Respond to the discussion questions in a minimum of one short paragraph and a maximum of two paragraphs (min 100 words; max 200 words)
dream86
Abnormal-Psychology-17th-Edition-B01DV759Q8.pdf
Abnormal Psychology Seventeenth Edition
Jill M. Hooley Harvard University
James N. Butcher University of Minnesota
Matthew K. Nock Harvard University
Susan Mineka Northwestern University
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Library of Congress Cataloging-in-Publication Data
Names: Hooley, Jill M., author. | Butcher, James Neal, author. | Nock, Matthew, author. | Mineka, Susan, author. Title: Abnormal psychology. Description: Seventeenth edition / Jill M. Hooley, James N. Butcher, Matthew K. Nock, Susan Mineka. | Boston : Pearson, [2017] | Revision of: Abnormal psychology / James N. Butcher, University of Minnesota, Susan Mineka, Northwestern University, Jill M. Hooley, Harvard University. Sixteenth edition. | Includes bibliographical references and index. Identifiers: LCCN 2015041946 | ISBN 9780133852059 | ISBN 0133852059 Subjects: LCSH: Psychology, Pathological—Textbooks. | Psychiatry—Textbooks
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iii
1 Abnormal Psychology: Overview and Research Approaches 1
2 Historical and Contemporary Views of Abnormal Behavior 32
3 Causal Factors and Viewpoints 60
4 Clinical Assessment and Diagnosis 106
5 Stress and Physical and Mental Health 136
6 Panic, Anxiety, Obsessions, and Their Disorders 173
7 Mood Disorders and Suicide 220
8 Somatic Symptom and Dissociative Disorders 269
9 Eating Disorders and Obesity 303
10 Personality Disorders 341
11 Substance-Related Disorders 384
12 Sexual Variants, Abuse, and Dysfunctions 421
13 Schizophrenia and Other Psychotic Disorders 459
14 Neurocognitive Disorders 503
15 Disorders of Childhood and Adolescence (Neurodevelopmental Disorders) 532
16 Psychological Treatment 570
17 Contemporary and Legal Issues in Abnormal Psychology 607
Brief Contents
iv
Features xiii What’s New in DSM-5? A Quick Guide xv Preface xvii About the Authors xxiii
1 Abnormal Psychology: Overview and Research Approaches 1
What Do We Mean by Abnormality? 3 Indicators of Abnormality 3
The World Around Us Extreme Generosity or Pathological Behavior? 6
Thinking Critically about DSM-5 What Is the DSM and Why Was It Revised? 7
The DSM-5 and the Definition of Mental Disorder 7
Classification and Diagnosis 8 What Are the Disadvantages of Classification? 8 How Can We Reduce Prejudicial Attitudes Toward People Who Are Mentally Ill? 9
Culture and Abnormality 10
How Common Are Mental Disorders? 12 Prevalence and Incidence 12 Prevalence Estimates for Mental Disorders 13 The Global Burden of Disease 15 Treatment 15 Mental Health Professionals 16
Research Approaches in Abnormal Psychology 16
Sources of Information 17 Case Studies 17 Self-Report Data 18 Observational Approaches 18
Forming and Testing Hypotheses 19 Sampling and Generalization 20 Internal and External Validity 21 Criterion and Comparison Groups 21
Correlational Research Designs 22 Measuring Correlation 22 Statistical Significance 23 Effect Size 24 Meta-Analysis 24 Correlations and Causality 24 Retrospective versus Prospective Strategies 24
The Experimental Method in Abnormal Psychology 25 Studying the Efficacy of Therapy 26 Single-Case Experimental Designs 27
Developments in Research Do Magnets Help with Repetitive-Stress Injury? 27
Animal Research 29
Unresolved Issues Are We All Becoming Mentally Ill? The Expanding Horizons of Mental Disorder 29 Summary 30
Key Terms 31
2 Historical and Contemporary Views of Abnormal Behavior 32
Historical Views of Abnormal Behavior 33 Demonology, Gods, and Magic 34 Hippocrates’ Early Medical Concepts 34
Developments in Thinking Melancholia Through the Ages 35
Early Philosophical Conceptions of Consciousness 36 Later Greek and Roman Thought 36 Early Views of Mental Disorders in China 37 Views of Abnormality During the Middle Ages 37
Toward Humanitarian Approaches 39 The Resurgence of Scientific Questioning in Europe 39 The Establishment of Early Asylums 40 Humanitarian Reform 41 Nineteenth-Century Views of the Causes and Treatment of Mental Disorders 45 Changing Attitudes Toward Mental Health in the Early Twentieth Century 45
The World Around Us Chaining Mental Health Patients 46
Mental Hospital Care in the Twentieth Century 46
The Emergence of Contemporary Views of Abnormal Behavior 48
Biological Discoveries: Establishing the Link Between the Brain and Mental Disorder 48 The Development of a Classification System 49 Development of the Psychological Basis of Mental Disorder 50
Developments in Research The Search for Medications to Cure Mental Disorders 50
The Evolution of the Psychological Research Tradition: Experimental Psychology 53
Unresolved Issues Interpreting Historical Events 56 Summary 58
Key Terms 59
3 Causal Factors and Viewpoints 60 Risk Factors and Causes of Abnormal Behavior 61
Necessary, Sufficient, and Contributory Causes 61 Feedback and Bidirectionality in Abnormal Behavior 63 Diathesis–Stress Models 63
Contents
Contents v
Assessment Interviews 115 The Clinical Observation of Behavior 116 Psychological Tests 117
Developments in Practice The Automated Practice: Use of the Computer in Psychological Testing 118
The Case of Andrea C.: Experiencing Violence in the Workplace 125
Developments in Practice Computer-Based MMPI-2 Report for Andrea C. 126
The Integration of Assessment Data 128 Ethical Issues in Assessment 128
Classifying Abnormal Behavior 129 Differing Models of Classification 129 Formal Diagnostic Classification of Mental Disorders 130
Unresolved Issues The DSM-5: Issues in Acceptance of Changed Diagnostic Criteria 133 Summary 134
Key Terms 135
5 Stress and Physical and Mental Health 136
What Is Stress? 137 Stress and the DSM 138 Factors Predisposing a Person to Stress 138 Characteristics of Stressors 139 Measuring Life Stress 140 Resilience 140
Stress and Physical Health 141 The Stress Response 142 The Mind–Body Connection 143 Understanding the Immune System 143
Stress and Immune System Functioning 145 Stress and Cytokines 145 Chronic Stress and Inflammation 146 Stress and Premature Aging 147
The World Around Us Racial Discrimination and Cardiovascular Health in African Americans 147
Emotions and Health 149 Personality 149 Depression 150 Anxiety 151 Social Isolation and Lack of Social Support 151 Positive Emotions 151 The Importance of Emotion Regulation 153
Treatment of Stress-Related Physical Disorders 153 Biological Interventions 153 Psychological Interventions 153
Stress and Mental Health 155 Adjustment Disorder 155 Adjustment Disorder Caused by Unemployment 156 Posttraumatic Stress Disorder 156
Perspectives to Understanding the Causes of Abnormal Behavior 66
The Biological Perspective 66 Genetic Vulnerabilities 67
Developments in Thinking Nature, Nurture, and Psychopathology: A New Look at an Old Topic 71
Brain Dysfunction and Neural Plasticity 72 Imbalances of Neurotransmitters and Hormones 73 Temperament 75 The Impact of the Biological Viewpoint 76
The Psychological Perspective 76 The Psychodynamic Perspective 77
Developments in Thinking The Humanistic and Existential Perspectives 82
The Behavioral Perspective 83 The Cognitive-Behavioral Perspective 86 What the Adoption of a Perspective Does and Does Not Do 89
The Social Perspective 90 Early Deprivation or Trauma 90 Problems in Parenting Style 93 Marital Discord and Divorce 95 Low Socioeconomic Status and Unemployment 96 Maladaptive Peer Relationships 97 Prejudice and Discrimination in Race, Gender, and Ethnicity 98 The Impact of the Social Perspective 99
The Cultural Perspective 99 Universal and Culture-Specific Symptoms of Disorders 99 Culture and Over- and Undercontrolled Behavior 100
The World Around Us Culture and Attachment Relationships 101
Unresolved Issues Theoretical Perspectives and the Causes of Abnormal Behavior 102 Summary 103
Key Terms 104
4 Clinical Assessment and Diagnosis 106
The Basic Elements in Assessment 107 The Relationship Between Assessment and Diagnosis 107 Taking a Social or Behavioral History 108 Ensuring Culturally Sensitive Assessment Procedures 109 The Influence of Professional Orientation 109 Reliability, Validity, and Standardization 110 Trust and Rapport Between the Clinician and the Client 110
Assessment of the Physical Organism 111 The General Physical Examination 111 The Neurological Examination 111 The Neuropsychological Examination 114
Psychosocial Assessment 115
vi Contents
Biological Causal Factors 191 Psychological Causal Factors 192
Developments in Research Nocturnal Panic Attacks 194
Treatments 195
Generalized Anxiety Disorder 197
DSM-5 Criteria for. . . Generalized Anxiety Disorder 198
Prevalence, Age of Onset, and Gender Differences 199 Comorbidity with Other Disorders 199 Psychological Causal Factors 199 Biological Causal Factors 201 Treatments 202
Obsessive-Compulsive and Related Disorders 203 Obsessive-Compulsive Disorder 203
Thinking Critically about DSM-5 Why Is OCD No Longer Considered to Be an Anxiety Disorder? 203
DSM-5 Criteria for. . . Obsessive-Compulsive Disorder 205
Prevalence, Age of Onset, and Gender Differences 206 Comorbidity with Other Disorders 206 Psychological Causal Factors 206 Biological Causal Factors 208 Treatments 210 Body Dysmorphic Disorder 212
DSM-5 Criteria for. . . Body Dysmorphic Disorder 213
Hoarding Disorder 215 Trichotillomania 215
Cultural Perspectives 216
The World Around Us Taijin Kyofusho 216
Unresolved Issues The Choice of Treatments: Medications or Cognitive-Behavior Therapy? 217 Summary 218
Key Terms 219
7 Mood Disorders and Suicide 220 Mood Disorders: An Overview 221
Types of Mood Disorders 221
DSM-5 Criteria for. . . Major Depressive Disorder 222
The Prevalence of Mood Disorders 222
DSM-5 Criteria for. . . Manic Episode 223
Unipolar Depressive Disorders 224 Major Depressive Disorder 224 Persistent Depressive Disorder 227
DSM-5 Criteria for. . . Persistent Depressive Disorder 228
Other Forms of Depression 228
Thinking Critically about DSM-5 Was It Wise to Drop the Bereavement Exclusion for Major Depression? 229
Developments in Thinking A New DSM-5 Diagnosis: Premenstrual Dysphoric Disorder 229
Thinking Critically about DSM-5 Changes to the Diagnostic Criteria for PTSD 157
Acute Stress Disorder 158
Posttraumatic Stress Disorder: Causes and Risk Factors 158
DSM-5 Criteria for… Posttraumatic Stress Disorder 159
Prevalence of PTSD in the General Population 160 Rates of PTSD after Traumatic Experiences 160 Causal Factors in Posttraumatic Stress Disorder 162 Individual Risk Factors 162 Biological Factors 163 Sociocultural Factors 164 Long-Term Effects of Posttraumatic Stress 165
Prevention and Treatment of Stress Disorders 165 Prevention 165
The World Around Us Does Playing Tetris After a Traumatic Event Reduce Flashbacks? 166
Treatment for Stress Disorders 167 Trauma and Physical Health 168
The World Around Us Virtual Reality Exposure Treatment for PTSD in Military Personnel 169
Unresolved Issues Why Is the Study of Trauma So Contentious? 170 Summary 170
Key Terms 172
6 Panic, Anxiety, Obsessions, and Their Disorders 173
The Fear and Anxiety Response Patterns 174 Fear 174 Anxiety 175
Overview of the Anxiety Disorders and Their Commonalities 176
Specific Phobias 177
DSM-5 Criteria for. . . Specific Phobia 177
Prevalence, Age of Onset, and Gender Differences 179 Psychological Causal Factors 179 Biological Causal Factors 181 Treatments 181
Social Phobia 183 Prevalence, Age of Onset, and Gender Differences 183 Psychological Causal Factors 184
DSM-5 Criteria for. . . Social Anxiety Disorder (Social Phobia) 184
Biological Causal Factors 185 Treatments 186
Panic Disorder 187
DSM-5 Criteria for. . . Panic Disorder 188
Agoraphobia 188 Prevalence, Age of Onset, and Gender Differences 189
DSM-5 Criteria for. . . Agoraphobia 189
Comorbidity with Other Disorders 190 The Timing of a First Panic Attack 190
Contents vii
Developments in Research What Can Neuroimaging Tell Us about Conversion Disorder? 280
Treatment of Conversion Disorder 280
Developments in Practice Treatment of a Patient Who Was Mute 281
Factitious Disorder 281
DSM-5 Criteria for. . . Factitious Disorder 282
Distinguishing Between Different Types of Somatic Symptom and Related Disorders 283
Dissociative Disorders: An Overview 283
Depersonalization/Derealization Disorder 284
DSM-5 Criteria for. . . Depersonalization/ Derealization Disorder 286
Dissociative Amnesia 286
DSM-5 Criteria for. . . Dissociative Amnesia 288
Thinking Critically about DSM-5 Where Does Conversion Disorder Belong? 289
Dissociative Identity Disorder 290
DSM-5 Criteria for. . . Dissociative Identity Disorder 291
The World Around Us DID, Schizophrenia, and Split Personality: Clearing Up the Confusion 292
Causal Factors and Controversies about DID 292 Current Perspectives 296
Cultural Factors, Treatments, and Outcomes in Dissociative Disorders 297
Cultural Factors in Dissociative Disorders 297 Treatment and Outcomes in Dissociative Disorders 297
Unresolved Issues DID and the Reality of “Recovered Memories” 299 Summary 300
Key Terms 302
9 Eating Disorders and Obesity 303 Clinical Aspects of Eating Disorders 304
Anorexia Nervosa 304
DSM-5 Criteria for. . . Anorexia Nervosa 305 Bulimia Nervosa 307
DSM-5 Criteria for. . . Bulimia Nervosa 307 Binge-Eating Disorder 308
DSM-5 Criteria for. . . Binge-Eating Disorder 309 Age of Onset and Gender Differences 310
Thinking Critically about DSM-5 Other Forms of Eating Disorders 311
Prevalence of Eating Disorders 311 Medical Complications of Eating Disorders 312 Course and Outcome 313 Diagnostic Crossover 313 Association of Eating Disorders with Other Forms of Psychopathology 314 Eating Disorders Across Cultures 315
Causal Factors in Unipolar Mood Disorders 230 Biological Causal Factors 230 Psychological Causal Factors 235
Developments in Research Why Do Sex Differences in Unipolar Depression Emerge During Adolescence? 243
Bipolar and Related Disorders 246 Cyclothymic Disorder 246 Bipolar Disorders (I and II) 246
Causal Factors in Bipolar Disorders 249 Biological Causal Factors 249 Psychological Causal Factors 251
Sociocultural Factors Affecting Unipolar and Bipolar Disorders 251
Cross-Cultural Differences in Depressive Symptoms 252 Cross-Cultural Differences in Prevalence 252
Treatments and Outcomes 252 Pharmacotherapy 253 Alternative Biological Treatments 255 Psychotherapy 256
Suicide: The Clinical Picture and the Causal Pattern 259 Who Attempts and Dies by Suicide? 260 Psychological Disorders 261
The World Around Us Warning Signs for Suicide 262
Other Psychosocial Factors Associated with Suicide 262 Biological Factors 263 Theoretical Models of Suicidal Behavior 263
Suicide Prevention and Intervention 264 Treatment of Mental Disorders 264 Crisis Intervention 264 Focus on High-Risk Groups and Other Measures 265
Unresolved Issues Is There a Right to Die? 265 Summary 266
Key Terms 268
8 Somatic Symptom and Dissociative Disorders 269
Somatic Symptom and Related Disorders: An Overview 270
Somatic Symptom Disorder 271
DSM-5 Criteria for. . . Somatic Symptom Disorder 271
Causes of Somatic Symptom Disorder 272 Treatment of Somatic Symptom Disorder 275
Illness Anxiety Disorder 276
DSM-5 Criteria for. . . Illness Anxiety Disorder 276
Conversion Disorder (Functional Neurological Symptom Disorder) 276
DSM-5 Criteria for. . . Conversion Disorder 277
Range of Conversion Disorder Symptoms 277 Important Issues in Diagnosing Conversion Disorder 278 Prevalence and Demographic Characteristics 278 Causes of Conversion Disorders 279
viii Contents
DSM-5 Criteria for. . . Schizoid Personality Disorder 350
Schizotypal Personality Disorder 351
DSM-5 Criteria for. . . Schizotypal Personality Disorder 352
Cluster B Personality Disorders 352 Histrionic Personality Disorder 352
DSM-5 Criteria for. . . Histrionic Personality Disorder 353
Narcissistic Personality Disorder 354
DSM-5 Criteria for. . . Narcissistic Personality Disorder 354
Antisocial Personality Disorder 355
DSM-5 Criteria for. . . Antisocial Personality Disorder 356
Borderline Personality Disorder 359
Thinking Critically about DSM-5 Nonsuicidal Self- Injury: Distinct Disorder or Symptom of Borderline Personality Disorder? 360
DSM-5 Criteria for. . . Borderline Personality Disorder 361
Cluster C Personality Disorders 364 Avoidant Personality Disorder 364
DSM-5 Criteria for. . . Avoidant Personality Disorder 365
Dependent Personality Disorder 365
DSM-5 Criteria for. . . Dependent Personality Disorder 366
Obsessive-Compulsive Personality Disorder 367
DSM-5 Criteria for. . . Obsessive-Compulsive Personality Disorder 368
General Sociocultural Causal Factors for Personality Disorders 368
Treatments and Outcomes for Personality Disorders 369 Adapting Therapeutic Techniques to Specific Personality Disorders 369 Treating Borderline Personality Disorder 370
The World Around Us Marsha Linehan Reveals Her Own Struggle with Borderline Personality Disorder 371
Treating Other Personality Disorders 371
Psychopathy 372 Dimensions of Psychopathy 372
Developments in Research Are You Working for a Psychopath? 375
The Clinical Picture in Psychopathy 376 Causal Factors in Psychopathy 377 A Developmental Perspective on Psychopathy 379 Treatments and Outcomes in Psychopathic Personality 380
Unresolved Issues DSM-5: How Can We Improve the Classification of Personality Disorders? 381 Summary 381
Key Terms 383
The World Around Us Ethnic Identity and Disordered Eating 316
Risk and Causal Factors in Eating Disorders 317 Biological Factors 317 Sociocultural Factors 318 Family Influences 320 Individual Risk Factors 320
Treatment of Eating Disorders 324 Treatment of Anorexia Nervosa 324 Treatment of Bulimia Nervosa 325
Developments in Practice New Options for Adults with Anorexia Nervosa 326
Treatment of Binge-Eating Disorder 327
The Problem of Obesity 328 Medical Issues 329 Definition and Prevalence 329 Weight Stigma 329
The World Around Us Do Negative Messages about Being Overweight Encourage Overweight People to Eat More or Less? 330
Obesity and the DSM 330
Risk and Causal Factors in Obesity 330 The Role of Genes 330 Hormones Involved in Appetite and Weight Regulation 331 Sociocultural Influences 332 Family Influences 333 Stress and “Comfort Food” 334 Pathways to Obesity 334
Treatment of Obesity 335 Lifestyle Modifications 335 Medications 336 Bariatric Surgery 336 The Importance of Prevention 337
Unresolved Issues The Role of Public Policy in the Prevention of Obesity 338 Summary 339
Key Terms 340
10 Personality Disorders 341 Clinical Features of Personality Disorders 342
Challenges in Personality Disorders Research 344 Difficulties in Diagnosing Personality Disorders 345 Difficulties in Studying the Causes of Personality Disorders 346
Thinking Critically about DSM-5 Why Were No Changes Made to the Way Personality Disorders Are Diagnosed? 347
Cluster A Personality Disorders 348 Paranoid Personality Disorder 348
DSM-5 Criteria for. . . Paranoid Personality Disorder 349
Schizoid Personality Disorder 349
Contents ix
The World Around Us Should Marijuana Be Marketed and Sold Openly as a Medication? 415
Gambling Disorder 416
DSM-5 Criteria for. . . Gambling Disorder 417
Unresolved Issues Exchanging Addictions: Is This an Effective Treatment Approach? 418 Summary 418
Key Terms 420
12 Sexual Variants, Abuse, and Dysfunctions 421
Sociocultural Influences on Sexual Practices and Standards 422
Case 1: Degeneracy and Abstinence Theory 423 Case 2: Ritualized Homosexuality in Melanesia 424 Case 3: Homosexuality and American Psychiatry 424
Paraphilic Disorders 426 Fetishistic Disorder 426
DSM-5 Criteria for. . . Several Different Paraphilic Disorders 427 Transvestic Disorder 428 Voyeuristic Disorder 429 Exhibitionistic Disorder 429 Frotteuristic Disorder 430 Sexual Sadism Disorder 430 Sexual Masochism Disorder 431 Causal Factors and Treatments for Paraphilias 432
Gender Dysphoria 433
DSM-5 Criteria for. . . Gender Dysphoria in Children 433
DSM-5 Criteria for. . . Gender Dysphoria in Adolescents and Adults 434 Treatment for Gender Dysphoria 435 Transsexualism 435 Treatment for Transsexualism 436
Sexual Abuse 437 Childhood Sexual Abuse 437 Pedophilic Disorder 439
Thinking Critically about DSM-5 Pedophilia and Hebephilia 440 Incest 440 Rape 441 Treatment and Recidivism of Sex Offenders 444
The World Around Us Megan’s Law 444
Sexual Dysfunctions 446 Sexual Dysfunctions in Men 447
DSM-5 Criteria for. . . Different Sexual Dysfunctions 448 Sexual Dysfunctions in Women 452
Unresolved Issues How Harmful Is Childhood Sexual Abuse? 455 Summary 456
Key Terms 458
11 Substance-Related Disorders 384 Alcohol-Related Disorders 385
The Prevalence, Comorbidity, and Demographics of Alcohol Abuse and Dependence 386
DSM-5 Criteria for. . . Alcohol Use Disorder 388 The Clinical Picture of Alcohol-Related Disorders 388
Developments in Research Fetal Alcohol Syndrome: How Much Drinking Is Too Much? 390
Causal Factors in the Abuse of and Dependence on Alcohol 392
Biological Causal Factors in Alcohol Abuse and Dependence 392 Psychosocial Causal Factors in Alcohol Abuse and Dependence 394
The World Around Us Binge Drinking in College 396 Sociocultural Causal Factors 397
Treatment of Alcohol-Related Disorders 397 Use of Medications in Treating Alcohol Abuse and Dependency 397 Psychological Treatment Approaches 398 Controlled Drinking versus Abstinence 399 Alcoholics Anonymous 399 Outcome Studies and Issues in Treatment 400 Relapse Prevention 401
Drug Abuse and Dependence 402
Opium and Its Derivatives 403 Biological Effects of Morphine and Heroin 403 Social Effects of Morphine and Heroin 404 Causal Factors in Opiate Abuse and Dependence 405 Neural Bases for Physiological Addiction 405 Addiction Associated with Psychopathology 406 Treatments and Outcomes 406
Stimulants 406 Cocaine 406 Amphetamines 408 Methamphetamine 409 Caffeine and Nicotine 409
Thinking Critically about DSM-5 Can Changes to the Diagnostic Criteria Result in Increased Drug Use? 409
Sedatives 411 Effects of Barbiturates 411 Causal Factors in Barbiturate Abuse and Dependence 412 Treatments and Outcomes 412
Hallucinogens 412 LSD 412 Mescaline and Psilocybin 413 Ecstasy 413 Marijuana 414
x Contents
Urban Living 492 Immigration 492 Cannabis Use and Abuse 493 A Diathesis–Stress Model of Schizophrenia 494
Treatments and Outcomes 495 Clinical Outcome 495 Pharmacological Approaches 496 Psychosocial Approaches 498
Unresolved Issues Why Are Recovery Rates in Schizophrenia Not Improving? 500 Summary 501
Key Terms 502
14 Neurocognitive Disorders 503 Brain Impairment in Adults 504
Thinking Critically about DSM-5 Is the Inclusion of Mild Neurocognitive Disorder a Good Idea? 505
Clinical Signs of Brain Damage 505 Diffuse Versus Focal Damage 506 The Neurocognitive/Psychopathology Interaction 508
Delirium 509 Clinical Picture 509
DSM-5 Criteria for. . . Delirium 510
Treatments and Outcomes 510
Major Neurocognitive Disorder 510
DSM-5 Criteria for. . . Major Neurocognitive Disorder 511
Parkinson’s Disease 512 Huntington’s Disease 512
Alzheimer’s Disease 512 Clinical Picture 513 Prevalence 514 Causal Factors 515
Developments in Research Depression Increases the Risk of Alzheimer’s Disease 517
Neuropathology 517 Treatment and Outcome 519 Early Detection 519
Developments in Research New Approaches to the Treatment of Alzheimer’s Disease 520
The World Around Us Exercising Your Way to a Healthier Brain? 521
Supporting Caregivers 521
Neurocognitive Disorder Resulting from HIV Infection or Vascular Problems 522
Neurocognitive Disorder Associated with HIV-1 Infection 522 Neurocognitive Disorder Associated with Vascular Disease 523
Neurocognitive Disorder Characterized by Profound Memory Impairment (Amnestic Disorder) 523
13 Schizophrenia and Other Psychotic Disorders 459
Schizophrenia 460 Origins of the Schizophrenia Construct 460 Epidemiology 461
Clinical Picture 462 Delusions 462
DSM-5 Criteria for. . . Schizophrenia 463 Hallucinations 464
The World Around Us Stress, Caffeine, and Hallucinations 465 Disorganized Speech 465 Disorganized Behavior 466 Negative Symptoms 466 Subtypes of Schizophrenia 467
Other Psychotic Disorders 467 Schizoaffective Disorder 467
DSM-5 Criteria for. . . Schizoaffective Disorder 467 Schizophreniform Disorder 467
DSM-5 Criteria for. . . Schizophreniform Disorder 468 Delusional Disorder 468 Brief Psychotic Disorder 468
DSM-5 Criteria for. . . Delusional Disorder 468
DSM-5 Criteria for. . . Brief Psychotic Disorder 469
Genetic and Biological Factors 469 Genetic Factors 469
The World Around Us The Genain Quadruplets 471 Prenatal Exposures 476
Developments in Thinking Could Schizophrenia Be an Immune Disorder? 477 Genes and Environment in Schizophrenia: A Synthesis 477 A Neurodevelopmental Perspective 478
Thinking Critically about DSM-5 Attenuated Psychosis Syndrome 480
Structural and Functional Brain Abnormalities 481 Neurocognition 481 Social Cognition 482 Loss of Brain Volume 483 Affected Brain Areas 483 White Matter Problems 484 Brain Functioning 485 Cytoarchitecture 486 Brain Development in Adolescence 487 Synthesis 487 Neurochemistry 488
Psychosocial and Cultural Factors 490 Do Bad Families Cause Schizophrenia? 490 Families and Relapse 491
Contents xi
Intellectual Disability 556 Levels of Intellectual Disability 557 Causal Factors in Intellectual Disability 558 Organic Intellectual Disability Syndromes 559 Treatments, Outcomes, and Prevention 562
Special Considerations in the Treatment of Children and Adolescents 563
Special Factors Associated with Treatment of Children and Adolescents 563
The World Around Us The Impact of Child Abuse on Psychological Disorders 565
Family Therapy as a Means of Helping Children 565 Child Advocacy Programs 566
Unresolved Issues How Should Society Deal with Delinquent Behavior? 566 Summary 567
Key Terms 569
16 Psychological Treatment 570 An Overview of Treatment 571
Why Do People Seek Therapy? 571 Who Provides Psychotherapeutic Services? 573 The Therapeutic Relationship 573
Measuring Success in Psychotherapy 574 Objectifying and Quantifying Change 574 Would Change Occur Anyway? 576 Can Therapy Be Harmful? 576
The World Around Us When Therapy Harms 576
What Therapeutic Approaches Should Be Used? 577 Evidence-Based Treatment 577 Medication or Psychotherapy? 578 Combined Treatments 578
Psychosocial Approaches to Treatment 579 Behavior Therapy 579 Cognitive and Cognitive-Behavioral Therapy 582 Humanistic-Experiential Therapies 584 Psychodynamic Therapies 587 Couples and Family Therapy 590 Eclecticism and Integration 591 Rebooting Psychotherapy 591
Sociocultural Perspectives 592 Social Values and Psychotherapy 592 Psychotherapy and Cultural Diversity 592
Biological Approaches to Treatment 593 Antipsychotic Drugs 593 Antidepressant Drugs 594 Antianxiety Drugs 597 Lithium and Other Mood-Stabilizing Drugs 598
Thinking Critically about DSM-5 What Are Some of the Clinical Implications of the Recent Changes? 599
Nonmedicinal Biological Treatments 600
Disorders Involving Head Injury 524 Clinical Picture 525 Treatments and Outcomes 527
The World Around Us Brain Damage in Professional Athletes 528
Unresolved Issues Should Healthy People Use Cognitive Enhancers? 529 Summary 530
Key Terms 531
15 Disorders of Childhood and Adolescence (Neurodevelopmental Disorders) 532
Special Considerations in Understanding Disorders of Childhood and Adolescence 534
Psychological Vulnerabilities of Young Children 534 The Classification of Childhood and Adolescent Disorders 534
Anxiety and Depression in Children and Adolescents 535 Anxiety Disorders of Childhood and Adolescence 535 Childhood Depression and Bipolar Disorder 537
Developments in Research Bipolar Disorder in Children and Adolescents: Is There an Epidemic? 539
Disruptive, Impulse-Control, and Conduct Disorder 540 Oppositional Defiant Disorder 541 Conduct Disorder 541
DSM-5 Criteria for. . . Conduct Disorder 541
Causal Factors in ODD and CD 542 Treatments and Outcomes 543
Elimination Disorders 544 Enuresis 544 Encopresis 545
Neurodevelopmental Disorders 545 Attention-Deficit/Hyperactivity Disorder 545
DSM-5 Criteria for. . . Attention-Deficit/ Hyperactivity Disorder 546
Autism Spectrum Disorder 549
DSM-5 Criteria for. . . Autism Spectrum Disorder 551
Tic Disorders 552
Developments in Practice Can Video Games Help Children with Neurodevelopmental Disorders? 553
Specific Learning Disorders 554 Causal Factors in Learning Disorder 555 Treatments and Outcomes 555
Thinking Critically about DSM-5 What Role Should Cultural Changes Have in Developing Medical Terminology? 556
xii Contents
The World Around Us Controversial Not Guilty Pleas: Can Altered Mind States or Personality Disorder Limit Responsibility for a Criminal Act? 619
The Insanity Defense 622 Competence to Stand Trial 625 Does Having Mental Health Problems Result in Convicted Felons Being Returned to Prison After Being Released? 626
Organized Efforts for Mental Health 627 U.S. Efforts for Mental Health 627 International Efforts for Mental Health 629
Challenges for the Future 629 The Need for Planning 630 The Individual’s Contribution 630
Unresolved Issues The HMOs and Mental Health Care 631 Summary 633
Key Terms 634
Glossary 635
References 658
Credits 730
Name Index 737
Subject Index 753
The World Around Us Deep Brain Stimulation for Treatment-Resistant Depression 603
Unresolved Issues Do Psychiatric Medications Help or Harm? 604 Summary 605
Key Terms 606
17 Contemporary and Legal Issues in Abnormal Psychology 607
Perspectives on Prevention 608 Universal Interventions 609 Selective Interventions 610 Indicated Interventions 613
Inpatient Mental Health Treatment in Contemporary Society 613
The Mental Hospital as a Therapeutic Community 613 Aftercare Programs 615 Deinstitutionalization 615
Controversial Legal Issues and the Mentally Ill 617 Civil Commitment 617
The World Around Us Important Court Decisions for Patient Rights 617
Assessment of “Dangerousness” 618
xiii
Features
Developments in Research
Do Magnets Help with Repetitive-Stress Injury? 27
The Search for Medications to Cure Mental Disorders 50
Nocturnal Panic Attacks 194
Why Do Sex Differences in Unipolar Depression Emerge During Adolescence? 243
What Can Neuroimaging Tell Us about Conversion Disorder? 280
Are You Working for a Psychopath? 375
Fetal Alcohol Syndrome: How Much Drinking Is Too Much? 390
Depression Increases the Risk of Alzheimer’s Disease 517
New Approaches to the Treatment of Alzheimer’s Disease 520
Bipolar Disorder in Children and Adolescents: Is There an Epidemic? 539
Developments in Thinking
Melancholia Through the Ages 35
Nature, Nurture, and Psychopathology: A New Look at an Old Topic 71
The Humanistic and Existential Perspectives 82
A New DSM-5 Diagnosis: Premenstrual Dysphoric Disorder 229
Could Schizophrenia Be an Immune Disorder? 477
Developments in Practice
The Automated Practice: Use of the Computer in Psychological Testing 118
Computer-Based MMPI-2 Report for Andrea C. 126
Treatment of a Patient Who Was Mute 281
New Options for Adults with Anorexia Nervosa 326
Can Video Games Help Children with Neurodevelopmental Disorders? 553
The World Around Us
Extreme Generosity or Pathological Behavior? 6
Chaining Mental Health Patients 46
Culture and Attachment Relationships 101
Racial Discrimination and Cardiovascular Health in African Americans 147
Does Playing Tetris After a Traumatic Event Reduce Flashbacks? 166
Virtual Reality Exposure Treatment for PTSD in Military Personnel 169
Taijin Kyofusho 216
Warning Signs for Suicide 262
DID, Schizophrenia, and Split Personality: Clearing Up the Confusion 292
Ethnic Identity and Disordered Eating 316
Do Negative Messages about Being Overweight Encourage Overweight People to Eat More or Less? 330
Marsha Linehan Reveals Her Own Struggle with Borderline Personality Disorder 371
Binge Drinking in College 396
Should Marijuana Be Marketed and Sold Openly as a Medication? 415
Megan’s Law 444
Stress, Caffeine, and Hallucinations 465
The Genain Quadruplets 471
Exercising Your Way to a Healthier Brain? 521
Brain Damage in Professional Athletes 528
The Impact of Child Abuse on Psychological Disorders 565
When Therapy Harms 576
Deep Brain Stimulation for Treatment-Resistant Depression 603
Important Court Decisions for Patient Rights 617
Controversial Not Guilty Pleas: Can Altered Mind States or Personality Disorder Limit Responsibility for a Criminal Act? 619
Unresolved Issues
Are We All Becoming Mentally Ill? The Expanding Horizons of Mental Disorder 29
Interpreting Historical Events 56
Theoretical Perspectives and the Causes of Abnormal Behavior 102
The DSM-5: Issues in Acceptance of Changed Diagnostic Criteria 133
Why Is the Study of Trauma So Contentious? 170
The Choice of Treatments: Medications or Cognitive-Behavior Therapy? 217
Is There a Right to Die? 265
DID and the Reality of “Recovered Memories” 299
The Role of Public Policy in the Prevention of Obesity 338
DSM-5: How Can We Improve the Classification of Personality Disorders? 381
Exchanging Addictions: Is This an Effective Treatment Approach? 418
How Harmful Is Childhood Sexual Abuse? 455
Why Are Recovery Rates in Schizophrenia Not Improving? 500
xiv Features
DSM-5 Criteria for… Gambling Disorder 417
DSM-5 Criteria for… Several Different Paraphilic Disorders 427
DSM-5 Criteria for… Gender Dysphoria in Children 433
DSM-5 Criteria for… Gender Dysphoria in Adolescents and Adults 434
DSM-5 Criteria for… Different Sexual Dysfunctions 448
DSM-5 Criteria for… Schizophrenia 463
DSM-5 Criteria for… Schizoaffective Disorder 467
DSM-5 Criteria for… Schizophreniform Disorder 468
DSM-5 Criteria for… Delusional Disorder 468
DSM-5 Criteria for… Brief Psychotic Disorder 469
DSM-5 Criteria for… Delirium 510
DSM-5 Criteria for… Major Neurocognitive Disorder 511
DSM-5 Criteria for… Conduct Disorder 541
DSM-5 Criteria for… Attention-Deficit/Hyperactivity Disorder 546
DSM-5 Criteria for… Autism Spectrum Disorder 551
Thinking Critically About DSM-5
What Is the DSM and Why Was It Revised? 7
Changes to the Diagnostic Criteria for PTSD 157
Why Is OCD No Longer Considered to Be an Anxiety Disorder? 203
Was It Wise to Drop the Bereavement Exclusion for Major Depression? 229
Where Does Conversion Disorder Belong? 289
Other Forms of Eating Disorders 311
Why Were No Changes Made to the Way Personality Disorders Are Diagnosed? 347
Nonsuicidal Self-Injury: Distinct Disorder or Symptom of Borderline Personality Disorder? 360
Can Changes to the Diagnostic Criteria Result in Increased Drug Use? 409
Pedophilia and Hebephilia 440
Attenuated Psychosis Syndrome 480
Is the Inclusion of Mild Neurocognitive Disorder a Good Idea? 505
What Role Should Cultural Changes Have in Developing Medical Terminology? 556
What Are Some of the Clinical Implications of the Recent Changes? 599
Should Healthy People Use Cognitive Enhancers? 529
How Should Society Deal with Delinquent Behavior? 566
Do Psychiatric Medications Help or Harm? 604
The HMOs and Mental Health Care 631
DSM-5 Boxes
DSM-5 Criteria for… Posttraumatic Stress Disorder 159
DSM-5 Criteria for… Specific Phobia 177
DSM-5 Criteria for… Social Anxiety Disorder (Social Phobia) 184
DSM-5 Criteria for… Panic Disorder 188
DSM-5 Criteria for… Agoraphobia 189
DSM-5 Criteria for… Generalized Anxiety Disorder 198
DSM-5 Criteria for… Obsessive-Compulsive Disorder 205
DSM-5 Criteria for… Body Dysmorphic Disorder 213
DSM-5 Criteria for… Major Depressive Disorder 222
DSM-5 Criteria for… Manic Episode 223
DSM-5 Criteria for… Persistent Depressive Disorder 228
DSM-5 Criteria for… Somatic Symptom Disorder 271
DSM-5 Criteria for… Illness Anxiety Disorder 276
DSM-5 Criteria for… Conversion Disorder 277
DSM-5 Criteria for… Factitious Disorder 282
DSM-5 Criteria for… Depersonalization/Derealization Disorder 286
DSM-5 Criteria for… Dissociative Amnesia 288
DSM-5 Criteria for… Dissociative Identity Disorder 291
DSM-5 Criteria for… Anorexia Nervosa 305
DSM-5 Criteria for… Bulimia Nervosa 307
DSM-5 Criteria for… Binge-Eating Disorder 309
DSM-5 Criteria for… Paranoid Personality Disorder 349
DSM-5 Criteria for… Schizoid Personality Disorder 350
DSM-5 Criteria for… Schizotypal Personality Disorder 352
DSM-5 Criteria for… Histrionic Personality Disorder 353
DSM-5 Criteria for… Narcissistic Personality Disorder 354
DSM-5 Criteria for… Antisocial Personality Disorder 356
DSM-5 Criteria for… Borderline Personality Disorder 361
DSM-5 Criteria for… Avoidant Personality Disorder 365
DSM-5 Criteria for… Dependent Personality Disorder 366
DSM-5 Criteria for… Obsessive-Compulsive Personality Disorder 368
DSM-5 Criteria for… Alcohol Use Disorder 388
xv
Many changes occurred from DSM-IV-TR to DSM-5. Here is a summary of some of the most impor-tant revisions. Many of these changes are high- lighted in the “Thinking Critically about DSM-5” boxes throughout this edition.
• The chapters of the DSM have been reorganized to reflect a consideration of developmental and lifespan issues. Disorders that are thought to reflect develop- mental perturbations or that manifest early in life (e.g., neurodevelopmental disorders and disorders such as schizophrenia) are listed before disorders that occur later in life.
• The multiaxial system has been abandoned. No distinc- tion is now made between Axis I and Axis II disorders.
• DSM-5 allows for more gender-related differences to be taken into consideration for mental health problems.
• It is extremely important for the clinician to understand the client’s cultural background in appraising mental health problems. DSM-5 contains a structured inter- view that focuses on the patient’s cultural background and characteristic approach to problems.
• The term intellectual disability is now used instead of the term mental retardation.
• A new diagnosis of autism spectrum disorder now encompasses autism, Asperger’s disorder, and other forms of pervasive developmental disorder. The diag- nosis of Asperger’s disorder has been eliminated from the DSM.
