6: Anxiety Disorders
Common Features of Anxiety Disorders
What Is Anxiety?
The Fight-or-Flight Response Gone Awry
Comorbidity of Anxiety Disorders
Generalized Anxiety Disorder
What is Generalized Anxiety Disorder?
Understanding Generalized Anxiety Disorder
Neurological Factors
Psychological Factors: Hypervigilance and the Illusion of Control
Social Factors: Stressors
Feedback Loops in Understanding Generalized Anxiety Disorder
Treating Generalized Anxiety Disorder
Targeting Neurological Factors: Medication
Targeting Psychological Factors
Targeting Social Factors
Feedback Loops in Treating Generalized Anxiety Disorder
Panic Disorder and Agoraphobia
The Panic Attack—A Key Ingredient of Panic Disorder
What Is Panic Disorder?
What Is Agoraphobia?
Understanding Panic Disorder and Agoraphobia
Neurological Factors
Psychological Factors
Social Factors: Stressors, a Sign of the Times, and “Safe People”
Feedback Loops in Understanding Panic Disorder and Agoraphobia
Treating Panic Disorder and Agoraphobia
Targeting Neurological Factors: Medication
Targeting Psychological Factors
Targeting Social Factors: Group and Couple Therapy
Feedback Loops in Treating Panic Disorder and Agoraphobia
Social Anxiety Disorder (Social Phobia)
What Is Social Anxiety Disorder?
Understanding Social Anxiety Disorder
Neurological Factors
Psychological Factors
Social Factors
Feedback Loops in Understanding Social Anxiety Disorder
Treating Social Anxiety Disorder
Targeting Neurological Factors: Medication
Targeting Psychological Factors: Exposure and Cognitive Restructuring
Targeting Social Factors: Groups Interactions
Feedback Loops in Treating Social Anxiety Disorder
Specific Phobia
What Is Specific Phobia?
Specifics About Specific Phobia
Understanding Specific Phobia
Neurological Factors
Psychological Factors
Social Factors: Modeling and Culture
Feedback Loops in Understanding Specific Phobia
Treating Specific Phobia
Targeting Neurological Factors: Medication
Targeting Psychological Factors
Targeting Social Factors: A Limited Role for Observational Learning
Feedback Loops in Treating Specific Phobia
Separation Anxiety Disorder
What Is Separation Anxiety Disorder?
CURRENT CONTROVERSY: Separation Anxiety Disorder: Anxiety Disorder or Developmental Difference?
Understanding and Treating Separation AnxietyDisorder
Follow-up on Earl Campbell
Chapter 7: Obsessive-Compulsive-Related and Trauma-Related Disorders
Obsessive-Compulsive Disorder and Related Disorders
What Is Obsessive-Compulsive Disorder?
What Is Body Dysmorphic Disorder?
Understanding Obsessive-Compulsive Disorder
Neurological Factors
Psychological Factors
Social Factors
Feedback Loops in Understanding Obsessive-Compulsive Disorder
Treating Obsessive-Compulsive Disorder
Targeting Neurological Factors: Medication
Targeting Psychological Factors
Targeting Social Factors: Family Therapy
Feedback Loops in Treating Obsessive-Compulsive Disorder
Trauma-Related Disorders
What Are the Trauma-Related Disorders?
What Is Posttraumatic Stress Disorder?
What Is Acute Stress Disorder?
Understanding Trauma-Related Disorders: PTSD
Neurological Factors
Psychological Factors: History of Trauma, Comorbidity, and Conditioning
Social Factors: Socioeconomic Factors, Social Support, and Culture
Feedback Loops in Understanding Posttraumatic Stress Disorder
Treating Posttraumatic Stress Disorder
Targeting Neurological Factors: Medication
Targeting Psychological Factors
CURRENT CONTROVERSY: Eye Movement Desensitization andReprocessing (EMDR) Treatment for Posttraumatic Stress Disorder
Targeting Social Factors: Safety, Support, and Family Education
Feedback Loops in Treating Posttraumatic Stress Disorder
Follow-up on Howard Hughes
Chapter 8: Dissociative and SomaticSymptom Disorders
Dissociative Disorders
Dissociative Disorders: An Overview
Normal Versus Abnormal Dissociation
Types of Dissociative Disorders
Dissociative Amnesia
What Is Dissociative Amnesia?
Understanding Dissociative Amnesia
Depersonalization-Derealization Disorder
What Is Depersonalization-Derealization Disorder?
Understanding Depersonalization-Derealization Disorder
Dissociative Identity Disorder
What Is Dissociative Identity Disorder?
Criticisms of the DSM-5 Criteria
Understanding Dissociative Identity Disorder
Treating Dissociative Disorders
Targeting Neurological Factors: Medication
Targeting Psychological and Social Factors: Coping and Integration
Feedback Loops in Treating Dissociative Disorders
Somatic Symptom Disorders
Somatic Symptom Disorders: An Overview
Somatic Symptom Disorder
What Is Somatic Symptom Disorder?
Understanding Somatic Symptom Disorder
Conversion Disorder
What Is Conversion Disorder?
Criticisms of the DSM-5 Criteria
Understanding Conversion Disorder
Illness Anxiety Disorder
CURRENT CONTROVERSY: Omission of Hypochondriasis fromDSM-5: Appropriate or Overreaction?
What Is Illness Anxiety Disorder?
Illness Anxiety Disorder, Anxiety Disorders, and OCD: Shared Features
Understanding Illness Anxiety Disorder
Treating Somatic Symptom Disorders
Targeting Neurological Factors
Targeting Psychological Factors: Cognitive-Behavior Therapy
Targeting Social Factors: Support and Family Education
Feedback Loops in Treating Somatic Symptom Disorders
Follow-up on Anna O.
Chapter 9: Substance Use Disorders
Substance Use: When Use Becomes a Disorder
Substance Use Versus Intoxication
Substance Use Disorders
Substance Use Disorder as a Category or ona Continuum?
Use Becomes a Problem
Comorbidity
Polysubstance Abuse
Prevalence and Costs
Culture and Context
Stimulants
What Are Stimulants?
Cocaine and Crack
Amphetamines
Methamphetamine
Ritalin
MDMA (Ecstasy)
Understanding Stimulants
Brain Systems and Neural Communication: Dopamine and Abuse
Psychological Factors: From Learning to Coping
Social Factors
Depressants
What Are Depressants?
Alcohol
Sedative-Hypnotic Drugs
Understanding Depressants
Neurological Factors
Psychological Factors
Social Factors
Other Abused Substances
What Are Other Abused Substances?
Opioids: Narcotic Analgesics
Hallucinogens
Dissociative Anesthetics
Understanding Other Abused Substances
Neurological Factors
Psychological Factors
Social Factors
Feedback Loops in Understanding Substance Use Disorders
Treating Substance Use Disorders
Goals of Treatment
CURRENT CONTROVERSY: Once an Alcoholic, Always an Alcoholic?
Targeting Neurological Factors
Detoxification
Medications
Targeting Psychological Factors
Motivation
Cognitive-Behavior Therapy
Twelve-Step Facilitation (TSF)
Targeting Social Factors
Residential Treatment
Group-Based Treatment
Family Therapy
Feedback Loops in Treating Substance Use Disorders
Chapter 10: Eating Disorders
Anorexia Nervosa
What Is Anorexia Nervosa?
Anorexia Nervosa According to DSM-5
Two Types of Anorexia Nervosa: Restricting and Binge Eating/Purging
Medical, Psychological, and Social Effects of Anorexia Nervosa
Medical Effects of Anorexia
Psychological and Social Effects of Starvation
Bulimia Nervosa
What Is Bulimia Nervosa?
Medical Effects of Bulimia Nervosa
Is Bulimia Distinct From Anorexia?
Binge Eating Disorder and“Other” Eating Disorders
What Is Binge Eating Disorder?
CURRENT CONTROVERSY: Is Binge Eating Disorder Diagnosisa Good Idea?