• Changes to the diagnostic criteria for attention deficit disorder now mean that symptoms that occur before age 12 (rather than age 7) have diagnostic significance.
• A new diagnosis, called disruptive mood dysregula- tion disorder, has been added. This will be used to diagnose children up to age 18 who show persistent irritability and frequent episodes of extreme and uncontrolled behavior.
• The subtypes of schizophrenia have been eliminated.
• The special significance afforded to bizarre delusions with regard to the diagnosis of schizophrenia has been removed.
• Bipolar and related disorders are now described in a separate chapter of the DSM and are no longer listed with depressive disorders.
• Premenstrual dysphoric disorder has been promoted from the appendix of DSM-IV-TR and is now listed as a new diagnosis.
• A new diagnosis of persistent depressive disorder now subsumes dysthymia and chronic major depressive disorder.
• The bereavement exclusion has been removed in the diagnosis of major depressive episode.
• The diagnosis of phobia no longer requires that the per- son recognize that his or her anxiety is unreasonable.
• Panic disorder and agoraphobia have been unlinked and are now separate diagnoses in DSM-5.
• Obsessive-compulsive disorder is no longer classi- fied as an anxiety disorder. DSM-5 contains a new chapter that covers obsessive-compulsive and related disorders.
• New disorders in the obsessive-compulsive and related disorders category include hoarding disorder and exco- riation (skin-picking) disorder.
• Posttraumatic stress disorder is no longer considered to be an anxiety disorder. Instead, it is listed in a new chapter that covers trauma- and stressor-related disorders.
• The diagnostic criteria for posttraumatic stress disor- der have been significantly revised. The definition of what counts as a traumatic event has been clarified and made more explicit. DSM-5 now also recognizes four-symptom clusters rather than the three noted in DSM-IV-TR.
• Dissociative fugue is no longer listed as a separate diagnosis. Instead, it is listed as a form of dissociative amnesia.
• The DSM-IV-TR diagnoses of hypochondriasis, somato- form disorder, and pain disorder have been removed and are now subsumed into the new diagnosis of somatic symptom disorder.
• Binge-eating disorder has been moved from the appendix of DSM-IV-TR and is now listed as an offi- cial diagnosis.
• The frequency of binge-eating and purging episodes has been reduced for the diagnosis of bulimia nervosa.
What’s New in DSM-5? A Quick Guide
xvi What’s New in DSM-5? A Quick Guide
• Substance-related disorders are divided into two sepa- rate groups: substance use disorders and substance- induced disorders.
• A new disorder, gambling disorder, has been included in substance-related and addictive disorders.
• Included for the first time in Section III of DSM-5 are several new disorders regarded as being in need of fur- ther study. These include attenuated psychosis syn- drome, nonsuicidal self-injury disorder, Internet gaming disorder, and caffeine use disorder.
• Amenorrhea is no longer required for the diagnosis of anorexia nervosa.
• The DSM-IV-TR diagnoses of dementia and amnestic disorder have been eliminated and are now sub- sumed into a new category called major neurocogni- tive disorder.
• Mild neurocognitive disorder has been added as a new diagnosis.
• No changes have been made to the diagnostic criteria for personality disorders, although an alternative model is now offered as a guide for future research.
xvii
We are so excited about this course and hope that you are too! We (the authors) all took this course when we were undergraduate students because we were curious about abnormal aspects of human behavior. Why do some people become so depressed they can’t get out of bed? Why do others have trouble controlling their use of alcohol and drugs? Why do some people become violent toward others, and in other cases toward themselves? We continue to be intensely curi- ous about, and fascinated by, the answers to these and many other questions about abnormal human behavior. The purpose of this book is to provide a comprehensive (and hopefully engaging) introduction to the primary psy- chological disorders studied within abnormal psychology.
As you will learn, there are many different types of psychological disorders, and each is caused by the interac- tion of many different factors and can be considered from many different perspectives. We thought a lot about how best to present this information in a way that will be clear and engaging and will allow you to gain a solid, funda- mental understanding of psychological disorders. As such, we use a biopsychosocial approach to provide a sophisti- cated appreciation of the total context in which abnormali- ties of behavior occur. This means that we present and describe the wide range of biological, psychological, and social factors that work together to lead to the develop- ment of psychological disorders. In addition, we discuss treatment approaches that target each of these different factors.
For ease of understanding we also present material on each disorder in a logical and consistent way. More specifi- cally, we focus on three significant aspects: (1) the clinical picture, where we describe the symptoms of the disorder and its associated features; (2) factors involved in the development of the disorder; and (3) treatment approaches. In each case, we examine the evidence for biological, psy- chosocial (i.e., psychological and interpersonal), and socio- cultural (the broader social environment of culture and subculture) influences. Because we wish never to lose sight of the person, we try to integrate as much case material as we can into each chapter. An additional feature of this book is a heavy focus on treatment. Although treatment is discussed in every chapter in the context of specific disor- ders, we also include a separate chapter that addresses issues in treatment more broadly. This provides students with increased understanding of a wide range of treatment approaches and permits more in-depth coverage than is possible in specific disorder–based chapters.
Abnormal Psychology has a long and distinguished tradi- tion as an undergraduate text. Ever since James Coleman wrote the first edition many years ago, this textbook has been considered the most comprehensive in the field. Along the way there have been many changes. This is very much the case with this new edition. Perhaps the most exciting change, however, is the addition of Harvard Professor Matthew Nock to the author team. Matt, a recent MacArthur Award (aka, “Genius Grant”) recipient, brings his bril- liance, scholarship, and wry sense of humor to the book, providing fresh approaches and new perspectives. We are delighted that he has joined the author team and welcome him with great enthusiasm!
The Hooley-Butcher-Nock-Mineka author team is in a unique position to provide students with an integrated and comprehensive understanding of abnormal psychol- ogy. Each author is a noted researcher, an experienced teacher, and a licensed clinician. Each brings different areas of expertise and diverse research interests to the text. We are committed to excellence. We are also committed to making our text accessible to a broad audience. Our approach emphasizes the importance of research as well as the need to translate research findings into informed and effective clinical care for all who suffer from mental disor- ders. In this new edition, we seek to open up the fascinat- ing world of abnormal psychology, providing students with comprehensive and up-to-date knowledge in a clear and engaging way. We hope that this newest edition con- veys some of the passion and enthusiasm for the topic that we still experience every day.
Why Do You Need This New Edition? The book you are reading is the seventeenth edition of Abnormal Psychology. Why so many revisions? And why not just use an old copy of the fifteenth or sixteenth edi- tion? The reason is that our field is constantly making advances in our understanding of abnormal psychology. New research is being published all the time. As authors, it is important to us that these changes and new ways of thinking about the etiology, assessment, and treatment of psychological disorders are accurately presented in this text. Although many of the ideas and diagnostic concepts in the field of abnormal psychology have persisted for hundreds of years, changes in thinking often occur. And, at
Preface
xviii Preface
makes it easier for readers to identify what they should be learning in each section. At the end of each chapter a summary of the learning objectives is also provided. In Review questions at the end of major sections within chapters also provide additional opportunities for self- assessment and increased learning.
What’s New This new edition of Abnormal Psychology has been rede- signed to reflect the newest and most relevant research findings, presented in a way that is engaging to the new- est generation of students. We’ve done a lot of updating! Our focus has been on streamlining material throughout the book to decrease the length of each chapter while retaining all of the important information that students should be learning.
We have also done our best to include the most excit- ing changes and advances occurring in our field. For example, throughout the text, we have significantly increased the focus on the manifestation and treatment of psychological disorders around the globe, using data from a recently completed cross-national series of studies in more than 20 different countries. In Chapter 3, we have added a new and more accessible description of why cor- relation does not equal causation—and what does! In Chapter 5, we now adopt a more broad and integrative approach to the health consequences of stress, including a focus on the mechanisms through which stress is thought to cause physical health problems. Chapter 7 has been updated substantially and now includes more information about some of the problems most relevant to college stu- dents, such as suicide and self-injury.
New case studies have also been added throughout the book. Chapter 8, for example, has four new case stud- ies, as well as two new highlight boxes. These illustrate recent neuroimaging research on patients with conversion disorder, as well as a very creative new approach to the treatment of this fascinating disorder. Chapter 11 has sig- nificant new material on how alcohol and drugs affect the brain, what causes hangovers, and information on new synthetic drugs that have recently hit the streets. In Chap- ter 13, the most current genetic findings concerning schizo- phrenia are described, and new developments in our understanding of the nature of dopamine abnormality in schizophrenia are discussed. A new Developments in Thinking highlight box also presents new ideas about the possibility that schizophrenia might be an immune func- tion disorder. Chapter 15 has been reorganized and updated throughout; for instance, it now includes cutting- edge findings on the potential causes and most effective treatments for autism spectrum disorders. And throughout the book we have included information about some of the newest ways in which researchers and clinicians are
some point, events occur that force a rethinking of familiar topics. A major example here is the revision of the manual that is used to classify mental disorders (called the DSM-5). This new edition of Abnormal Psychology includes the most up-to-date information about DSM-5 diagnostic categories, classifications, and criteria.
Every time we work on a revision of Abnormal Psychol- ogy we are reminded of how dynamic and vibrant our field is. Developments in areas such as genetics, brain imaging, behavioral observation, and classification, as well changes in social and government policy and in legal decisions, add to our knowledge base and stimulate new treatments for those whose lives are touched by mental disorders.
If you’re wondering what exactly is so new in this edi- tion of Abnormal Psychology, here are seven big revisions that we have made.
1. We have a new author! Matt Nock brings a fresh and new perspective to this authoritative and established text.
2. The seventeenth edition of Abnormal Psychology in- cludes the most up-to-date and in-depth information about biological influences on the entire spectrum of behavioral abnormalities, while still maintaining a comprehensive and balanced biopsychosocial ap- proach to understanding abnormal behavior.
3. As a result of the publication of DSM-5, the diagnostic criteria for many disorders have changed. This edition includes detailed boxes listing the current DSM-5 diag- nostic criteria for all the disorders covered in the book. Specific highlight boxes and discussions in the text also alert you to some of the most important changes in DSM-5.
4. Other feature boxes provide opportunities for critical thinking by illustrating some of the controversies asso- ciated with the changes that were (or were not) made. Throughout the text we also provide readers with dif- ferent perspectives on the likely implications that these changes will have (or are having) for clinical diagnosis and research in psychopathology.
5. Reflecting the ever-changing field of abnormal psy- chology, hundreds of new references have been added, highlighting the newest and most important research findings.
6. Changes have been made in many chapters to improve the flow of the writing and enhance learning. The pre- sentation of material in many chapters has also been reorganized to provide a more logical and coherent narrative.
7. Finally, at the beginning of each chapter, clearly de- fined learning objectives provide the reader with an overview of topics and issues that will be included in the chapter. These learning objectives also appear again in the specific sections to which they apply. This
Preface xix
and how far we have yet to go in our understanding of psychological disorders. The topics covered here provide insight into the future of the field and expose students to some controversial topics.
Pedagogy LEARNINg OBJECTIVES Each chapter begins with learning objectives. These orient the reader to the material that will be presented in each specific chapter. Learning objectives are also repeated by the section they apply to and summarized at the end of each chapter. This provides students with an excellent tool for study and review. In this edition, sections of many chapters have also been reor- ganized and material has been streamlined whenever pos- sible. All the changes that have been made are designed to improve the flow of the writing and enhance pedagogy.
CASE STUDIES Extensive case studies of individuals with various disorders are integrated in the text through- out the book. Some are brief excerpts; others are detailed analyses. These cases bring important aspects of the dis- orders to life. They also remind readers that the problems of abnormal psychology affect the lives of people—people from all kinds of diverse backgrounds who have much in common with all of us.
IN REVIEW QUESTIONS Review questions appear at the end of each major section within the chapter, providing regular opportunities for self-assessment as students read and further reinforce their learning.
DSM-5 BOXES Throughout the book these boxes contain the most up-to-date (DSM-5) diagnostic criteria for all of the disorders discussed. In a convenient and visually ac- cessible form, they provide a helpful study tool that re- flects current diagnostic practice. They also help students understand disorders in a real-world context.
RESEARCH CLOSE-UP TERMS Appearing throughout each chapter, these terms illuminate research methodolo- gies. They are designed to give students a clearer under- standing of some of the most important research concepts in the field of abnormal psychology.
CHAPTER SUMMARIES Each chapter ends with a summary of the essential points of the chapter organized around the learning objectives presented at the start of the chapter. These summaries use bulleted lists rather than formal paragraphs. This makes the information more ac- cessible for students and easier to scan.
KEy TERMS Key terms are identified in each chapter. Key terms are also listed at the end of every chapter with page numbers referencing where they can be found in the body of the text. Key terms are also defined in the Glossary at the end of the text.
treating psychological disorders, such as via the use of new smartphone apps, brain stimulation treatments, and assistive therapeutic robots! These are just a handful of the many changes we have made to give readers the most cur- rent perspectives possible. We want students to stay ahead of the curve and to provide them with the most up-to-date information we can. We also want to give students a sense of how and in what ways various fields are likely moving.
This edition also retains features that were very well received in the last edition. To assist both instructors and students, we continue to feature specialized boxes, high- lighting many of the key changes that were made in DSM-5. In this edition, however, we also provide a detailed but accessible description of the RDoC approach.
As before, chapters begin with learning objectives. These orient the reader to the material that will be pre- sented in each specific chapter. Learning objectives are also repeated by the section they apply to and summarized at the end of each chapter. Most chapters also begin with a case study (many of which are new) that illustrates the mental health problems to be addressed in the chapter. This serves to capture students’ interest and attention right from the outset. Numerous new references, photographs, and illustrations have also been added. In short, outdated mate- rial has been replaced, current findings have been included, and new developments have been identified. Importantly, all of this has been accomplished without adding length to the book! We hope you enjoy this new edition.
Features and Pedagogy The extensive research base and accessible organization of this book are supported by high-interest features and helpful pedagogy to further engage students and support learning. We also hope to encourage students to think in depth about the topics they are learning about through specific high- light features that emphasize critical thinking.
Features FEATURE BOXES Special sections, called Developments in Research, Developments in Thinking, Developments in Practice, and The World Around Us, highlight topics of particular interest, focusing on applications of research to everyday life, current events, and the latest research meth- odologies, technologies, and findings.
CRITICAL THINKINg Many of the revisions to DSM-5 were highly contentious and controversial. A feature box called “Thinking Critically about DSM-5” introduces stu- dents to the revised DSM and encourages them to think critically about the implications of these changes.
UNRESOLVED ISSUES All chapters include end-of- chapter sections that demonstrate how far we have come
xx Preface
anorexia nervosa, PTSD, alcoholism, schizophrenia, autism, ADHD, bipolar disorder, social phobia, hypochondriasis, borderline personality disorder, and adjustment to physical illness. These video segments are available on DVD.
Volume 1: ISBN 0131933329
Volume 2: ISBN 0136003036
Volume 3: ISBN 0132308916
MyPsychLab (0205952372) Available at www.MyPsychLab.com, MyPsychLab is an online homework, tutorial, and assessment program that truly engages students in learning. It helps students better prepare for class, quizzes, and exams—resulting in better performance in the course. It provides educators a dynamic set of tools for gauging individual and class performance:
Customizable—MyPsychLab is customizable. Instructors choose what students’ course looks like. Homework, applications, and more can easily be turned on and off.
Blackboard Single Sign-on—MyPsychLab can be used by itself or linked to any course management system. Blackboard single sign-on provides deep linking to all New MyPsychLab resources.
Pearson eText and Chapter Audio—Like the printed text, students can highlight relevant passages and add notes. The Pearson eText can be accessed through laptops, iPads, and tablets. Download the free Pearson eText app to use on tablets. Students can also listen to their text with the Audio eText.
Assignment Calendar & gradebook—A drag and drop assignment calendar makes assigning and completing work easy. The automatically graded assessment provides instant feedback and flows into the gradebook, which can be used in the MyPsychLab or exported.
Personalized Study Plan—Students’ personalized plans promote better critical thinking skills. The study plan organizes students’ study needs into sections, such as Remembering, Understanding, Applying, and Analyzing.
Instructor’s Manual (0134319451) A comprehensive tool for class preparation and manage- ment, each chapter includes teaching objectives; a chapter overview; a detailed lecture outline; a list of key terms; teaching resources, including lecture launchers, class activities, demonstrations, assignments, teaching tips, and handouts; a list of video, media, and Web resources; and a sample syllabus. Available for download on the Instruc- tor’s Resource Center at www.pearsonhighered.com.
Supplements Package REVELTM EXPERIENCE DESIgNED FOR THE WAy TODAy’S STU- DENTS READ, THINK, AND LEARN When students are engaged deeply, they learn more effectively and per- form better in their courses. This simple fact inspired the creation of REVEL: an immersive learning experience de- signed for the way today’s students read, think, and learn. Built in collaboration with educators and students nation- wide, REVEL is the newest, fully digital way to deliver re- spected Pearson content.
REVEL enlivens course content with media interac- tives and assessments—integrated directly within the authors’ narrative—that provide opportunities for students to read about and practice course material in tandem. This immersive experience boosts student engagement, which leads to better understanding of concepts and improved performance throughout the course.
Learn more about REVEL www.pearsonhighered.com/revel The seventeenth edition includes integrated videos and
media content throughout, allowing students to explore topics more deeply at the point of relevancy.
Revel also offers the ability for students to assess their content mastery by taking multiple-choice quizzes that offer instant feedback and by participating in a variety of writing assignments such as peer-reviewed questions and auto-graded assignments.
Speaking Out: Interviews with People Who Struggle with Psychological Disorders This set of video segments allows students to see firsthand accounts of patients with various disorders. The inter- views were conducted by licensed clinicians and range in length from 8 to 25 minutes. Disorders include major depressive disorder, obsessive-compulsive disorder,
Preface xxi
patience and support during this time. Matthew Nock would like to thank his wife, Keesha, and their children Matt Jr., Maya, and Georgina, for their patience (and toler- ance). He is also grateful to Franchesca Ramirez and Nicole Murman for their assistance in the preparation of this edi- tion. Finally, Susan Mineka thanks her graduate students, friends, and family for their patience and support.
The authors would like to express our most extreme gratitude, respect, and appreciation to our amazing development editor, Stephanie Ventura. Her insightful rec- ommendations, editorial excellence, and all-around awe- someness made her a delight to work with. (Note: If they had let her edit this section, she would have caught that we just ended a sentence with a preposition. She’s that good.) A big thank you also goes to Amber Chow, our acquisi- tions editor, for her leadership, guidance, advice, and sup- port of this book. Without Amber’s ability to manage every challenge that arose, this book might still be in the produc- tion stages. In addition, we are grateful to Carrie Brandon for all of her hard work, support, and especially for her instrumental role in creating new video for this edition. Another special thank you goes to Cecilia Turner, our pro- gram manager, for her expert coordination of all aspects of this project as well as to Donna Simons and Sherry Lewis for their skillful management of the production of this book. We also thank Laura Chadwick for her efforts to secure all the permissions necessary for the figures and photographs.
Many experts, researchers, and users of this book pro- vided us with comments on individual chapters. We are extremely grateful for their input and feedback. Their knowledge and expertise help us keep this text current and accurate.
We are also especially grateful to the many reviewers who have given us invaluable feedback on this and previous editions of Abnormal Psychology: Joe Davis, CSU/ SWC; Dan Fox, University of Houston; Marvin Lee, Tennessee State University; Stevie McKenna, Rutgers University; Loreto Prieto, Iowa State University; Hugh Riley, Baylor University; Edward Selby, Rutgers University; Tasia Smith, University of Florida; Stephanie Stein, Central Washington University; David Topor, Harvard University; Anthony Zoccolillo, Texas A&M; Angela Bragg, Mount Hood Community College; Greg Carey, University of Colorado; Louis Castonguay, Pennsylvania State University; Richard Cavasina, California University of Pennsylvania; Dianne Chambless, University of Pennsylvania; Lee Anna Clark, The University of Iowa; Barbara Cornblatt; William Paul Deal, University of Mississippi; Raymond L. Eastman, Stephen F. Austin State University; John F. Edens, Sam Houston State University; Colleen Ehrnstrom, University of Colorado at Boulder; William Fals-Stewart, The State University of New York at Buffalo; John P. Forsyth, The
Test Bank (0134474767) The Test Bank is composed of approximately 2,000 fully referenced multiple-choice, completion, short-answer, and concise essay questions. Each question is accompanied by a page reference, difficulty level, skill type (factual, con- ceptual, or applied), topic, and a correct answer. Available for download on the Instructor’s Resource Center at www. pearsonhighered.com.
MyTest (0134319478) A powerful assessment-generation program that helps instructors easily create and print quizzes and exams. Ques- tions and tests can be authored online, allowing instructors ultimate flexibility and the ability to efficiently manage assessments anytime, anywhere. Instructors can easily access existing questions and edit, create, and store questions using a simple drag-and-drop technique and Word-like controls. Data on each question provides information on difficulty level and the page number of the corresponding text discus- sion. For more information, go to www.PearsonMyTest.com.
Lecture PowerPoint Slides (0134319443) The PowerPoint slides provide an active format for present- ing concepts from each chapter and feature relevant figures and tables from the text. Available for download on the Instructor’s Resource Center at www.pearsonhighered.com.
Enhanced Lecture PowerPoint Slides with Embedded Videos (0134474791) have been embedded with select Speak- ing Out video pertaining to each disorder chapter, enabling instructors to show videos within the context of their lecture.
PowerPoint Slides for Photos, Figures, and Tables (013447483X) contain only the photos, figures, and line art from the text. Available for download on the Instructor’s Resource Center at www.pearsonhighered.com.
Acknowledgments It takes each member of the author team more than a year of focused work to produce a new edition of this textbook. During this time, family and friends receive much less attention than they deserve. We are aware that a few lines of acknowledgment in a preface do little to compensate those close to us for all the inconveniences and absences they have endured. Nonetheless, Jill Hooley is ever grate- ful to Kip Schur for his patience, love, support, and ability to retain a sense of humor throughout the revision process. She also wishes to thank Tina Chou for her help with pro- ducing an image for Chapter 10. James Butcher would like to thank his wife, Carolyn L. Williams, and his children, Holly Butcher, Sherry Butcher, and Jay Butcher, for their
xxii Preface
State University of New York at Albany; Louis R. Franzini, San Diego State University; David H. Gleaves, Texas A&M University; Michael Green, University of California at Los Angeles; Steven Haynes, University of Hawaii at Manoa; Kathi Heffner, Ohio University; Daniel Holland, University of Arkansas at Little Rock; Steven Hollon, Vanderbilt University; Joanne Hoven Stohs, California State University Fullerton; Robert Howland, University of Pittsburgh, School of Medicine; Jean W. Hunt, Cumberland College; Alexandrea Hye-Young Park, Virginia Tech; William G. Iacono, University of Minnesota; Jessica Jablonski, University of Delaware; Erick Janssen, Indiana University; Sheri Johnson, University of Miami; Ann Kane, Barnstable High; Alan Kazdin, Yale University; Lynne Kemen, Hunter College; Carolin Keutzer, University of Oregon; John F. Kihlstrom, University of California at Berkeley; Gerald Koocher, Simmons College; David Kosson, Chicago Medical School; Marvin Lee, Tennessee State University; Brett Litz, Boston University; Brendan Maher, Harvard University; Richard McNally, Harvard University; Edwin Megargee, Florida State University; William Miller, University of New Mexico; Robin Morgan, Indiana
University Southeast; Michael Neboschick, College of Charleston; Matthew Nock, Harvard University; Chris Patrick, Florida State University; Marcus Patterson, University of Massachusetts; John Daniel Paxton, Lorain County Community College; Walter Penk, Memorial Veterans Hospital, Bedford, MA; Diego Pizzagalli, Harvard University; Lauren Polvere, Concordia University; Andy Pomerantz, Southern Illinois University, Edwardsville; Harvey Richman, Columbus State University; Barry J. Ries, Minnesota State University; Lizabeth Roemer, University of Massachusetts at Boston; Rick Seime, Mayo Clinic; Frances Sessa, Pennsylvania State University, Abington; Brad Schmidt, Ohio State University; Kandy Stahl, Stephen F. Austin State University; Stephanie Stein, Central Washington University; Xuan Stevens, Florida International University; Eric Stice, University of Texas at Austin; Marcus Tye, Dowling College; Beverly Vchulek, Columbia College; Michael E. Walker, Stephen F. Austin State University; Clifton Watkins, University of North Texas; Nathan Weed, Central Michigan University; and Kenneth J. Zucker, Centre for Addiction and Mental Health, Ontario, Canada.
xxiii
Jill M. Hooley Harvard University
Jill M. Hooley is a professor of psychology at Harvard University. She is also the head of the experimental psychopathology and clinical psychology program at Harvard. Dr. Hooley was born in England and received a BSc in psychology from the University of Liverpool. This was followed by research work at Cambridge Uni- versity. She then attended Magdalen College, Oxford, where she completed her DPhil. After a move to the United States and additional training in clinical psychology at SUNY Stony Brook, Dr. Hooley took a position at Harvard, where she has been a fac- ulty member since 1985.
Dr. Hooley has a long-standing interest in psychosocial pre- dictors of psychiatric relapse in patients with severe psychopa- thology such as schizophrenia and depression. Her research has been supported by grants from the National Institute of Mental Health and by the Borderline Personality Disorder Research Foun- dation. She uses fMRI to study emotion regulation in people who are vulnerable to depression and in people who are suffering from borderline personality disorder. Another area of research interest is nonsuicidal self-harming behaviors such as skin cutting or burning.
In 2000, Dr. Hooley received the Aaron T. Beck Award for Excellence in Psychopathology Research. She is also a past presi- dent of the Society for Research in Psychopathology. The author of many scholarly publications, Dr. Hooley was appointed Associate Editor for Clinical Psychological Science in 2012. She is also an asso- ciate editor for Applied and Preventive Psychology and serves on the editorial boards of several journals including the Journal of Con- sulting and Clinical Psychology, the Journal of Family Psychology, Family Process, and Personality Disorders: Theory, Research and Treat- ment. In 2015 Dr. Hooley received the Zubin Award for Lifetime Achievement in Psychopathology Research from the Society for Research in Psychopathology.
At Harvard, Dr. Hooley has taught graduate and undergrad- uate classes in introductory psychology, abnormal psychology, schizophrenia, mood disorders, clinical psychology, psychiatric diagnosis, and psychological treatment. Reflecting her commit- ment to the scientist-practitioner model, she also does clinical work specializing in the treatment of people with depression, anxiety disorders, and personality disorders.
About the Authors
James N. Butcher Professor Emeritus, University of Minnesota
James N. Butcher was born in West Virginia. He enlisted in the army when he was 17 years old and served in the airborne infan- try for 3 years, including a 1-year tour in Korea during the Korean War. After military service, he attended Guilford College, graduat- ing in 1960 with a BA in psychology. He received an MA in exper- imental psychology in 1962 and a PhD in clinical psychology from the University of North Carolina at Chapel Hill. He was awarded Doctor Honoris Causa from the Free University of Brussels, Belgium, in 1990 and an honorary doctorate from the University of Florence, Florence, Italy, in 2005. He is currently professor emer- itus in the Department of Psychology at the University of Minne- sota. He was associate director and director of the clinical psychology program at the university for 19 years. He was a mem- ber of the University of Minnesota Press’s MMPI Consultative Committee, which undertook the revision of the MMPI in 1989. He was formerly the editor of Psychological Assessment, a journal of the American Psychological Association, and serves as consulting editor or reviewer for numerous other journals in psychology and psychiatry. Dr. Butcher was actively involved in developing and organizing disaster response programs for dealing with human problems following airline disasters during his career. He organized a model crisis intervention disaster response for the Minneapolis-St. Paul Airport and organized and supervised the psychological services offered following two major airline disasters: North- west Flight 255 in Detroit, Michigan, and Aloha Airlines on Maui. He is a fellow of the Society for Personality Assessment. He has published 60 books and more than 250 articles in the fields of abnormal psychology, cross-cultural psychology, and personality assessment.
xxiv About the Authors
Susan Mineka Northwestern University
Susan Mineka, born and raised in Ithaca, New York, received her undergraduate degree magna cum laude in psychology at Cornell University. She received a PhD in experimental psychology from the University of Pennsylvania and later completed a formal clinical retraining program from 1981 to 1984. She taught at the University of Wisconsin–Madison and at the University of Texas at Austin before moving to Northwestern University in 1987. Since 1987 she has been a professor of psychology at Northwestern, and from 1998 to 2006 she served as director of clinical training there. She has taught a wide range of undergraduate and graduate courses, including introduc- tory psychology, learning, motivation, abnormal psychology, and cognitive-behavior therapy. Her current research interests include cognitive and behavioral approaches to understanding the etiology, maintenance, and treatment of anxiety and mood disorders. She is currently a Fellow of the American Psychological Association, the American Psychological Society, and the Academy of Cognitive Therapy. She has served as editor of the Journal of Abnormal Psychol- ogy (1990–1994). She also served as associate editor for Emotion from 2002 to 2006 and is on the editorial boards of several of the leading journals in the field. She was also president of the Society for the Science of Clinical Psychology (1994–1995) and was president of the Midwestern Psychological Association (1997). She also served on the American Psychological Association’s Board of Scientific Affairs (1992–1994, chair 1994), on the Executive Board of the Soci- ety for Research in Psychopathology (1992–1994, 2000–2003), and on the Board of Directors of the American Psychological Society (2001–2004). During 1997 and 1998 she was a fellow at the Center for Advanced Study in the Behavioral Sciences at Stanford.
Matthew K. Nock Harvard University
Matthew Nock was born and raised in New Jersey. Matt received his BA from Boston University (1995), followed by two masters (2000, 2001) and a PhD from Yale University (2003). He also com- pleted a clinical internship at Bellevue Hospital and the New York University Child Study Center (2003). Matt joined the faculty of Harvard University in 2003 and has been there ever since, cur- rently serving as a Professor in the Department of Psychology. While an undergraduate, Matt became very interested in the ques- tion of why people do things to intentionally harm themselves and he has been conducting research aimed at answering this question ever since. His research is multidisciplinary in nature and uses a range of methodological approaches (e.g., epidemio- logic surveys, laboratory-based experiments, and clinic-based studies) to better understand how these behaviors develop, how to predict them, and how to prevent their occurrence. His work is funded by research grants from the National Institutes of Health, Department of Defense, and several private foundations. Matt’s research has been published in over 100 scientific papers and book chapters and has been recognized through the receipt of awards from the American Psychological Association, the Association for Behavioral and Cognitive Therapies, and the American Associa- tion of Suicidology. In 2011 he received a MacArthur Fellowship (aka, “Genius Grant”) in recognition of his research on suicide and self-harm. At Harvard, Matt teaches courses on various topics including psychopathology, statistics, research methods, and cul- tural diversity. He has received numerous teaching and mentoring awards including the Roslyn Abramson Teaching Award and the Petra Shattuck Prize.
1
Chapter 1
Abnormal Psychology: Overview and Research Approaches
Learning Objectives
1.1 Explain how we define abnormality and classify mental disorders.
1.2 Describe the advantages and disadvantages of classification.
1.3 Explain how culture affects what is considered abnormal and describe two different culture-specific disorders.
1.4 Distinguish between incidence and prevalence and identify the most common and prevalent mental disorders.
1.5 Discuss why abnormal psychology research can be conducted in almost any setting.
1.6 Describe three different approaches used to gather information about mental disorders.
1.7 Explain why a control (or comparison group) is necessary to adequately test a hypothesis.
1.8 Discuss why correlational research designs are valuable, even though they cannot be used to make causal inferences.
1.9 Explain the key features of an experimental design.
2 Chapter 1
Scott Scott was born into an affluent family. There were no problems when he was born and he seemed to develop normally when he was a child. He went to a prestigious college and completed his degree in mathematics. Shortly afterwards, however, he began to isolate him- self from his family and he abandoned his plans for graduate studies. He traveled to San Francisco, took an apartment in a run-down part of the city, became increasingly suspicious of people around him, and developed strange ideas about brain transfer technology. Shortly before Christmas, he received a package from a friend. As he opened the package, he reported that his “head exploded” and he began to hear voices, even though no one was around. The voices began to tell him what to do and what not to do. His con- cerned parents came out to visit him, but he refused to seek any help or return home to live with them. Shortly after, he left the city and, living as a homeless person, moved around the country, even- tually making his way back to the East Coast. Throughout that time he was hearing voices every day—sometimes as many as five or six different ones. Eventually Scott’s worried family located him and per- suaded him to seek treatment. Although he has been hospitalized several times and been on many different medications in the inter- vening years, Scott still has symptoms of psychosis. His voices have never entirely gone away and they still dictate his behavior to a con- siderable extent. Now age 49, he lives in a halfway house, and works part-time shelving books in a university library.
Abnormal psychology is concerned with understanding the nature, causes, and treatment of mental disorders. The topics and problems within the field of abnormal psychol- ogy surround us every day. You have only to read a news- paper, flip through a magazine, surf the web, or sit through a movie to be exposed to some of the issues that clinicians and researchers deal with on a day-to-day basis. All too often, some celebrity is in the news because of a drug or alcohol problem, a suicide attempt, an eating disorder, or some other psychological difficulty. Countless books pro- vide personal accounts of struggles with schizophrenia, depression, phobias, and panic attacks. Films and TV shows portray aspects of abnormal behavior with varying degrees of accuracy. And then there are the tragic news sto- ries of mothers who kill their children, in which problems with depression, schizophrenia, or postpartum difficulties seem to be implicated.
Abnormal psychology can also be found much closer to home. Walk around any college campus, and you will see flyers about peer support groups for people with eating dis- orders, depression, and a variety of other disturbances. You may even know someone who has experienced a clinical problem. It may be a cousin with a cocaine habit, a room- mate with bulimia, or a grandparent who is developing Alzheimer’s disease. It may be a coworker of your mother’s who is hospitalized for depression, a neighbor who is afraid to leave the house, or someone at your gym who works out intensely despite being worrisomely thin. It may even be the disheveled street person in the aluminum foil hat who shouts, “Leave me alone!” to voices only he can hear.
The issues of abnormal psychology capture our inter- est, demand our attention, and trigger our concern. They also compel us to ask questions. To illustrate further, let’s consider two clinical cases.
Monique Monique is a 24-year-old law student. She is attractive, neatly dressed, and clearly very bright. If you were to meet her, you would think that she had few problems in her life; but Monique has been drinking alcohol since she was 14, and she smokes marijuana every day. Although she describes herself as “just a social drinker,” she drinks four or five glasses of wine when she goes out with friends and also drinks several glasses of wine a night when she is alone in her apartment in the evening. She frequently misses early morning classes because she feels too hung over to get out of bed. On several occasions her drinking has caused her to black out. Although she denies having any problems with alcohol, Monique admits that her friends and family have become very con- cerned about her and have suggested that she seek help. Monique, however, says, “I don’t think I am an alcoholic because I never drink in the mornings.” The previous week she decided to stop smoking marijuana entirely because she was concerned that she might have a drug problem. However, she found it impossible to stop and is now smoking regularly again.
Perhaps you found yourself asking questions as you read about Monique and Scott. For example, because Monique doesn’t drink in the mornings, you might have
Fergie has spoken about her past struggles with substance abuse, specifically crystal meth.
Abnormal Psychology: Overview and Research Approaches 3
controversial than you might expect. We also outline basic information about the extent of behavioral abnormalities in the population at large.
The second part of this chapter is devoted to research. We make every effort to convey to you how abnormal behavior is studied. Research is at the heart of progress and knowledge in abnormal psychology. The more you know and understand about how research is conducted, the more educated and aware you will be about what research find- ings do and do not mean.
What Do We Mean by Abnormality? 1.1 Explain how we define abnormality and classify
mental disorders.
It may come as a surprise to you that there is still no univer- sal agreement about what is meant by abnormality or disor- der. This is not to say we do not have definitions; we do. However, a truly satisfactory definition will probably always remain elusive (Lilienfeld et al., 2013; Stein et al., 2010).
Indicators of Abnormality Why does the definition of a mental disorder present so many challenges? A major problem is that there is no one behavior that makes someone abnormal. However, there are some clear elements or indicators of abnormality (Lilienfeld et al., 2013; Stein et al., 2010). No single indica- tor is sufficient in and of itself to define or determine abnor- mality. Nonetheless, the more that someone has difficulties in the following areas, the more likely he or she is to have some form of mental disorder:
1. Subjective distress: If people suffer or experience psy- chological pain we are inclined to consider this as indicative of abnormality. People with depression clearly report being distressed, as do people with anxi- ety disorders. But what of the patient who is manic and whose mood is one of elation? He or she may not be experiencing any distress. In fact, many such patients dislike taking medications because they do not want to lose their manic “highs.” You may have a test tomor- row and be exceedingly worried. But we would hardly label your subjective distress abnormal. Although sub- jective distress is an element of abnormality in many cases, it is neither a sufficient condition (all that is needed) nor even a necessary condition (a feature that all cases of abnormality must show) for us to consider something as abnormal.
2. Maladaptiveness: Maladaptive behavior is often an indicator of abnormality. The person with anorexia may restrict her intake of food to the point where she
wondered whether she could really have a serious alcohol problem. She does. This is a question that concerns the cri- teria that must be met before someone receives a particular diagnosis. Or perhaps you wondered whether other peo- ple in Monique’s family likewise have drinking problems. They do. This is a question about what we call family aggregation—that is, whether a disorder runs in families.
You may also have been curious about what is wrong with Scott and why he is hearing voices. Questions about the age of onset of his symptoms as well as predisposing factors may have occurred to you. Scott has schizophrenia, a disorder that often strikes in late adolescence or early adulthood. Also, as Scott’s case illustrates, it is not espe- cially unusual for someone who develops schizophrenia to develop in a seemingly normal manner before suddenly becoming ill.
These cases, which describe real people, give some indication of just how profoundly lives can be derailed because of mental disorders. It is hard to read about diffi- culties such as these without feeling compassion for the people who are struggling. Still, in addition to compassion, clinicians and researchers who want to help people like Monique and Scott must have other attributes and skills. If we are to understand mental disorders, we must learn to ask the kinds of questions that will enable us to help the patients and families who have mental disorders. These questions are at the very heart of a research-based approach that looks to use scientific inquiry and careful observation to understand abnormal psychology.
Asking questions is an important aspect of being a psychologist. Psychology is a fascinating field, and abnor- mal psychology is one of the most interesting areas of psy- chology (although we are undoubtedly biased). Psychologists are trained to ask questions and to conduct research. Though not all people who are trained in abnor- mal psychology (this field is sometimes called psychopa- thology) conduct research, they still rely heavily on their scientific skills and ability both to ask questions and to put information together in coherent and logical ways. For example, when a clinician first sees a new client or patient, he or she asks many questions to try and understand the issues or problems related to that person. The clinician will also rely on current research to choose the most effective treatment. The best treatments of 20, 10, or even 5 years ago are not invariably the best treatments of today. Knowl- edge accumulates and advances are made—and research is the engine that drives all of these developments.
In this chapter, we outline the field of abnormal psy- chology and the varied training and activities of the peo- ple who work within its demands. First we describe the ways in which abnormal behavior is defined and classified so that researchers and mental health professionals can communicate with each other about the people they see. Some of the issues here are probably more complex and
4 Chapter 1
4. Violation of the standards of society: All cultures have rules. Some of these are formalized as laws. Others form the norms and moral standards that we are taught to follow. Although many social rules are arbitrary to some extent, when people fail to follow the conven- tional social and moral rules of their cultural group, we may consider their behavior abnormal. For example, driving a car or watching television would be consid- ered highly abnormal for the Amish of Pennsylvania. However, both of these activities reflect normal every- day behavior for most other Pennsylvania residents.
Of course, much depends on the magnitude of the violation and on how commonly the rule is violated by others. As illustrated in the preceding example, a be- havior is most likely to be viewed as abnormal when it violates the standards of society and is statistically deviant or rare. In contrast, most of us have parked il- legally at some point. This failure to follow the rules is so statistically common that we tend not to think of it as abnormal. Yet when a mother drowns her children there is instant recognition that this is abnormal behavior.
5. Social discomfort: Not all rules are explicit. And not all rules bother us when they are violated. Nonethe- less, when someone violates an implicit or unwritten social rule, those around him or her may experience a sense of discomfort or unease. Imagine that you are sitting in an almost empty bus. There are rows of unoccupied seats. Then someone comes in and sits down right next to you. How do you feel? Is the per- son’s behavior abnormal? Why? The person is not breaking any formal rule. He or she has paid for a ticket and is permitted to sit anywhere he or she likes. But your sense of social discomfort (“Why did this person sit right next to me when there are so many empty seats available?”) will probably incline you to think that this is an example of abnormal behavior. In other words, social discomfort is another potential way that we can recognize abnormality. But again, much depends on circumstances. If the person who gets on the bus is someone you know well, it might be more unusual if he or she did not join you.