Disordered Eating: “Other” Eating Disorders
Understanding Eating Disorders
Neurological Factors: Setting the Stage
Brain Systems
Neural Communication: Serotonin
Genetics
Psychological Factors: Thoughts of and Feelings About Food
Thinking About Weight, Appearance, and Food
Operant Conditioning: Reinforcing Disordered Eating
Personality Traits as Risk Factors
Dieting, Restrained Eating, and Disinhibited Eating
Other Psychological Disorders as Risk Factors
Social Factors: The Body in Context
The Role of Family and Peers
The Role of Culture
Eating Disorders Across Cultures
The Power of the Media
Objectification Theory: Explaining the Gender Difference
Feedback Loops in Understanding Eating Disorders
Treating Eating Disorders
Targeting Neurological and Biological Factors: Nourishing the Body
A Focus on Nutrition
Medical Hospitalization
Medication
Targeting Psychological Factors: Cognitive-Behavior Therapy
CBT for Anorexia
CBT for Bulimia
Efficacy of CBT for Treating Eating Disorders
Targeting Social Factors
Interpersonal Therapy
Family Therapy
Psychiatric Hospitalization
Prevention Programs
Feedback Loops in Treating Eating Disorders
Follow-up on Marya Hornbacher
Chapter 11: Gender and Sexual Disorders
Gender Dysphoria
What Is Gender Dysphoria?
Understanding Gender Dysphoria
Neurological Factors
Psychological Factors: A Correlation with Play Activities?
Social Factors: Responses From Others
Treating Gender Dysphoria
Targeting Neurological and Other Biological Factors: Altered Appearance
Targeting Psychological Factors: Understanding the Choices
Targeting Social Factors: Family Support
Paraphilic Disorders
What Are Paraphilic Disorders?
Paraphilic Disorders Involving Nonconsenting People
Sexual Sadism Disorder and Sexual Masochism Disorder: Pain and Humiliation
Paraphilic Disorders Involving Nonhuman Objects
Assessing Paraphilic Disorders
Criticisms of the DSM-5 Paraphilic Disorders
Understanding Paraphilic Disorders
Neurological Factors
Psychological Factors: Conditioned Arousal
Social Factors: More Erotica?
Treating Paraphilic Disorders
Targeting Neurological and Other Biological Factors: Medication
CURRENT CONTROVERSY: Sex Offenders: Is Surgical Castrationan Ethical Solution?
Targeting Psychological Factors: Cognitive-Behavior Therapy
Targeting Social Factors
Sexual Dysfunctions
An Overview of Sexual Functioning and Sexual Dysfunctions
The Normal Sexual Response Cycle
Sexual Dysfunctions According to DSM-5
Sexual Desire Disorders and Sexual Arousal Disorders
Orgasmic Disorders
Sexual Pain Disorder: Genito-Pelvic Pain/Penetration Disorder
Criticisms of the Sexual Dysfunctions in DSM-5
Understanding Sexual Dysfunctions
Neurological and Other Biological Factors
Psychological Factors in Sexual Dysfunctions
Social Factors
Feedback Loops in Understanding Sexual Dysfunctions
Treating Sexual Dysfunctions
Targeting Neurological and Other Biological Factors: Medications
Targeting Psychological Factors: Shifting Thoughts, Learning Behaviors
Targeting Social Factors: Couples Therapy
Feedback Loops in Treating Sexual Dysfunctions
Chapter 12: Schizophrenia and Other Psychotic Disorders
What Are Schizophrenia and Other Psychotic Disorders?