6. Irrationality and unpredictability: As we have already noted, we expect people to behave in certain ways. Although a little unconventionality may add some spice to life, there is a point at which we are likely to consider a given unorthodox behavior abnormal. If a person sitting next to you suddenly began to scream and yell obscenities at nothing, you would probably regard that behavior as abnormal. It would be unpre- dictable, and it would make no sense to you. The disor- dered speech and the disorganized behavior of patients with schizophrenia are often irrational. Such behaviors are also a hallmark of the manic phases of bipolar disor- der. Perhaps the most important factor, however, is our
becomes so emaciated that she needs to be hospital- ized. The person with depression may withdraw from friends and family and may be unable to work for weeks or months. Maladaptive behavior interferes with our well-being and with our ability to enjoy our work and our relationships. But not all disorders involve maladaptive behavior. Consider the con artist and the contract killer, both of whom have antisocial personality disorder. The first may be able glibly to talk people out of their life savings, the second to take someone’s life in return for payment. Is this behavior maladaptive? Not for them, because it is the way in which they make their respective livings. We consider them abnormal, however, because their behavior is maladaptive for and toward society.
3. Statistical deviancy: The word abnormal literally means “away from the normal.” But simply consider- ing statistically rare behavior to be abnormal does not provide us with a solution to our problem of defining abnormality. Genius is statistically rare, as is perfect pitch. However, we do not consider people with such uncommon talents to be abnormal in any way. Also, just because something is statistically common doesn’t make it normal. The common cold is certainly very common, but it is regarded as an illness nonetheless.
On the other hand, intellectual disability (which is statistically rare and represents a deviation from normal) is considered to reflect abnormality. This tells us that in defining abnormality we make value judg- ments. If something is statistically rare and undesirable (as is severely diminished intellectual functioning), we are more likely to consider it abnormal than something that is statistically rare and highly desirable (such as genius) or something that is undesirable but statisti- cally common (such as rudeness).
As with most accomplished athletes, Venus and Serena Williams’ physical ability is abnormal in a literal and statistical sense. Their behavior, however, would not be labeled as being abnormal by psychologists. Why not?
Abnormal Psychology: Overview and Research Approaches 5
poisonous snakes as pets) not immediately regarded as mentally ill? Just because we may be a danger to ourselves or to others does not mean we are mentally ill. Conversely, we cannot assume that someone diag- nosed with a mental disorder must be dangerous. Although people with mental illness do commit seri- ous crimes, serious crimes are also committed every day by people who have no signs of mental disorder. Indeed, research suggests that in people with mental illness, dangerousness is more the exception than the rule (Corrigan & Watson, 2005).
One final point bears repeating. Decisions about abnormal behavior always involve social judgments and are based on the values and expectations of society at large. This means that culture plays a role in determining what is and is not abnormal. In addition, because society is con- stantly shifting and becoming more or less tolerant of cer- tain behaviors, what is considered abnormal or deviant in one decade may not be considered abnormal or deviant a decade or two later. At one time, homosexuality was classi- fied as a mental disorder. But this is no longer the case (it was removed from the formal classification system in 1974). A generation ago, pierced noses and navels were regarded as highly deviant and prompted questions about a person’s mental health. Now, however, such adornments are commonplace and attract little attention. What other behaviors can you think of that are now considered normal but were regarded as deviant in the past?
evaluation of whether the person can control his or her behavior. Few of us would consider a roommate who began to recite speeches from King Lear to be abnormal if we knew that he was playing Lear in the next cam- pus Shakespeare production—or even if he was a dra- matic person given to extravagant outbursts. On the other hand, if we discovered our roommate lying on the floor, flailing wildly, and reciting Shakespeare, we might consider calling for assistance if this was entirely out of character and we knew of no reason why he should be behaving in such a manner.
7. Dangerousness: It seems quite reasonable to think that someone who is a danger to him- or herself or to another person must be psychologically abnormal. Indeed, therapists are required to hospitalize suicidal clients or contact the police (as well as the person who is the target of the threat) if they have a client who makes an explicit threat to harm another person. But, as with all of the other elements of abnormality, if we rely only on dangerousness as our sole feature of abnormality, we will run into problems. Is a soldier in combat mentally ill? What about someone who is an extremely bad driver? Both of these people may be a danger to others. Yet we would not consider them to be mentally ill. Why not? And why is someone who engages in extreme sports or who has a dangerous hobby (such as free diving, race car driving, or keeping
How important is dangerousness to the definition of mental illness? If we are a risk to ourselves or to others, does this mean we are mentally ill?
Tattoos, which were once regarded as highly deviant, are now quite commonplace and considered fashionable by many.
As you think about these issues, consider the person described in the World Around Us box. He is certainly an unusual human being. But is his behavior abnormal? Do you think everyone will agree about this?
6 Chapter 1
The World Around Us Extreme Generosity or Pathological Behavior?
Zell Kravinsky was a brilliant student who grew up in a working- class neighborhood in Philadelphia. He won prizes at school, and at the age of 12, he began investing in the stock market. Despite his abilities, his Russian immigrant parents were, in the words of a family friend, “steadfast in denying him any praise.” Kravinsky eventually completed two Ph.D. degrees and indulged his growing interest in real estate. By the time he was 45 years old, he was married with children. His assets amounted to almost $45 million.
Although Kravinsky had a talent for making money, he found it difficult to spend it. He drove an old car, did not give his children pocket money, and lived with his family in a modest home. As his fortune grew, however, he began to talk to his friends about his plans to give all of his assets to charity. His phi- lanthropy began in earnest when he and his wife gave two gifts, totaling $6.2 million, to the Centers for Disease Control Founda- tion. They also donated an apartment building to a school for the disabled in Philadelphia. The following year the Kravinskys gave real estate gifts worth approximately $30 million to Ohio State University.
Kravinsky’s motivation for his donations was to help oth- ers. According to one of his friends, “He gave away the money because he had it and there were people who needed it. But it changed his way of looking at himself. He decided the purpose of his life was to give away things.” After he had put some money aside in trust for his wife and his children, Kravinsky’s personal assets were reduced to a house (on which he had a substantial mortgage), two minivans, and around $80,000 in stocks and cash. He had essentially given away his entire fortune.
Kravinsky’s donations did not end when his financial assets became depleted. He began to be preoccupied with the idea of nondirected organ donations, in which an altruistic person gives an organ to a total stranger. When he learned that he could live quite normally with only one kidney, Kravinsky decided that the personal costs of giving away one of his kidneys were minimal compared to the benefits received by the kidney recipient. His wife, however, did not share his view. Although she had con- sented to bequeathing substantial sums of money to worthwhile charities, when it came to her husband offering his kidney, she could not support him.
For Kravinsky, however, the burden of refusing to help alleviate the suffering of someone in need was almost unbear- able, even if it meant sacrificing his very own organs. He called the Albert Einstein Medical Center and spoke to a transplant coordinator. He met with a surgeon and then with a psychia- trist. Kravinsky told the psychiatrist that his wife did not support his desire to donate one of his kidneys. When the psychiatrist told him that he was doing something he did not have to do, Kravinsky’s response was that he did need to make this sacri- fice: “You’re missing the whole point. It’s as much a necessity as food, water, and air.”
Three months later, Kravinsky left his home in the early hours of the morning, drove to the hospital, and donated his right kidney. He informed his wife after the surgery was over. In spite of the turmoil that his kidney donation created within his family, Kravinsky’s mind turned back to philanthropy almost immediately. “I lay there in the hospital, and I thought about all my other good organs. When I do something good, I feel that I can do more. I burn to do more. It’s a heady feeling.” By the time he was discharged, he was wondering about giving away his one remaining kidney.
After the operation, Kravinsky experienced a loss of direc- tion. He had come to view his life as a continuing donation. However, now that his financial assets and his kidney were gone, what could he provide to the less fortunate? Sometimes he imagines offering his entire body for donation. “My organs could save several people if I gave my whole body away.” He acknowledges that he feels unable to hurt his family through the sacrifice of his life.
Several years after the kidney donation, Kravinsky still remains committed to giving away as much as possible. How- ever, his actions have caused a tremendous strain in his marriage. In an effort to maintain a harmonious relationship with his wife, he is now involved in real estate and has bought his family a larger home. (Taken from I. Parker, 2004.)
Is Zell Kravinsky a courageous man of profound moral com- mitment? Or is his behavior abnormal and indicative of a mental disorder? Explain how you reached the conclusion you did.
Is Zell Kravinsky’s behavior abnormal, or is he a man with profound moral conviction and courage?
Abnormal Psychology: Overview and Research Approaches 7
thought to reflect a dysfunction in biological, psychological, or developmental processes that are necessary for mental functioning. DSM-5 also recognizes that mental disorders are usually associated with significant distress or disability in key areas of functioning such as social, occupational, or other activities. Predictable or culturally approved responses to common stressors or losses (such as death of a loved one) are excluded. It is also important that this dys- functional pattern of behavior not stem from social devi- ance or conflicts that the person has with society as a whole.
This new DSM-5 definition of mental illness was based on input from various DSM-5 work groups as well as other sources (Broome & Bortolotti, 2010; First & Wakefield, 2010; Stein et al., 2010). Although this definition will still not sat- isfy everyone, it brings us even closer to a good working
The DSM-5 and the Definition of Mental Disorder In the United States, the accepted standard for defining various types of mental disorders is the American Psychi- atric Association’s Diagnostic and Statistical Manual of Men- tal Disorders. This manual, commonly referred to as the DSM, is revised and updated from time to time. The current version, called DSM-5, was published in 2013. It is 947 pages long and contains a total of 541 diagnostic categories (Blashfield et al., 2014). This recent revision of the DSM has been the topic of much debate and controversy. In the Thinking Critically about DSM-5 box we explain more about the DSM and discuss why a revision was necessary.
Although the DSM is widely used, it is not the only psychiatric classification system. The International Classifi- cation of Diseases (called ICD-10 because it is now in its 10th revision) is produced by the World Health Organization (WHO). Chapter V of this document covers mental and behavioral disorders (WHO, 2015b). Although the ICD-10 has much in common with DSM-5, it also many differ- ences, with similar disorders having different names, for example. The ICD-10 is used in many countries outside the United States and ICD-11 is currently in development.
Within DSM-5, a mental disorder is defined as a syn- drome that is present in an individual and that involves clinically significant disturbance in behavior, emotion regu- lation, or cognitive functioning. These disturbances are
DSM-5 Thinking Critically about DSM-5 What Is the DSM and Why Was It Revised? The Diagnostic and Statistical Manual of Mental Disorders (DSM)
provides all the information necessary (descriptions, lists of
symptoms) to diagnose mental disorders. As such, it provides
clinicians with specific diagnostic criteria for each disorder. This
creates a common language so that a specific diagnosis means
the same thing to one clinician as it does to another. In addition,
providing descriptive information about the type and number of
symptoms needed for each diagnosis helps ensure diagnostic
accuracy and consistency (reliability). The DSM is also impor-
tant for research. If patients could not be diagnosed reliably, it
would be impossible to compare different treatments for
patients with similar conditions. Although the DSM does not
include information about treatment, clinicians need to have an
accurate diagnosis in order to select the most appropriate treat-
ment for their patients.
Since DSM-I was first published in 1952, the DSM has been
revised from time to time. Revisions are important because they
allow new scientific developments to be incorporated into how we
think about mental disorders. The revision process for DSM-5
had the goals of maintaining continuity with the previous edition
(DSM-IV) as well as being guided by new research findings. But
another guiding principle was that no constraints should be
placed on the level of change that could be made. If this strikes
you as a little contradictory, you are correct. Striking the right bal-
ance between change and continuity presented considerable
challenges. It also created a great deal of controversy. As part of
the revision process, experts in specific disorders were invited to
join special DSM-5 work groups and make specific recommenda-
tions for change. In some cases, the debates were so heated that
people resigned from their work groups! Now that DSM-5 is here,
not everyone is happy with some of the changes that have been
made. On the other hand, many of the revisions that have been
made make a lot of sense. In the chapters that follow we highlight
key changes in DSM-5. We also try to help you think critically
about the reasons behind the specific modifications that were
proposed and understand why they were accepted.
8 Chapter 1
A final effect of classification system usage is somewhat more mundane. As others have pointed out, the classifica- tion of mental disorders has social and political implica- tions (see Keeley et al., 2015; Kirk & Kutchins, 1992). Simply put, defining the domain of what is considered to be patho- logical establishes the range of problems that the mental health profession can address. As a consequence, on a purely pragmatic level, it furthermore delineates which types of psychological difficulties warrant insurance reim- bursement and the extent of such reimbursement.
What Are the Disadvantages of Classification? Of course, a number of potential disadvantages are associated with the use of a discrete classification system. Classification, by its very nature, provides information in a shorthand form. However, using any form of shorthand inevitably leads to a loss of information. If we know the specific history, personality traits, idiosyncrasies, and familial relations of a person with a particular type of disorder (e.g., from reading a case sum- mary), we naturally have much more information than if we were simply told the individual’s diagnosis (e.g., schizophre- nia). In other words, as we simplify through classification, we inevitably lose an array of personal details about the actual person who has the disorder.
Moreover, although things are improving, there can still be some stigma (disgrace) associated with having a psychi- atric diagnosis. Stigma, of course, is hardly the fault of the diagnostic system itself. But even today, people are gener- ally far more comfortable disclosing that they have a physi- cal illness such as diabetes than they are admitting to any mental disorder. This is in part due to the fear (real or imag- ined) that speaking candidly about having a psychological disorder will result in unwanted social or occupational con- sequences or frank discrimination. Be honest. Have you ever described someone as “nuts,” “crazy,” or “a psycho”? Now think of the hurt that people with mental disorders experi- ence when they hear such words. In one study, 96 percent of patients with schizophrenia reported that stigma was a rou- tine part of their lives (Jenkins & Carpenter-Song, 2008). In spite of the large amount of information that is now availa- ble about mental health issues, the level of knowledge about mental illness (sometimes referred to as mental health liter- acy) is often very poor (Thornicroft et al., 2007).
Stigma is a deterrent to seeking treatment for mental health problems. This is especially true for younger people, for men, and for ethnic minorities (Clement et al., 2015). Stigma is also a disproportionately greater deterrent to treatment seeking for two other groups: military personnel and (ironically) mental health professionals. Would you have predicted this? Why do you think this is the case?
Related to stigma is the problem of stereotyping. Ste- reotypes are automatic beliefs concerning other people that
description. Keep in mind that any definition of abnormal- ity or mental disorder must be somewhat arbitrary. Rather than thinking of the DSM as a finished product, it should always be regarded as a work in progress, with regular updates and modifications to be expected. Although earlier versions of the DSM used Roman numerals to refer to each specific edition (e.g., DSM-IV), Arabic numerals are now being used instead of Roman numerals (5 versus V) to facil- itate updating (e.g., DSM-5.1, DSM-5.2) in the future.
in review • Why is abnormality so difficult to define?
• What characteristics help us recognize abnormality?
Classification and Diagnosis 1.2 Describe the advantages and disadvantages of
classification.
If defining abnormality is so contentious and so difficult, why do we try to do it? One simple reason is that most sci- ences rely on classification (e.g., the periodic table in chem- istry and the classification of living organisms into kingdoms, phyla, classes, and so on in biology). At the most fundamental level, classification systems provide us with a nomenclature (a naming system). This gives clinicians and researchers both a common language and shorthand terms for complex clinical conditions. Without having a common set of terms to describe specific clinical conditions, clinicians would have to talk at length about each patient individu- ally to provide an overview of the patient’s problems. But if there is a shared understanding of what the term “schizo- phrenia” means, for example, communication across pro- fessional boundaries is simplified and facilitated.
Another advantage of classification systems is that they enable us to structure information in a more helpful manner. Classification systems shape the way information is organ- ized. For example, most classification systems typically place diagnoses that are thought to be related in some way close together. In DSM-5, the section on anxiety disorders includes disorders (such as panic disorder, specific phobia, and agora- phobia) that share the common features of fear and anxiety.
Organizing information within a classification system also allows us to study the different disorders that we clas- sify and therefore to learn new things. In other words, clas- sification facilitates research, which gives us more information and facilitates greater understanding, not only about what causes various disorders but also how they might best be treated. For example, thinking back to the cases you read about, Monique has alcohol and drug use disorders, and Scott has schizophrenia. Knowing what disorder each of them has is clearly very helpful, because Scott’s treatment would be very different from Monique’s.
Abnormal Psychology: Overview and Research Approaches 9
Respectful and appropriate language should instead be used. At one time, it was quite common for mental health professionals to describe a given patient as “a schizophrenic” or “a manic-depressive.” Now, however, it is widely acknowledged that it is more accurate (not to mention more considerate) to use what is called person-first language and say, “a person with schizophrenia,” or “a person with bipo- lar disorder.” Simply put, the person is not the diagnosis.
How Can We Reduce Prejudicial Attitudes Toward People Who Are Mentally Ill? Negative reactions to people with mental illness are com- mon and may be a fairly widespread phenomenon throughout the world. Using focus groups, Arthur and col- leagues (2010) asked community residents in Jamaica about the concept of stigma. Some participants came from rural communities, others from more urban areas. Regard- less of their gender, level of education, or where they lived, most participants described highly prejudicial attitudes toward those with mental illnesses. One middle-class male participant said, “We treat them as in a sense second class citizens, we stay far away from them, ostracize them, we just treat them bad” (see Arthur et al., 2010, p. 263). Fear of people who are mentally ill was also commonly expressed. A rural-dwelling middle-class man described a specific sit- uation in the following way, “There is a mad lady on the
we unavoidably learn as a result of growing up in a par- ticular culture (e.g., people who wear glasses are more intelligent; New Yorkers are rude). Because we may have heard about certain behaviors that can accompany mental disorders, we may automatically and incorrectly infer that these behaviors will also be present in any person we meet who has a psychiatric diagnosis. Negative stereotypes about psychiatric patients are also perpetuated in movies. If you have ever seen a horror movie you know that a com- mon dominant theme involves the homicidal maniac. And an analysis of 55 horror films made between 2000 and 2012 has shown that it is people with psychosis who are most often portrayed as murderers (Goodwin, 2014). Stereotyp- ing is also reflected in the comment “People like you don’t go back to work” in the case example of James McNulty.
James McNulty
I have lived with bipolar disorder for more than 35 years—all of my adult life. The first 15 years were relatively conventional, at least on the surface. I graduated from an Ivy League university, started my own business, and began a career in local politics. I was married, the father of two sons. I experienced mood swings during these years, and as I got older the swings worsened. Eventually, I became so ill that I was unable to work, my marriage ended, I lost my business, and I became homeless.
At this point I had my most powerful experience with stigma. I was 38 years old. I had recently been discharged after a psychiatric hospitalization for a suicide attempt, I had no place to live, my savings were exhausted, and my only possession was a 4-year-old car. I con- tacted the mental health authorities in the state where I then lived and asked for assistance in dealing with my mental illness. I was told that to qualify for assistance I would need to sell my car and spend down the proceeds. I asked how I was supposed to get to work when I recovered enough to find a job. I was told, “Don’t worry about going back to work. People like you don’t go back to work.” (McNulty, 2004)
Finally, stigma can be perpetuated by the problem of labeling. A person’s self-concept may be directly affected by being given a diagnosis of schizophrenia, depression, or some other form of mental illness. How might you react if you were told something like this? Furthermore, once a group of symptoms is given a name and identified by means of a diagnosis, this diagnostic label can be hard to shake even if the person later makes a full recovery.
It is important to keep in mind, however, that diagnos- tic classification systems do not classify people. Rather, they classify the disorders that people have. And stigma may be less a consequence of the diagnostic label than a result of the dis- turbed behavior that got the person the diagnosis in the first place. In some situations, a diagnosis may even reduce stigma because it provides at least a partial explanation for a person’s otherwise inexplicable behavior (Ruscio, 2004). Nonetheless, when we note that someone has an illness, we should take care not to define him or her by that illness.
Are attitudes toward people who are mentally ill in Jamaica more benign than they are in more industrialized countries?
10 Chapter 1
was “doing much better now.” In other trials, the biographi- cal description made no mention of any mental illness when the person on the slide was being described. Students who took part in the study reported more distress and had more muscle tension in their brows when they imagined inter- acting with a person with schizophrenia than when they imagined interacting with a person who did not have schiz- ophrenia. Heart rate changes also suggested they were expe- riencing the imagined interactions with the patients as being more unpleasant than the interactions with the nonpatients. Finally, research participants who had more psychophysio- logical reactivity to the slides of the patients reported higher levels of stigma toward these patients. These findings sug- gest that people may tend to avoid those with mental illness because the psychophysiological arousal these encounters create is experienced as unpleasant.
in review • What is stigma? How common is it?
• What challenges are involved in reducing stigma toward people with mental illness?
Culture and Abnormality 1.3 Explain how culture affects what is considered
abnormal and describe two different culture- specific disorders.
Just as we must consider changing societal values and expectations in defining abnormality, so too must we con- sider differences across cultures. In fact, this is explicitly acknowledged in the DSM-5 definition of disorder. Within a given culture, many shared beliefs and behaviors exist that are widely accepted and that may constitute one or more customary practices. For instance, many people in Christian countries believe that the number 13 is unlucky. The origins of this may be linked to the Last Supper, at which 13 people were present. Many of us try to be especially cautious on Friday the 13th. Some hotels and apartment buildings avoid having a 13th floor altogether. Similarly, there is frequently no bed numbered 13 in hospital wards.
The Japanese, in contrast, are not worried about the number 13. Rather, they attempt to avoid the number 4. This is because in Japanese the sound of the word for “four” is similar to the sound of the word for “death” (see Tseng, 2001, pp. 105–106).
There is also considerable variation in the way different cultures describe psychological distress. For example, there is no word for “depressed” in the languages of certain Native Americans, Alaska Natives, and Southeast Asian cultures (Manson, 1995). Of course, this does not mean that members from such cultural groups do not experience clinically signifi- cant depression. As the accompanying case illustrates,
road named […]. Even the police are afraid of her because she throws stones at them. She is very, very terrible” (p. 261). Moreover, even when more kindly attitudes were expressed, fear was still a common response. One person put it simply, “You are fearful even though you may be sympathetic” (p. 262). In short, the results of this study suggest that stereotyping, labeling, and stigma toward people with mental illness are not restricted to industrial- ized countries. Although we might wish that it were other- wise, prejudicial attitudes are common. This highlights the need for anti-stigma campaigns.
For a long time, it was thought that educating people that mental illnesses were “real” brain disorders might be the solution. Sadly, however, this does not seem to be the case. Although there have been impressive increases in the proportion of people who now understand that mental dis- orders have neurobiological causes, this increased aware- ness has not resulted in decreases in stigma. In one study, Pescosolido and colleagues (2010) asked people in the com- munity to read a vignette (brief description) about a person who showed symptoms of mental illness. Some people read a vignette about a person who had schizophrenia. Others read a vignette about someone with clinical depression or alcohol dependence. Importantly, no diagnostic labels were used to describe these people. The vignettes simply pro- vided descriptive information. Nonetheless, the majority of the people who were surveyed in this study expressed an unwillingness to work with the person described in the vignette. They also did not want to have to socialize with them and did not want them to marry into their family. Moreover, the level of rejection that was shown was just as high as it was in a similar survey that was done 10 years earlier. Over that same 10-year period, however, many more people embraced a neurobiological understanding about the causes of mental illness. So what this study tells us is that just because people understand that mental illness is caused by problems in the brain doesn’t mean that they are any less prejudiced toward those with mental illness. This is a disappointing conclusion for everyone who hoped that more scientific research into the biology of mental ill- ness would lead to the elimination of stigma.
Stigma does seem to be reduced by having more contact with people in the stigmatized group (Corrigan et al., 2014; Couture & Penn, 2003). However, there may be barriers to this. Simply imagining interacting with a person who has a mental disorder can lead to distress and also to unpleasant physical reactions. In an interesting study, Graves and col- leagues (2005) asked college students enrolled in a psychol- ogy course to imagine interacting with a person whose image was shown to them on a slide. As the slide was being presented, subjects were given some scripted biographical information that described the person. In some scripts, the target person was described as having been diagnosed with schizophrenia, although it was also mentioned that he or she
Abnormal Psychology: Overview and Research Approaches 11
coats are ragged; they’re thinner. They just wander aimlessly; even the ewes don’t seem to care about the little ones.” Physical examination and laboratory tests are normal. Mr. GH continues to take two tablets of acetaminophen daily for mild arthritic pain. Although he describes himself as a “recovering alcoholic,” Mr. GH reports not having con- sumed alcohol during the last 23 years. He denies any prior episodes of depression or other psychiatric problems. (Manson, 1995, p. 488)
however, the way some disorders present themselves may depend on culturally sanctioned ways of articulating distress.
Depression in a Native American Elder
JGH is a 71-year-old member of a Southwestern tribe who has been brought to a local Indian Health Service hospital by one of his grand- daughters and is seen in the general medical outpatient clinic for mul- tiple complaints. Most of Mr. GH’s complaints involve nonlocalized pain. When asked to point to where he hurts, Mr. GH indicates his chest, then his abdomen, his knees, and finally moves his hands “all over.” Barely whispering, he mentions a phrase in his native language that translates as “whole body sickness.” His granddaughter notes that he “has not been himself” recently. Specifically, Mr. GH, during the past 3 or 4 months, has stopped attending or participating in many events previously important to him and central to his role in a large extended family and clan. He is reluctant to discuss this change in behavior as well as his feelings. When questioned more directly, Mr. GH acknowledges that he has had difficulty falling asleep, sleeps intermittently through the night, and almost always awakens at dawn’s first light. He admits that he has not felt like eating in recent months but denies weight loss, although his clothes hang loosely in many folds. Trouble concentrating and remembering are eventually dis- closed as well. Asked why he has not participated in family and clan events in the last several months, Mr. GH describes himself as “too tired and full of pain” and “afraid of disappointing people.” Further pressing by the clinician is met with silence. Suddenly the patient states, “You know, my sheep haven’t been doing well lately. Their
There is no word for “depressed” in the languages of certain Native American tribes. Members of these communities tend to describe their symptoms of depression in physical rather than emotional terms.
As is apparent in the case of JGH, culture can shape the clinical presentation of disorders like depression, which are present across cultures around the world (see Draguns & Tanaka-Matsumi, 2003). In China, for instance, individu- als with depression frequently focus on physical concerns (fatigue, dizziness, headaches) rather than verbalizing their feelings of melancholy or hopelessness (Kleinman, 1986; Parker et al., 2001). This focus on physical pain rather than emotional pain is also noteworthy in Mr. GH’s case.
Despite progressively increasing cultural awareness, we still know relatively little concerning cultural interpreta- tion and expression of abnormal psychology (Arrindell, 2003). The vast majority of the psychiatric literature origi- nates from Euro-American countries—that is, Western Europe, North America, and Australia/New Zealand (Patel & Kim, 2007; Patel & Sumathipala, 2001). To exacerbate this underrepresentation, research published in languages other than English tends to be disregarded (Draguns, 2001).
Prejudice toward people with mental illness seems to be found worldwide. However, some types of psychopathology appear to be highly culture specific: They are found only in certain areas of the world and seem to be highly linked to culturally bound concerns. A case in point is taijin kyofusho. This syndrome, which is an anxiety disorder, is quite preva- lent in Japan. It involves a marked fear that one’s body, body parts, or body functions may offend, embarrass, or otherwise make others feel uncomfortable. Often, people with this dis- order are afraid of blushing or upsetting others by their gaze, facial expression, or body odor (Levine & Gaw, 1995).
Some disorders are highly culture specific. For example, taijin kyofusho is a disorder that is prevalent in Japan. It is characterized by the fear that one may upset others by one’s gaze, facial expression, or body odor.
12 Chapter 1
the nature and extent of the psychological difficulties within a given area, state, or country because they are responsible for determining how resources such as fund- ing of research projects or services provided by community mental health centers may be most effectively allocated. It would obviously be imprudent to have a treatment center filled with clinicians skilled in the treatment of anorexia nervosa (a very severe but relatively rare clinical problem) if there were few clinicians skilled in treating anxiety or depression, which are much more prevalent disorders.
Second, estimates of the frequency of mental disor- ders in different groups of people may provide valuable clues as to the causes of these disorders. For example, data from the United Kingdom have shown that schizophrenia is about three times more likely to develop in ethnic minorities than in the white population (Kirkbridge et al., 2006). Rates of schizophrenia in southeast London are also high relative to other parts of the country. This is prompt- ing researchers to explore why this might be. Possible fac- tors may be social class and neighborhood deprivation, as well as diet or exposure to infections or environmental contaminants.
Prevalence and Incidence Before we can further discuss the impact of mental disor- ders upon society, we must clarify the way in which psy- chological problems are counted. Epidemiology is the study of the distribution of diseases, disorders, or health- related behaviors in a given population. Mental health epi- demiology is the study of the distribution of mental disorders. A key component of an epidemiological survey is determining the frequencies of mental disorders. There are several ways of doing this. The term prevalence refers to the number of active cases in a population during any given period of time. Prevalence figures are typically expressed as percentages (i.e., the percentage of the popu- lation that has the disorder). Furthermore, there are several different types of prevalence estimates that can be made.
Point prevalence refers to the estimated proportion of actual, active cases of a disorder in a given population at a given point in time. For example, if we were to conduct a study and count the number of people who have major depressive disorder (i.e., clinical depression) on January 1 of next year, this would provide us with a point prevalence estimate of active cases of depression. A person who expe- rienced depression during the months of November and December but who managed to recover by January 1 would not be included in our point prevalence calculation. The same is true of someone whose depression did not begin until January 2.
If, on the other hand, we wanted to calculate a 1-year prevalence figure, we would count everyone who experi- enced depression at any point in time throughout the entire
Another culturally rooted expression of distress, found in people of Latino descent, especially those from the Car- ibbean, is ataque de nervios or an “attack of nerves” (Lizardi et al., 2009; Lopez & Guarnaccia, 2005). This is a clinical syndrome that does not seem to correspond to any specific diagnosis within the DSM. The symptoms of an ataque de nervios, which is often triggered by a stressful event such as divorce or bereavement, include crying, trembling, and uncontrollable screaming. There is also a sense of being out of control. Sometimes the person may become physically or verbally aggressive. Alternately, the person may faint or experience a seizure-like fit. Once the ataque is over, the person may promptly resume his or her normal manner, with little or no memory of the incident.
As noted earlier, abnormal behavior is behavior that deviates from the norms of the society in which the person lives. Experiences such as hearing the voice of a dead rela- tive might be regarded as normative in one culture (e.g., in many Native American tribes) yet abnormal in another cul- tural milieu. Nonetheless, certain unconventional actions and behaviors are almost universally considered to be the product of mental disorder.
Many years ago, the anthropologist Jane Murphy (1976) studied abnormal behavior in the Yoruba of Africa and the Yupik-speaking Eskimos living on an island in the Bering Sea. Both societies had words that were used to denote abnormality or “craziness.” In addition, the clusters of behaviors that were considered to reflect abnormality in these cultures were behaviors that most of us would also regard as abnormal. These included hearing voices, laugh- ing at nothing, defecating in public, drinking urine, and believing things that no one else believes. Why do you think these behaviors are universally considered to be abnormal?
in review • In what ways can culture shape the clinical presentation of men-
tal disorders?
• Are the same disorders always found worldwide, regardless of culture?
How Common Are Mental Disorders? 1.4 Distinguish between incidence and prevalence and
identify the most common and prevalent mental disorders.
How many and what sort of people have diagnosable psy- chological disorders today? This is a significant question for a number of reasons. First, such information is essential when planning and establishing mental health services. Mental health planners require a precise understanding of
Abnormal Psychology: Overview and Research Approaches 13
Because DSM-5 is so new, no comprehensive lifetime prevalence data using this revised version of the DSM are yet available. However, the lifetime prevalence of having any DSM-IV disorder is 46.4 percent. This means that almost half of the Americans who were questioned had been affected by mental illness at some point in their lives (Kessler, Berglund, Demler, et al., 2005). Although this fig- ure may seem high, it may actually be an underestimate, as the NCS-R study did not assess for eating disorders, schiz- ophrenia, or autism, for example. Neither did it include measures of most personality disorders. As you can see from Table 1.1, the most prevalent category of psychologi- cal disorders is anxiety disorders. The most common indi- vidual disorders are major depressive disorder, alcohol abuse, and specific phobias (e.g., fear of small animals, insects, flying, heights). Social phobias (e.g., fear of public speaking) are similarly very common (see Table 1.2).
year. As you might imagine, this prevalence figure would be higher than the point prevalence figure because it would cover a much longer time. It would moreover include those people who had recovered before the point prevalence assessment as well as those whose disorders did not begin until after the point prevalence estimate was made.
Finally, we may also wish to obtain an estimate of the number of people who have had a particular disorder at any time in their lives (even if they are now recovered). This would provide us with a lifetime prevalence esti- mate. Because they extend over an entire lifetime and include both currently ill and recovered individuals, life- time prevalence estimates tend to be higher than other kinds of prevalence estimates.
An additional term with which you should be familiar is incidence. This refers to the number of new cases that occur over a given period of time (typically 1 year). Inci- dence figures tend to be lower than prevalence figures because they exclude preexisting cases. In other words, if we were assessing the 1-year incidence of schizophrenia, we would not count people whose schizophrenia began before our given starting date (even if they were still ill) because they are not “new” cases of schizophrenia. On the other hand, someone who was quite well previously but then developed schizophrenia during our 1-year window would be included in our incidence estimate.
Prevalence Estimates for Mental Disorders Now that you have an understanding of some basic terms, let’s turn to the 1-year prevalence rates for several impor- tant disorders. The most comprehensive source of preva- lence estimates for adults in the United States diagnosed with mental disorders is the National Comorbidity Survey Replication (NCS-R). It sampled the entire adult American population using a number of sophisticated methodologi- cal strategies (Kessler et al., 2004; Kessler, Berglund, Borges, et al., 2005; Kessler & Merikangas, 2004). Table 1.1 shows 1-year and lifetime prevalence estimates of the DSM-IV mental disorders assessed from the NCS-R study.
Table 1.1 Prevalence of Mental Disorders in Adults in the United States
1-Year (%) Lifetime (%)
Any anxiety disorder 18.1 28.8
Any mood disorder 9.5 20.8
Any substance-abuse disorder 3.8 14.6
Any disorder 26.2 46.4
SOURCES: Based on Kessler, R. C., Berglund, P., Borges, G., Nock, M., & Wang, P. S. (2005a). Trends in suicide ideation, plans, gestures, and attempts in the United States. JAMA, 293(20), 2487–95.; Kessler, R. C., Chiu, W. T., Demler, O., & Walters, E. E. (2005c). Prevalence, severity, and comorbidity of 12-month DSM-IV disorders in the National Comorbidity Survey Replication. Arch. Gen. Psychiatry, 62, 617–27.
Table 1.2 Most Common Individual Mental Disorders in the United States
Disorder 1-Year Prevalence (%)
Lifetime Prevalence (%)
Major depressive disorder 6.7 16.6
Alcohol abuse 3.1 13.2
Specific phobia 8.7 12.5
Social phobia 6.8 12.1
Conduct disorder 1.0 9.5
SOURCES: Based on Kessler, R. C., Berglund, P., Borges, G., Nock, M., & Wang, P. S. (2005a). Trends in suicide ideation, plans, gestures, and attempts in the United States. JAMA, 293(20), 2487–95.; Kessler, R. C., Chiu, W. T., Demler, O., & Walters, E. E. (2005c). Prevalence, severity, and comorbidity of 12-month DSM-IV disorders in the National Comorbidity Survey Replication. Arch. Gen. Psychiatry, 62, 617–27.
Although lifetime (and 12-month) rates of mental disor- ders appear to be quite high, it is important to remember that, in some cases, the duration of the disorder may be relatively brief (e.g., depression that lasts for a few weeks after the breakup of a romantic relationship). Furthermore, many peo- ple who meet criteria for a given disorder will not be seriously affected by it. For instance, in the NCS-R study, almost half (48 percent) of the people diagnosed with a specific phobia had disorders that were rated as mild in severity, and only 22 percent of phobias were regarded as severe (Kessler, Chiu, et al., 2005). Meeting diagnostic criteria for a particular disor- der and being seriously impaired by that disorder are not nec- essarily synonymous. In the NCS-R data, 12-month rates of serious mental illness are estimated to be 5.8 percent for adults and 8.0 percent among adolescents (Kessler et al., 2012).
One problem with the NCS-R data is that they are now well over a decade old. Fortunately, another survey, called the National Survey on Drug Use and Health (NSDUH), is conducted every year. Although this survey does not include information about specific disorders, it can be used to provide the most recent information. As you can see from Figure 1.1, the most up-to-date estimates show that
14 Chapter 1
the 1-year prevalence of serious mental illness (excluding substance use disorders) in adults in the United States is 4.1 percent overall. This is not too far from the 5.8 percent rate reported in the NCS-R (which did include substance use disorders). You can also see from the figure that rates of serious mental illness are higher in some groups than in others.
A final finding from the NCS-R study concerns the widespread occurrence of comorbidity among diagnosed disorders (Kessler, Chiu, et al., 2005). Comorbidity is the term used to describe the presence of two or more disor- ders in the same person. Comorbidity is especially high in people who have severe forms of mental disorders. In the NCS-R study, half of the individuals with a disorder rated as serious on a scale of severity (mild, moderate, and seri- ous) had two or more additional disorders. An illustra- tion of this would be a person who drinks excessively and who is simultaneously depressed and suffering from an anxiety disorder. In contrast, only 7 percent of the people who had a mild form of a disorder also had two or more other diagnosable conditions. What this indicates is that comorbidity is much more likely to occur in people who have the most serious forms of mental disorders. When the condition is mild, comorbidity is the exception rather than the rule.
Disorders do not always occur in isolation. A person who abuses alcohol may also be depressed or pathologically anxious. This is an example of comorbidity.
Pe rc
en t
Prevalence of Serious Mental Illness Among U.S. Adults (2012) 9
8
7
6
4.1 4.1 4.4 4.2 4.2
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*NH/OPI = Native Hawaiian/Other Pacific Islander **AI/AN = American Indian/Alaska Native
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8.5
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Figure 1.1 Prevalence of Serious Mental Illness Among U.S. Adults (2012) Rates of severe mental illness are higher in women, people ages 26 to 49, and some minority groups.
(Data courtesy of SAMHSA)
Abnormal Psychology: Overview and Research Approaches 15
Treatment Although they may not be available to everyone, many treatments for psychological disorders exist. These include medications as well as different forms of psychotherapy. Each chapter of this book that covers specific disorders also includes a section describing how those disorders are treated. In addition, in Chapter 16 we discuss different approaches to treatment more broadly and describe differ- ent types of therapy in detail. However, it is important to emphasize that not all people with psychological disorders receive treatment. In some cases, people deny or minimize their suffering. Others try to cope on their own and may manage to recover without ever seeking aid from a mental health professional. As we noted earlier, stigma is a factor that makes some people especially reluctant to seek help (Clement et al., 2015). Even when they recognize that they have a problem, it is typical for individuals to wait a long time before deciding to seek help. Half of individuals with depression delay seeking treatment for more than 6 to 8 years. For anxiety disorders, the delay ranges from 9 to 23 years (Wang, Berglund, et al., 2005)!
When people with mental disorders do seek help, they are often treated by their family physician rather than by a mental health specialist (Wang, Berglund, et al., 2005). It is also the case that the vast majority of mental health treatment
The Global Burden of Disease Mental and substance use disorders are often disabling conditions. Worldwide, they account for over 7 percent of the global burden of disease. This is more than the burden of disease caused by HIV/AIDS, tuberculosis, diabetes, or transportation injuries. Because they are so common, anxi- ety disorders, depressive disorders, and substance use dis- orders together account for 184 million disability adjusted years of life (DALYs), where one DALY can be thought of as the loss of 1 year of otherwise “healthy” life. The disor- der that results in the biggest global burden is depression, which accounts for more than 40 percent of the DALYs (see Figure 1.2). In terms of lost economic output caused by people with mental disorders being temporarily or perma- nently unable to work, estimates are that, worldwide, men- tal disorders will cost 16 trillion U.S. dollars (about 25 percent of global GDP in 2010) during the next 20 years. This is a staggering figure. It also does not include the costs of treatment or the personal (emotional) costs that living with a mental disorder can cause for the person and his or her family (Whiteford et al., 2013). All of this points to the need to find better ways to provide mental health services, especially in developing countries. In war-torn or resource- constrained environments, however, this presents numer- ous challenges.