The Symptoms of Schizophrenia
Positive Symptoms
Negative Symptoms
Cognitive Deficits: The Specifics
Deficits in Attention
Deficits in Working Memory
Deficits in Executive Functioning
Cognitive Deficits Endure Over Time
Limitations of DSM-5 Criteria
Deficit/Nondeficit Subtypes
Distinguishing Between Schizophrenia and Other Disorders
Psychotic Symptoms in Schizophrenia, Mood Disorders, and Substance-Related Disorders
Other Psychotic Disorders
CURRENT CONTROVERSY: Attenuated Psychosis Syndrome: The Diagnosis That Wasn’t
Schizophrenia Facts in Detail
Prevalence
Comorbidity
Course
Gender Differences
Culture
Prognosis
Understanding Schizophrenia
Neurological Factors in Schizophrenia
Brain Systems
Neural Communication
Genetics
Psychological Factors in Schizophrenia
Mental Processes and Cognitive Difficulties: Attention, Memory, and Executive Functions
Beliefs and Attributions
Emotional Expression
Social Factors in Schizophrenia
Understanding the Social World
Stressful Environments
Immigration
Economic Factors
Cultural Factors: Recovery in Different Countries
Feedback Loops in Understanding Schizophrenia
Treating Schizophrenia
Targeting Neurological Factors in Treating Schizophrenia
Medication
Brain Stimulation: ECT
Targeting Psychological Factors in Treating Schizophrenia
Cognitive-Behavior Therapy
Treating Comorbid Substance Abuse: Motivational Enhancement
Targeting Social Factors in Treating Schizophrenia
Family Education and Therapy
Group Therapy: Social Skills Training
Inpatient Treatment
Minimizing Hospitalizations: Community-Based Interventions
Feedback Loops in Treating Schizophrenia
Chapter 13: Personality Disorders
Diagnosing Personality Disorders
What Are Personality Disorders?
Assessing Personality Disorders
DSM-5 Personality Clusters
Criticisms of the DSM-5 Category of Personality Disorders
Understanding Personality Disorders in General
Neurological Factors in Personality Disorders: Genes and Temperament
Psychological Factors in Personality Disorders: Temperament and the Consequences of Behavior
Social Factors in Personality Disorders: Insecurely Attached
Feedback Loops in Understanding Personality Disorders
Treating Personality Disorders: General Issues
Targeting Neurological Factors in Personality Disorders
Targeting Psychological Factors in Personality Disorders
Targeting Social Factors in Personality Disorders
Odd/Eccentric PersonalityDisorders
Paranoid Personality Disorder
Schizoid Personality Disorder
Schizotypal Personality Disorder
What Is Schizotypal Personality Disorder?
Understanding Schizotypal Personality Disorder
Treating Odd/Eccentric Personality Disorders
Dramatic/Erratic Personality Disorders
Antisocial Personality Disorder
Understanding Antisocial Personality Disorder and Psychopathy
Treating Antisocial Personality Disorder and Psychopathy
CURRENT CONTROVERSY: Should Psychopaths Receive Treatment?
Borderline Personality Disorder
Understanding Borderline Personality Disorder
Treating Borderline Personality Disorder: New Treatments
Histrionic Personality Disorder
What Is Histrionic Personality Disorder?
Distinguishing Between Histrionic Personality Disorder and Other Disorders
Treating Histrionic Personality Disorder
Narcissistic Personality Disorder
What Is Narcissistic Personality Disorder?
Treating Narcissistic Personality Disorder
Fearful/Anxious Personality Disorders
Avoidant Personality Disorder
What Is Avoidant Personality Disorder?
Distinguishing Between Avoidant Personality Disorder and Other Disorders
Dependent Personality Disorder
Obsessive-Compulsive Personality Disorder
What Is Obsessive-Compulsive Personality Disorder?
Distinguishing Between Obsessive-Compulsive Personality Disorder and OCD
Understanding Fearful/Anxious Personality Disorders
Treating Fearful/Anxious Personality Disorders
Follow-up on Rachel Reiland
Chapter 14: Neurodevelopmental and Disruptive Behavior Disorders
Intellectual Disability (Intellectual Developmental Disorder)
What Is Intellectual Disability?
CURRENT CONTROVERSY: Changing Mental Retardation to Intellectual Disability: Will Such a Switch Be Beneficial?
Understanding Intellectual Disability
Neurological Factors: Teratogens and Genes
Psychological Factors: Problem Behaviors
Social Factors: Understimulation
Treating Intellectual Disability
Targeting Neurological Factors: Prevention
Targeting Psychological and Social Factors: Communication
Targeting Social Factors: Accommodation in the Classroom—It’sthe Law
Autism Spectrum Disorder
What Is Autism Spectrum Disorder?