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Other mental disorders Drug use disorders Alcohol use disorders Idiopathic intellectual disability Pervasive developmental disorders Childhood behavioral disorders Eating disorders Bipolar disorder Schizophrenia Anxiety disorders Depressive disorders
Figure 1.2 The Burden of Mental Illness for Different Disorders Across the Lifespan Disability adjusted life years (DALYs) for various mental and substance use disorders are shown according to age. DALYs represent the total (worldwide) number of otherwise healthy years of life that are lost or profoundly impacted because of the disorder. Depression causes the greatest total disability. This is because depression is a relatively common disorder.
(Adapted from Whiteford et al., 2013. Global burden of disease attributable to mental and substance use disorders: findings from the Global Burden of Disease Study 2010. Lancet, 382, 1580.)
16 Chapter 1
with the patient several times a week. A clinical social worker may help the patient resolve family problems, and a psychiatric nurse may check in with the patient on a daily basis to provide support and help the patient cope better in the hospital environment. The intensity of treatment that is typical in a hospital setting is designed to help the patient get better as rapidly as possible.
Patients treated in outpatient settings may also work with a team of professionals. However, the number of men- tal health specialists involved is typically much smaller. In some cases a patient will receive all treatment from a psy- chiatrist, who will prescribe medication and also provide psychotherapy. Other patients will receive medications from a psychiatrist and see a psychologist or a clinical social worker for regular therapy sessions. In other cases, depend- ing on the type and severity of the problem, a patient (client is the preferred term in some settings) may see a counseling psychologist, a psychoanalyst, or a counselor who special- izes in the treatment of drug and alcohol problems.
in review • What is epidemiology?
• What is the difference between prevalence and incidence?
• What are the most common mental disorders?
• How is illness severity associated with comorbidity?
Research Approaches in Abnormal Psychology 1.5 Discuss why abnormal psychology research can be
conducted in almost any setting.
As is apparent from the NCS-R study, the lives of large numbers of people are affected by mental disorders. To learn all that we can about these conditions, we need to conduct research. In this way, we can study the characteris- tics or nature of disorders. Through research we can learn about the symptoms of a disorder, its prevalence, whether it tends to be either acute (short in duration) or chronic (long in duration), and the problems and deficits that often accompany it.
Research allows us to further understand the etiology (or causes) of disorders. Finally, we need research to pro- vide the best care for the patients who are seeking assis- tance with their difficulties. All of the authors of this book are trained clinicians. As such, we turn to the research lit- erature to help us provide the most effective and up-to- date care for the patients whom we see.
Students new to the field of abnormal psychology often assume that all answers may be revealed through scrutinizing past case studies. However, when we study individual cases and derive inferences from them, we are
is now administered on an outpatient (as opposed to an inpatient) basis (O’Donnell et al., 2000). Outpatient treat- ment requires that a patient visit a mental health facility practitioner; however, the patient does not have to be admitted to the hospital or stay there overnight. A patient may attend a community mental health center, see a pri- vate therapist, or receive treatment through the outpatient department of a hospital.
Hospitalization and inpatient care are the preferred options for people who need more intensive treatment than can be provided on an outpatient basis. Various sur- veys indicate that admission to mental hospitals has decreased substantially during the past 45 years. The development of medications that control the symptoms of the most severe disorders is one reason for this change. Budget cuts have also forced many large state or county facilities to close. The limitations that insurance companies place on hospital admissions also contribute. If a hospital stay is not authorized by the insurance company, patients must seek treatment elsewhere.
Patients needing inpatient care are usually admitted to the psychiatric units of general hospitals, or to private psy- chiatric hospitals specializing in particular mental disor- ders. Stays in inpatient facilities tend to be much shorter than they were in the past (see Case et al., 2007; Lay et al., 2007). Patients receive additional treatment on an outpa- tient basis.
This trend away from the use of traditional hospitali- zation began several decades ago. Over time, there has been an enormous decrease in inpatient beds. For example, in 1955 there were 339 beds available in state mental hospi- tals per 100,000 people in the population. By the year 2000, that figure had dropped to just 22 (Lamb & Weinberger, 2005). One unfortunate consequence of this is that the number of prison inmates being treated for severe mental illness has increased dramatically. When people with severe mental illness (who may have no financial resources and no health insurance) are unable to find adequate treat- ment in the community, this increases the likelihood that they will end up coming to the attention of law enforce- ment personnel. In short, the movement away from long- stay inpatient hospitalization (which is referred to as deinstitutionalization) has had many unintended conse- quences, especially for the most disadvantaged members of our society. Deinstitutionalization is discussed further in Chapter 2.
Mental Health Professionals When patients receive inpatient treatment, several differ- ent mental health professionals often work as a team to provide the necessary care. A psychiatrist may prescribe medications and monitor the patient for side effects. A clin- ical psychologist may provide individual therapy, meeting
Abnormal Psychology: Overview and Research Approaches 17
methodology in turn evolves. In the sections that follow, we introduce some fundamental research concepts so that you may begin to think critically like a clinical scientist. For further help, in some chapters we use a Research Close-Up to draw your attention to some key terms that are central to the comprehension of psychological research.
Sources of Information 1.6 Describe three different approaches used to gather
information about mental disorders.
As humans, we often direct our attention to the people around us. If you were asked to describe your best friend, your father, or even the professor teaching your abnormal psychology class, you would undoubtedly have plenty to say. As is the case in virtually all other sciences, the founda- tion of psychological knowledge stems from observation. Indeed, a large amount of early knowledge was distilled from case studies in which specific individuals were described in great detail.
Case Studies Astute clinicians such as the German psychiatrist Emil Kraepelin (1856–1926) and the Swiss psychiatrist Eugen Bleuler (1857–1939) provided us with detailed accounts of patients whom a modern-day reader would easily recog- nize as having disorders such as schizophrenia and manic depression. Alois Alzheimer (1864–1915) depicted a patient with an unusual clinical picture that subsequently became known as Alzheimer’s disease. Sigmund Freud (1856– 1939), the founder of psychoanalysis, published multiple clinical cases describing what we now recognize as phobia (the case of “Little Hans”) and obsessive-compulsive disor- der (“the Rat Man”). Such portrayals make for fascinating reading, even today.
Much can be learned when skilled clinicians use the case study method. Still, the information presented in them is subject to bias because the writer of the case study selects what information to include and what information to omit. Another concern is that the material in a case study is often relevant only to the individual being described. This means that the conclusions of a case study have low generalizability—that is, they cannot be used to draw con- clusions about other cases even when those cases involve people with a seemingly similar abnormality. When there is only one observer and one subject, and when the obser- vations are made in a relatively uncontrolled context and are anecdotal and impressionistic in nature, the conclu- sions we can draw are very narrow and may be mistaken. Nonetheless, case studies are an excellent way to illustrate clinical material. They can also provide some limited support for a particular theory or provide some negative
as likely to develop errors in our thinking as we are to obtain knowledge. One such error is that we often attend only to data that confirm our view of how things are. For example, Dr. Smart might believe that drinking milk causes schizophrenia. When we ask Dr. Smart why he holds this view, he might say it is because every patient he has ever treated who has schizophrenia has drunk milk at some time in his or her life. Given that Dr. Smart has treated a lot of patients with schizophrenia and clearly has a great deal of experience with the disorder, we might be persuaded that he is right. Then along comes Dr. Notsofast. Dr. Notsofast decides to conduct a research study. He studies two groups of people: One group has schizophrenia; the other group does not have schizophrenia. Dr. Notsofast asks all of them about their milk-drinking habits. He finds that everyone has drunk milk at some point in his or her life and that there are no differences between the two groups with respect to their milk-drinking histories. As this simple example illustrates, research prevents us from being mis- led by natural errors in thinking. In short, research protects investigators from their own biases in perception and inference (Raulin & Lilienfeld, 2015).
Abnormal psychology research can be conducted in a variety of settings outside the research laboratory, including clinics, hospitals, schools, or prisons.
Abnormal psychology research can take place in clin- ics, hospitals, schools, prisons, and even highly unstruc- tured contexts such as naturalistic observations of the homeless on the street. It is not the setting that determines whether a given research project may be undertaken. As Kazdin aptly points out (1998), “methodology is not merely a compilation of practices and procedures. Rather it is an approach toward problem solving, thinking, and acquiring knowledge.” As such, research methodology (that is, the scientific processes and procedures we use to conduct research) is constantly evolving.
As new techniques become available (brain-imaging techniques and new statistical procedures, to name a few),
18 Chapter 1
the lab for analysis. This, too, is a form of observational data; it tells us something that we want to know using a variable that is relevant to our interests.
Technology has advanced, and we are now developing methods to study behaviors, moods, and cognitions that have long been considered inaccessible. For example, brain-imaging techniques such as functional magnetic res- onance imaging (fMRI) are now routinely used to study the working brain. We can study blood flow to various parts of the brain during memory tasks. We can even look at which brain areas influence imagination.
With other techniques such as transcranial magnetic stimulation (TMS; see Figure 1.3), which generates a magnetic field on the surface of the head, we can stimu- late underlying brain tissue (see Eldaief et al., 2013). This can be done painlessly and noninvasively while the person receiving the TMS sits in an armchair. Using TMS, we can even take a particular area of the brain “off-line” for a few seconds and measure the behavioral consequences. In short, we can now collect observa- tional data that would have been impossible to obtain in the past.
evidence that can challenge a prevailing idea or assump- tion. Importantly, case studies can be a valuable source of new ideas and serve as a stimulus for research, and they may provide insight into unusual clinical conditions that are too rare to be studied in a more systematic way.
Self-Report Data If we wish to study behavior in a more rigorous manner, how do we go about doing so? One approach is to collect self-report data from the people we wish to learn more about. This might involve having our research partici- pants complete questionnaires of various types. Another way of collecting self-report data is from interviews. The researcher asks a series of questions and then records what the person says.
Asking people to report on their subjective experi- ences might appear to be an excellent way to collect information. However, as a research approach it has some limitations. Self-report data can sometimes be mis- leading. One problem is that people may not be very good reporters of their own subjective states or experi- ences. For example, when asked in an interview, one child may report that he has 20 “best friends.” Yet, when we observe him, he may always be playing alone. Because people will occasionally lie, misinterpret the question, or desire to present themselves in a particularly favorable (or unfavorable) light, self-report data cannot always be regarded as highly accurate and truthful. This is something that anyone who has ever tried online dat- ing knows only too well! And if you still need convinc- ing, ask three people to tell you their weight. Then ask them to step on a scale. How likely is it that the weight they self-report will be the weight that appears when they step on the scale? What reasons do you think might explain the discrepancy?
Observational Approaches When we collect information in a way that does not involve asking people directly (self-report), we are using some form of observational approach. Exactly how we go about this depends on what it is we seek to under- stand. For example, if we are studying aggressive chil- dren, we may wish to have trained observers record the number of times children who are classified as being aggressive hit, bite, push, punch, or kick their playmates. This would involve direct observation of the children’s behavior.
We may also collect information about biological vari- ables (such as heart rate) in our sample of aggressive chil- dren. Alternatively, we could collect information about stress hormones, such as cortisol, by asking the observed children to spit into a plastic container (because cortisol is found in saliva). We would then send the saliva samples to
Wire coil
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Figure 1.3 Researchers use technology, such as transcranial magnetic stimulation (TMS), to study how the brain works. TMS generates a magnetic field on the surface of the head through which underlying brain tissue is stimulated. Researchers can evaluate and measure behavioral consequences of this noninvasive and painless brain stimulation.
Abnormal Psychology: Overview and Research Approaches 19
have had cosmetic breast augmentation (Sarwer et al., 2007). Consider for a moment why this association might exist. Possible explanations might include higher rates of psychopathology in women who seek breast augmenta- tion, unrealistic expectations about the positive effects that the surgery would have on their lives, postoperative com- plications that could lead to depressed mood, and other factors such as preoperative body image dissatisfaction.
In practice, much clinical research involves a mix of self-report and observational methods. Also, keep in mind that when we refer to observing behavior we mean much more than simply watching people. Observing behavior, in this context, refers to careful scrutiny of the conduct and manner of specific individuals (e.g., healthy people, people with depression, people with anxiety, people with schizo- phrenia). We may study social behavior in a sample of patients with depression by enlisting trained observers to record the frequency with which the patients smile or make eye contact. We may also ask the patients themselves to fill out self-report questionnaires that assess social skills. If we think that sociability in patients with depression may be related to (or correlated with) their severity of depression, we may further ask patients to complete self-report meas- ures designed to assess that severity. We may even measure levels of certain substances in patients’ blood, urine, or cere- brospinal fluid (the clear fluid that bathes the brain and that can be obtained by performing a lumbar puncture). Finally, we could possibly study the brains of patients with depression directly via brain-imaging approaches. These diverse sources of information would provide us with potentially valuable data, the basis of scientific inquiry.
in review • What are the strengths and limitations of case studies?
• Why is it desirable not to rely solely on self-report data as a source of information?
• What is the difference between self-report and observational data?
• What range of measures could be considered to reflect obser- vational data?
Forming and Testing Hypotheses 1.7 Explain why a control (or comparison group) is
necessary to adequately test a hypothesis.
Research is all about asking questions. To make sense of behavior, researchers generate hypotheses. A hypothesis is an effort to explain, predict, or explore something. What distinguishes scientific hypotheses from the vague specu- lation that we all routinely engage in is that scientists attempt to test their hypotheses. In other words, they try to design research studies that will help them approach a fuller understanding of how and why things happen.
Anecdotal accounts such as case studies can be very valuable in helping us develop hypotheses, although case studies are not well suited for testing the hypotheses that they may have inspired. Other sources of hypotheses are unusual or unexpected research findings. One example is the higher-than-expected rate of suicide in women who
Although men generally have lower rates of depression than women, the rate of depression for Jewish men and women is equal. Why would this be? A correlation between higher rates of depression and lower rates of alcohol abuse in Jewish men provides interesting ground for further study.
Another observation in search of an explanation is the finding that, although men generally have lower rates of depression than women, this is not true of Jewish men. Why should Jewish men be more at risk for depression than non-Jewish men? One hypothesis is that there may be an interesting (and inverse) relationship between depres- sion and alcohol use (Levav et al., 1997). Jewish men have lower rates of alcohol abuse and alcohol dependence than do non-Jewish men. Consistent with this idea, a study of members of Orthodox synagogues in London found no alcoholism and similar rates of depression in females and males (i.e., a 1:1 gender ratio instead of the typical 2:1 ratio; Loewenthal et al., 1995). Although much more remains to be uncovered, the hypothesis that higher rates of depres- sion in Jewish men may be related to their lower rates of
20 Chapter 1
are drawn from this underlying population. To do this, we would use a technique called sampling. What this means is that we would try to select people who are representa- tive of the much larger group of individuals with panic dis- order (in the same way that jury selection involves having a representative sample of eligible voters).
Ideally, we would like our smaller sample (our study group) to mirror the larger group (the underlying popula- tion) in all important ways (e.g., in severity and duration of disorder and in demographics such as age, gender, and mar- ital status). If we could do everything perfectly, our research sample would be randomly selected from the larger popula- tion of people with panic disorder, which is tantamount to ensuring that every person in that population would have an equal chance of being included in our study. Such a pro- cedure would automatically adjust for potential biases in sample selection. In practice, however, this does not happen, and researchers must simply do the best they can given real- world constraints (including the fact that some people don’t wish to participate in a research study!).
Because finding research participants is not always easy, researchers sometimes use “samples of convenience” in their studies. This means that they study groups of peo- ple who are easily accessible to them and who are readily available. Have you noticed how much research is con- ducted using college students? Is this because college stu- dents are intrinsically fascinating people to study? Or are other factors in play here?
alcohol abuse appears to merit further study (see Loewenthal et al., 2003).
Hypotheses are vital because they frequently deter- mine the therapeutic approaches used to treat a particular clinical problem. The ideas we have about what might be causing a client’s difficulties will naturally shape the form of intervention we use when we provide treatment. For instance, suppose we are confronted with someone who washes his or her hands 60 to 100 times a day, causing seri- ous injury to the skin and underlying tissues (this is an example of obsessive-compulsive disorder). If we believe that this behavior is a result of subtle problems in certain neural circuits, we may try to identify which circuits are dysfunctional in the hope of ultimately finding a means of correcting them (perhaps with medication).
On the other hand, if we view the excessive hand washing as reflecting a symbolic cleansing of sinful and unacceptable thoughts, we may try to unearth and address the sources of the person’s excessive guilt and concern with morality. Finally, if we regard the hand washing as merely the product of unfortunate conditioning or learn- ing, we may devise a means to extinguish the problematic behavior. In other words, our working hypotheses regard- ing the causes of different disorders very much shape the approaches we use when we study and treat the disorders.
Sampling and Generalization We can occasionally glean instructive leads from careful scrutiny of a single case. However, this strategy rarely yields enough information to allow us to reach firm con- clusions. Research in abnormal psychology is concerned with gaining enhanced understanding and, where possi- ble, control of abnormal behavior (i.e., the ability to alter it in predictable ways). Edward, for instance, may accost women in supermarkets and try to lick their feet because his mother always gave him attention when, as a child, he tried on her shoes. In contrast, George may engage in the same behavior for an entirely different reason. We need to study a larger group of individuals with the same problem in order to discover which of our observations or hypothe- ses possess scientific credibility. The more people we study, the more confident we can be about our findings.
Whom should we include in our research study? In general, we want to study groups of individuals who have similar abnormalities of behavior. If we wanted to study people with panic disorder, a first step would be to deter- mine criteria such as those provided in the current DSM for identifying people affected with this clinical disorder. We would then need to find people who fit our criteria. Ideally, we would study everyone in the world who met our criteria because these people constitute our population of interest. This, of course, is impossible to do, so instead we would try to get a representative sample of people who
Why is so much research conducted using college students? What are the advantages and disadvantages of this?
An even more convenient strategy is to recruit partici- pants online using approaches such as Amazon’s Mechanical Turk. MTurk is an online labor market that connects “requesters” with “workers” who then complete surveys or other research-related tasks in return for a small pay- ment (Shapiro et al., 2013). Although this makes life easier for researchers, there is (as usual) no free lunch. As you might expect, MTurk workers are not a representative sam- ple of the population as a whole. Is your grandmother an
Abnormal Psychology: Overview and Research Approaches 21
group of people who do not exhibit the disorder being stud- ied but who are comparable in all other major respects to the criterion group (i.e., people with the disorder being studied). By “comparable” we might mean that the two groups are similar in age, number of males and females, educational level, and similar demographic variables. Typically, the com- parison group is psychologically healthy, or “normal,” according to certain specified criteria. We can then compare the two groups on the variables of interest.
To further illustrate the idea of criterion and control groups, let us return to our example about schizophrenia and milk. Dr. Smart’s hypothesis was that drinking milk causes schizophrenia. However, when a group of patients with schizophrenia (the criterion group or the group of interest) was compared with a group of patients who did not have schizophrenia (the control group), it was clear that there were no differences in milk drinking between the two groups.
Using the controlled research approaches we have just described, researchers have learned much about many dif- ferent psychological disorders. We can also use extensions of this approach not only to compare one cohort of patients with healthy controls but also to compare groups of patients with different disorders.
For example, Cutting and Murphy (1990) studied how well (1) patients with schizophrenia, (2) patients with depression or mania, and (3) healthy controls performed on a questionnaire testing social knowledge. This involved a series of multiple-choice questions that presented a social problem (e.g., “How would you tell a friend politely that he had stayed too long?”). Possible answer choices included responses such as “There’s no more coffee left” and “You’d better go. I’m fed up with you staying too long.” (In case you are wondering, both of these are incor- rect choices; the preferred answer for this example was, “Excuse me. I’ve got an appointment with a friend.”)
Consistent with the literature showing that social def- icits are associated with schizophrenia, the patients with schizophrenia did worse on this test relative to both the healthy controls and the patients with depression or mania. The finding that the patients with schizophrenia did more poorly than the patients with depression or mania allowed the researchers to rule out the possibility that simply being a psychiatric patient is linked to poor social knowledge.
in review • Explain what the term representative sample means.
• What is a sample of convenience?
• What is the difference between internal and external validity? How can external validity be maximized?
• Why are comparison or control groups so important?
MTurk worker? Almost certainly not. Workers tend to be younger, overeducated, underemployed, less religious, and more liberal than people in the general population. In the United States, blacks and Hispanics are underrepre- sented and Asians are overrepresented in the MTurk worker pool relative to their presence in the population as a whole (Paolacci & Chandler, 2014).
Internal and External Validity From a research perspective, the more representative our sample is, the better able we are to generalize (or extend the findings from our study) to the larger group. The extent to which we can generalize our findings beyond the study itself is called external validity. A research study that involves both males and females from all age groups, income levels, and educational levels is more representa- tive of the underlying population (and will have greater external validity) than research using only female college students, for example. And when we study a group of peo- ple who all share a defining characteristic (e.g., a specific disorder), we may then be able to infer that additional commonalities that they share (such as a family history of depression or low levels of certain neurotransmitters) may be related to the disorder itself. Of course, this is based on the assumption that the characteristic in question is not widely shared by people who do not have the disorder.
Unlike external validity, which concerns the degree to which research findings from a specific study can be gener- alized to other samples, contexts, or times, internal validity reflects how confident we can be in the results of a particu- lar given study. In other words, internal validity is the extent to which a study is methodologically sound, free of confounds, or other sources of error, and able to be used to draw valid conclusions. For example, suppose that a researcher is interested in how heart rate changes when participants are told that they are about to be given an elec- tric shock. Imagine also how much faith you might have in the results of the research if participants who have just completed the study are allowed to chat in the waiting area with people who are just about to participate. What if the latter learn that, in reality, no shocks are given at all? How might this information change how subjects respond? Fail- ure to control the exchange of information in this way clearly jeopardizes the integrity of the study and is a threat to its internal validity. Some subjects (those who have not been given prior information) will expect to receive real shocks; others will not because, unbeknownst to the exper- imenter, information has been leaked to them beforehand.
Criterion and Comparison Groups To test their hypotheses, researchers use a comparison group (sometimes called a control group). This may be defined as a
22 Chapter 1
people (people with specific disorders, people who have had traumatic experiences, people who win lotteries, etc.) whom we can then study. Using these types of research designs, we are able to identify factors that appear to be associated with depression, alcoholism, binge eating, or alternate psychological states of distress (for a more com- prehensive description of this kind of research approach, see Kazdin, 1998).
Measuring Correlation Correlational research takes things as they are and deter- mines associations among observed phenomena. Do mea- sures vary together in a direct, corresponding manner (known as a positive correlation—see Figure 1.5) such as in the example we mentioned earlier showing that breast augmentation surgery was correlated with increased risk of suicide? Or conversely, is there an inverse correlation, or negative correlation, between the variables of interest (such as high socioeconomic status and decreased risk of psychopathology)? Or finally, are the variables in question entirely independent of one another, or uncorrelated, such that a given state or level of one variable fails to predict reliably the degree of the other variable, as was the case with our example about milk and schizophrenia?
The strength of a correlation is measured by a correlation coefficient, which is denoted by the symbol r. A correlation runs from 0 to 1, with a number closer to 1 representing a stronger association between the two variables. The + sign or – sign indicates the direction of the association between the variables. For example, a positive correlation means that higher scores on one variable are associated with
Correlational Research Designs 1.8 Discuss why correlational research designs are
valuable, even though they cannot be used to make causal inferences.
A major goal of researchers in abnormal psychology is to learn about the causes of different disorders. For ethical and practical reasons, however, we often cannot do this directly. Perhaps we want to learn about factors that result in depression. We may hypothesize that the stress of losing a parent early in life may be important in this regard. Need- less to say, we cannot create such situations and then see what unfolds!
Instead, the researcher uses what is known as a correlational research design. A correlational research design involves studying the world as it is. Unlike a true experimental research design (described later), correla- tional research does not involve any manipulation of vari- ables. Rather, the researcher selects certain groups of interest (e.g., people who have recently been exposed to a great deal of stress, or people who lost a parent when they were growing up). She would then compare the groups on a variety of different measures (including, in this example, levels of depression).
Any time we study differences between individuals who have a particular disorder and those who do not, we are utilizing this type of correlational research design (see Figure 1.4). Essentially, we are capitalizing on the fact that the world works in ways that create natural groupings of
Sample
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Figure 1.4 Correlational Research Designs In correlational research, data are collected from two different samples or groups and are then compared.
(Adapted from Petrie & Sabin, 2000. Medical Statistics at a Glance. Oxford, UK: Blackwell Science Ltd.)
Abnormal Psychology: Overview and Research Approaches 23
of 100. Researchers adopt this conventional level of signifi- cance and consider correlations that have a p < .05 to be statistically significant and worthy of attention. Of course, this does not mean that the result in question could not have occurred by chance; it simply means that it is not very likely.
Statistical significance is influenced not only by the magnitude or size of the correlation between the two vari- ables but also by the sample size. A correlation of .30 will not be significant if the sample size is 20 people but will be significant if the sample size is 50 people. Correlations based on very large samples (e.g., 1,000 people) can be very small and yet still reach statistical significance. Conversely, correlations drawn from small samples need to be very large to reach statistical significance.
higher scores on the other variable, as might be the case for hours spent studying and grade point average. A negative correlation means that, as scores on one variable go up, scores on the other variable tend to go down. An example here might be the association between hours spent partying and grade point average.
Statistical Significance If you read a research article, you are likely to see correla- tions reported in the text. Next to the correlation you will almost certainly see a notation that reads p < .05. This is the level of statistical significance. But what does this mean? Simply put, it means that the probability that the correlation would occur purely by chance is less than 5 out
B C
Strong positive correlation between two variables
(e.g., weight and calorie intake)
Astrological sign
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(e.g., weight and astrological sign)
Weak positive correlation between two variables (e.g., weight and hours of video game playing)
Time spent exercising
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(e.g., weight and exercise)
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Figure 1.5 Scatterplots of data illustrating positive, negative, and no correlation between two variables. Dots indicate a given person’s score on the two variables of interest. A strong positive correlation (r 5 11.0) means that high scores on one variable are associated with high scores on the second variable, creating a forward-sloping straight line. For example, we would expect there to be a positive correlation between weight and the number of calories eaten per day. When there is a strong negative correlation (r 5 21.0), high scores on the first variable are associated with low scores on the second variable, creating a backward-sloping straight line. A relevant example here would be the association between weight and time spent exercising per day. When there is no correlation (r = 0), scores on the independent variable tell us nothing about scores on the dependent variable. An example here might involve weight and astrological sign.
24 Chapter 1
intellectual development, or depression and reported prior stressors. This in no way affirms that one factor is the cause of the other.
Consider, for example, the positive correlation that exists between ice cream consumption and drowning. Does this mean that eating ice cream compromises swim- ming ability and so leads to drowning? Or that people who are about to drown themselves like to have one final ice cream cone before they enter the water? Both of these alter- natives are clearly absurd. Much more likely is that some unknown third variable might be causing both events to happen. This is known as the third variable problem. What might the third variable be in this example? After a moment’s reflection, you might realize that a very plausi- ble third variable is hot summer weather. Ice cream con- sumption increases in the summer months. So, too, does the number of people who drown because more people swim during the summer than at any other time. The cor- relation between ice cream consumption and drowning is a spurious one, caused by the fact that both variables are cor- related with the weather.
To use an example from abnormal psychology, it was once thought that masturbation caused insanity. This hypothesis no doubt arose from the fact that, historically, patients in mental asylums could often be seen masturbat- ing in full view of others. Of course, we now know that masturbation and insanity were correlated not because masturbation caused insanity but because sane people are much more likely to masturbate in private than in public. In other words, the key factor linking the insanity and mas- turbation (and the unmeasured third variable) was that of impaired social awareness.
Even though correlational studies may not be able to pinpoint causal relationships, they can be a powerful and rich source of inference. They often suggest causal hypoth- eses (increased height may cause increased weight; increased weight is unlikely to cause increased height), generate questions for further research, and occasionally provide crucial data that may confirm or refute specific hypotheses. Much of what we know about mental disor- ders is derived from correlational studies. The fact that we cannot manipulate many of the variables we study does not mean that we cannot learn a great deal from such approaches.
Retrospective versus Prospective Strategies Correlational research designs can be used to study differ- ent groups of patients as they are at the time of the study (i.e., concurrently). For example, if we used brain imaging to look at the size of certain brain structures in patients with schizophrenia and in healthy controls, we would be using this type of approach. But if we wanted to learn what
Effect Size The fact that statistical significance is influenced by sample size creates a problem when we want to compare findings across studies. Suppose that Dr. Green reports a significant association between two variables in her study. But, in a second study, Dr. Blue reports no significant correlation between these same two variables. This is not an uncom- mon occurrence in the scientific literature, and it often cre- ates a lot of confusion about whose results are “correct.” But if Dr. Green has a larger sample size than Dr. Blue, the same-size correlation will be significant in Dr. Green’s study but not reach statistical significance in Dr. Blue’s study. To avoid the problems inherent in just focusing on statistical significance, and to facilitate comparison of results across different studies (which invariably have dif- ferent sample sizes), researchers often report a statistic called the effect size. The effect size reflects the size of the association between two variables independent of the sam- ple size. An effect size of zero means there is no association between the variables. Because it is independent of sample size, the effect size can be used as a common metric and is very valuable when we want to compare the strength of findings across different studies. If the effect size is about the same in the studies of both Dr. Green and Dr. Blue, we can conclude that they really had similar findings, regard- less of the fact that the results were significant in one study but not in the other.
Meta-Analysis When researchers want to summarize research findings in a specific area, they often do a literature search and write a review. In drawing their conclusions they will rely on sig- nificance levels, noting whether more studies than not found a significant association between two variables, such as smoking and health. A far better approach, however, is to conduct a meta-analysis. A meta-analysis is a statistical approach that calculates and then combines the effect sizes from all of the studies. Within a meta-analysis, each sepa- rate study can be thought of as being equivalent to an indi- vidual participant in a conventional research design. Because it uses effect sizes, a meta-analysis provides a bet- ter way to summarize research findings than is possible with a literature review.
Correlations and Causality When it comes to correlations, one thing is very important to remember: Correlation does not mean causation. Just because two variables are correlated does not tell us any- thing about why they are correlated. This is true regardless of the size of the correlation. Many research investigations in abnormal psychology reveal that two (or more) things regularly occur together, such as poverty and diminished
Abnormal Psychology: Overview and Research Approaches 25
A prototypical illustration might be a study that follows, from infancy to adulthood, the children of mothers with schizophrenia. By collecting data on the children at regular intervals, researchers can compare those who later develop schizophrenia with those who do not, with the goal of identifying important differentiating factors. In another example of a longitudinal design, researchers have shown that adolescents who report suicidal thoughts at age 15 are much more likely to have psychological problems and to have attempted suicide by age 30 than people who do not have suicidal ideas in their teens (Reinherz et al., 2006).
in review • What is the difference between a positive and a negative correlation? • If two variables are correlated, does this mean that one variable
causes the other? If so, why? If not, why not?
The Experimental Method in Abnormal Psychology 1.9 Explain the key features of an experimental design.
As you have already learned, even when we find strong positive or negative associations between variables, corre- lational research does not allow us to draw any conclu- sions about directionality (i.e., does variable A cause B, or does B cause A?). This is known as the direction of effect problem. To draw conclusions about causality and resolve questions of directionality, an experimental research approach must be used. In such cases, scientists control all factors except one—the factor that could have an effect on a variable or outcome of interest. They then actively manipulate (or influence) that one factor. The factor that is manipulated is referred to as the independent variable. If the outcome of interest, called the dependent variable, is observed to change as the manipulated factor is changed, then that independent variable can be regarded as a cause of the outcome (see Figure 1.6).
In Romania, children who are abandoned by their parents are traditionally raised in orphanages rather than in foster care. To study the cognitive effects of institutional versus other forms of care, researchers randomly assigned 136 children who had been institutionalized as babies to either remain in these institutions or be raised by foster families (see Nelson et al., 2007). These foster parents had been recruited for the study by the researchers. Another sample of children who lived with their birth families was also studied for comparison purposes. All the children received cognitive testing when they were 30, 42, and 54 months old. In this study, the independent variable is the living situation of the child (orphanage or foster care). The dependent variable is intellectual functioning.
our patients were like before they developed a specific dis- order, we might adopt a retrospective research strategy. This involves looking back in time. In other words, we would try to collect information about how the patients behaved early in their lives with the goal of identifying fac- tors that might have been associated with what went wrong later. In some cases, our source material might be limited to a patient’s recollections, the recollections of fam- ily members, material from diaries, or other records. A challenge with this technique is the potential for memories to be both faulty and selective.
Certain difficulties are involved with attempting to reconstruct the pasts of people already experiencing a dis- order. Apart from the fact that a person who currently has a mental disorder may not be the most accurate or objec- tive source of information, such a strategy invites investi- gators to discover what they already presume they will discover concerning background factors theoretically linked to a disorder. It invites biased procedure, uncon- scious or otherwise.
For instance, reports of a link between early sexual abuse and various forms of psychopathology began to emerge in the 1980s. After these reports came out, many therapists proceeded to suggest to their patients with such conditions that perhaps they too had been abused. For certain overzealous therapists, the fact that many patients had no memories of any abuse was taken as evi- dence that the painful memories had simply been “repressed.” In other cases, a patient’s simply having such common problems as difficulty sleeping or being easily startled was taken as evidence of past abuse. Over time, many patients became as convinced as their thera- pists that they must have been abused and that this accounted for their current difficulties. But for many patients, it simply was not the case that they had been abused. This underscores the pitfalls inherent in trying to reinterpret a person’s past (or past behavior) in light of his or her current problems. Adherence to fundamental scientific principles is as crucial in the clinical domain as it is in the research laboratory.
Another approach is to use a prospective research strategy, which involves looking ahead in time. Here the idea is to identify individuals who have a higher-than- average likelihood of becoming psychologically disor- dered and to focus research attention on them before any disorder manifests. We can have much more confidence in our hypotheses about the causes of a disorder if we have been tracking influences and measuring them prior to the development of the illness in question. When our hypoth- eses correctly predict the behavioral problems that a group of individuals will later develop, we are much closer to establishing a causal relationship. A study that follows people over time and that tries to identify factors that pre- date the onset of a disorder employs a longitudinal design.
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method has proved to be indispensable. It is a relatively straightforward process to establish: A proposed treat- ment is given to a designated group of patients and with- held from a similar group of patients. Should the treated group show significantly more improvement than the untreated group, we can have confidence in the treat- ment’s efficacy. We may not, however, know why the treatment works, although investigators are becoming increasingly sophisticated in fine-tuning their experiments to tease out the means by which therapeutic change is induced (e.g., Kazdin & Nock, 2003; Kleim et al., 2013; Ramseyer et al., 2014). The Developments in Research fea- ture provides a nice example of a treatment research study. The findings of this study also show just how powerful placebo effects can be.
In treatment research it is important that the two groups (treated and untreated) be as equivalent as possible except for the presence or absence of the proposed active treatment. To facilitate this, patients are typically randomly assigned to the treatment condition or the no-treatment condition. Random assignment means that every research participant has an equal chance of being placed in the treat- ment or the no-treatment condition. Once a treatment has been established as effective, it can then be provided for members of the original control (untreated) group, leading to improved functioning for all those involved.
Sometimes, however, this “waiting list” control group strategy is deemed inadvisable for ethical or other rea- sons. Withholding a treatment that has been established as beneficial just to evaluate a new form of treatment may deprive control subjects of valuable clinical help for longer than would be considered appropriate. For this reason, stringent safeguards need to be in place regarding the potential costs versus benefits of conducting the particular research project.
In certain cases, an alternative research design may be called for in which two (or more) treatments are compared
Did the children assigned to foster care fare better than the children who remained in institutions? The answer is yes. At both the 42-month and the 54-month assessments, the children in foster families had significantly higher scores on the measure of cognitive functioning than the children who remained institutionalized. We can therefore conclude that there was something about being raised in a foster fam- ily that was responsible for the increased intellectual devel- opment of these children. Sadly, however, the cognitive development of both groups of children was much lower than the intellectual functioning of children who were raised in typical families. The results of this unique study therefore tell us that, although foster care helps abandoned children, these children remain at a disadvantage relative to children who are raised by their biological families. However, based at least partially on the findings from this remarkable study, Romania no longer allows children without severe disabili- ties to be placed in institutional care.
Random assignment
Random assignment
Administer treatment
Baseline assessment
Compare responses between
two groups Administer
control
Assess response
Assess responseSample
Population
Figure 1.6 Experimental Research Designs In experimental research, participants are assessed at baseline and then randomly assigned to different groups (e.g., a treatment and a control condition). After the experiment or treatment is completed, data collected from the two different groups are then compared.
(Adapted from Petrie & Sabin, 2000. Medical Statistics at a Glance. Oxford, UK: Blackwell Science Ltd.)
Studying the Efficacy of Therapy Researchers in abnormal psychology are often interested in learning which treatments work for specific disorders. Used in the context of treatment research, the experimental
Abnormal Psychology: Overview and Research Approaches 27
in differing yet comparable groups. This method is termed a standard treatment comparison study. Typically, the efficacy of the control condition has been previously established; thus, patients who are assigned to this condi- tion are not disadvantaged. Instead, the question is whether patients who receive the new treatment improve to a greater extent than those receiving the control (estab- lished) treatment. Such comparative-outcome research has much to recommend it and is being increasingly employed (Kendall et al., 2004).
Single-Case Experimental Designs Does experimental research always involve testing hypoth- eses by manipulating variables across groups? The simple
Developments in Research Do Magnets Help with Repetitive-Stress Injury?
Magnets are often marketed to people who have chronic hand or wrist pain. This type of problem is known as repetitive-stress injury (RSI) and can be caused by extensive computer use. But do magnets really relieve the chronic pain that is associated with RSI? Testimonials notwithstanding, the only way to answer this question is by controlled research.
Pope and McNally (2002) randomly assigned college stu- dents with RSI to one of three groups. One group was asked to wear wristbands containing magnets for a 30-minute period (magnet group). A second group was also given seemingly identi- cal bracelets to wear. In this case, however, and unknown both to the participants and to the assistant running the study, the mag- nets had been removed from the wristbands (sham group). A third group of subjects did not receive any magnets (no-treatment group).
You should note here that this study is an example of what we call a double-blind study. In other words, neither the subjects nor the experimenter who was working with the subjects knew who got the genuine magnets. The use of the wristbands with the magnets removed is called a placebo treatment condition (the word pla- cebo comes from the Latin meaning “I shall please”). Placebo treat- ment conditions enable experimenters to control for the possibility that simply believing one is getting an effective type of treatment produces a therapeutic benefit. Finally, the no-treatment control group enables the experimenters to see what happens when they do not provide any treatment (or expectation of treatment) at all.
At the start of the study, all of the student participants com- pleted a 4-minute typing test. This provided a measure of how many words they could type in this time period. Then, 30 min- utes after wearing the magnets or fake wristbands (or, for the no-treatment subjects, after waiting 30 minutes), all participants completed another 4-minute typing test. In addition, those who had been assigned to either the genuine or the placebo magnet
group were asked to rate their degree of pain relief (from no improvement to complete relief) using an 8-point scale.
What were the results? As might be expected, those peo- ple who had been assigned to the no-treatment group did not report that their level of pain changed in any appreciable way. This is hardly surprising because nothing had been done to them at all. They typed an average of about four more words on the second test (the posttest) than on the first (the pretest).
Did the people who wore the magnets do better than this? The answer is yes. Those who wore the genuine magnets reported that their pain was diminished. They also typed an aver- age of 19 more words on the second typing test than they had on the first! In other words, with respect to both their self-report data (their pain improvement ratings) and their behavioral data (how rapidly they could type), they clearly did better than the no- treatment group.
Before you rush out to buy magnetic bracelets, however, let us look at the performance of the people who received the fake bracelets. Like the subjects who wore the genuine mag- nets, these participants also reported that their pain had improved. And, in fact, on the behavioral typing test, subjects in the placebo treatment group typed even more words on the second test (an average of 26 more words) than subjects who wore the real magnets did. With respect to their self-reports and their behavioral data, therefore, the group who wore the fake bracelets improved just as much as the group who wore the real magnets! On the basis of this study, then, we must conclude that magnet therapy works via the placebo effect, not because there is any genuine clinical benefit that comes from the magnets themselves. If you believe that the magnet will help your RSI, you do not actually need a magnet to bring about any clinical improvement. And this, in a nutshell, is why we need controlled research trials.
answer is no. We have already noted the importance of case studies as a source of ideas and hypotheses. In addi- tion, case studies can be used to develop and test therapy techniques within a scientific framework. Such approaches are called single-case research designs (Hayes, 1998; Kazdin, 1998). A central feature of such designs is that the same individual is studied over time. Behavior or perfor- mance at one point in time can then be compared to behav- ior or performance at a later time, after a specific intervention or treatment has been introduced. For exam- ple, using a single-case design, Wallenstein and Nock (2007) were able to show that exercise helped a 26-year-old female patient to significantly decrease the frequency of her nonsuicidal self-injuring behaviors, which included self-hitting and head-banging.
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trichotillomania (pronounced tri-ko-til-lo-mania). Kris’s hair pulling was so severe that she had a bald area on her scalp that was approximately 2.5 inches in diameter.
The researchers used an ABAB experimental design (see Figure 1.7) to test a treatment for reducing Kris’s hair pulling. In each phase, they used a video camera to observe Kris while she was alone in her room watching television. During the baseline phase (Phase A), observers measured the percentage of time that Kris spent either touching or manipulating her hair (42.5 per- cent of the time) as well as pulling hair (7.6 percent of the time).
In the treatment phase (Phase B), a 2.5-lb weight was put around Kris’s wrist when she settled down to watch television. When she was wearing the wrist weight, Kris’s hair manipulation and hair pulling were reduced to zero. This, of course, suggested that Kris’s behavior had changed because she was wearing a weight on her wrist. To verify this, the wrist weight was withdrawn in the second A phase (i.e., ABA). Kris immediately started to touch and manipulate her hair again (55.9 percent). She also showed an increase in hair pulling (4 percent of the time).
When the wrist weight was reintroduced in the second B phase (ABAB), Kris’s hair manipulation and pulling once again decreased, at least for a while. Although additional treatments were necessary (see Rapp et al., 2000), Kris’s hair pulling was eventually eliminated entirely. Most important for our discussion, the ABAB design allowed the researchers to systematically explore, using experimental tech- niques and methods, the treatment approaches that might be ben- eficial for patients with trichotillomania.
One of the most basic experimental designs in single- case research is called the ABAB design. The different let- ters refer to different phases of the intervention. The first A phase serves as a baseline condition. Here we simply collect data on or from the participant. Then, in the first B phase, we introduce our treatment. Perhaps the person’s behavior changes in some way. Even if there is a change, however, we are not justified in concluding that it was due to the introduction of our treatment. Other factors might have coincided with its introduction, so any asso- ciation between the treatment and the behavior change might be spurious. To establish whether it really was the treatment that was important, we therefore withdraw the treatment and see what happens. This is the reasoning behind the second A phase (i.e., at the ABA point). Finally, to demonstrate that the behavior observed during the B phase is attainable once again, we reinstate our treatment and see if the behavioral changes we saw in the first B phase become apparent again. To further clarify the logic behind the ABAB design, let’s consider the case of Kris (see Rapp et al., 2000).
Kris
Kris was a 19-year-old female with severe intellectual impairments. Since the age of 3 she had pulled her hair out. This disorder is called
Base- line
2.5-lb weights
2.5-lb weights
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en ta
ge o
f ti
m e
m an
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at in
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Hair manipulation 80
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Figure 1.7 An ABAB Experimental Design: Kris’s Treatment In the A phase, baseline data are collected. In the B phase, a treatment is introduced. This treat- ment is then withdrawn (second A phase) and then reinstated (second B phase). In this example, hair manipulation declines with use of wrist weights, returns to pretreatment (baseline) levels when they are withdrawn, and declines again when they are reintroduced.
(Data adapted from Rapp et al., 2000. Treatment of hair pulling and hair manipulation maintained by digital-tactile stimulation. Behavior Therapy, 31, pp. 381–93.)
Abnormal Psychology: Overview and Research Approaches 29
This observation led Seligman and his colleagues to argue that human depression (which he believed was analogous to the reaction of the helpless dogs) is a reaction to uncon- trollable stressful events in which one’s behavior has no effect on one’s environment, leading to helplessness,
Animal Research An additional way in which we can use the experimental method is by conducting research with animals. Although ethical considerations are still critical in animal research, we are able to perform studies using animal subjects that would not be possible to implement with humans (such as subjecting them to controlled environmental conditions or having them be raised by a different mother).
Of course, one major assumption is that the findings from animal studies can be generalized to humans. Experi- ments of this kind are generally known as analogue studies, in which we study not the true item of interest but an approximation to it. Analogue studies may also involve humans (e.g., when we try to study depression by study- ing healthy research participants whom we have made mildly and transiently sad).
One current model of depression, called “hopelessness depression,” has its origins in early research conducted with animals (Seligman, 1975). Laboratory experiments with dogs had demonstrated that, when subjected to repeated experiences of painful, unpredictable, and ines- capable electric shock, the dogs lost their ability to learn a simple escape response to avoid further shock in a differ- ent situation later on. They just sat and endured the pain.
Animal research allows behavioral scientists to manipulate and study behavior under controlled conditions that would not be possible to replicate using humans as subjects. However, results of this research may not hold up when extended to humans outside the laboratory in a real-world setting.
Unresolved Issues Are We All Becoming Mentally Ill? The Expanding Horizons of Mental Disorder
The concept of mental disorder, as we have seen, suffers from the lack of a truly objective means of determining what is disor- dered and what is not. Moreover, inclusion of a disorder in the DSM is a prerequisite for health insurers’ reimbursement of ser- vices rendered. It is therefore in the financial interests of mental health professionals to be more and more inclusive concerning the kinds of problems that might be regarded as “mentally disor- dered.” Not surprisingly, there is often pressure to include in the DSM more and more kinds of socially undesirable behavior.
The DSM has been growing in size for many years as new disorders are added. But it is in the interests of the public at large to keep a close eye on proposed expansions of what is consid- ered “mentally disordered.” Failure to do so could eventually lead to a situation in which much of human behavior—save for the most bland, conformist, and conventional of conduct—would be declared a manifestation of a mental disorder. For example, when DSM-5 was being developed, some groups lobbied for “apathy syndrome” and “parental alienation syndrome” to be considered as new disorders. But is being unmotivated or having a troubled relationship with your parents really a disorder? In the end, these proposals were rejected.
Accepted into DSM-5, however, were several newly proposed disorders that might still cause some to raise an eyebrow. These include “caffeine use disorder” and “Internet gaming disorder.”
These have been added to DSM-5 in a special section that is reserved for disorders still in need of further study. Although this does not mean that they are being formally accepted as official disorders, it is certainly a first step. What do you think of this? How close do you think we are getting to the point where all of us, by virtue of drinking too much coffee or spending too much time gaming are at risk of being considered mentally ill?
Internet gaming disorder is now listed in DSM-5 as a new disorder in need of further study.
30 Chapter 1
Summary 1.1 Explain how we define abnormality and classify
mental disorders.
• A precise definition of abnormality remains elusive. Elements that can be helpful in considering whether something is abnormal include subjective distress, maladaptiveness, statistical deviancy, violation of soci- etal norms, social discomfort, irrationality and unpre- dictability, and dangerousness.
• The DSM employs a category type of classification similar to that used in medicine. Disorders are regarded as discrete clinical entities, though not all clinical disorders may be best considered in this way.
• Even though it is not without problems, the DSM pro- vides us with working criteria that help clinicians and researchers identify and study specific difficulties that affect the lives of many people. It is far from a “fin- ished product.” However, familiarity with the DSM is essential to significant study of the field.
1.2 Describe the advantages and disadvantages of classification.
• Classifying disorders provides a common language as well as a communication shorthand. It also allows us to structure information in an efficient manner and provides us with an organizational framework. This facilitates research and treatment. In addition, classifi- cation defines the domain of what is considered to be pathological. From a practical perspective, it delineates the types of psychological difficulties that warrant insurance reimbursement and identifies the disorders that mental health professionals treat.
• When we classify, we lose detailed personal informa- tion about the person with the disorder. Classifica- tion can also facilitate stigma, stereotyping, and labeling, although we should keep in mind that these
problems are not caused by the classification system itself. Fear of being viewed negatively or being dis- criminated against may lead some people to avoid seeking treatment.
1.3 Explain how culture affects what is considered abnormal and describe two different culture- specific disorders.
• Culture shapes the presentation of clinical disorders in some cases. Culture also provides the backdrop against which we must evaluate whether a particular behavior is abnormal or not.
• Certain disorders appear to be highly culture specific. Taijin kyofusho is an anxiety disorder that is quite prev- alent in Japan. It involves fear that one’s body, body parts, or body functions may offend, embarrass, or make others feel uncomfortable. Ataque de nervios is another culturally rooted expression of distress. It is found in people of Latino descent, especially those from the Caribbean. This condition does not have a clear counterpart in the DSM. Symptoms can include crying, trembling, fainting, uncontrollable screaming, and a general feeling of loss of control.
1.4 Distinguish between incidence and prevalence and identify the most common and prevalent mental disorders.
• Epidemiology involves the study of the distribution and frequency of disorders. Incidence is the number of new cases that occur in a given period of time. Preva- lence refers to the total number cases in a population during any specified period of time.
• Just under 50 percent of people will experience some form of mental disorder during the course of their life- times. Mood disorders and anxiety disorders are par- ticularly common.
passivity, and depression. In other words, the findings from these animal studies provided the impetus for what first became known as the “learned helplessness theory of depression” (Abramson et al., 1978; Seligman, 1975) and is now termed “the hopelessness theory of depression” (Abramson et al., 1989). These theories of depression are not without their difficulties. Nevertheless, it is useful to remain aware of the broader message: Even though prob- lems may arise when we generalize too readily from ani- mal to human models of psychopathology, the learned helplessness analogy has generated much research and has
allowed us to refine and develop our understanding of depression.
in review • How is experimental research different from correlational research?
• In experimental research, which variable (independent or de- pendent) is manipulated?
• What is a placebo?
• Explain the process of performing an ABAB design. Why are such designs helpful to clinicians and researchers?
Abnormal Psychology: Overview and Research Approaches 31
group must be comparable in all major respects (age, educational level, proportion of males and females, etc.) to the criterion group (e.g., people with the disor- der we want to learn about), except for the fact that they do not exhibit the disorder of interest. The control group could be psychologically healthy people, or could comprise people with a different disorder.
• Only when they are using a suitable control or com- parison group can researchers compare the two groups on the variables of interest to see if there are significant differences.
1.8 Discuss why correlational research designs are valuable, even though they cannot be used to make causal inferences.
• Correlational research examines factors as they cur- rently are, allowing us to identify factors that appear to be associated with certain disorders.
• Just because two variables are correlated does not mean that there is a causal relationship between them. Correlation does not equal causation.
1.9 Explain the key features of an experimental design.
• Experimental research involves manipulating one variable (the independent variable) and observing the effect this manipulation produces with regard to another variable (the dependent variable).
• Because the experimenter is changing the experimen- tal conditions, experimental research designs permit causal inferences to be made.
• Although most experiments involve the study of groups, single-case experimental designs (e.g., ABAB designs) may also be used to make causal inferences in individual instances.
1.5 Discuss why abnormal psychology research can be conducted in almost any setting.
• Studying and drawing inferences from past case stud- ies alone often leads to erroneous thinking as we often focus on data that confirm our ideas of how things are.
• Research prevents us from being misled by natural errors in thinking and can be conducted in clinics, hos- pitals, schools, prisons, and on the street. It is not the setting that determines whether a given research pro- ject may be undertaken. The importance lies in the researcher’s methodology.
1.6 Describe three different approaches used to gather information about mental disorders.
• Information about mental disorders can be collected through case studies, self-report data, and observa- tional approaches.
• Case studies can be a valuable source of new ideas and serve as a stimulus for research. They also may pro- vide insight into unusual clinical conditions that are too rare to be studied in a more systematic way.
• Self-report data allows us to study behavior in a more rigorous manner. This type of research often involves having research participants complete questionnaires of various types or conducting interviews.
• When we collect information in a way that does not involve asking people directly, we are using some form of observational approach. Exactly how we go about this depends on what it is we seek to understand.
1.7 Explain why a control (or comparison group) is necessary to adequately test a hypothesis.
• Unless there is a control or comparison group, research- ers cannot test their hypothesis adequately. The control
ABAB design, p. 28 abnormal psychology, p. 2 acute, p. 16 analogue studies, p. 29 bias, p. 17 case study, p. 17 chronic, p. 16 comorbidity, p. 14 comparison or control group, p. 21 correlation, p. 22 correlation coefficient, p. 22 correlational research, p. 22 criterion group, p. 21 dependent variable, p. 25 direct observation, p. 18 double-blind study, p. 27
effect size, p. 24 epidemiology, p. 12 etiology, p. 16 experimental research, p. 25 external validity, p. 21 family aggregation, p. 3 generalizability, p. 17 hypothesis, p. 19 incidence, p. 13 independent variable, p. 25 internal validity, p. 21 labeling, p. 9 lifetime prevalence, p. 13 longitudinal design, p. 25 meta-analysis, p. 24 negative correlation, p. 22
nomenclature, p. 8 1-year prevalence, p. 12 placebo treatment, p. 27 point prevalence, p. 12 positive correlation, p. 22 prevalence, p. 12 prospective research, p. 25 random assignment, p. 26 retrospective research, p. 25 sampling, p. 20 self-report data, p. 18 single-case research design, p. 27 statistical significance, p. 23 stereotyping, p. 8 stigma, p. 8 third variable problem, p. 24
Key Terms
32
Chapter 2
Historical and Contemporary Views of Abnormal Behavior
Learning Objectives
2.1 Explain how abnormal behavior has been viewed throughout history.
2.2 Describe the effect that humanism had on abnormal psychology.
2.3 Identify developments that led to the contemporary view of abnormal psychology.
Historical and Contemporary Views of Abnormal Behavior 33
highlight some views of psychopathology and some of the treatments administered, from ancient times to the twenty-first century. In a broad sense, we will see a pro- gression of beliefs from what we now consider supersti- tion to those based on scientific awareness—from a focus on supernatural explanations to knowledge of natural causes. The course of this evolution has at times been marked by periods of advancement or unique, individ- ual contributions, followed by long years of inactivity or unproductive, backward steps.
Although human life appeared on earth some 3 mil- lion or more years ago, written records extend back only a few thousand years. Thus, our knowledge of our early ancestors is limited. Two Egyptian papyri dating from the sixteenth century b.c. provide some clues to the earliest treatments of diseases and behavior disorders (Okasha & Okasha, 2000). The Edwin Smith papyrus (named after its nineteenth-century discoverer) contains detailed descrip- tions of the treatment of wounds and other surgical opera- tions. In it, the brain is described—possibly for the first time in history—and the writing clearly shows that the brain was recognized as the site of mental functions. The Ebers papyrus offers another perspective on treatment. It covers internal medicine and the circulatory system but relies more on incantations and magic for explaining and curing diseases with unknown causes. Although surgical techniques may have been used, they were probably cou- pled with prayers, which reflected the prevailing view of the origin of mental illness.
Antisocial personality disorders, though not well addressed in psychiatry until the nineteenth century, have posed major problems to all societies. There is evidence from legal and religious literature that some people with personality problems posed serious challenges to earlier societies going back the beginning of civilization. In ancient Mesopotamia (before the eighth century b.c.) there was a clear recognition of the types of mental health problems that are currently described as personality disorders in contemporary diagnostic manuals, the ICD-10 and DSM-5. Antisocial personality problems were described on cunei- form tablets detailing an ancient Mesopotamian incanta- tion that were found at the palace of Ashurbanipal in what is now Iraq (the tablets are currently in the British Museum). Those tablets include descriptions of antisocial behaviors such as irritability and aggressiveness; lack of remorse; hurting, mistreating or stealing from others; fail- ing to conform to social norms with respect to lawful behaviors; impulsivity or failure to plan ahead; and show- ing irresponsible behaviors that mental health practitio- ners today encounter and recognize as personality disorders. The behavioral problems were dealt with not through medicine but through religious rites or incanta- tions that were made by people who sought exorcism from antisocial traits and behaviors by repeating explicit
An Artist in Bedlam The most famous patient committed to the historic Bethlem Hos- pital in England (better known as Bedlam) during its long existence was a well-known and talented young artist, Richard Dadd (1817– 1886). Dadd was born in Chatham, England, in 1817. His father was a successful chemist. Dadd attended the Kings School in Rochester and also studied art at the Royal Academy School in London. He showed a strong aptitude for drawing and painting and was admitted to the prestigious Royal Academy of Arts at the early age of 20. When he was 25, he was invited to accompany Sir Thomas Phillips, the former mayor of Newport, on a grand tour through Europe, Greece, Turkey, Syria, and Egypt to serve as the draftsman and painter for the expedition. During the trip, Dadd produced a number of exceptional paintings of people and places he encountered on the journey. The voyage was reportedly difficult and stressful, and at one point, during a trip up the Nile River, Dadd underwent a remarkable personality change, becoming delusional and increasingly aggressive and violent toward people he met. He was reported to have expressed an urge to kill the Pope. He experienced delusional beliefs—for example, that he had come under the influence of the Egyptian god Osiris.
When he returned from the trip in 1843, he was diagnosed as being mentally unsound because of his hallucinations and his strange, delusional beliefs. In an effort to restore him to health, his family took him to recuperate in a countryside village in Kent, England. The records indicate that one day he came to the con- clusion that his father was the Devil in disguise, and on a walk in the countryside Dadd killed his father with a knife. He attempted to escape by fleeing to France; however, his aggressive behavior continued, and he attempted to kill a tourist with a razor. He was arrested by the police and was eventually returned to England. He was committed to Bethlem Royal Hospital, where he was held in the criminal ward for dangerous inmates. He remained in Beth- lem Hospital for almost 20 years and was eventually transferred to Broadmoor Hospital, where he died in 1886. During his stay in both the Bethlem and Broadmoor hospitals he was allowed and encouraged to paint by the staff as part of his treatment. During this time he produced a number of paintings, many of which can be seen today in art museums.
Although he appears to have experienced symptoms of a mood disorder including acute mania (see Chapter 7), it is likely that Dadd suffered from paranoid schizophrenia (see Chapter 14 for further discussion). Interestingly, two of his siblings appeared to suffer from the same symptom pattern; thus, he may have been genetically predisposed to this condition (see Greysmith, 1979, and MacGregor, 1989, for a discussion of his life and artwork).
Historical Views of Abnormal Behavior 2.1 Explain how abnormal behavior has been viewed
throughout history.
Our historical efforts to understand abnormal psychol- ogy include both humor and tragedy. In this chapter, we
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smite thee with madness.” Apparently this punishment was thought to involve the withdrawal of God’s protection and the abandonment of the person to the forces of evil. In such cases, every effort was made to rid the person of the evil spirit. The primary type of treatment for demonic pos- session was exorcism, which included various techniques for casting an evil spirit out. These techniques varied but typically included magic, prayer, incantation, noisemak- ing, and the use of horrible-tasting concoctions made from sheep’s dung and wine.
Hippocrates’ Early Medical Concepts The Greek temples of healing ushered in the Golden Age of Greece under the Athenian leader Pericles (461–429 b.c.). This period saw considerable progress in the understand- ing and treatment of mental disorders, in spite of the fact that Greeks of the time considered the human body sacred so little could be learned of human anatomy or physiol- ogy. During this period the Greek physician Hippocrates (460–377 b.c.), often referred to as the father of modern medicine, received his training and made substantial con- tributions to the field.
Hippocrates denied that deities and demons inter- vened in the development of illnesses and instead insisted that mental disorders, like other diseases, had natural causes and appropriate treatments. He believed that the brain was the central organ of intellectual activity and that mental disorders were due to brain pathology. He also emphasized the importance of heredity and predisposition and pointed out that injuries to the head could cause sen- sory and motor disorders.
Hippocrates classified all mental disorders into three general categories—mania, melancholia, and phrenitis (brain fever)—and gave detailed clinical descriptions of the specific disorders included in each category. He relied heavily on clinical observation, and his descriptions, which were based on daily clinical records of his patients, were surprisingly thorough.
Maher and Maher (1994) pointed out that the best known of the earlier paradigms for explaining personal- ity or temperament is the doctrine of the four humors, associated with the name of Hippocrates and later with the Roman physician Galen. The four elements of the material world were thought to be earth, air, fire, and water, which had attributes of heat, cold, moistness, and dryness. These elements combined to form the four essential fluids of the body—blood (sanguis), phlegm, bile (choler), and black bile (melancholic). The fluids combined in different proportions within different indi- viduals, and a person’s temperament was determined by which of the humors was dominant. From this view came
phrases. A recent article by Abdul-Hamid and Stein (2013) provides interesting evidence of the comparability of these ancient views of behavior problems to contemporary diagnostic manuals and their management of them through religious rites.
The Ashurbanipal cuneiform tablet from Mesopotamia around 800 b.c. includes descriptions of antisocial behaviors such as irritability and aggressiveness; mistreating or stealing from others; and irresponsible behaviors that mental health practitioners today encounter and recognize as personality disorders.
Demonology, Gods, and Magic References to abnormal behavior in early writings show that the Chinese, Egyptians, Hebrews, and Greeks often attributed such behavior to a demon or god who had taken possession of a person. Whether the “possession” was assumed to involve good spirits or evil spirits usu- ally depended on the affected individual’s symptoms. If a person’s speech or behavior appeared to have a reli- gious or mystical significance, it was usually thought that he or she was possessed by a good spirit or god. Such people were often treated with considerable awe and respect, for individuals believed they had supernat- ural powers.
Most possessions, however, were considered to be the work of an angry god or an evil spirit, particularly when a person became excited or overactive and engaged in behavior contrary to religious teachings. Among the ancient Hebrews, for example, such possessions were thought to represent the wrath and punishment of God. Moses is quoted in the Bible as saying, “The Lord shall
Historical and Contemporary Views of Abnormal Behavior 35
one of the earliest and longest lasting typologies of human behavior: the sanguine, the phlegmatic, the cho- leric, and the melancholic. Each of these “types” brought with it a set of personality attributes. For example, the person of sanguine temperament was optimistic, cheer- ful, and unafraid.
Hippocrates considered dreams to be important in understanding a patient’s personality. On this point, he was a harbinger of a basic concept of modern psychody- namic psychotherapy. The treatments advocated by Hip- pocrates were far in advance of the exorcistic practices then prevalent. For the treatment of melancholia (see the Developments in Thinking box), for example, he pre- scribed a regular and tranquil life, sobriety and abstinence
Developments in Thinking Melancholia Through the Ages
Although the modern mental health sciences have made great strides in defining, describing, classifying, determining the causes of, and treating psychological disorders, we should not ignore or minimize the contributions to understanding these conditions that were made by many individuals in antiquity. Actually, some men- tal health problems that are receiving a great deal of research and clinical attention today have been recognized and well described for millennia. One recent study of surviving letters from patients who were hospitalized in Edinborough Asylum between 1873 and 1906 concluded that mental health problems in the nineteenth century were very similar to those in our day (Beveridge, 1997). One such disorder is depression.
Perhaps no other mental disorder received so much atten- tion from early scholars as depression, or (as it has been referred to in the past) melancholia. Efforts to understand melancholia have been undertaken by physicians, philosophers, writers, painters, and religious leaders in Western civilization for over 2,000 years. Moreover, conditions similar to depression are described in surviving writings from ancient Egypt (Okasha & Okasha, 2000). These disorders might have been viewed vari- ously as medical conditions or religious states or human frailties; however, the symptom structure and behavior described were unmistakable.
Radden (2000) published an interesting compendium of important writings on melancholia that span 24 centuries, some highlights of which are provided here.
• Investigations into the nature of depression, beginning with
Aristotle and Galen during the Greek and Roman eras, provide
lucid descriptions of the disorder melancholia.
• Even in the Middle Ages, when scholarship and inquiry were hindered by a period of religious persecution that included the Spanish Inquisition, scholars were interested in mental states such as melancholia. Hildegard (1098–1179), a nun known as
the “first published woman physician,” carried the Greek views of melancholia further by noting, among other things, that melancholia took different forms in men and women. Johann Weyer (1515–1588) provided astute descriptions of melancholia and examined characteristics of persons who might be so affected, even though these observations were often couched in terms of demonic possession—perhaps as a concession to leaders of the Inquisition in order to avoid persecution.
• The pre-modern view of melancholia as a disorder (without the taint of demonic possession or ancient Greek humors) was introduced by Philippe Pinel (1745–1826). A French physician widely recognized for his contributions to the humane treat- ment of people with mental disorders, Pinel also advanced our scholarly understanding of mental disorders such as melan- cholia by improving a classification schema and examining the causes of the disorder.
• Two early modern contributors to our understanding of depression were Wilhelm Griesinger (1817–1868) and Emil Kraepelin (1856–1926). Griesinger’s views on the underlying biological basis for disorders such as melancholia focused the field of psychiatry on the need to seek biological determi- nants for disorders. Kraepelin is credited with preparing the way for the modern view of psychiatry. His classification schema is still cited today in contemporary writings as semi- nal in the evolution of diagnostic classification systems. He also identified manic depression as a major category of depression.
Even though much of our understanding of depression and our development of effective treatment methods has emerged during the past three decades, our debt to the ancients who struggled with describing and understanding this disorder needs to be recognized.
from all excesses, a vegetable diet, celibacy, exercise short of fatigue, and bleeding if indicated. He also recognized the importance of the environment and often removed his patients from their families.
Hippocrates’ emphasis on the natural causes of dis- eases, on clinical observation, and on brain pathology as the root of mental disorders was truly revolutionary. Like his contemporaries, however, Hippocrates had little knowledge of physiology. He believed that hysteria (the appearance of physical illness in the absence of organic pathology) was restricted to women and was caused by the uterus wandering to various parts of the body, pining for children. For this “disease,” Hippocrates recommended marriage as the best remedy.
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Plato shared the belief that mental disorders were in part divinely caused.
The celebrated Greek philosopher Aristotle (384–322 b.c.), who was a pupil of Plato, wrote extensively on men- tal disorders. Among his most lasting contributions to psy- chology are his descriptions of consciousness. He held the view that “thinking” as directed would eliminate pain and help to attain pleasure. On the question of whether mental disorders could be caused by psychological factors such as frustration and conflict, Aristotle discussed the possibility and rejected it; his lead on this issue was widely followed. Aristotle generally subscribed to the Hippocratic theory of disturbances in the bile. For example, he thought that very hot bile generated amorous desires, verbal fluency, and suicidal impulses.
Later Greek and Roman Thought Hippocrates’ work was continued by some of the later Greek and Roman physicians. Particularly in Alexandria, Egypt (which became a center of Greek culture after its founding in 332 b.c. by Alexander the Great), medical prac- tices developed to a higher level, and the temples dedi- cated to Saturn were first-rate sanatoria. Pleasant surroundings were considered of great therapeutic value for patients with mental illness, who were provided with constant activities including parties, dances, walks in the temple gardens, rowing along the Nile, and musical con- certs. Physicians of this time also used a wide range of therapeutic measures including dieting, massage, hydro- therapy, gymnastics, and education, as well as some less desirable practices such as bleeding, purging, and mechan- ical restraints.
Asclepiades (c. 124–40 b.c.) was a Greek physician born at Prusa in Bithynia in Asia Minor and practiced med- icine in Rome toward the end of the second century b.c. He developed a theory of disease that was based on the flow of atoms through the pores in the body and came up with treatments, such as massage, special diets, bathing, exer- cise, listening to music, and rest and quiet, to restore to the body (Stone, 1937).
One of the most influential Greek physicians was Galen (A.D. 130–200), who practiced in Rome. Although he elabo- rated on the Hippocratic tradition, he did not contribute much that was new to the treatment or clinical descriptions of mental disorders. Rather, he made a number of original contributions concerning the anatomy of the nervous sys- tem. (These findings were based on dissections of animals; human autopsies were still not allowed.) Galen also took a scientific approach to the field, dividing the causes of psy- chological disorders into physical and mental categories. Among the causes he named were injuries to the head, excessive use of alcohol, shock, fear, adolescence, menstrual changes, economic reversals, and disappointment in love.
The earliest use of the concept “delirium” to describe symptoms of mental disorders that result from fever or physical injury or brain trauma occurred in the first cen- tury A.D. by Celsus (Adamis et al., 2007).
Early Philosophical Conceptions of Consciousness The Greek philosopher Plato (429–347 b.c.) studied indi- viduals with mental disturbances who had committed criminal acts and how to deal with them. He wrote that such persons were, in some “obvious” sense, not responsi- ble for their acts and should not receive punishment in the same way as normal persons. He also made provision for mental cases to be cared for in the community.
Plato viewed psychological phenomena as responses of the whole organism, reflecting its internal state and natural appetites. In The Republic, Plato emphasized the importance of individual differences in intellectual and other abilities and took into account sociocultural influ- ences in shaping thinking and behavior. His ideas regard- ing treatment included a provision for “hospital” care for individuals who developed beliefs that ran counter to those of the broader social order. There they would be engaged periodically in conversations comparable to psychotherapy to promote the health of their souls (Milns, 1986). Despite these modern ideas, however,
Hippocrates’ (460–377 b.c.) belief that mental disease was the result of natural causes and brain pathology was revolutionary for its time.
Historical and Contemporary Views of Abnormal Behavior 37
negative forces that both complement and contradict each other. If the two forces are balanced, the result is physical and mental health; if they are not, illness results. Thus, treat- ments focused on restoring balance (Tseng, 1973, p. 570).
Chinese medicine reached a relatively sophisticated level during the second century, and Chung Ching, who has been called the Hippocrates of China, wrote two well- known medical works around A.D. 200. Like Hippocrates, he based his views of physical and mental disorders on clinical observations, and he implicated organ pathologies as primary causes. However, he also believed that stressful psychological conditions could cause organ pathologies, and his treatments, like those of Hippocrates, utilized both drugs and the regaining of emotional balance through appropriate activities.
As in the West, Chinese views of mental disorders regressed to a belief in supernatural forces as causal agents. From the later part of the second century through the early part of the ninth century, ghosts and devils were impli- cated in “ghost-evil” insanity, which presumably resulted from possession by evil spirits. The “Dark Ages” in China, however, were neither so severe (in terms of the treatment of patients with mental illness) nor as long lasting as in the West. A return to biological, somatic (bodily) views and an emphasis on psychosocial factors occurred in the centuries that followed. During the past 50 years, China has been experiencing a broadening of ideas in mental health ser- vices and has been incorporating many ideas from Western psychiatry (Zhang & Lu, 2006).
Views of Abnormality During the Middle Ages During the Middle Ages (about A.D. 500 to A.D. 1500), the more scientific aspects of Greek medicine survived in the Islamic countries of the Middle East. The first mental hospi- tal was established in Baghdad in A.D. 792; it was soon fol- lowed by others in Damascus and Aleppo (Polvan, 1969). In these hospitals, individuals with mental disturbances received humane treatment. One outstanding figure in ancient medicine was Avicenna from Persia (c. 980–1037). Referred to as the “prince of physicians” (Campbell, 1926), he was the author of The Canon of Medicine, perhaps the most widely studied medical work ever written. In his writ- ings, Avicenna frequently referred to hysteria, epilepsy, manic reactions, and melancholia. The following case study illustrates Avicenna’s unique approach to the treatment of a young prince suffering from mental disorder.
An Early Treatment Case
A certain prince was afflicted with melancholia and suffered from the delusion that he was a cow. . . . He would low like a cow, causing annoyance to everyone, . . . crying, “Kill me so that a good stew may
Roman medicine reflected the characteristic pragma- tism of the Roman people. Roman physicians wanted to make their patients comfortable and thus used pleasant physical therapies such as warm baths and massage. They also followed the principle of contrariis contrarius (or “opposite by opposite”) by, for example, having their patients drink chilled wine while they were in a warm tub.
Galen (A.D. 130–200) believed that psychological disorders could have either physical causes, such as injuries to the head, or mental causes, such as disappointment in love.
Early Views of Mental Disorders in China China was one of the earliest developed civilizations in which medicine and attention to mental disorders were introduced (Soong, 2006). The following passage is taken from an ancient Chinese medical text supposedly written by Huang Ti (c. 2674 b.c.), the third legendary emperor:
The person suffering from excited insanity initially feels sad, eating and sleeping less; he then becomes grandiose, feeling that he is very smart and noble, talking and scold- ing day and night, singing, behaving strangely, seeing strange things, hearing strange voices, believing that he can see the devil or gods. (Tseng, 1973, p. 570)
Even at this early date, Chinese medicine was based on a belief in natural rather than supernatural causes for ill- nesses. For example, in the concept of yin and yang, the human body, like the cosmos, is divided into positive and
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ranging from madness and possession to alcohol abuse and epilepsy. They found sin implicated in only nine cases (16 percent). To understand better this elusive period of history, let us look at two events of the times, mass mad- ness and exorcism, to see how they are related to views of abnormal behavior.
MASS MADNESS During the last half of the Middle Ages in Europe, a peculiar trend emerged in efforts to under- stand abnormal behavior. It involved mass madness—the widespread occurrence of group behavior disorders that were apparently cases of hysteria. Whole groups of people were affected simultaneously. Dancing manias (epidemics of raving, jumping, dancing, and convulsions) were reported as early as the tenth century. One such episode that occurred in Italy early in the thirteenth century was known as tarantism—a disorder that included an uncon- trollable impulse to dance that was often attributed to the bite of the southern European tarantula or wolf spider. This dancing mania later spread to Germany and the rest of Europe, where it was known as Saint Vitus’s dance.
Isolated rural areas were also afflicted with outbreaks of lycanthropy—a condition in which people believed themselves to be possessed by wolves and imitated their behavior. In 1541 a case was reported in which a person suffering from lycanthropy told his captors, in confidence, that he was really a wolf but that his skin was smooth on the surface because all the hairs were on the inside (Stone, 1937). To cure him of his delusions, his extremities were amputated, following which he died, still uncured.
Mass madness occurred periodically all the way into the seventeenth century but had reached its peak during the fourteenth and fifteenth centuries—a period noted for social oppression, famine, and epidemic diseases. During this time, Europe was ravaged by a plague known as the Black Death, which killed millions (according to some esti- mates, 50 percent of the population of Europe died) and severely disrupted social organization. Undoubtedly, many of the peculiar cases of mass madness were related to the depression, fear, and wild mysticism engendered by the terrible events of this period. People simply could not believe that frightening catastrophes such as the Black Death could have natural causes and thus could be within their power to control, prevent, or even create.
Today, so-called mass hysteria occurs occasionally; the affliction usually mimics some type of physical disorder such as fainting spells or convulsive movements. A case of apparent mass hysteria occurred among hundreds of West Bank Palestinian girls in April 1983. This episode threat- ened to have serious political repercussions because some Arab leaders initially thought that the girls had been poi- soned by Israelis. Health officials later concluded that psy- chological factors had played a key role in most of the cases (Hefez, 1985).
be made of my flesh.” Finally . . . he would eat nothing. . . . Avicenna was persuaded to take the case. . . . First of all he sent a message to the patient bidding him be of good cheer because the butcher was coming to slaughter him, whereat . . . the sick man rejoiced. Some time afterward Avicenna, holding a knife in his hand, entered the sickroom saying, “Where is this cow that I may kill it?” The patient lowed like a cow to indicate where he was. By Avicenna’s orders he was laid on the ground bound hand and foot. Avicenna then felt him all over and said, “He is too lean, and not ready to be killed; he must be fattened.” Then they offered him suitable food of which he now partook eagerly, and gradually he gained strength, got rid of his delusion, and was completely cured. (Browne, 1921, pp. 88–89)
Ancient Persian physician Avicenna (c. 980–1037) approached the treatment of mental disorders with humane practices unknown to Western medical practitioners of the time.
During the Middle Ages in Europe, scientific inquiry into abnormal behavior was limited, and the treatment of individuals who were psychologically disturbed was char- acterized more often by ritual or superstition than by attempts to understand an individual’s condition. In con- trast to Avicenna’s era in the Islamic countries of the Mid- dle East or to the period of enlightenment during the seventeenth and eighteenth centuries, the Middle Ages in Europe were largely devoid of scientific thinking and humane treatment for those with mental illness.
Mental disorders were quite prevalent throughout the Middle Ages in Europe, especially toward the end of the period, when medieval institutions, social structures, and beliefs began to change drastically. During this time, super- natural explanations of the causes of mental illness grew in popularity. Within this environment, it obviously was dif- ficult to make great strides in the understanding and treat- ment of abnormal behavior. Although the influence of theology was growing rapidly, “sin” was not always cited as a causal factor in mental illness. For example, Kroll and Bachrach (1984) examined 57 episodes of mental illness
Historical and Contemporary Views of Abnormal Behavior 39
some people with mental illness were punished as witches. Otherwise, as we will see in the next section, why did some physicians and thinkers go to great lengths to expose the fallacies of the connection? In the case of witchcraft and mental illness, the confusion may be due, in part, to confusion about demonic possession. Even Robert Burton (1576–1640), an enlightened scholar, in his classic work The Anatomy of Melancholia (1621), considered demonic possession a poten- tial cause of mental disorder. There were two types of demonically possessed people: Those physically possessed were considered mad, whereas those spiritually possessed were likely to be considered witches. Over time, the dis- tinctions between these two categories may have blurred in the eyes of historians, resulting in the perception that witchcraft and mental illness were connected more fre- quently in the medieval mind than was the case.
The changing view of the relationship between witch- craft and mental illness points to an even broader issue— the difficulties of interpreting historical events accurately. We will discuss this concept in more depth in the Unre- solved Issues section at the end of this chapter.
in review • What aspects of Hippocrates’ alternative approach to mental
disorders were truly revolutionary?
• What were the historical views of the disorder of melancholia (known as depression today)?
• What was the role of supernatural beliefs in efforts to understand mental disorders during the Middle Ages?
• What is mass madness? Give some examples of this phenomenon.
Toward Humanitarian Approaches 2.2 Describe the effect that humanism had on
abnormal psychology.
During the latter part of the Middle Ages and the early Renaissance, scientific questioning reemerged and a move- ment emphasizing the importance of specifically human interests and concerns began—a movement (still with us today) that can be loosely referred to as humanism. Conse- quently, the superstitious beliefs that had hindered the understanding and therapeutic treatment of mental disor- ders began to be challenged.
The Resurgence of Scientific Questioning in Europe Paracelsus (1490–1541), a Swiss physician, was an early critic of superstitious beliefs about possession. He insisted that the dancing mania was not a possession but a form of
Ilechukwu (1992) describes an epidemic of mass hyste- ria that occurred in Nigeria in 1990 in which many men feared that their genitals had simply vanished. This fear of genital retraction accompanied by a fear of death is referred to as koro and has been widely documented in Southeast Asia. The afflicted persons believe this genital disappear- ance was caused by a supernatural occurrence in which they were robbed of their genitalia in order to benefit other people magically. Ilechukwu attributes some of this panic to male resentment of women’s success during a period of social strain and the symbolic equation between masculine sexuality and economic, social, and creative prowess.
EXORCISM AND WITCHCRAFT In the Middle Ages in Europe, management of people who were mentally dis- turbed was left largely to the clergy. Monasteries served as refuges and places of confinement. During the early medi- eval period, people with mental disturbances were typi- cally treated with kindness. “Treatment” consisted of prayer, holy water, sanctified ointments, the breath or spit- tle of the priests, the touching of relics, visits to holy places, and mild forms of exorcism. In some monasteries and shrines, exorcisms were performed by the gentle “laying on of hands.” Such methods were often joined with vaguely understood medical treatments derived mainly from Galen, which gave rise to prescriptions such as the follow- ing: “For a fiend-sick man: When a devil possesses a man, or controls him from within with disease, a spewdrink of lupin, bishopswort, henbane, garlic. Pound these together, add ale and holy water” (Cockayne, 1864–1866).
Interestingly, there has been a recent resurgence of superstition. For example, one can find those who believe that supernatural forces cause psychological problems and that “cures” should involve exorcism to rid people of unwanted characteristics or “spells.” Fries (2001) reported on the tragedy of a woman who drowned her 4-year-old daughter in an exorcism ritual. The mother was attempting to rid her daughter of the demons that the mother believed possessed her. In another example, CBS News (2003) reported an incident in which a boy with autism was killed in an exorcism at a church in Milwaukee.
It had long been thought that during the Middle Ages many people with mental disturbances were accused of being witches and thus were punished and often killed (e.g., Zilboorg & Henry, 1941). But several more recent interpretations have questioned the extent to which this was so (Maher & Maher, 1985; Phillips, 2002). For example, in a review of the literature, Schoeneman (1984) notes that “the typical accused witch was not a mentally ill person but an impoverished woman with a sharp tongue and a bad temper” (p. 301). He concluded that “witchcraft was, in fact, never considered a variety of possession either by witch hunters, the general populace, or modern historians” (p. 306). To say “never” may be overstating the case; clearly,
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ahead of his time. He was scorned by his peers, many of whom called him “Weirus Hereticus” and “Weirus Insa- nus.” His works were banned by the Church and remained so until the twentieth century.
The clergy, however, were also beginning to question the practices of the time. For example, St. Vincent de Paul (1576–1660), at the risk of his life, declared, “Mental disease is no different than bodily disease and Christianity demands of the humane and powerful to protect, and the skillful to relieve the one as well as the other” (Castiglioni, 1924).
In the face of such persistent advocates of science, who continued their testimonies throughout the next two centu- ries, demonology and superstition gave ground. These advocates gradually paved the way for the return of obser- vation and reason, which culminated in the development of modern experimental and clinical approaches.