Understanding Autism Spectrum Disorder
Neurological Factors
Psychological Factors: Cognitive Deficits
Social Factors: Communication Problems
Treating Autism Spectrum Disorder
Targeting Neurological Factors
Targeting Psychological Factors: Applied Behavior Analysis
Targeting Social Factors: Communication
Specific Learning Disorder: Problems with the Three Rs
What Is Specific Learning Disorder?
Understanding Specific Learning Disorder
Neurological Factors
Psychological Factors
Social Factors
Treating Dyslexia
Disorders of Disruptive Behaviorand Attention
What Is Conduct Disorder?
Adolescent-Onset Type
Childhood-Onset Type
What Is Oppositional Defiant Disorder?
Understanding Disorders of Disruptive Behavior and Attention
Neurological Factors
Psychological Factors: Recognizing Facial Expressions, Low Self-Esteem
Social Factors: Blame and Credit
Feedback Loops in Understanding Attention-Deficit/Hyperactivity Disorder
Treating Disorders of Disruptive Behavior and Attention: Focus on ADHD
Targeting Neurological Factors: Medication
Targeting Psychological Factors: Treating Disruptive Behavior
Targeting Social Factors: Reinforcement in Relationships
Feedback Loops in Treating Attention-Deficit/Hyperactivity Disorder
Chapter 15: Neurocognitive Disorders
Normal Versus Abnormal Aging and Cognitive Functioning
Cognitive Functioning in Normal Aging
Intelligence
Memory
Processing Speed, Attention, and Working Memory
Psychological Disorders and Cognition
Depression
Anxiety Disorders
Schizophrenia
Medical Factors That Can Affect Cognition
Diseases and Illnesses
Stroke
Head Injury
Substance-Induced Changes in Cognition
Delirium
What Is Delirium?
Understanding Delirium: A Side Effect?
Delirium Caused by Substance Use
Delirium Caused by a General Medical Condition
Treating Delirium: Rectify the Cause
Dementia (and Mild Versus Major Neurocognitive Disorders)
What Is Dementia?
Mild and Major Neurocognitive Disorders
CURRENT CONTROVERSY: Mild and Major Neurocognitive Disorders
Dementia and Alzheimer’s Disease
Understanding Dementia
Alzheimer’s Disease
Vascular Dementia
Dementia Due to Other Medical Conditions
Treating Dementia
Targeting Neurological Factors
Targeting Psychological Factors
Targeting Social Factors
Diagnosing Mrs. B.’s Problems
Chapter 16: Ethical and Legal Issues
Ethical Issues
An Ethical Principle: The Role of Confidentiality
Ambiguities Regarding Confidentiality
Limits of Confidentiality: HIPAA in Action
Legal Restrictions on Confidentiality
Privileged Communication
Informed Consent to Participate in Research on Mental Illness: Can Patients Truly Be Informed?
Criminal Actions and Insanity
While Committing the Crime: Sane or Insane?
From the M’Naghten Test to the Durham Test
The American Legal Institute Test
Insanity Defense Reform Acts
The Insanity Defense: Current Issues
Assessing Insanity for the Insanity Defense
States’ Rights: Doing Away with the Insanity Defense
CURRENT CONTROVERSY: Criminal Behavior: Does Abnormal Neural Functioning Make It More Excusable?
With the Insanity Defense, Do People Really “Get Away with Murder”?
After Committing the Crime: Competent to Stand Trial?
Dangerousness: Legal Consequences
Evaluating Dangerousness
Actual Dangerousness
Confidentiality and the Dangerous Patient: Duty to Warn and Duty to Protect
Maintaining Safety: Confining the Dangerously Mentally Ill Patient
Criminal Commitment
Civil Commitment
Sexual Predator Laws
Legal Issues Related to Treatment
Right to Treatment
Right to Refuse Treatment
Competence to Refuse Treatment
Mental Health and Drug Courts
The Wheels of Justice: Follow-upon Andrew Goldstein
Glossary
References
Permissions and Attributions
Name Index
Subject Index
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