The Establishment of Early Asylums From the sixteenth century on, special institutions called asylums—sanctuaries or places of refuge meant solely for the care of people with mental illness—grew in number. The early asylums were begun as a way of removing from society troublesome individuals who could not care for themselves. Although scientific inquiry into abnormal behavior was on the increase, most early asylums, often referred to as “madhouses,” were not pleasant places or “hospitals” but primarily residences or storage places for people who were insane. The unfortunate residents lived and died amid conditions of incredible filth and cruelty.
The first asylum established in Europe was probably in Spain in 1409 (Villasante, 2003), although this point has been the subject of considerable discussion (Polo, 1997; Trope, 1997). Little is known about the treatment of patients in this asylum. In 1547 the monastery of St. Mary of Bethlem in London (initially founded as a monastery in 1247; see O’Donoghue, 1914) was officially made into an asylum by Henry VIII. Its name soon was contracted to “Bedlam,” and it became widely known for its deplorable conditions and practices. The more violent patients were exhibited to the public for one penny a look, and the more harmless inmates were forced to seek charity on the streets of London. Tuke (1882) describes Ned Ward’s account, in History of the Insane in the British Isles, of a visit to Bedlam:
Accordingly we were admitted in thro’ an iron gate, within which sat a brawny Cerberus, of an Idico-colour, leaning upon a money-box; we turned in through another Iron-Barricado, where we heard such a rattling of chains, drumming of doors, ranting, hollowing, singing, and run- ning, that I could think of nothing but Don Quevedo’s Vision where the lost souls broke loose and put Hell in an uproar. The first whimsey-headed wretch of this lunatic family that we observed, was a merry fellow in a straw cap, who was talking to himself, “that he had an army of Eagles at his command,” then clapping his hand upon his
disease, and that it should be treated as such. He also pos- tulated a conflict between the instinctual and spiritual natures of human beings, formulated the idea of psychic causes for mental illness, and advocated treatment by “bodily magnetism,” later called hypnosis (Mora, 1967). Although Paracelsus rejected demonology, his view of abnormal behavior was colored by his belief in astral influ- ences (lunatic is derived from the Latin word luna, or “moon”). He was convinced that the moon exerted a super- natural influence over the brain—an idea, incidentally, that persists even today.
Johann Weyer (1515–1588), a German physician and writer who wrote under the Latin name of Joannus Wierus, was so deeply disturbed by the imprisonment, torture, and burning of people accused of witchcraft that he made a careful study of the entire problem. About 1583 he pub- lished a book, On the Deceits of the Demons, that contains a step-by-step rebuttal of the Malleus Maleficarum, a witch- hunting handbook published in 1486 for use in recognizing and dealing with those suspected of being witches. In his book, Weyer argued that a considerable number, if not all, of those imprisoned, tortured, and burned for witchcraft were really sick in mind or body and that, consequently, great wrongs were being committed against innocent peo- ple. Weyer’s work enjoyed the approval of a few outstand- ing physicians and theologians of his time. Mostly, however, it met with vehement protest and condemnation.
Weyer was one of the first physicians to specialize in mental disorders, and his wide experience and progressive views justify his reputation as the founder of modern psy- chopathology. Unfortunately, however, he was too far
Johann Weyer (1515–1588), a sixteenth-century German physician, became so concerned over the torture and imprisonment of people accused of being witches that he wrote a book rebutting the church’s witch-hunting handbook, the Malleus Maleficarum.
Historical and Contemporary Views of Abnormal Behavior 41
needed to choose rationality over insanity. Thus, the treat- ment techniques were aggressive, aimed at restoring a “physical balance in the body and brain.” These tech- niques, though based on the scientific views of the day, were designed to intimidate patients. They included pow- erful drugs, water treatments, bleeding and blistering, electric shocks, and physical restraints. For example, a vio- lent patient might be plunged into ice water or a listless patient into hot water; frenzied patients might be adminis- tered drugs to exhaust them; or patients might be bled in order to drain their system of “harmful” fluids.
Humanitarian Reform Clearly, by the late eighteenth century, most mental hospi- tals in Europe and America were in significant need of reform. The humanitarian treatment of patients received great impetus from the work of Philippe Pinel (1745–1826) in France.
PINEL’S EXPERIMENT In 1792, shortly after the first phase of the French Revolution, Pinel was placed in charge of La Bicêtre, a hospital in Paris. In this capacity, he received the grudging permission of the Revolutionary Commune to remove the chains from some of the inmates as an exper- iment to test his views that patients with mental illness should be treated with kindness and consideration—as sick people, not as vicious beasts or criminals. Had his experiment proved a failure, Pinel might have lost his head, but fortunately it was a great success. Chains were removed; sunny rooms were provided; patients were per- mitted to exercise on the hospital grounds; and kindness was extended to these poor beings, some of whom had been chained in dungeons for 30 or more years. The effect was almost miraculous. The previous noise, filth, and abuse were replaced by order and peace. Interestingly, a historical document, subsequently found in the French Archives, raises some question about the date at which humanitarian reforms were begun in France. The docu- ment, provided by Jean-Baptiste Pussin (Pinel’s predeces- sor at La Bicêtre), indicated that he had been the head of the hospital beginning in 1784 and had removed some of the chains from patients and employed slightly more humane straitjackets instead. He also pointed out in the document that he had issued orders forbidding the staff from beating patients (Weiner, 1979).
TUKE’S WORK IN ENGLAND At about the same time that Pinel was reforming La Bicêtre, an English Quaker named William Tuke (1732–1822) established the York Retreat, a pleasant country house where patients with mental illness lived, worked, and rested in a kindly, reli- gious atmosphere (Narby, 1982). This retreat represented the culmination of a noble battle against the brutality, igno- rance, and indifference of Tuke’s time.
head, swore by his crown of moonshine, he would battle all the Stars in the Skies, but he would have some claret. . . . We then moved on till we found another remarkable fig- ure worth our observing, who was peeping through his wicket, eating of bread and cheese, talking all the while like a carrier at his supper, chewing his words with his victuals, all that he spoke being in praise of bread and cheese: “bread was good with cheese, and cheese was good with bread, and bread and cheese was good together”; and abundance of such stuff; to which my friend and I, with others stood listening; at last he coun- terfeits a sneeze, and shot such a mouthful of bread and cheese amongst us, that every spectator had some share of his kindness, which made us retreat. (pp. 76–77)
Such asylums for those with mental illness were grad- ually established in other countries, including Mexico (1566) and France (1641). An asylum was established in Moscow in 1764, and the notorious Lunatics’ Tower in Vienna was constructed in 1784. This structure was a show- place in Old Vienna, an ornately decorated round tower within which were square rooms. The doctors and “keep- ers” lived in the square rooms, while the patients were con- fined in the spaces between the walls of the rooms and the outside of the tower, where they were put on exhibit to the public for a small fee. These early asylums were primarily modifications of penal institutions, and the inmates were treated more like beasts than human beings.
In the United States, the Pennsylvania Hospital in Philadelphia, completed under the guidance of Benjamin Franklin in 1756, provided some cells or wards for patients with mental illness. The Public Hospital in Williamsburg, Virginia, constructed in 1768, was the first hospital in the United States devoted exclusively to patients with mental illness. The treatment of patients with mental illness in the United States was no better than that offered by European institutions, however. Zwelling’s 1985 review of the Public Hospital’s treatment methods shows that, initially, the phi- losophy of treatment involved the belief that the patients
Constructed in 1768, the Public Hospital in Williamsburg, Virginia was the first hospital in the United States devoted exclusively to patients with mental illness.
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occurred in Kingston, Jamaica, prompted an audit of colo- nial facilities and practices. In Kingston, an article written by a former patient disclosed that the staff used “tanking” to control and punish patients with mental illness. During tanking, “lunatics” were routinely held under water in a bathing tank by nurses and sometimes other patients until they were near death (Swartz, 2010).
RUSH AND MORAL MANAGEMENT IN AMERICA The success of Pinel’s and Tuke’s humanitarian experiments revolutionized the treatment of patients with mental ill- ness throughout the Western world. In the United States, this revolution was reflected in the work of Benjamin Rush (1745–1813), the founder of American psychiatry and also one of the signers of the Declaration of Independence. While he was associated with the Pennsylvania Hospital in 1783, Rush encouraged more humane treatment of patients with mental illness; wrote the first systematic treatise on
The Quakers believed in treating all people, even the insane, with kindness and acceptance. Their view that kind acceptance would help people with mental illness recover sparked the growth of more humane psychiatric treatment during a period when such patients were ignored and mis- treated (Glover, 1984).
The Quaker retreat at York has continued to provide humane mental health treatment for over 200 years (Borthwick et al., 2001), even though the mental hospital movement spawned by its example evolved into large mental hospitals that became crowded and often offered less-than-humane treatment in the late nineteenth and early twentieth centuries. (See the photograph of the York Retreat today.)
As word of Pinel’s amazing results spread to England, Tuke’s small force of Quakers gradually gained the sup- port of English medical practitioners such as Thomas Wakley and Samuel Hitch. In 1841 Hitch introduced trained nurses into the wards at the Gloucester Asylum and put trained supervisors at the head of the nursing staffs. These innova- tions, quite revolutionary at the time, not only improved the care of patients but also changed public attitudes toward people with mental disturbances. In 1842, follow- ing Wakley’s lobbying for change, the Lunacy Inquiry Act was passed, which included a requirement that asylums and houses be effectively inspected every 4 months (Roberts, 1981) to ensure proper diet and the elimination of the use of restraints.
In 1845, the Country Asylums Act was passed in England, which required every county to provide asylum to “paupers and lunatics” (Scull, 1996). Britain’s policy of providing more humane treatment of people with mental illness was substantially expanded to the colonies (Australia, Canada, India, West Indies, South Africa, etc.) after a widely publicized incident of maltreatment of patients that
This painting depicts Philippe Pinel supervising the unchaining of inmates at La Bicêtre hospital. Pinel’s experiment represented both a great reform and a major step in devising humanitarian methods of treating mental disorders.
This picture shows a male ward of Bethlem Hospital under the new, more humane treatment approach. Walford (1878) pointed out that by 1815, there was no more “show for a penny” at Bethlem Hospital, and patients were afforded more humane living facilities and activities.
The historic mental health facility, the York Retreat, continues to provide services in York, England, over 200 years since it was founded by William Tuke in 1796. This mental health facility is sponsored by the Quakers and provides a broad range of services in both inpatient and outpatient care.
Historical and Contemporary Views of Abnormal Behavior 43
mental hygiene movement, which advocated a method of treatment that focused almost exclusively on the physical well-being of hospitalized patients with mental illness. Although the patients’ comfort levels improved under the mental hygienists, the patients received no help for their mental problems and thus were subtly condemned to help- lessness and dependency.
Advances in biomedical science also contributed to the demise of moral management and the rise of the mental hygiene movement. These advances fostered the notion that all mental disorders would eventually yield to biological explanations and biologically based treat- ments (Luchins, 1989). Thus, the psychological and social environment of a patient was considered largely irrele- vant; the best one could do was keep the patient comfort- able until a biological cure was discovered. Needless to say, the anticipated biological cure-all did not arrive, and by the late 1940s and early 1950s, discharge rates were down to about 30 percent. Its negative effects on the use of moral management notwithstanding, the mental hygiene movement has accounted for many humanitarian accomplishments.
BENJAMIN FRANKLIN’S EARLY DISCOVERY OF THE POTENTIAL CURATIVE EFFECTS OF ELECTRIC SHOCK In school, most people learn about Benjamin Franklin’s early experimentation with electricity in the early eighteenth century. His kite-flying during electric storms and its influence on the physical sciences is com- mon knowledge. However, most people (even mental health professionals) are not aware that his work with electricity was among the earliest efforts to explore elec- tric shock to treat mental illness, an insight he gained accidentally. His proposals for using electricity to treat melancholia (depression) grew out of his observations that a severe shock he had experienced altered his memo- ries (see the informative discussion by Finger & Zaromb, 2006). Franklin published articles describing his experi- ence and suggested that physicians further study this method for treating melancholia. Shortly afterward, one of his friends, a physician named Ingenhousz, reported a similar incident in which he observed alterations in his thinking following a shock he had received. He too called for clinical trials to study this phenomenon as a possible treatment for psychiatric patients. Although these early efforts suggested that electroshock was a potentially valu- able treatment approach, medical research on the procedure was slow to develop. Rudolf Gottfried Arndt (1835–1900) from Germany treated a larger number of psychotic patients with electrotherapy (Arndt, 1878; see also discus- sion by Steinberg, 2013), but it was not until the twentieth century that Cerletti and Bini (1938), at the University of Rome, brought professional attention to electric shock as a treatment for depression.
psychiatry in America, Medical Inquiries and Observations upon Diseases of the Mind (1812); and was the first American to organize a course in psychiatry (see Gentile & Miller, 2009). But even he did not escape entirely from the estab- lished beliefs of his time. His medical theory was tainted with astrology, and his principal remedies were bloodlet- ting and purgatives. In addition, he invented and used a device called the “tranquilizing chair,” which was proba- bly more torturous than tranquil for patients. The chair was thought to lessen the force of the blood on the head while the muscles were relaxed. Despite these limitations, we can consider Rush an important transitional figure between the old era and the new.
During the early part of this period of humanitarian reform, the use of moral management—a wide-ranging method of treatment that focused on a patient’s social, individual, and occupational needs—became relatively widespread. This approach, which stemmed largely from the work of Pinel and Tuke, began in Europe during the late eighteenth century and in America during the early nineteenth century.
Moral management in asylums emphasized the patients’ moral and spiritual development and the reha- bilitation of their “character” rather than their physical or mental disorders, in part because very little effective treat- ment was available for these conditions at the time. The treatment or rehabilitation of the physical or mental disor- ders was usually attempted through manual labor and spiritual discussion, along with humane treatment.
Moral management achieved a high degree of effec- tiveness—which is all the more amazing because it was done without the benefit of the antipsychotic drugs used today and because many of the patients were probably suf- fering from syphilis, a then-incurable disease of the central nervous system. In the 20-year period between 1833 and 1853, Worcester State Hospital’s discharge rate for patients who had been ill less than a year before admission was 71 percent. Even for patients with a longer preadmission disorder, the discharge rate was 59 percent (Bockhoven, 1972). In London, Walford (1878) reported that during a 100-year period ending in 1876, the “cure” rate was 45.7 per- cent for the famed Bedlam Hospital.
Despite its reported effectiveness in many cases, moral management was nearly abandoned by the latter part of the nineteenth century. The reasons were many and varied. Among the more obvious ones were ethnic prejudice against the rising immigrant population in hospitals, lead- ing to tension between staff and patients; the failure of the movement’s leaders to train their own replacements; and the overextension of hospital facilities, which reflected the misguided belief that bigger hospitals would differ from smaller ones only in size.
Two other reasons for the demise of moral manage- ment are, in retrospect, truly ironic. One was the rise of the
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(see the Unresolved Issues section at the end of this chapter). Her advocacy of the humane treatment of people with mental illness stood in stark contrast to the cruel treat- ment common at the time.
DIX AND THE MENTAL HYGIENE MOVEMENT Doro- thea Dix (1802–1887) was an energetic New Englander who became a champion of poor and “forgotten” people who had been consigned to prisons and mental institutions for decades during the nineteenth century. Dix, herself a child of very difficult and impoverished circumstances (Viney, 1996), later became an important driving force in humane treatment for psychiatric patients. She worked as a school- teacher as a young adult but was later forced into early retirement because of recurring attacks of tuberculosis. In 1841, she began to teach in a women’s prison. Through this contact she became acquainted with the deplorable condi- tions in jails, almshouses, and asylums. In a “Memorial” submitted to the U.S. Congress in 1848, she stated that she had seen
more than 9000 idiots, epileptics and insane in the United States, destitute of appropriate care and protection . . . bound with galling chains, bowed beneath fetters and heavy iron bails attached to drag-chains, lacerated with ropes, scourged with rods and terrified beneath storms of execration and cruel blows; now subject to jibes and scorn and torturing tricks; now abandoned to the most outra- geous violations. (Zilboorg & Henry, 1941, pp. 583–584)
As a result of what she had seen, Dix carried on a zealous campaign between 1841 and 1881 that aroused people and legislatures to do something about the inhu- man treatment accorded to people with mental illness. Through her efforts, the mental hygiene movement grew in America: Millions of dollars were raised to build suit- able hospitals, and 20 states responded directly to her appeals. Not only was she instrumental in improving conditions in American hospitals but she also directed the opening of two large institutions in Canada and com- pletely reformed the asylum system in Scotland and sev- eral other countries. She is credited with establishing 32 mental hospitals, an astonishing record given the igno- rance and superstition that still prevailed in the field of mental health at that time. Dix rounded out her career by organizing the nursing forces of the Union Army during the Civil War. A resolution presented by the U.S. Con- gress in 1901 characterized her as “among the noblest examples of humanity in all history” (Karnesh, with Zucker, 1945, p. 18).
Later critics have claimed that establishing hospitals for people with mental illness and increasing the number of patients in them spawned overcrowded facilities and custodial care (Bockhoven, 1972; Dain, 1964). These critics have further claimed that housing patients in institutions away from society interfered with the treatment of the day (moral therapy) and deferred the search for more appropriate and effective treatments for mental disorders (Bockhoven, 1972). These criticisms, however, do not con- sider the context in which Dix’s contributions were made
Dorothea Dix (1802–1887) was a tireless reformer who made great strides in changing public attitudes toward people with mental illness.
THE MILITARY AND PEOPLE WITH MENTAL ILLNESS Mental health treatment was also advanced by military medicine. The first mental health facility for treating war casualties with mental disabilities was opened by the Con- federate Army during the American Civil War (Deutsch, 1944; Gabriel, 1987). An even more extensive and influen- tial program of military psychiatry evolved in Germany during the late 1800s. Lengweiler (2003) reviewed the evo- lution of military psychiatry in Germany between the Franco-Prussian War in 1870 and World War I in 1914. During this period, psychiatrists, a number of whom made great contributions to the field of abnormal psychol- ogy (e.g., Emil Kraepelin and Richard von Krafft-Ebing), worked with the military administration, conducting research and training doctors to detect mental health problems that could interfere with performance of duty. One early research program illustrates the interplay between medicine and the military administration. Kraepelin, who viewed alcohol as a key cause of psycho- logical problems among soldiers, conducted a research project evaluating the extent to which alcohol consump- tion adversely affected the soldiers’ ability to fire their rifles effectively.
Historical and Contemporary Views of Abnormal Behavior 45
general public, however, the asylum was an eerie place and its occupants a strange and frightening lot. Little was done by the psychiatrists to educate the public or reduce the general fear of insanity. A principal reason for this silence, of course, was that early psychiatrists had few treatment strategies or effective procedures to help patients.
Nineteenth-Century Views of the Causes and Treatment of Mental Disorders In the early part of the nineteenth century, mental hospitals were controlled essentially by laypersons because of the prominence of moral management in the treatment of “lunatics.” Medical professionals—or “alienists,” as psy- chiatrists were called at this time in reference to their treat- ing the “alienated,” or insane—had a relatively inconsequential role in the care of the insane and the man- agement of the asylums of the day. Moreover, effective treatments for mental disorders were unavailable, the only measures being such procedures as drugging, bleeding, and purging, which produced few objective results. How- ever, during the latter part of the century, alienists gained control of the insane asylums and incorporated the tradi- tional moral management therapy into their other rudi- mentary physical medical procedures.
Over time, the alienists acquired more status and influ- ence in society and became influential as purveyors of morality, touting the benefits of Victorian morality as important to good mental health. Mental disorders were only vaguely understood, and conditions such as melan- cholia (depression) were considered to be the result of nervous exhaustion. That is, psychiatrists of the time thought that emotional problems were caused by the expenditure of energy or by the depletion of bodily ener- gies as a result of excesses in living. The mental deteriora- tion or “shattered nerves” that supposedly resulted from a person’s using up precious nerve force came to be referred to as “neurasthenia,” a condition that involved pervasive feelings of low mood, lack of energy, and physical symp- toms that were thought to be related to “lifestyle” prob- lems brought on by the demands of civilization. These vague symptoms, viewed by the alienists/psychiatrists as a definable medical condition, were then considered treat- able by medical men of the times.
Changing Attitudes Toward Mental Health in the Early Twentieth Century It is difficult to partition modern views of abnormal behav- ior into discrete, uniform attitudes or to trace their histori- cal precedents without appearing arbitrary and overly simplistic. However, a brief, selective overview here will bring us into the contemporary era and set the scene for our discussion of the major viewpoints and causal consid- erations discussed in Chapter 3. By the end of the nine- teenth century, the mental hospital or asylum—“the big house on the hill”—with its fortress-like appearance, had become a familiar landmark in America. In it, patients with mental illness lived under relatively harsh conditions despite the inroads made by moral management. To the
In the first half of the twentieth century, hospital care for people with mental illness afforded very little in the way of effective treatment. In many cases, the care was considered to be harsh, punitive, and inhumane.
Gradually, however, important strides were made toward changing the general public’s attitude toward patients with mental illness. In America, the pioneering work of Dix was followed by that of Clifford Beers (1876–1943), whose book A Mind That Found Itself was first published in 1908. Beers, a Yale graduate, described his own mental collapse and told of the bad treatment he received in three typical institutions of the day. Although chains and other torture devices had long since been given up, the straitjacket was still widely used as a means of “quieting” excited patients. Beers experienced this treatment and supplied a vivid description of what such painful immobilization of the arms means to an overwrought mental patient in a widely read descrip- tion of his experiences.
After Beers recovered in the home of a kind attendant, he launched a campaign to make people realize that such treatment was no way to handle the sick. He soon won the interest and support of many public-spirited individuals, including the eminent psychologist William James and the “dean of American psychiatry,” Adolf Meyer.
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marked the beginning of an important period of change. In that year, Mary Jane Ward published a very influential book, The Snake Pit, which was popularized in a movie of the same name. This work called attention to the plight of patients with mental illness and helped to create concern over the need to provide more humane mental health care in the community in place of the overcrowded mental hos- pitals. Also in 1946, the National Institutes of Mental Health was organized and provided active support for research and training through psychiatric residencies and (later) clinical psychology training programs. Moreover, the Hill-Burton Act, a program that funded community mental health hospitals, was passed during this period. This legislation, along with the Community Mental Health Act of 1963, helped to create a far-reaching set of programs to develop outpatient psychiatric clinics, inpatient facilities in general hospitals, and community consultation and rehabilitation programs. Baker and colleagues (2012) dis- cussed the broad extension of clinical psychology after World War II with the increased development of mental health services for veterans returning from the war.
The need for reform in psychiatric hospitals was a prom- inent concern of many professionals and laypersons alike
Mental Hospital Care in the Twentieth Century The twentieth century began with a continued period of growth in asylums for people with mental illness; however, the fate of patients with mental illness during that century was neither uniform nor entirely positive (see the World Around Us box). At the beginning of the twentieth century, with the influence of enlightened people such as Clifford Beers, mental hospitals grew substantially in number— predominantly to house persons with severe mental disor- ders such as schizophrenia, depression, organic mental disorders, tertiary syphilis and paresis (syphilis of the brain), and severe alcoholism. By 1940 the public mental hospitals housed over 400,000 patients, roughly 90 percent of whom resided in large state-funded hospitals; the remainder resided in private hospitals (Grob, 1994). Dur- ing this period, hospital stays were typically quite lengthy, and many individuals with mental illness were destined to be hospitalized for many years. For the first half of the twentieth century, hospital care was accompanied by little in the way of effective treatment, and the care was often harsh, punitive, and inhumane. The year 1946, however,
The World Around Us Chaining Mental Health Patients
Because of limited mental health treatment resources in some countries, it is not uncommon for people with mental illness to be chained. Westermeyer and Kroll (1978) conducted an epidemio- logic study on the use of restraints for people with mental illness in 27 villages in Laos. They reported that people with mental ill- ness who were aggressive toward others or who were consid- ered to be a danger to themselves were sometimes restrained by being chained to posts. The woman from Laos in the photograph shown here suffered from a psychotic disorder and reportedly felt compelled to sweep her platform for 6 or 7 hours a day. She
was restrained at a Buddhist temple in order to keep her from wandering into the jungle (Westermeyer, 2001).
Treatment of patients at the Mohammad Ali Shah Shrine in eastern Afghanistan involves being fed only a small piece of bread, a raw chili, and water each day for 21 days. Their family is charged 20 pounds a month. Many patients are chained as a means of controlling their behavior.
Many temples in some countries provide homes for individu- als who are psychologically disturbed, although the care is typically inadequate. For example, Erwady, India, near Madras, has 15 pri- vately run homes, many of which are without electricity, tap water, toilet facilities, and beds. In 2000, six people died from waterborne disease at one of the Erwady asylums, prompting the government to direct an inquiry into the conditions of the mental health asylums. Later, fire swept through a palm-thatched shed that housed people with mental illness at one Erwady asylum, killing 25 patients and injuring 5 others, many of whom were chained to heavy stones or pillars (Associated Press, 2001). At the time of the fire, the asylum housed 46 residents; only 16 of the patients escaped uninjured.
What social factors today might prompt people in some societies to engage in the extreme action of chaining indi- viduals with mental health problems? How would Philippe Pinel during the eighteenth century or Clifford Beers in the early twentieth century view these contemporary chaining events?Chained patient from Laos
Historical and Contemporary Views of Abnormal Behavior 47
The original impetus behind the deinstitutionalization policy was that it was considered more humane (and cost effective) to treat disturbed people outside of large mental hospitals because doing so would prevent people from acquiring negative adaptations to hospital confinement. Many professionals were concerned that the mental hospi- tals were becoming permanent refuges for disturbed peo- ple who were “escaping” from the demands of everyday living and were settling into a chronic sick role with a per- manent excuse for letting other people take care of them. There was great hope that new medications would pro- mote a healthy readjustment and enable former patients to live more productive lives outside the hospital. In a recent review on the influence of deinstitutionalization on dis- charged patients, Kunitoh (2013) found that, although many symptoms and social behavioral problems remained unchanged, both living skills and quality of life were improved after discharge. However, many former patients have not fared well in community living and authorities now frequently speak of the “abandonment” of chronic patients to a cruel and harsh existence. Evidence of this failure to treat psychiatric patients successfully in the com- munity can be readily seen in our cities: Many of the peo- ple living on the streets in large cities today are homeless and have mental illnesses. The problems caused by deinsti- tutionalization appear to be due, in no small part, to the failure of society to develop ways to fill the gaps in mental health services in the community (Grob, 1994).
during the 1950s and 1960s. A great deal of professional attention was given to the need to improve conditions in mental hospitals following the publication of another influ- ential book, Asylums, by the sociologist Erving Goffman (1961). This book further exposed the inhumane treatment of patients with mental illness and provided a detailed account of neglect and maltreatment in mental hospitals. The move- ment to change the mental hospital environment was also enhanced significantly by scientific advances in the last half of the twentieth century, particularly the development of effective medications for many disorders—for example, the use of lithium in the treatment of manic depressive disorders (Cade, 1949) and the introduction of phenothiazines for the treatment of schizophrenia. (See Developments in Research and Chapter 17 for further discussion.)
During the latter decades of the twentieth century, our society had seemingly reversed its position with respect to the means of providing humane care for people with mental illness in the hospital environment. Vigorous efforts were made to close down mental hospitals and return people who were psychiatrically disturbed to the community, ostensibly as a means of providing more integrated and humane treat- ment than was available in the “isolated” environment of the psychiatric hospital and because of the success of medi- cations (chlorpromazine) that emerged in the 1950s to allevi- ate psychotic symptoms (Alanen et al., 2009). Large numbers of psychiatric hospitals were closed, and there was a signifi- cant reduction in state and county mental hospital popula- tions, from over half a million in 1950 (Lerman, 1981) to about 100,000 by the early 1990s (Narrow et al., 1993). These reductions are all the more impressive given that the U.S. population increased substantially during those years. This movement, referred to as deinstitutionalization, although motivated by benevolent goals, has also created great diffi- culties for many people with psychological challenges and for many communities as well (see Chapter 17).
As a phenomenon, deinstitutionalization is an interna- tional movement. For example, there has been a shift in the locus of care of patients with chronic psychiatric illnesses from psychiatric hospitals to community-based residential services in Hong Kong (Chan, 2001), in the Netherlands (Pijl et al., 2001), and in Finland (Korkeila et al., 1998). Some countries have experienced extensive deinstitution- alization during the past 20 years. For example, in England and Wales during the last decades of the twentieth century, only 14 of 130 psychiatric institutions remained open; and Australia showed a 90 percent reduction in hospital beds during the same period (Goldney, 2003). In a follow-up study of patients from 22 hospitals in Italy, D’Avanzo and colleagues (2003) report that all were closed and 39 percent of the patients in these hospitals had been discharged to nursing homes, 29 percent to residential facilities, and 29 percent to other psychiatric hospitals; only 2 percent were returned to their families.
Freed from the confines of institutionalized care, or abandoned by society? Many homeless people suffer from one or more mental disorders. Deinstitutionalization, though motivated by benevolent goals, has created great difficulties for many individuals with psychological disturbances who have been released to a cruel and harsh existence.
The mental institution, once thought to be the most humane way to manage the problems of people with severe mental illnesses, came to be seen as obsolete or as an evil alternative, more of a problem than a solution to men- tal health problems. By the end of the twentieth century,
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Biological Discoveries: Establishing the Link Between the Brain and Mental Disorder Advances in the study of biological and anatomical factors as underlying both physical and mental disorders devel- oped during this period. A major biomedical breakthrough, for example, came with the discovery of the organic factors underlying general paresis—syphilis of the brain. One of the most serious mental illnesses of the day, general paresis produced paralysis and insanity and typically caused death within 2 to 5 years as a result of brain deterioration. This scientific discovery, however, did not occur overnight; it required the combined efforts of many scientists and researchers for nearly a century.
GENERAL PARESIS AND SYPHILIS The discovery of a cure for general paresis began in 1825, when the French physician A. L. J. Bayle (1799–1858) differentiated general paresis as a specific type of mental disorder. Bayle gave a complete and accurate description of the symptom pattern of paresis and convincingly presented his reasons for believing paresis to be a distinct disorder. Many years later, in 1897, the Viennese psychiatrist Richard von Krafft-Ebing conducted experiments involving the inoculation of patients with paresis with matter from syphilitic sores. None of the patients developed secondary symptoms of syphilis, which led to the conclusion that they must previ- ously have been infected. This crucial experiment estab- lished the relationship between general paresis and syphilis. It was almost a decade later, in 1906, when August von Wassermann devised a blood test for syphilis. This devel- opment made it possible to check for the presence of the deadly bacteria in the bloodstream of an individual before the more serious consequences of infection appeared.
Finally, in 1917, Julius von Wagner-Jauregg, chief of the psychiatric clinic of the University of Vienna, intro- duced the malarial fever treatment of syphilis and pare- sis because he knew that the high fever associated with malaria killed off the bacteria. He infected nine patients with paresis with the blood of a malaria-infected soldier and found marked improvement in paretic symptoms in three patients and apparent recovery in three others. By 1925 several hospitals in the United States were incorpo- rating the new malarial treatment for paresis into their hospital treatments. One of the earliest controlled stud- ies of malarial treatment for paresis was conducted by Bahr and Brutsch in Indiana in 1928. They found that out of the 100 patients studied, 37 percent of patients with paresis showed significant recovery, 25 percent had been discharged, and 21 percent of those had returned to their previous or similar occupations. Today, of course, we have penicillin as an effective, simpler treatment of syphilis, but the early malarial treatment represented
inpatient mental hospitals had been substantially replaced by community-based care, day treatment hospi- tals, and outreach.
The twentieth century closed on a note of uncertainty with respect to the best ways to manage the needs of severely disturbed psychiatric patients. It is clear that closing mental hospitals and providing treatment for severely disturbed people in the community has not proved to be the panacea it was touted to be only a few years ago (Whitaker, 2009). As we will discuss further in Chapter 17, deinstitutionalization has created problems for both patients and society as a whole. The role of the psychiatric hospital in helping those with severe psychi- atric problems is likely to undergo further evolution as society again finds itself unable to deal effectively with the problems that severe mental illness can create if ignored or left unattended (see Grob, 1994).
in review • Describe the changing views toward mental illness that evolved
as scientific thinking came to have greater influence in Europe in the sixteenth and seventeenth centuries.
• Discuss the development of the psychiatric hospital.
• Describe the historical development of humanitarian reform, and give some of the reasons why it occurred.
• Describe the changes in social attitudes that brought about major changes in the way persons with mental disorders have been treated.
The Emergence of Contemporary Views of Abnormal Behavior 2.3 Identify developments that led to the contemporary
view of abnormal psychology.
While the mental hygiene movement was gaining ground in the United States during the latter years of the nine- teenth century, great technological discoveries occurred both at home and abroad. These advances helped usher in what we know today as the scientific, or experimentally oriented, view of abnormal behavior and the application of scientific knowledge to the treatment of individuals with mental disturbances. In this section we describe four major themes in abnormal psychology that spanned the nine- teenth and twentieth centuries and generated powerful influences on our contemporary perspectives in abnormal behavior: (1) biological discoveries, (2) the development of a classification system for mental disorders, (3) the emergence of psychological causation views, and (4) experimental psychological research developments.
Historical and Contemporary Views of Abnormal Behavior 49
were eventually discredited, although lobotomy is still used in some rare cases.
It is important to note here that although the discovery of the organic bases of mental disorders addressed the “how” behind causation, it did not, in most cases, address the “why.” This is sometimes true even today. For example, although we know what causes certain “presenile” mental disorders—brain pathology—we do not yet know why some individuals are afflicted and others are not. Nonethe- less, we can predict quite accurately the courses of these dis- orders. This ability is due not only to a greater understanding of the organic factors involved but also, in large part, to the work of a follower of Griesinger, Emil Kraepelin.
The Development of a Classification System Emil Kraepelin (1856–1926), another German psychiatrist, played a dominant role in the early development of the biological viewpoint. His textbook Compendium der Psychiat- rie, published in 1883, not only emphasized the importance of brain pathology in mental disorders but also made several related contributions that helped establish this viewpoint. The most important of these contributions was
the first clear-cut conquest of a mental disorder by medi- cal science. The field of abnormal psychology had come a long way—from superstitious beliefs to scientific proof of how brain pathology can cause a specific disorder. This breakthrough raised great hopes in the medical community that organic bases would be found for many other mental disorders—perhaps for all of them.
BRAIN PATHOLOGY AS A CAUSAL FACTOR With the emergence of modern experimental science in the early part of the eighteenth century, knowledge of anatomy, physiology, neurology, chemistry, and general medicine increased rapidly. Scientists began to focus on diseased body organs as the cause of physical ailments. It was the next logical step for these researchers to assume that men- tal disorder was an illness based on the pathology of an organ—in this case, the brain. In 1757 Albrecht von Haller (1708–1777), in his Elementa physiologae corporis humani, emphasized the importance of the brain in psychic func- tions and advocated postmortem dissection to study the brains of the insane. The first systematic presentation of this viewpoint, however, was made by the German psy- chiatrist Wilhelm Griesinger (1817–1868). In his textbook The Pathology and Therapy of Psychic Disorders, published in 1845, Griesinger insisted that all mental disorders could be explained in terms of brain pathology. Following the dis- covery that brain deterioration resulted in general paresis, other successes followed. Alois Alzheimer and other inves- tigators established the brain pathology in cerebral arterio- sclerosis and in the senile mental disorders. Eventually, in the twentieth century, the organic pathologies underlying the toxic mental disorders (disorders caused by toxic sub- stances such as lead), certain types of mental retardation, and other mental illnesses were discovered.
Along with the advancements in mental health treat- ment in the twentieth century came some unfortunate missteps. During the early years of the twentieth century, Henry Cotton, a psychiatrist at a New Jersey hospital, developed a theory that mental health problems such as schizophrenia could be cured by removing the infections that he believed caused the condition. He used surgical procedures to remove all of a person’s teeth or body parts such as tonsils, parts of the colon, testicles, or ova- ries in order to reduce the infection (Scull, 2005). In the 1920s through the 1940s, an American psychiatrist, Walter Freeman, followed the strategies developed by Italian psychiatrist Egas Moniz to treat severe mental disorders using surgical procedures called lobotomies. Freeman modified the surgery used by Moniz, using an ice pick to sever the neural connections in the brain after entering through the patient’s eye sockets (see discussion on lobotomy by El-Hai, 2005). These surgical efforts to treat mental disorder were considered to be ineffective and inappropriate by many in the profession at the time and
Emil Kraepelin (1856–1926) was a German psychiatrist who developed an early synthesis and classification system of the hundreds of mental disorders by grouping diseases together based on common patterns of symptoms. Kraepelin also demonstrated that mental disorders showed specific patterns in the genetics, course, and outcome of disorders.
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predetermined and predictable as the course of measles. Thus, the outcome of a given type of disorder could pre- sumably be predicted even if it could not yet be controlled. Such claims led to widespread interest in the accurate description and classification of mental disorders.
Development of the Psychological Basis of Mental Disorder Despite the emphasis on biological research, understanding of the psychological factors in mental disorders was progress- ing as well. The first major steps were taken by Sigmund Freud (1856–1939), the most frequently cited psychological
his system of classification of mental disorders, which became the forerunner of today’s DSM classification (see Chapters 1 and 4). Kraepelin noted that certain symptom patterns occurred together regularly enough to be regarded as specific types of mental disease. He then pro- ceeded to describe and clarify these types of mental disor- ders, working out a scheme of classification that is the basis of our present system. Integrating all of the clinical material underlying this classification was a Herculean task and represented a major contribution to the field of psychopathology.
Kraepelin saw each type of mental disorder as distinct from the others and thought that the course of each was as
Developments in Research The Search for Medications to Cure Mental Disorders
For centuries physicians have sought a medicinal cure for mental disorders. One of the earliest known treatises on the use of drugs to treat mental disorders is the work of the Roman physician Galen (a.d. 130–200). His writing details both the concoction of various medications and the clinical use of drug therapy with patients experiencing mental disorders. Most of his medications were laxatives and emetics (purgatives) that were used to cleanse the body of nonhuman materials believed to be causing the per- son’s ills. During the Middle Ages, another notable but highly con- troversial physician-chemist named Paracelsus (1490–1541) experimented with various chemicals as medications to treat human disorders. He even used a substance referred to as “mummy powder” (ground up particles of mummies) and various other, seemingly more potent substances such as mercury.
A more recent phase in the development of psychotropic medicine began in the 1950s. The root Rauwolfia serpentina had been used for centuries as an herbal folk medicine in India, where it had been prescribed for a wide array of afflictions, including insanity. In the early 1950s the active ingredient in Rauwolfia, reserpine, was isolated by a Swiss drug company, and in 1953 psychiatrist R. A. Hakim wrote a prize-winning paper on using Rauwolfia to treat psychosis (as cited in Gupta et al., 1943). Today reserpine has been surpassed as a treatment for psychoses because of the development of other drugs and because of its side effects, and it is mostly used in the treatment of hypertension.
The second psychoactive drug to emerge in the 1950s as a treatment for severe mental disorder was chlorpromazine. A German chemist named Bernthsen, searching for compounds that would operate as dyes, first developed the drug in the latter part of the nineteenth century. He synthesized a compound that is referred to as phenothiazine. Paul Erlich, a medical researcher and father of the field of chemotherapy, thought that this com- pound might be effective in treating human diseases by killing nonhuman cells while preserving human tissue. The drug was first tried as a means of treating malaria, and by the 1930s it was being employed as an anesthetic. In 1951, the French surgeon Henri Laborit employed the drug as an “artificial hibernator” to
prevent shock among surgical patients. It was not until 1952 that two French psychiatrists, Jean Delay and Pierre Deniker, finding that the drug reduced psychotic symptoms, began to use chlor- promazine to treat psychiatric patients.
The almost magical impact of antipsychotic medication was immediately felt in the psychiatric community in the United States. By 1956, the first year of widespread use of reserpine and chlor- promazine, the impact on psychiatric hospitalization had begun to show a remarkable effect. The previously increasing admission rate to psychiatric hospitals leveled off at 560,000 psychiatric inpa- tients in the United States. This number had dropped to 490,000 by 1964 and to 300,000 by 1971. Currier (2000) reported that the number of inpatient psychiatric beds decreased sharply during the past generation, both in absolute numbers and as a percentage of total hospital beds in seven countries including the United States. The drop in available hospital beds between and 1960 and 1994 was from 4 per thousand to less than 1.3 per thousand of the population. In the United States, the available bed reductions were fostered by the movement for deinstitutionalization and the devel- opment of managed care. In Europe and other regions, the num- ber of beds decreased largely as a result of intense government pressure to curtail health care budgets. Interestingly, the need for psychiatric inpatient care has remained despite the closing of pub- lic mental health hospitals. Hutchins and colleagues (2011) point out that the number of private mental hospitals doubled between 1976 and 1992 and that two-thirds of all psychiatric hospitals and half of all inpatient beds were in private facilities.
The effectiveness of drugs in reducing psychotic symptoms has also led researchers to develop more specific causal hypoth- eses for mental disorders such as schizophrenia. Researchers have noted that antipsychotic drugs such as the phenothiazines modify the levels of dopamine, a neurotransmitter associated with schizophrenia. These observations have led theoreticians to the “dopamine hypothesis”—that the metabolism of dopamine is associated with the cause of schizophrenia.
Sources: Frankenburg (1994); Green (1951); Moriarty et al. (1984); Pachter (1951).
Historical and Contemporary Views of Abnormal Behavior 51
years—in fact, mesmerism, as his technique came to be known, was as much a source of heated discussion in the early nineteenth century as psychoanalysis became in the early twentieth century. This discussion led to renewed interest in hypnosis itself as an explanation of the “cures” that took place.
theorist of the twentieth century (Street, 1994). During five decades of observation, treatment, and writing, Freud developed a comprehensive theory of psychopa- thology that emphasized the inner dynamics of uncon- scious motives (often referred to as psychodynamics) that are at the heart of the psychoanalytic perspective. The methods he used to study and treat patients came to be called psychoanalysis. We can trace the ancestral roots of psychoanalysis to a somewhat unexpected place—the study of hypnosis, especially in its relation to hysteria. (For a contemporary discussion of hysteria, see Brown, 2006.) Hypnosis, an induced state of relaxation in which a person is highly open to suggestion, first came into widespread use in late-eighteenth- and early-nineteenth-century France.
MESMERISM Our efforts to understand psychological causation of mental disorder start with Franz Anton Mesmer (1734–1815), an Austrian physician who further developed the ideas of Paracelsus (the influential sixteenth-century physician and scholar; see Developments in Research) about the influence of the planets on the human body. Mesmer believed that the planets affected a universal magnetic fluid in the body, the distribution of which determined health or disease. In attempting to find cures for mental disorders, Mesmer concluded that all people possessed magnetic forces that could be used to influence the distribution of the magnetic fluid in other people, thus effecting cures.
Mesmer attempted to put his views into practice in Vienna and various other cities, but it was in Paris in 1778 that he gained a broad following. There, he opened a clinic in which he treated all kinds of diseases by using “animal magnetism.” In a dark room, patients were seated around a tub containing various chemicals, and iron rods protrud- ing from the tub were applied to the affected areas of the patients’ bodies. Accompanied by music, Mesmer appeared in a lilac robe, passing from one patient to another and touching each one with his hands or his wand. By this means, Mesmer was reportedly able to remove hysterical anesthesias and paralyses. He also dem- onstrated most of the phenomena later connected with the use of hypnosis.
Mesmer was eventually branded a charlatan by his medical colleagues and an appointed body of noted scholars that included the American scientist Benjamin Franklin (Van Doren, 1938). The committee conducted what have been referred to as the first psychological experiments (Dingfelder, 2010), or tests such as tricking a woman into believing that she had been influenced by magnetism. The committee concluded that the real source of Mesmer’s power was in the patients and not in “mag- netism.” Mesmer was forced to leave Paris and quickly faded into obscurity. His methods and results, however, were at the center of scientific controversy for many
Franz Anton Mesmer (1734–1815) believed that the distribution of magnetic fluid in the body was responsible for determining health or disease. He further thought that all people possessed magnetic forces that could be used to influence the distribution of fluid in others, thus effecting cures. In this painting of his therapy, Mesmer stands on the far right, holding a wand. He was eventually branded a fraud by his colleagues. His theories did, however, demonstrate most of the phenomena later connected with the use of hypnosis.
Even after mesmerism was discredited in France, this method of inducing a trance and its perceived potential for treating illness had a long life in the United States. The magical powers of mesmerism were introduced in 1836 and intrigued a number of Americans, ranging from the poet Emerson to the physician Benjamin Rush, with specu- lations about its higher mental powers and its potential application as an anesthetic for surgical procedures (Schmit, 2005). A number of lecturers traveled the United States illustrating its medical use and giving demonstra- tions, including to the U.S. Congress. The early mesmer- ists, though considered to be “quacks” by many physicians, had an influence on medical practice until the introduction of ether as a surgical anesthetic (Schmit, 2005). In spite of its limitations, mesmerism clearly had an influence on psy- chology and hypnosis for many years and came to be influ- ential in spiritual movements such as Christian Science in the nineteenth century.
THE NANCY SCHOOL Ambrose August Liébeault (1823–1904), a French physician who practiced in the town of Nancy, used hypnosis successfully in his practice. Also in Nancy at the time was a professor of medicine, Hippolyte Bernheim (1840–1919), who became interested in the rela- tionship between hysteria and hypnosis. His interest was piqued by Liébeault’s success in using hypnosis to cure a patient whom Bernheim had been treating unsuccessfully by more conventional methods for 4 years (Selling, 1943).
52 Chapter 2
patients experiencing hysteria and came away convinced that powerful mental processes could remain hidden from consciousness.
On his return to Vienna, Freud worked in collaboration with another Viennese physician, Josef Breuer (1842–1925), who had incorporated an interesting innovation into the use of hypnosis with his patients. Unlike hypnotists before them, Freud and Breuer directed patients to talk freely about their problems while under hypnosis. The patients usually displayed considerable emotion and, on awaken- ing from their hypnotic states, felt a significant emotional release, which was called a catharsis. This simple innova- tion in the use of hypnosis proved to be of great signifi- cance: It not only helped patients discharge their emotional tensions by discussing their problems but also revealed to the therapist the nature of the difficulties that had brought about certain symptoms. The patients, on awakening, saw no relationship between their problems and their hysteri- cal symptoms.
It was this approach that led to the discovery of the unconscious—the portion of the mind that contains expe- riences of which a person is unaware—and with it the belief that processes outside of a person’s awareness can play an important role in determining behavior. In 1893, Freud and Breuer published a joint paper titled On the Psy- chical Mechanisms of Hysterical Phenomena, which was one of the great milestones in the study of the dynamics of the conscious and unconscious. Freud soon discovered, more- over, that he could dispense with hypnosis entirely. By encouraging patients to say whatever came into their minds without regard to logic or propriety, Freud found that patients would eventually overcome inner obstacles to remembering and would discuss their problems freely.
Bernheim and Liébeault worked together to develop the hypothesis that hypnotism and hysteria were related and that both were due to suggestion (Brown & Menninger, 1940). Their hypothesis was based on two lines of evidence: (1) The phenomena observed in hysteria—such as paraly- sis of an arm, inability to hear, and anesthetic areas in which an individual could be stuck with a pin without feel- ing pain (all of which occurred when there was apparently nothing organically wrong)—could be produced in normal subjects by means of hypnosis and (2) the same symptoms also could be removed by means of hypnosis. Thus, it seemed likely that hysteria was a sort of self-hypnosis. The physicians who accepted this view ultimately came to be known as adherents of the Nancy School.
Meanwhile, Jean Charcot (1825–1893), who was head of the Salpêtrière Hospital in Paris and the leading neu- rologist of his time, had been experimenting with some of the phenomena described by the mesmerists. As a result of his research, Charcot disagreed with the findings of the Nancy School and insisted that degenerative brain changes led to hysteria. In this, Charcot was eventually proved wrong, but work on the problem by so outstanding a sci- entist did a great deal to awaken medical and scientific interest in hysteria.
The dispute between Charcot and the Nancy School was one of the major debates of medical history, and many harsh words were spoken on both sides. The adher- ents to the Nancy School finally triumphed. This first rec- ognition of a psychologically caused mental disorder spurred more research on the behavior underlying hyste- ria and other disorders. Soon it was suggested that psy- chological factors were also involved in anxiety states, phobias, and other psychopathologies. Eventually, Charcot himself was won over to the new point of view and did much to promote the study of psychological factors in various mental disorders.
The debate over whether mental disorders are caused by biological or psychological factors continues to this day. The Nancy School–Charcot debate represented a major step forward for psychology, however. Toward the end of the nineteenth century, it became clear that mental disorders could have psychological bases, biological bases, or both. But a major question remained to be answered: How do the psychologically based mental disorders actu- ally develop?
THE BEGINNINGS OF PSYCHOANALYSIS The first sys- tematic attempt to answer this question was made by Sig- mund Freud (1856–1939). Freud was a brilliant, young Viennese neurologist who received an appointment as lec- turer on nervous diseases at the University of Vienna. In 1885 he went to study under Charcot and later became acquainted with the work of Liébeault and Bernheim at Nancy. He was impressed by their use of hypnosis with
Psychoanalysis was introduced to North America at a famous meeting at Clark University in Worcester, Massachusetts, in 1909. Among those present were (back row) A. A. Brill, Ernest Jones, and Sandor Ferenczi; (front row) Sigmund Freud, G. Stanley Hall, and Carl Jung.
Historical and Contemporary Views of Abnormal Behavior 53
Wundt (1832–1920) and William James (1842–1910). Although the early work of these experimental psychologists did not bear directly on clinical practice or on our understanding of abnormal behavior, this tradition was clearly influential a few decades later in molding the thinking of the psycholo- gists who brought these rigorous attitudes into the clinic. (For a discussion of the history of clinical psychology, see Benjamin, 2014, and Shriver, 2015.)
THE EARLY PSYCHOLOGY LABORATORIES In 1879 Wilhelm Wundt established the first experimental psy- chology laboratory at the University of Leipzig. While studying the psychological factors involved in memory and sensation, Wundt and his colleagues devised many basic experimental methods and strategies. Wundt directly influenced early contributors to the empirical study of abnormal behavior such as William James, G. Stanley Hall, and a student of Wundt’s, J. McKeen Cattell (1860–1944) (Benjamin, 2014); they followed his experi- mental methodology and also applied some of his research strategies to study clinical problems. For exam- ple, Cattell brought Wundt’s experimental methods to the United States and used them to assess individual differ- ences in mental processing. He and other students of Wundt’s work established research laboratories through- out the United States.
It was not until 1896, however, that another of Wundt’s students, Lightner Witmer (1867–1956), combined research with application and established the first American psy- chological clinic at the University of Pennsylvania. At Witmer’s clinic both research and therapy were conducted, with a focus on the problems of children with mental defi- ciencies. Witmer, considered to be the founder of clinical psychology (McReynolds, 1996, 1997), was influential in encouraging others to become involved in this new profes- sion. Other clinics were soon established. One clinic of great importance was the Chicago Juvenile Psychopathic Institute (later called the Institute of Juvenile Research), established in 1909 by William Healy (1869–1963). Healy was the first to view juvenile delinquency as a symptom of urbanization, not as a result of inner psychological problems. In so doing, he was among the first to recog- nize a new area of causation—environmental, or sociocul- tural, factors.
By the first decade of the twentieth century, psycho- logical laboratories and clinics were burgeoning, and a great deal of research was being generated (Goodwin, 2011). The rapid and objective communication of scientific findings was perhaps as important in the development of modern psychology as the collection and interpretation of research findings. This period saw the origin of many sci- entific journals for the propagation of research and theo- retical discoveries, and as the years have passed, the number of journals has grown. The American Psychological
Two related methods enabled him to understand patients’ conscious and unconscious thought processes. One method, free association, involved having patients talk freely about themselves, thereby providing informa- tion about their feelings, motives, and so forth. A second method, dream analysis, involved having patients record and describe their dreams. These techniques helped analysts and patients gain insights and achieve a better understanding of the patients’ emotional prob- lems. Freud devoted the rest of his long and energetic life to the development and elaboration of psychoana- lytic principles. His views were formally introduced to American scientists in 1909, when he was invited to deliver a series of lectures at Clark University by the eminent psychologist G. Stanley Hall (1844–1924), who was then president of the university. These lectures created a great deal of controversy and helped popularize psy- choanalytic concepts with scientists as well as with the general public.
We will discuss the psychoanalytic viewpoint further in Chapter 3. Freud’s lively and seminal views attracted a substantial following over his long career, and interest in his ideas persists today, more than 100 years after he began writing. Numerous other clinician-theorists—such as Carl Jung, Alfred Adler, and Harry Stack Sullivan—launched “spin-off” theories that have elaborated on the psychoana- lytic viewpoint. More will also be said of these views in Chapter 3. Here we will examine the early development of psychological research and explore the evolution of the behavioral perspective on abnormal behavior.
The Evolution of the Psychological Research Tradition: Experimental Psychology The origins of much of the scientific thinking in contempo- rary psychology lie in early rigorous efforts to study psycho- logical processes objectively, as demonstrated by Wilhelm
54 Chapter 2
Watson, a man of impressive energy and demeanor, saw great possibilities in behaviorism, and he was quick to point them out to his fellow scientists and a curious public. He boasted that through conditioning he could train any healthy child to become whatever sort of adult one wished. He also challenged the psychoanalysts and the more bio- logically oriented psychologists of his day by suggesting that abnormal behavior was the product of unfortunate, inadvertent earlier conditioning and could be modified through reconditioning.
By the 1930s Watson had had an enormous impact on American psychology. Watson’s approach placed heavy emphasis on the role of the social environment in conditioning personality development and behavior, both normal and abnormal. Today’s behaviorally ori- ented psychologists still accept many of the basic tenets of Watson’s doctrine, although they are more cautious in their claims.
Operant Conditioning While Pavlov and Watson were studying stimulus–response conditioning, E. L. Thorndike (1874–1949) and subsequently B. F. Skinner (1904–1990) were exploring a different kind of conditioning, one in which the consequences of behavior influence behavior. Behavior that operates on the environment may be instru- mental in producing certain outcomes, and those out- comes, in turn, determine the likelihood that the behavior will be repeated on similar occasions. For example, Thorndike studied how cats could learn a particular response, such as pulling a chain, if that response was fol- lowed by food reinforcement. This type of learning came to be called instrumental conditioning and was later renamed operant conditioning by Skinner. Both terms are still used today. In Skinner’s view, behavior is “shaped” when something reinforces a particular activity of an organism—which makes it possible “to shape an animal’s behavior almost as a sculptor shapes a lump of clay” (Skinner, 1951, pp. 26–27).
Association publishes numerous scientific journals, many of which focus on research into abnormal behavior and personality functioning.
THE BEHAVIORAL PERSPECTIVE Although psycho- analysis dominated thought about abnormal behavior at the end of the nineteenth century and in the early twentieth century, another school—behaviorism—emerged out of experimental psychology to challenge its supremacy. Behavioral psychologists believed that the study of sub- jective experience—through the techniques of free asso- ciation and dream analysis—did not provide acceptable scientific data because such observations were not open to verification by other investigators. In their view, only the study of directly observable behavior—and the stimuli and reinforcing conditions that “control” it—could serve as a basis for formulating scientific principles of human behavior.
The behavioral perspective is organized around a cen- tral theme: the role of learning in human behavior. Although this perspective was initially developed through research in the laboratory rather than through clinical prac- tice, its implications for explaining and treating maladap- tive behavior soon became evident.
Classical Conditioning The origins of the behavioral view of abnormal behavior and its treatment are tied to experimental work on the type of learning known as classical conditioning—a form of learning in which a neutral stimulus is paired repeatedly with an uncondi- tioned stimulus that naturally elicits an unconditioned behavior. After repeated pairings, the neutral stimulus becomes a conditioned stimulus that elicits a conditioned response. This work began with the discovery of the con- ditioned reflex by Russian physiologist Ivan Pavlov (1849–1936). Around the turn of the twentieth century, Pavlov demonstrated that dogs would gradually begin to salivate in response to a nonfood stimulus such as a bell after the stimulus had been regularly accompanied by food.
Pavlov’s discoveries in classical conditioning excited a young American psychologist, John B. Watson (1878–1958), who was searching for objective ways to study human behavior. Watson reasoned that if psychology was to become a true science, it would have to abandon the sub- jectivity of inner sensations and other “mental” events and limit itself to what could be objectively observed. What better way to do this than to observe systematic changes in behavior brought about simply by rearranging stimulus conditions? Watson thus changed the focus of psychology to the study of overt behavior rather than the study of theoretical mentalistic constructs, an approach he called behaviorism.
Ivan Pavlov (1849–1936), a pioneer in demonstrating the part conditioning plays in behavior, is shown here with the staff and some of the apparatus used to condition reflexes in dogs.
Historical and Contemporary Views of Abnormal Behavior 55
B. F. Skinner (1904–1990) formulated the concept of operant conditioning, in which reinforcers can be used to make a response more or less probable and frequent. some of the key contributors to the field of abnormal psy-
chology, see Table 2.1.
in review • Compare the views of the Nancy School with those of Charcot.
How did this debate influence modern psychology?
• Evaluate the impact of the work of Freud and that of Watson on psychology today.
• How did early experimental science help to establish brain pathology as a causal factor in mental disorders?
• Describe the historical development of the behavioral view in psychology.
Table 2.1 Major Figures in the Early History of Abnormal Psychology The Ancient World
Hippocrates (460–377 b.c.) A Greek physician who believed that mental disease was the result of natural causes and brain pathology rather than demonology.
Plato (429–347 b.c.) A Greek philosopher who believed that patients with mental illness should be treated humanely and should not be held responsible for their actions.
Aristotle (384–322 b.c.) A Greek philosopher and a pupil of Plato who believed in the Hippocratic theory that various agents, or humors, within the body, when imbalanced, were responsible for mental disorders. Aristotle rejected the notion of psychological factors as causes of mental disorders.
Galen (a.d. 130–200) A Greek physician who contributed much to our understanding of the nervous system. Galen divided the causes of mental disorders into physical and mental categories.
The Middle Ages
Avicenna (c. 980–1037) An ancient Persian physician who promoted principles of humane treatment for people with mental disturbances at a time when Western approaches to mental illness were inhumane.
Hildegard (1098–1179) A remarkable woman, known as the “Sybil of the Rhine,” who used curative powers of natural objects for healing and wrote treatises about natural history and medicinal uses of plants.
Hippocrates Galen
Avicenna
In this chapter we have touched on several important trends in the evolution of the field of abnormal psychology and have recounted the contributions of numerous indi- viduals from history who have shaped our current views. The vast amount of information available can cause confu- sion and controversy when efforts are made to obtain an integrated view of behavior and causation. We may have left supernatural beliefs behind, but we have moved into something far more complex in trying to determine the role of natural factors—be they biological, psychological, or sociocultural—in abnormal behavior. For a recap of
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The Sixteenth Through the Eighteenth Centuries
Paracelsus (1490–1541) A Swiss physician who rejected demonology as a cause of abnormal behavior. Paracelsus believed in psychic causes of mental illness.
Teresa of Avila (1515–1582) A Spanish nun, since canonized, who argued that mental disorder was an illness of the mind.
Johann Weyer (1515–1588) A German physician who argued against demonology and was ostracized by his peers and the Church for his progressive views.
Robert Burton (1576–1640) An Oxford scholar who wrote a classic, influential treatise on depression, The Anatomy of Melancholia, in 1621.
William Tuke (1732–1822) An English Quaker who established the York Retreat, where patients with mental illness lived in humane surroundings.
Philippe Pinel (1745–1826) A French physician who pioneered the use of moral management in La Bicêtre and La Salpêtrière hospitals in France, where patients with mental illness were treated in a humane way.
Benjamin Rush (1745–1813) An American physician and the founder of American psychiatry, who used moral management, based on Pinel’s humanitarian methods, to treat people with mental disturbances.
The Nineteenth and Early Twentieth Centuries
Dorothea Dix (1802–1887) An American teacher who founded the mental hygiene movement in the United States, which focused on the physical well-being of patients with mental illness in hospitals.
Clifford Beers (1876–1943) An American who campaigned to change public attitudes toward patients with mental illness after his own experiences in mental institutions.
Franz Anton Mesmer (1734–1815) An Austrian physician who conducted early investigations into hypnosis as a medical treatment.
Emil Kraepelin (1856–1926) A German psychiatrist who developed the first diagnostic system.
Sigmund Freud (1856–1939) The founder of the school of psychological therapy known as psy- choanalysis.
Wilhelm Wundt (1832–1920) A German scientist who established the first experimental psychology laboratory in 1879 and subsequently influenced the empirical study of abnormal behavior.
J. McKeen Cattell (1860–1944) An American psychologist who adopted Wundt’s methods and studied individual differences in mental processing.
Lightner Witmer (1867–1956) An American psychologist who established the first psychological clinic in the United States, focusing on problems of children with mental deficiencies. He also founded the journal The Psychological Clinic in 1907.
William Healy (1869–1963) An American psychologist who established the Chicago Juvenile Psychopathic Institute and advanced the idea that mental illness was due to environmental, or sociocultural, factors.
Ivan Pavlov (1849–1936) A Russian physiologist who published classical studies in the psychol- ogy of learning.
John B. Watson (1878–1958) An American psychologist who conducted early research into learning principles and came to be known as the father of behaviorism.
B. F. Skinner (1904–1990) An American learning theorist who developed the school of learning known as operant conditioning and was influential in incorporating behavioral principles into influencing behavioral change.
Benjamin Rush
Dorothea Dix
Sigmund Freud
John B. Watson B.F. Skinner
Unresolved Issues Interpreting Historical Events
Understanding current events and phenomena depends to a substantial degree on having an accurate understanding of the historical development of knowledge. Many psychologists hold the view that psychological theorizing can be advanced by greater use of historical data (McGuire, 1994). This chapter has attempted to provide a historical perspective on some of the concepts you will encounter in the chapters that follow. You might think that looking back in history to get a picture of events that occurred long ago would not be a difficult task—that it would be a simple
matter of reviewing some history books and some publications from the time in question. However, different and conflicting views as to the importance and relevance of historical events in contem- porary psychology have emerged. The traditional view maintains that historical events are stepping stones for understanding con- temporary events, while a “New History” approach minimizes this cumulative and often celebratory approach and questions the cumulative knowledge aspect. Instead, this approach favors con- sidering history as “national habits or characteristics of a culture
Historical and Contemporary Views of Abnormal Behavior 57
that does not necessarily serve as cumulative force in the advancement of knowledge” (for an interesting discussion of his- torical approaches see Lovett, 2006). The distinction here is whether past developments in acquiring knowledge and under- standing build on each other to create a more accurate picture or whether such developments should be viewed independently in their own context.
Regardless of one’s view of the historical approach, those who try to understand the historical context of particular phe- nomena or ideas are sometimes confronted with what Burton (2001) referred to as the tenacity of historical misinformation. He pointed out that there is one discouraging theme in the history of science—the widespread acceptance of false accounts. He noted that it is not uncommon for psychological findings and theories to be exaggerated or distorted and that the exaggera- tions frequently spread much further through public sources than do the authentic facts. For example, he noted the wide- spread acceptance, and inclusion in many textbooks, of inac- curate restatements of the widely cited study of Little Albert’s fear of furry objects:
Little Albert
Little Albert was the famous toddler who, originally unafraid of rats, exhibited such a fear when J. B. Watson and Rayner (1920) paired the presence of a rat with a loud noise. Harris (1979), Samelson (1980), and Gilovich (1991) are among the critics who have noted how frequently and consistently this case is misrep- resented and exaggerated. J. B. Watson and Rayner described pairing the loud noise with the rat and later testing Albert’s reac- tion to a rat and a rabbit, as well as to blocks, a seal coat, cotton wool, the hair of Watson and some assistants, and a Santa Claus mask. Albert never reacted to the blocks or the assistants’ hair, always reacted to the rat, and reacted to the other objects with various degrees of agitation that were sometimes vividly described but sometimes merely (and vaguely) termed “negative reaction.” According to Harris (1979, p. 153), secondary sources have erroneously reported the testing of “a fur pelt, . . . a man’s beard, . . . a cat, a pup, a fur muff, . . . a white furry glove, . . . Albert’s aunt, who supposedly wore fur, . . . either the fur coat or the fur neckpiece of Albert’s mother, . . . and even a teddy bear.” (pp. 228–229)
Another factor that can affect the quality of historical informa- tion is that our views of history and our understanding of events are sometimes open to reinterpretation. As Schudson (1995) points out, “Collective memory, more than individual memory, at least in liberal pluralistic societies, is provisional. It is always open to contestation” (p. 16). Any number of obstacles can stand in the way of our gaining an accurate picture of the attitudes and behaviors of people who lived hundreds of years ago. This has certainly been the case with our views of the Middle Ages (Kroll & Bachrach, 1984).
The foremost problem in retrospective psychological analy- sis is that we cannot rely on direct observation, a hallmark of psychological research. Instead, we must turn to written docu- ments or historical surveys of the times. Although these sources are often full of fascinating information, they may not reveal directly the information we seek; we must therefore extrapolate
“facts” from the information we have, which is not always an easy task. We are restricted in our conclusions by the documents or sources available to us. Attempting to learn about people’s atti- tudes and subtle social perceptions hundreds of years ago by examining surviving church documents or biographical accounts is less than ideal. First, we inevitably view these documents out of the context in which they were written. Second, we do not know whether the authors had ulterior motives or what the real purposes of the documents were. For example, some histori- ans have concluded erroneously that people of the Middle Ages considered sin to be a major causal factor in mental illness. This misconception may have been due in part to zealous authors invoking “God’s punishment” against the victims of mental ill- nesses who happened to be their enemies. Apparently, if the victims happened to be friends, sin was typically not mentioned as a causal factor (Kroll & Bachrach, 1984). Such writings, of course, are biased, but we may have no way of knowing this. The fewer the sources surveyed, the more likely that any existing bias will go undetected.
In other cases, concepts important to historical interpre- tation may have quite a different meaning to us today than they had in the past, or the meaning may simply be unclear. Kroll and Bachrach (1984) point out that the concept of “pos- session,” so critical to our views of the Middle Ages, is a very vague and complex concept for which we have no helpful natu- ral models. Our language fails us, except for colorful analogies and metaphors. Just as the term nervous breakdown means different things to different people, so too possession means and meant many different things and undoubtedly had a differ- ent range of meanings to medieval persons from what it has to us. This kind of uncertainty can make definitive assessments of things that happened during the Middle Ages difficult, if not impossible (Phillips, 2002).
Bias can come into play during interpretation also. Our interpretations of historical events or previously held beliefs can be colored by our own views of what is normal and what is abnormal. In fact, it is difficult to conduct a retrospective analy- sis without taking current perspectives and values as a start- ing point. For example, our modern beliefs about the Middle Ages have led, says Schoeneman (1984), to our contemporary misinterpretation that during the fifteenth and sixteenth centu- ries people with mental illness were typically accused of being witches. For most of us, this mistaken interpretation makes sense simply because we do not understand the medieval per- spective on witchcraft.
Although reevaluations of the Middle Ages have discredited the view that demonology, sin, and witchcraft played key roles in the medieval understanding of mental illness, it is also clear that in some cases these concepts were associated with mental illness. Where does the truth lie? It appears that the last word has not been written on the Middle Ages, nor on any period of our history for that matter. At best, historical views—and, there- fore, retrospective psychological studies—must be regarded as working hypotheses that are open to change as new perspec- tives are applied to history and as “new” historical documents are discovered.
Summary 2.1 Explain how abnormal behavior has been viewed
throughout history.
• Understanding of abnormal behavior has not evolved smoothly or uniformly over the centuries; the steps have been uneven, with great gaps in between, and unusual—even bizarre—views or beliefs have often sidetracked researchers and theorists.
• The dominant social, economic, and religious views of the times have had a profound influence over how people have viewed abnormal behavior.
• In the ancient world, superstitious explanations for mental disorders were followed by the emergence of medical concepts in many places such as Egypt and Greece; many of these concepts were developed and refined by Roman physicians.
• After the fall of Rome near the end of the fifth century A.D., superstitious views dominated popular thinking about mental disorders for over 1,000 years. In the fif- teenth and sixteenth centuries, it was still widely believed, even by scholars, that some of the people experiencing mental disturbances were possessed by a devil.
2.2 Describe the effect that humanism had on abnormal psychology.
• Great strides have been made in our understanding of abnormal behavior. For example, during the latter part of the Middle Ages and the early Renaissance, a spirit of scientific questioning reappeared in Europe, and several noted physicians spoke out against inhumane treatments. There was a general movement away from superstitions and “magic” toward reasoned, scientific studies.
• With recognition of a need for the special treatment of people with mental illness came the founding of vari- ous “asylums” toward the end of the sixteenth century. However, institutionalization led to the isolation and maltreatment of patients. Slowly this situation was recognized, and in the eighteenth century further efforts were made to help afflicted individuals by pro- viding them with better living conditions and humane treatment, although these improvements were the exception rather than the rule.
• The nineteenth and early twentieth centuries witnessed a number of scientific and humanitarian advances. The work of Philippe Pinel in France, of William Tuke in England, and of Benjamin Rush and Dorothea Dix in
the United States prepared the way for several impor- tant developments in contemporary abnormal psychol- ogy, such as moral management. Among these were the gradual acceptance of patients with mental illness as afflicted individuals who need and deserve profes- sional attention; the successful application of biomedi- cal methods to disorders; and the growth of scientific research into the biological, psychological, and socio- cultural roots of abnormal behavior.
• The reform of mental hospitals continued into the twentieth century, but during the last four decades of the century, there was a strong movement to close mental hospitals and release people into the commu- nity. This movement remains controversial in the early part of the twenty-first century.
2.3 Identify developments that led to the contemporary view of abnormal psychology.
• In the nineteenth century, great technological discov- eries and scientific advancements that were made in the biological sciences enhanced the understanding and treatment of individuals with mental illness. One major biomedical breakthrough came with the discov- ery of the organic factors underlying general paresis— syphilis of the brain—one of the most serious mental illnesses of the day.
• Beginning in the early part of the eighteenth century, knowledge of anatomy, physiology, neurology, chemistry, and general medicine increased rapidly. These advances led to the identification of the bio- logical, or organic, pathology underlying many physical ailments.
• The development of a psychiatric classification system by Kraepelin played a dominant role in the early development of the biological viewpoint. Kraepelin’s work (a forerunner to the DSM system) helped to establish the importance of brain pathology in mental disorders and made several related contributions that helped establish this viewpoint.
• The first major steps toward understanding psycho- logical factors in mental disorders occurred with mes- merism and the Nancy School, followed by the work of Sigmund Freud. During five decades of observa- tion, treatment, and writing, he developed a theory of psychopathology, known as psychoanalysis, that emphasized the inner dynamics of unconscious motives. During the past half-century, other clinicians
58
Historical and Contemporary Views of Abnormal Behavior 59
psychology. The behavioral perspective is organized around a central theme—that learning plays an impor- tant role in human behavior. Although this perspective was initially developed through research in the labora- tory (unlike psychoanalysis, which emerged out of clinical practice with disturbed individuals), it has been shown to have important implications for explaining and treating maladaptive behavior.
• Understanding the history of psychopathology—its forward steps and missteps alike—helps us under- stand the emergence of modern concepts of abnormal behavior.
have modified and revised Freud’s theory, which has thus evolved into new psychodynamic perspectives.
• Scientific investigation into psychological factors and human behavior began to make progress in the latter part of the nineteenth century. The end of the nine- teenth century and the early twentieth century saw experimental psychology evolve into clinical psychol- ogy with the development of clinics to study, as well as intervene in, abnormal behavior.
• Paralleling this development was the work of Pavlov in understanding learning and conditioning. Behav- iorism emerged as an explanatory model in abnormal
asylums, p. 40 behavioral perspective, p. 54 behaviorism, p. 54 catharsis, p. 52 classical conditioning, p. 54 deinstitutionalization, p. 47 dream analysis, p. 53 exorcisms, p. 39
free association, p. 53 insanity, p. 41 lycanthropy, p. 38 mass madness, p. 38 mental hygiene
movement, p. 43 mesmerism, p. 51 moral management, p. 43
Nancy School, p. 52 operant conditioning, p. 54 psychoanalysis, p. 51 psychoanalytic perspective, p. 51 Saint Vitus’s dance, p. 38 tarantism, p. 38 unconscious, p. 52
Key Terms
60
Learning Objectives
3.1 Distinguish between risk factors and causes of abnormal behavior.
3.2 List the perspectives that psychologists take to understand the causes of abnormal behavior.
3.3 Explain what the biological perspective tells us about abnormal behavior and also explain the biological causal factors of abnormal behavior.
3.4 Describe the most prominent psychological perspectives on abnormal psychology.
3.5 Describe three social factors known to contribute to abnormal behavior.
3.6 Explain how cultural differences can influence perceptions of abnormal behavior.
Chapter 3
Causal Factors and Viewpoints
Causal Factors and Viewpoints 61
Chapter 1, we can learn about relationships among vari- ables by observing them and measuring the extent to which two variables or events co-occur (i.e., co-vary or correlate). In trying to understand what causes different kinds of psy- chopathology, an important first step is to observe what variables are associated with such outcomes. A variable (X) that is associated with an outcome of interest (Y) is consid- ered to be a correlate of that outcome. For instance, the experience of physical abuse during childhood (X) is associ- ated with greater risk of depression later in life (Y), so abuse is said to be correlated with depression. But just knowing that two things are correlated doesn’t tell you if one caused the other (see Kraemer et al., 1997, and Figure 3.1). If, and only if, X is shown to precede Y in time can we infer that X is a risk factor for Y. That is, it is a factor or characteristic that is associated with an increased risk of developing con- dition Y. The next question we want to ask is if X can be changed. If it can, then it is considered to be a variable risk factor for outcome Y. If not, then it is considered a fixed marker of outcome Y, as is the case with a history of abuse during childhood. The key question for causality is whether changing X leads to a change in Y. If not, then X would be considered a variable marker of Y. If so, then and only then, would we consider X to be a causal risk factor for condition Y. Many correlates and risk factors may seem like they could be causes of our outcome of interest, but in order to know for sure, we must conduct studies to test the nature of these associations.
Necessary, Sufficient, and Contributory Causes With these distinctions in mind, it is important to note that there are different types of causal relations in the etiology, or causal pattern, of abnormal behavior. A necessary cause (X) is a characteristic that must exist for a disorder (Y) to occur. For example, general paresis (Y)—a degenerative brain disorder—cannot develop unless a person has previ- ously contracted syphilis (X). Or more generally, if Y occurs, then X must have preceded it. Another example is Huntington’s chorea—a rare degenerative brain disorder of the central nervous system—which can develop only if the person has the necessary gene (IT15, or the Hunting- ton’s gene—see Chapter 14). To date, most mental disor- ders have not been found to have necessary causes, although there continues to be a search for such causes.
A sufficient cause of a disorder is a condition that guarantees the occurrence of a disorder. For example, one current theory hypothesizes that hopelessness (X) is a suf- ficient cause of depression (Y) (Abramson et al., 1995, 1989). Or, more generally, if X occurs, then Y will also occur. According to this theory, if you are hopeless enough about your future, then you will become depressed. However, a sufficient cause may not be a necessary cause. Continuing
We saw in the last chapter that speculation about the causes of abnormal behavior goes back very far in human history. From early times, those who observed disordered behavior grappled with the question of its cause, and many people believed that abnormal behavior was the work of gods or demons. Hippocrates proposed a disease model suggesting that an imbalance in the four bodily humors produced abnormal behavior, with each humor connected with certain kinds of behavior. More recently, disorders such as schizophrenia and autism were thought to be caused by poor parenting practices or the adminis- tration of vaccines.
Each attempt at identifying a cause brought with it a theory, or model, of abnormal behavior. Today we are still puzzling over the causes of abnormal behavior, and specu- lation about causes continues to give rise to new models of abnormality. Since about 1900, several important schools of thought have developed elaborate models to explain the origins of abnormal behavior and to suggest how it might be treated. We discuss the most influential of these theo- retical perspectives in this chapter, paying special attention to the different types of causal factors that each perspective has identified. First, however, we need to address the very nature of the concept of causation as it is applied to abnor- mal behavior.
Risk Factors and Causes of Abnormal Behavior 3.1 Distinguish between risk factors and causes of
abnormal behavior.
Central to the field of abnormal psychology are questions about what causes people to experience mental distress and to behave maladaptively. If we knew the causes for given disorders, we might be able to prevent conditions that lead to them and perhaps reverse those that maintain them. We could also classify and diagnose disorders better if we clearly understood their causes rather than relying on clusters of symptoms, as we usually must do now.
Although understanding the causes of abnormal behavior is a desirable goal, it is enormously difficult to achieve because human behavior is so complex. Even the simplest human behavior, such as speaking or writing a single word, relies on various biological processes (e.g., the development of different brain regions), as well as thou- sands of prior social experiences. Attempting to under- stand a person’s life in causal terms is a task of enormous magnitude, whether it be a fairly normal or adaptive life or a life characterized by severe mental disorders.
One of the primary goals of clinical psychology, like science more generally, is to understand the nature of rela- tionships among variables of interest. As you learned in
62 Chapter 3
could increase the probability that a child will later have difficulty in handling close personal relationships or could increase the probability that being rejected in a relationship in adulthood will precipitate depression. We say here that parental rejection could be a contributory cause for the per- son’s later difficulties, but it is neither necessary nor suffi- cient (Abramson et al., 1989, 1995).
with the depression example, Abramson and colleagues (1989) acknowledge that hopelessness is not a necessary cause of depression; there are other causes of depression as well. Finally, what we study most often in psychopathol- ogy research are contributory causes. A contributory cause is one that increases the probability of a disorder develop- ing but is neither necessary nor sufficient for the disorder to occur. More generally, if X occurs, then the probability of Y occurring increases. For example, parental rejection
Does manipulation of X
change Y?
Variable risk factor
Can X be changed?
Risk factor
Does X precede Y?
Yes
No
Correlate
Is X associated
with Y?
Noncorrelate
No Concomitant/ consequence
No
No
Yes
Fixed marker
Variable marker
Causal risk factor
Yes
Yes
Figure 3.1 From Correlation to Causation Virtually all areas of science share an interest in understanding how variables are related to each other. Are they correlated? Does one actually cause the other? This helpful diagram created by Kraemer and colleagues (1997) is designed to help determine the status of potential causal factors. To use it, ask yourself: “Can it be shown that. . . .” Then start at the top-left box and work your way down.
Negative life events can contribute to the development of mental disorders, but may not be necessary or sufficient in themselves. The destruction caused by Hurricane Katrina is one example. Many, but not all, of those affected by the hurricane had elevated symptoms of mental disorders in the years following the storm.
In addition to distinguishing among necessary, suffi- cient, and contributory causes of abnormal behavior, we must also consider the time frame under which the differ- ent causes operate. Some causal factors occurring rela- tively early in life may not show their effects for many years; these would be considered distal risk factors (or dis- tal causal factors if the conditions described in Figure 3.1 are satisfied) that may contribute to a predisposition to develop a disorder. For example, loss of a parent early in life, or having abusive or neglectful parents as a child or adolescent, may serve as a distal contributory cause pre- disposing a person to depression or antisocial behaviors later in life. By contrast, other factors operate shortly before the occurrence of the symptoms of a disorder; these would be considered proximal risk factors. Some- times a proximal factor may be a condition that proves too much for a child or adult and triggers the onset of a disorder. A crushing disappointment at school or work or severe difficulties with a school friend or a marital part- ner are examples of more proximal factors that could lead to depression. In other cases, proximal factors might involve biological changes such as damage to certain parts of the left hemisphere of the brain, which can lead to depression.
A reinforcing contributory cause is a condition that tends to maintain maladaptive behavior that is already occurring.
Causal Factors and Viewpoints 63
Perceived Hostility
A boy with a history of disturbed interactions with his parents rou- tinely misinterprets the intentions of his peers as being hostile. He develops defensive strategies to counteract the supposed hostility of those around him such as rejecting the efforts of others to be friendly, which he misinterprets as patronizing. Confronted by the boy’s prickly behavior, those around him become defensive, hostile, and rejecting, thus confirming and strengthening the boy’s distorted expectations. What is the cause of this boy’s problems with his peers? His interac- tions with his parents? His tendency to misinterpret the intentions of others? His defensiveness? The response of his peers? Each seems to contribute; however, teasing these all apart and understanding if and how they contribute to his problems is an extremely challenging task. Welcome to the world of psychopathology research!
An example is the extra attention, sympathy, and relief from unwanted responsibility that may come when a per- son is ill; these pleasant experiences may unintentionally discourage recovery. Another example occurs when a depressed person’s behavior alienates friends and family, leading to a greater sense of rejection that reinforces the existing depression (Joiner & Timmons, 2009).
For many forms of psychopathology, we do not yet have a clear understanding of whether there are neces- sary or sufficient causes, although answering this ques- tion remains the goal of much current research. We do, however, have a good understanding of many of the risk factors for most forms of psychopathology. Some of the distal risk factors, to be discussed later in this chapter, set up vulnerability during childhood to some disorder later in life. Other more proximal risk factors appear to bring on a disorder directly, and still others may contribute to maintenance of a disorder. This complex picture is further complicated by the fact that what may be a proximal risk factor for a problem at one stage in life may also serve as a distal risk factor that sets up a predisposition for another disorder later in life. For example, the death of a parent can be a proximal risk factor of a child’s subsequent grief reaction, which might last a few months or a year; how- ever, the parent’s death may also serve as a distal risk fac- tor that increases the probability that when the child grows up he or she will become depressed in response to certain stressors.
Feedback and Bidirectionality in Abnormal Behavior Traditionally in the sciences, the task of determining cause-and-effect relationships has focused on isolating the condition X (cause) that can be demonstrated to lead to condition Y (effect). For example, when the alcohol content of the blood reaches a certain level, alcoholic intoxication occurs. When more than one causal factor is involved, as is often the case, the term causal pattern is used. Here, conditions A, B, C, and so on, lead to condi- tion Y. In either case, this concept of cause follows a sim- ple linear model in which a given variable or set of variables leads to a result either immediately or later. However, in the behavioral sciences, we deal with a multitude of interacting causes, and often have difficulty distinguishing between what is a cause and what is an effect. This occurs because effects can serve as feedback that can in turn influence the causes. In other words, the effects of feedback and the existence of mutual, two-way (bidirectional) influences must be taken into account.
Consider the following example, which illustrates that our concepts of causal relationships must take into account the complex factors of bidirectionality of feedback.
Diathesis–Stress Models Scientists try to understand how variables work together to cause outcomes of interest using conceptual models that distinguish between different types of causal factors. Many mental disorders are believed to develop when someone who has a preexisting vulnerability for that disorder experi- ences a major stressor. Models describing this kind of situa- tion are commonly known as diathesis–stress models of abnormal behavior (e.g., Ingram & Luxton, 2005; Meehl, 1962; Monroe & Simons, 1991). A vulnerability, or diathesis, is a predisposition toward developing a disorder that can derive from biological, psychological, or sociocultural causal factors. Stress, the response or experience of an individual to demands that he or she perceives as taxing or exceeding his or her personal resources, will be the focus of Chapter 5. Stress often occurs when an individual experi- ences chronic or episodic events that are undesirable and lead to behavioral, physiological, and cognitive accommo- dations (Schneiderman et al., 2005).
To translate these terms into the types of causal factors described earlier, the diathesis results from one or more relatively distal necessary or contributory causes, but is generally not sufficient to cause the disorder. Instead, there must be a more proximal factor (the stressor), which may also be contributory or necessary but is generally not suffi- cient by itself to cause the disorder except in someone with the diathesis. It is important to note that factors contribut- ing to the development of a diathesis are themselves some- times highly potent stressors, as when a child experiences the death of a parent and may thereby acquire a predispo- sition or diathesis for becoming depressed later in life.
Researchers have proposed several different ways in which a diathesis and stress may combine to produce a dis- order (Ingram & Luxton, 2005). In what is called the addi- tive model, the diathesis and the stress sum together, and when one is high the other can be low, and vice versa. Thus, a person with no diathesis or a very low level of diathesis
64 Chapter 3
In contrast to risk factors that increase the likelihood of negative outcomes, protective factors decrease the like- lihood of negative outcomes among those at risk (Kraemer et al., 1997). Note that a protective factor is not simply the absence of a risk factor, but instead is something that actively buffers against the likelihood of a negative out- come among those with some risk factor(s). One impor- tant protective factor in childhood is having a family environment in which at least one parent is warm and supportive, allowing the development of a good attach- ment relationship between the child and parent that can protect against the harmful effects of an abusive parent (Masten & Coatsworth, 1998).
Protective factors are not necessarily positive experi- ences. Indeed, sometimes exposure to stressful experi- ences that are dealt with successfully can promote a sense of self-confidence or self-esteem and thereby serve as a protective factor. Thus, some stressors paradoxically pro- mote coping. This “steeling” or “inoculation” effect is more likely to occur with moderate stressors than with mild or extreme stressors (Barlow, 2002; Hetherington, 1991; Rutter, 1987). Some protective factors have nothing to do with experiences at all but are simply some quality or attribute of a person. For example, adolescents who score high on emotional intelligence are less likely to show negative outcomes following childhood abuse (Cha & Nock, 2009).
Protective factors most often, but not always, lead to resilience—the ability to adapt successfully to even very difficult circumstances. An example is the child who per- severes and does well in school despite his or her parent’s drug addiction or physical abuse. More generally, the term resilience has been used to describe the phenomenon that “some individuals have a relatively good outcome despite suffering risk experiences that would be expected to bring about serious sequelae” (Rutter, 2007, p. 205). A more everyday way of thinking of resilience is in terms of “over- coming the odds” against you. There is increasing evi- dence that if a child’s fundamental systems of adaptation (such as intelligence and cognitive development, ability to self-regulate, motivation to achieve mastery, effective par- enting, and well-functioning neurobiological systems for handling stress) are operating normally, then most threat- ening circumstances will have minimal impact on him or her (Masten, 2001; Sapienza & Masten, 2011). Problems tend to arise when one or more of these systems of adapta- tion is weak to begin with (e.g., low intelligence or poorly functioning neurobiological systems for handling stress; Lester et al., 2006) or when a serious stressor damages one or more of these systems (e.g., when a parent dies). Prob- lems can also arise when the level of challenge far exceeds human capacity to adapt (e.g., exposure to chronic trauma in war or chronic maltreatment in abusive families; Ungar, 2015). We should also note, however, that resilience should
could still develop a disorder when faced with truly severe stress. In other words, individuals who have a high level of a diathesis may need only a small amount of stress before a disorder develops, but those who have a very low level of a diathesis may need to experience a large amount of stress for a disorder to develop. In what is called an interactive model, some amount of diathesis must be present before stress will have any effect. Thus, someone with no diathe- sis will never develop the disorder, no matter how much stress he or she experiences, whereas someone with the diathesis will demonstrate an increasing likelihood of developing the disorder with increasing levels of stress. More complex models are also possible because diatheses often exist on a continuum, ranging from zero to high lev- els. Each of these possibilities is illustrated in Figure 3.2.
(a)
HighLow
Pr ob
ab ili
ty o
f D
ep re
ss io
n
Level of Stress
High
Low
High Level of Diathesis
No Diathesis
HighLow
Pr ob
ab ili
ty o
f D
ep re
ss io
n
Level of Stress
High
Low
High Level of Diathesis
Medium Level of Diathesis
No Diathesis
(b)
Me diu
m Le
ve l o
f D iat
he sis
Figure 3.2 Diathesis–Stress Model (a) Interactive model of diathesis-stress interaction. (b) Additive model of diathesis–stress interaction.
(Adapted from S. M. Monroe & A. D. Simons (1991). Diathesis–stress theories in the context of life stress research: Implications for the depressive disorders. Psychological Bulletin, 110, 406–425.)
Causal Factors and Viewpoints 65
grandmother both had histories of recurrent clinical depression. The twins were separately adopted into two loving middle-class families without a history of depression. Melinda’s adoptive family provided a loving and supportive environment and supported her through school and college. Tracy’s adoptive parents, by contrast, soon divorced, and she was raised by her adoptive mother, who devel- oped a serious dependence on alcohol and who could not hold a job. Her mother’s living circumstances deteriorated and Tracy was forced to change schools four times. Because of her adoptive moth- er’s alcohol and other mental problems, she was unable to provide Tracy with a consistently loving and supportive environment, and when she was drunk she frequently punished Tracy for no good rea- son. Tracy somehow managed to graduate from high school and supported herself through a state college. Both Tracy and Melinda married after they graduated from college but, by age 27, both mar- riages resulted in divorce. Although Melinda developed some depressive symptoms for the first 6 weeks following the divorce, the depression was not severe and she quickly recovered. Tracy, by contrast, developed a major depressive episode that lasted for over a year.
not be thought of as an all-or-none capacity, and some research suggests that resilient children (that is, those who show high social competence despite high stress) may also experience considerable self-reported emo- tional distress. Moreover, children who show resilience in one domain may show significant difficulties in other domains.
A child growing up under conditions of adversity may be protected from problems later in life if he or she has a warm and supportive relationship with some adult, such as a grandparent. Encouraging children to learn, explore, ask questions, and try new experiences— while providing a safe and supportive environment—is an important aspect of a protective relationship.
In sum, we can distinguish between causes of abnor- mal behavior that lie within and are part of the biological makeup or prior experience of a person—diatheses, vul- nerabilities, or predispositions—and causes that pertain to current challenges in a person’s life—stressors. Typically, neither the diathesis nor the stress is by itself sufficient to cause the disorder, but in combination they can sometimes lead the individual to behave abnormally. In addition, we can examine protective factors, which may derive either from particular types of experiences or from certain quali- ties of the person, that can promote resilience in the face of vulnerability and stress. The following scenario illustrates some of these concepts.
Nature and Nurture
Melinda and Tracy were identical twins whose parents were killed in a car accident when they were a year old. Their mother and
In this example, both Tracy and Melinda have identical genetic makeup and therefore the same genetic diathesis for depression. Both had experienced the same distal stressor (death of parents at an early age), and the same proximal stressor (divorce) at age 27. However, Melinda had many protective factors growing up (loving and sup- portive family and adequate resources) that Tracy did not have (lack of a loving and supportive mother and inadequate resources). Thus, Melinda showed resilience in the face of her divorce but Tracy did not.
This discussion should make it very clear that diathesis– stress models need to be considered in a broad framework of multicausal developmental models. Specifically, in the course of development a child may acquire a variety of cumulative risk factors that may interact to determine his or her risk for psychopathology. These risk factors also interact with a variety of protective processes, and sometimes with stressors, to determine whether the child develops in a normal and adaptive way—as opposed to showing signs of maladaptive behavior and psychopa- thology—in childhood, adolescence, or adulthood. Note also that to understand what is abnormal, one must always have a good understanding of normal human develop- ment at biological, psychological, and sociocultural levels of analysis. This has been the focus of the rapidly growing field of developmental psychopathology, which concen- trates on determining what is abnormal at any point in development by comparing and contrasting it with the normal and expected changes that occur in the course of development. For example, an intense fear of the dark in a 3- to 5-year-old child may not be considered abnormal, given that most children have at least one specific fear that they bring into early adolescence. However, an intense fear
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in review • What are the three traditional perspectives that have dominated
the study of abnormal behavior in recent years?
• What is the central idea of the more current biopsychosocial per- spective?
The Biological Perspective 3.3 Explain what the biological perspective tells us
about abnormal behavior and also explain the biological causal factors of abnormal behavior.
As we saw in Chapter 2 in the discussion of general paresis and its link to syphilis, the traditional biological viewpoint focuses on mental disorders as diseases, many of the pri- mary symptoms of which are cognitive, emotional, or behavioral. Mental disorders are thus viewed as disorders of the central nervous system, the autonomic nervous sys- tem, and/or the endocrine system that are either inherited or caused by some pathological process. At one time, peo- ple who adopted this viewpoint hoped to find simple bio- logical explanations. Today, however, most people recognize that such explanations are rarely simple, and many also acknowledge that psychological and sociocul- tural causal factors play important roles as well.
The disorders first recognized as having biological or organic components were those associated with gross destruction of brain tissue. These disorders are neurologi- cal diseases—that is, they result from the disruption of brain functioning by physical or biochemical means and often involve psychological or behavioral aberrations. For example, damage to certain areas in the brain can cause memory loss, and damage to the left hemisphere that occurs during a stroke can cause depression.
However, most mental disorders are not caused by neurological damage per se. For example, abnormalities in neurotransmitter systems in the brain can lead to mental disorders without causing damage to the brain. Moreover, the bizarre content of delusions and other abnormal men- tal states like hallucinations can never be caused simply and directly by brain damage. Consider the example of a person with schizophrenia or general paresis who claims to be Napoleon. The content of such delusions must be the by-product of some sort of functional integration of differ- ent neural structures, some of which have been “pro- grammed” by personality and learning based on past experience (e.g., having learned who Napoleon was).
We focus here on four categories of biological factors that seem particularly relevant to the development of mal- adaptive behavior: (1) genetic vulnerabilities, (2) brain dysfunction and neural plasticity, (3) neurotransmitter and hormonal abnormalities in the brain or other parts of
of the dark that causes considerable distress and avoidance behavior in a high school or college-age student would be considered a phobia.
in review • What is a necessary cause? A sufficient cause? A contributory
cause?
• What is a diathesis–stress model of abnormal behavior?
• Define the terms protective factors and resilience. Give examples of each.
• Explain why diathesis–stress models need to be considered as multicausal developmental models.
Perspectives to Understanding the Causes of Abnormal Behavior 3.2 List the perspectives that psychologists take to
understand the causes of abnormal behavior.
Students are often perplexed by the fact that in the behav- ioral sciences several competing explanations are often offered for the same thing. For instance, what causes depression? There are many different perspectives from which we can study this question. One way is to take a biological perspective in which we try to understand how factors such as genetics, neurobiology, and hormonal responses can influence psychopathology, a strategy that has become increasingly common in recent years. Another is to take a psychological perspective and try to under- stand how dysfunctional thoughts, feelings, and behav- iors can lead to psychopathology. Yet another is to take a sociocultural perspective in which we try to understand how social and cultural factors can influence the way that we think about abnormal behavior. Of course, these differ- ent perspectives overlap, so an integrated approach is needed to provide a full understanding of the origins of various forms of psychopathology. Thus, in recent years, many theorists recognize the need for a more integrative, biopsychosocial viewpoint that acknowledges that bio- logical, psychological, and social factors all interact and play a role in psychopathology and treatment. Moreover, the cultural context in which each of these factors plays out influences how we think about behavior, both normal and abnormal.
With this in mind, we now turn to the major different perspectives themselves. We present the key ideas of each perspective, along with information about attempts to evaluate its validity. We also describe the kinds of causal factors that each model tends to emphasize.
Causal Factors and Viewpoints 67
Each human cell has 23 pairs of chromosomes (46 total) containing genetic materials that encode the hereditary plan for each individual. One copy of each chromosome comes from the mother and one from the father. Twenty-two of these chromosome pairs determine, by their biochemical action, an individual’s general anatomical and other physiological characteristics. The remaining pair, the sex chromosomes, determines the individual’s sex. If both of these are X chromosomes, the offspring is a female (XX). If the sex chromosome inherited from the father is a Y chro- mosome, the offspring is a male (XY). (See Figure 3.3.)
Research in developmental genetics has shown that abnormalities in the structure or number of chromosomes can be associated with major defects or disorders. For example, Down syndrome is a type of intellectual disabil- ity in which there is a trisomy (a set of three chromosomes instead of two) in chromosome 21 (see Chapter 15). Here the extra chromosome is the primary cause of the disorder. Anomalies may also occur in the sex chromosomes, pro- ducing a variety of complications, such as ambiguous sex- ual characteristics, that may predispose a person to develop abnormal behavior.
More typically, however, personality traits and mental disorders are not affected by chromosomal abnormalities per se. Instead they are more often influenced either by abnormalities in some of the genes on the chromosomes or by naturally occurring variations of genes known as polymorphisms. Although you will often hear about
the central nervous system, and (4) temperament. Each of these categories encompasses a number of conditions that influence the quality and functioning of our bodies and our behavior. They are often not independent of each other but rather interact with one another. Moreover, dif- ferent factors may play more or less important roles in dif- ferent people.
Genetic Vulnerabilities Genes are very long molecules of DNA (deoxyribonucleic acid) that are present at various locations on chromosomes. Chromosomes are the chain-like structures within a cell nucleus that contain the genes. Genes are the carriers of the information that we inherit from our parents (individuals have two copies of each gene—one from each of our parents), and each gene exists in two or more alternate forms called alleles. Genes don’t fully determine whether a person devel- ops a mental disorder; however, there is substantial evidence that most mental disorders show at least some genetic influ- ence (Plomin et al., 2013; Rutter, 2006a). Some of these genetic influences, such as broad temperamental features, are first apparent in newborns and children. For example, some chil- dren are just naturally more shy or anxious, whereas others are more outgoing (Fox et al., 2010; Kagan & Fox, 2006). However, some genetic sources of vulnerability do not mani- fest themselves until adolescence or adulthood, when most mental disorders appear for the first time.
Figure 3.3 Human Chromosome Pairs A normal human male has 23 pairs of chromosomes, including an X chromosome and a Y chromosome.
(Adapted from “Human Chromosome Pairs,” from Thomas D. Gelehrter et al. (1998). Principles of Medical Genetics. Reprinted with permission of Lippincott/Williams & Wilkins and Dr. Thomas D. Gelehrter.)
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Another example occurs in people at genetic risk for depression, who have been shown to be more likely to respond to stressful life events by becoming depressed than are people without the genetic risk factors who expe- rience the same stressful life events (Moffitt et al., 2005, 2006). In one landmark study of nearly 850 young adults who were followed since age 3, investigators found evi- dence for a genotype–environment interaction involving several variants on a specific gene involved in the trans- port of the neurotransmitter serotonin. The variants of this gene that a person had affected the likelihood that she or he would develop major depression in her or his 20s, but only when considered in interaction with life stress (Caspi et al., 2003). Specifically, individuals with one variant of the gene (two short alleles) who also expe- rienced four or more major life stressors had twice the probability of developing major depression than individ- uals with another variant of the gene (two long alleles) who also experienced four or more major life stressors (see Chapter 7 for more details). Since then, this basic pattern of results has been replicated in many studies (although not in all), with recent evidence suggesting that the effects are robust if sophisticated interview-based measures of life stress are used (Uher & McGuffin, 2010; see also Karg et al., 2011).
GEnotypE–EnvironmEnt CorrELationS In many cases, genes can actually shape the environmental experiences a child has, thus affecting the phenotype in important ways. For example, a child who is genetically predisposed to aggressive behavior may be rejected by his or her peers in early grades because of the aggressive behavior. Such rejection may lead the child to go on to associate with similarly aggressive and delinquent peers in later grades, leading to an increased likelihood of develop- ing a full-blown pattern of delinquency in adolescence. When the genotype shapes the environmental experiences a child has in this way, we refer to this phenomenon as a genotype–environment correlation (Plomin et al., 2013; Rutter, 2006a, 2007). Researchers have found three impor- tant ways in which an individual’s genotype may shape his or her environment (Jang, 2005; Plomin et al., 2013).
1. The child’s genotype may have what has been termed a passive effect on the environment, resulting from the genetic similarity of parents and children. For exam- ple, highly intelligent parents may provide a highly stimulating environment for their child, thus creating an environment that will interact in a positive way with the child’s genetic endowment for high intelli- gence. Conversely, parents who exhibit antisocial behavior tend to create a risky environment character- ized by family dysfunction, thereby increasing the probability of certain mental disorders in their children (Rutter, 2006b; see also Chapter 10).
discoveries that “the gene” for a particular disorder has been discovered, vulnerabilities to mental disorders are almost always polygenic, which means they are influenced by multiple genes or by multiple polymorphisms of genes, with any one gene having only very small effects (Kendler, 2005; Plomin et al., 2013). In other words, a genetically vulnerable person has usually inherited a large number of genes, or polymorphisms of genes, that operate together in an additive or interactive fashion to increase vulnerability. Collectively these genes may lead to structural abnormali- ties in the central nervous system, to abnormalities in the regulation of brain chemistry and hormonal balance, or to excesses or deficiencies in the reactivity of the autonomic nervous system, which is involved in mediating many of our emotional responses.
In the field of abnormal psychology, genetic influences rarely express themselves in a simple and straightforward manner. This is because behavior, unlike some physical characteristics such as eye color, is not determined exclu- sively by genetic endowment; it is a product of the organ- ism’s interaction with the environment. In other words, genes can affect behavior only indirectly. Gene “expres- sion” is normally not a simple outcome of the information encoded in DNA but is, rather, the end product of an intri- cate process that may be influenced by the internal (e.g., intrauterine) and external environment. Indeed, certain genes can actually be “turned on,” or activated, and “turned off,” or deactivated, in response to environmental influences such as stress.
thE rELationShip of GEnotypES to phEnotypES A person’s total genetic endowment is referred to as her or his genotype and, except for identical twins, no two humans ever begin life with the same genetic makeup. The observed structural and functional characteristics that result from an interaction of the genotype and the environ- ment are referred to as a person’s phenotype.
GEnotypE–EnvironmEnt intEraCtionS In most cases, genetic factors are not necessary and sufficient to cause mental disorders but instead can contribute to a vul- nerability or diathesis to develop psychopathology that only happens if there is a significant stressor in the person’s life (as in the diathesis–stress models described above). This is known as a genotype–environment interaction. One important example is illustrated by a disorder known as PKU-induced intellectual disability (see Chapter 15). Children with the genetic vulnerability to PKU react very differently to many common foods with phenylalanine than do normal children because they cannot metabolize the phenylalanine (an amino acid), and as its metabolic products build up, they damage the brain (Plomin et al., 2013; Rutter, 2006b). Fortunately, this syndrome can be pre- vented if the young child’s diet is changed so as to elimi- nate foods with phenylalanine.
Causal Factors and Viewpoints 69
twins are this high, so we can safely conclude that no mental disorders are completely heritable. Nevertheless, as we will see, there are relatively high concordance rates for identical twins in some of the more severe forms of psychopathology. These concordance rates are particu- larly meaningful when they differ from those found for nonidentical (i.e., dizygotic) twins. Dizygotic twins develop from two different fertilized eggs and so do not share any more genes than do siblings from the same par- ents. One would therefore expect concordance rates for a disorder to be much lower for dizygotic (DZ) than for monozygotic (MZ) twins if the disorder had a strong genetic component. Evidence for genetic transmission of a trait or a disorder can be obtained by comparing the concordance rates between identical and nonidentical twins. For most of the disorders we will discuss, concor- dance rates are indeed much lower for nonidentical twins than for identical twins.
Some researchers have argued that finding higher concordance rates for a disorder in monozygotic twins than in dizygotic twins is not conclusive evidence of a genetic contribution because it is always possible that iden- tical twins are treated more similarly by their parents and others than are nonidentical twins (Bouchard & Propping, 1993; Torgersen, 1993). However, research has provided evidence that the genetic similarity is more important than
2. The child’s genotype may evoke particular kinds of reactions from the social and physical environment— a so-called evocative effect. For example, active, happy babies evoke more positive responses from others than do passive, unresponsive infants (Lytton, 1980). Similarly, musically talented children may be picked out at school and given special opportunities (Plomin et al., 2013).
3. The child’s genotype may play a more active role in shaping the environment—a so-called active effect. In this case the child seeks out or builds an environment that is congenial—a phenomenon known as “niche building.” For example, extraverted children may seek the company of others, thereby enhancing their own tendencies to be sociable (Baumrind, 1991; Plomin et al., 2013).
mEthoDS for StuDyinG GEnEtiC infLuEnCES Although advances are beginning to be made in studying genetic factors that are associated with psychopathology, for the most part we are not yet able to isolate, on the genes themselves, specific defects for mental disorders. Instead, most of the information we have on the role of genetic fac- tors in mental disorders is based not on studies of genes but on studies of people who are related to each other. Three primary methods have traditionally been used in behavior genetics, the field that focuses on studying the heritability of mental disorders (as well as other aspects of psychological functioning): (1) the family history method, (2) the twin method, and (3) the adoption method. More recently, two additional methods, linkage studies and asso- ciation studies, have also been developed.
The family history (or pedigree) method requires that an investigator observe samples of relatives of each proband or index case (the subject, or carrier, of the trait or disorder in question) to see whether the incidence increases in proportion to the degree of hereditary rela- tionship. In addition, the incidence of the disorder in a normal population is compared (as a control) with its incidence among the relatives of the index cases. The main limitation of this method is that people who are more closely related genetically also tend to share more similar environments, which makes it difficult to disen- tangle genetic and environmental effects.
The twin method is the second approach used to study genetic influences on abnormal behavior. Identical (monozy- gotic) twins share the same genetic endowment because they develop from a single zygote, or fertilized egg. Thus, if a given disorder or trait were completely heritable, one would expect the concordance rate—the percentage of twins sharing the disorder or trait—to be 100 percent. That is, if one identical twin had a particular disorder, the other twin would as well. However, there are no forms of psy- chopathology where the concordance rates for identical
These identical twins from Bouchard’s University of Minnesota Study of Twins Reared Apart pose here with Dr. Nancy Segal, co-director of the project. Mark Newman (left) and Gerry Levey (right) were separated at birth and raised by different parents. Both were dedicated firefighters in different New Jersey towns and met after someone mistook one of them at a firemen’s convention for his twin. Both had highly similar patterns of baldness and were 6′4″ tall. They both loved Budweiser beer (which they both held by placing their pinky finger under the beer can) as well as Chinese and Italian food. Both had been smokers until recently, when one had quit. They both also liked hunting and fishing and always carried knives. These eerie similarities between identical twins reared apart have been observed in many other such twins as well (Segal, 2005).
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the similarity of the parents’ behavior (Plomin et al., 2013). Nevertheless, the ideal study of genetic factors in psycho- pathology involves identical twins who have been reared apart in significantly different environments. Unfortu- nately, finding such twins is extremely difficult (there are probably only a few hundred pairs in the United States), and so only a few such small studies have been done.
The adoption method, the third method used to study genetic influences, capitalizes on the fact that adoption cre- ates a situation in which individuals who do not share a common family environment are nonetheless genetically related. In one variation on this method, the biological par- ents of individuals who have a given disorder (and who were adopted away shortly after birth) are compared with the biological parents of individuals without the disorder (who also were adopted away shortly after birth) to deter- mine their rates of disorder. If there is a genetic influence, one expects to find higher rates of the disorder in the biological relatives of those with the disorder than in those without the disorder. In another variation, researchers compare the rates of disorder in the adopted-away off- spring of biological parents who have a disorder with those seen in the adopted-away offspring of normal biological parents. If there is a genetic influence, then there should be higher rates of disorder in the adopted-away offspring of the biological parents who have the disorder.
more similar, whether the influence occurs within the fam- ily (e.g., family discord and poverty) or in the environment (e.g., two high-quality schools, with one twin going to each). Nonshared environmental influences are those in which the children in a family differ. These would include unique experiences at school and also some unique features of upbringing in the home, such as a parent treating one child in a qualitatively different way from another. An example of nonshared influences occurs when parents who are quarreling and showing hostility to one another draw some children into the conflict while others are able to remain outside it. For many important psychological char- acteristics and forms of psychopathology, nonshared influ- ences have appeared to be more important—that is, experiences that are specific to a child may do more to influence his or her behavior and adjustment than experi- ences shared by all children in the family (Plomin et al., 2013; Rutter, 1991, 2006a).
LinkaGE anaLySiS anD aSSoCiation StuDiES More recent molecular genetic methods used to study genetic influences on mental disorders include linkage anal- ysis and association studies. Whereas the methods previ- ously described attempt to obtain quantitative estimates of the degree of genetic influence for different disorders, link- age analysis and association studies attempt to determine the actual location of genes responsible for mental disor- ders. Considerable excitement surrounds such work because identifying the location of genes for certain disor- ders could provide promising leads for new forms of treat- ment and even prevention of those disorders.
Linkage analysis studies of mental disorders capital- ize on several currently known locations on chromosomes of genes for other inherited physical characteristics or bio- logical processes (such as eye color or blood group). For example, researchers might conduct a large family pedi- gree study on schizophrenia, looking at all known rela- tives of a person with schizophrenia going back several generations. At the same time, however, they might also keep track of something like the eye color of each individ- ual (as well as which DSM diagnoses they have). Eye color might be chosen because it has a known genetic marker located on a particular chromosome. If the researchers found that the familial patterns for schizophrenia in one family pedigree (a sample of all relatives) were closely linked to the familial patterns for eye color in the same pedigree, they could infer that a gene affecting schizo- phrenia might be located very nearby on the chromosome that contains the known genetic marker for eye color. In other words, in this case one would expect all members of a particular family pedigree with schizophrenia to have the same eye color (e.g., blue), even though all members of a different family pedigree with schizophrenia might have brown eyes.
Although pitfalls can arise in interpreting each of these methods, if the results from studies using all three strate- gies converge, one can draw reasonably strong conclusions about the genetic influence on a disorder. The Develop- ments in Thinking box considers various misconceptions about studies of genetics and psychopathology.
SEparatinG GEnEtiC anD EnvironmEntaL infLuEnCES Because all of the three types of heritabil- ity studies separate heredity from environment to some extent, they also allow for testing the influence of environ- mental factors and even for differentiating “shared” and “nonshared” environmental influences. Shared environmen- tal influences are those that would make children in a family
Causal Factors and Viewpoints 71
given disorder. Researchers then compare the frequencies in these two groups of certain genetic markers that are known to be located on particular chromosomes (such as eye color or blood group). If one or more of the known genetic markers occur with much higher frequency in the individuals with the disorder than in the people without the disorder, the researchers infer that one or more genes associated with the disorder are located on the same chro- mosome. Ideally, the search for gene candidates for a given disorder starts with known genes for some biological pro- cess that is disrupted in the disorder (see Moffitt et al., 2005). For example, one study found that the genetic mark- ers for certain aspects of dopamine functioning were pres- ent significantly more frequently in the children with hyperactivity than in the children without hyperactivity. This led researchers to infer that some of the genes involved with hyperactivity are located near the known genetic
A number of published studies during the past 20 years using linkage analysis have provided evidence supporting, for example, the location of a gene for bipolar disorder on chromosome 11 and the location of genes for schizophrenia on particular parts of chromosomes 22, 6, 8, and 1. However, numerous other studies have failed to replicate these results. Therefore, most results are consid- ered inconclusive at the present time (Carey, 2003; Rutter, 2006a). Part of the problem in coming up with replicable results in such studies is that most of these disorders are influenced by many different genes spread over multiple chromosomes. To date, these linkage analysis techniques have been most successful in locating the genes for single- gene brain disorders such as Huntington’s disease (Plomin et al., 2013; Rutter, 2006a).
association studies start with two large groups of individuals, one group with and one group without a
Developments in Thinking Nature, Nurture, and Psychopathology: A New Look at an Old Topic
People have abundant misconceptions and stereotypes about studies of genetic influences on behavior, traits, and psychopa- thology, many stemming from outdated ideas that nature and nurture are separate rather than in constant interplay. Indeed, as we have seen in the examples of genotype–environment correla- tions and interactions, “In the great majority of cases, both psy- chological traits and mental disorders are multifactorial in origin—meaning that they involve some kind of combination, and interplay, among several genetic factors providing contributions to susceptibility or liability and several environmental factors that similarly play a part in the causal pathway” (Rutter, 2006a, p. 29). Several of the more important misconceptions are presented here (Plomin et al., 2013; Rutter, 1991, 2006a).
1. Misconception: Strong genetic effects mean that environ- mental influences must be unimportant. Fact: Even if we are discussing a trait or disorder that has a strong genetic influence, environmental factors can have a major impact on the level of that trait (Rutter, 2006a). Height, for example, is strongly genetically determined, and yet nutritional factors have a very large effect on the actual height a person attains. Between 1900 and 1960 the average height of boys reared in London increased about 4 inches, thanks only to improve- ments in diet (Tizard, 1975).
2. Misconception: Genes provide a limit to potential. Fact: One’s potential can change if one’s environment changes, as the height example above illustrates. Another example comes from children born to socially disadvantaged parents but who are adopted and reared with socially advantaged parents. These children have a mean IQ about 12 points higher than those reared in the socially disadvantaged environment (Capron & Duyme, 1989; see also Duyme et al., 2004).
3. Misconception: Genetic strategies are of no value for study- ing environmental influences. Fact: The opposite is true because genetic research strategies provide critical tests of environmental influences on personality and psychopathol- ogy (Rutter, 2006a). For example, because monozygotic twins have identical genes, concordance rates of less than 100 percent clearly illustrate the importance of environmental influences (Bouchard & Loehlin, 2001; Rutter, 2006a).
4. Misconception: Genetic effects diminish with age. Fact: Although many people assume that genetic effects should be maximal at birth, with environmental influences getting stron- ger with increasing age, it is now evident that this is not always true (Plomin, 1986; Rutter, 2006a). For height, weight, and IQ, dizygotic twins are almost as alike as monozygotic twins in early infancy, but over time dizygotic twins show greater differences than monozygotic twins. For whatever reasons, many genetic effects on psychological characteris- tics increase with age up to at least middle childhood or even young adulthood. Moreover, other genetic effects do not appear until much later in life, as in cases like Huntington’s disease, to be discussed in Chapter 14.
5. Misconception: Disorders that run in families must be genetic, and those that do not run in families must not be genetic. Fact: Many examples contradict these misconcep- tions. For example, teenage-onset juvenile delinquency tends to run in families, and yet this seems to be due pri- marily to environmental rather than genetic influences (Plomin et al., 2013; Rutter, 2006a). Conversely, autism is such a rare disorder that it doesn’t appear to run in families (only about 3 percent of siblings have the disorder), and yet there seems to be a very powerful genetic effect (Plomin et al., 2013; Rutter, 2006a).
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that were less negatively affected by brain injury that occurred early in development than those without the same positive prenatal experiences (Kolb et al., 2003). One example of negative effects of prenatal experiences comes from an experiment in which pregnant monkeys exposed to unpredictable loud sounds had infants that were jittery and showed neurochemical abnormalities (specifically, ele- vated levels of circulating catecholamines; Schneider, 1992). Many postnatal environmental events also affect the brain development of the infant and child (Nelson & Bloom, 1997; Thompson & Nelson, 2001). For example, the formation of new neural connections (or synapses) after birth is dramatically affected by the experiences a young organism has (Rosenzweig et al., 2002). Rats reared in enriched environments (as opposed to in isolation) show heavier and thicker cell development in certain portions of the cortex (as well as more synapses per neuron). Similar but less extensive changes can occur in older animals exposed to enriched environments. Physical exercise, such as running, also has been shown to lead to neurogenesis (the creation of new brain cells; Stranahan et al., 2007). Indeed, neural plasticity continues to some extent through- out the life span (so get up and go for a jog after you finish this chapter!).
Research on neural and behavioral plasticity, in combination with the work described earlier on genotype– environment correlations, makes it clear why developmen- tal psychopathologists have been devoting increasing attention to a developmental systems approach (Masten, 2006; Spencer et al., 2009), which acknowledges that genet- ics influences neural activity, which in turn influences behavior, which in turn influences the environment, but also that these influences are bidirectional. Thus, Figure 3.4 illustrates this first direction of influence but also shows how various aspects of our environment (physical, social, and cultural) also influence our behavior, which in turn
markers for dopamine functioning (Thapar et al., 2006; see also Plomin et al., 2013). For most mental disorders that are known to be influenced polygenically, association studies are more promising than linkage studies for identifying small effects of any particular gene.
In summary, studies using linkage and association methodologies hold tremendous promise for identifying new prevention or treatment approaches. However, at present that promise has not been fulfilled because of diffi- culties in producing replicable results.
Brain Dysfunction and Neural Plasticity Specific brain lesions with observable defects in brain tis- sue are rarely a primary cause of psychiatric disorders. However, advances in understanding how more subtle deficiencies of brain structure or function are implicated in many mental disorders have been increasing at a rapid pace in the past few decades. Some of these advances come from the increased availability of sophisticated new neuroimaging techniques to study the function and struc- ture of the brain (see Chapter 4 for more details). Research has revealed that genetic factors guide brain develop- ment—so these different pieces of the biological puzzle are all related (Hibar et al., 2015). However, we also know that genetic programs for brain development are not so rigid and deterministic as was once believed (Gottesman & Hanson, 2005; Thompson & Nelson, 2001). Instead, there is considerable neural plasticity—flexibility of the brain in making changes in organization and function in response to pre- and postnatal experiences, stress, diet, disease, drugs, maturation, and so forth. Existing neural circuits can be modified, or new neural circuits can be gen- erated (Fox et al., 2010; Kolb et al., 2003). The effects can be either beneficial or detrimental to the individual, depend- ing on the circumstances.
One example of the positive effects of prenatal experi- ences comes from an experiment in which pregnant rats housed in complex, enriched environments had offspring
Environment (physical, social, cultural)
Behavior
Neural activity
Genetic activity
Individual development
Bidirectional Influences
Figure 3.4 Bidirectional Influences A systems view of psychobiological development.
(Adapted from Gilbert Gottlieb. 1992. Individual Development and Evolution: The Genesis of Novel Behavior. New York: Oxford University Press. Reprinted by permission of Lawrence Erlbaum Associates.)
Causal Factors and Viewpoints 73
the presynaptic terminal and can destroy excess neu- rotransmitters there too.
There are many different kinds of neurotransmitters; some increase the likelihood that the postsynaptic neuron will “fire” (produce an impulse), and others inhibit the impulse. Whether the neural message is successfully trans- mitted to the postsynaptic neuron depends, among other things, on the concentration of certain neurotransmitters within the synapse.
imbaLanCES of nEurotranSmittEr SyStEmS The belief that imbalances in neurotransmitters in the brain can result in abnormal behavior is one of the basic tenets of the biological perspective today, although currently most researchers agree that this is only part of the causal pattern involved in the etiology of most disorders. Sometimes psy- chological stress can bring on neurotransmitter imbalances. These imbalances can be created in a variety of ways:
• There may be excessive production and release of the neurotransmitter substance into the synapses, causing a functional excess in levels of that neurotransmitter.
• There may be dysfunctions in the normal processes by which neurotransmitters, once released into the syn- apse, are deactivated. Ordinarily this deactivation occurs either through a process of reuptake of the released neurotransmitter from the synapse into the axon endings or through a process of degradation by certain enzymes that may be present in the synapse and in the presynaptic axon endings.
• Finally, there may be problems with the receptors in the postsynaptic neuron, which may be either abnor- mally sensitive or abnormally insensitive.
Neurons that are sensitive to a particular neurotrans- mitter tend to cluster together, forming neural paths between different parts of the brain known as chemical cir- cuits. As we will see, different disorders are thought to stem from different patterns of neurotransmitter imbal- ances in various brain areas (Lambert & Kinsley, 2005; Thompson, 2000). Medications used to treat various disor- ders are often believed to operate by correcting these imbalances. For example, the widely prescribed antide- pressants Prozac and Zoloft are designed to slow the reup- take of the neurotransmitter serotonin, thereby prolonging how long serotonin remains in the synapse (see Chapters 7 and 16).
Although over a hundred neurotransmitters have been discovered to date, five different kinds of neurotransmit- ters have been most extensively studied in relationship to psychopathology: (1) norepinephrine, (2) dopamine, (3) serotonin, (4) glutamate, and (5) gamma aminobutyric acid (known as GABA; Carlson, 2007; Lambert & Kinsley, 2005; Thompson, 2000). The first three belong to a class of neurotransmitters called monoamines because each is
affects our neural activity, and this in turn can even influ- ence genetic activity (Gottesman & Hanson, 2005; Gottlieb & Halpern, 2002; Masten, 2006).
Imbalances of Neurotransmitters and Hormones In order for the brain to function adequately, neurons, or nerve cells, must communicate effectively with one another. This communication is done through the trans- mission of electrical nerve impulses. Nerve impulses travel from the cell body or dendrites of one neuron (nerve cell) down the axon. Although there is only one axon for each neuron, axons have branches at their ends called axon endings. These are the sites where neurotransmitter substances are released into the synapse—a tiny fluid-filled space between the axon endings of one neuron (the presyn- aptic neuron) and the dendrites or cell body of another neu- ron (the postsynaptic neuron). These interneuronal transmissions are accomplished by neurotransmitters— chemical substances that are released into the synapse by the presynaptic neuron when a nerve impulse occurs. The neurotransmitter substances released into the synapse then act on the postsynaptic membrane of the dendrite (or cell body) of the receiving neuron, which has special- ized receptor sites where the neurotransmitter substances pass on their message. The neurotransmitters can stimu- late that postsynaptic neuron to either initiate an impulse or inhibit impulse transmission. Both kinds of messages are important.
Once the neurotransmitter substance is released into the synapse, it does not stay around indefinitely (other- wise, the receiving neuron would continue firing in the absence of a real impulse). Sometimes the neurotransmit- ters are quickly destroyed by an enzyme such as mono- amine oxidase, and sometimes they are returned to storage vesicles in the axon endings by a reuptake mechanism—a process of reabsorption by which the neurotransmitters are reabsorbed or effectively sucked back up into the axon ending. The enzyme monoamine oxidase is also present in
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One particularly important set of interactions occurs in the hypothalamic-pituitary-adrenal (hpa) axis. Activa- tion of this axis involves:
1. Messages in the form of corticotropin-releasing hormone (CRH) travel from the hypothalamus to the pituitary.
2. In response to CRH, the pituitary releases adrenocor- ticotropic hormone (ACTH), which stimulates the cortical part of the adrenal gland (located on top of the kidney) to produce epinephrine (adrenaline) and the stress hormone cortisol, which are released into the general circulation. Cortisol mobilizes the body to deal with stress.
3. Cortisol in turn provides negative feedback to the hypothalamus and pituitary to decrease their release of CRH and ACTH, which in turn reduces the release of adrenaline and cortisol. This negative feedback sys- tem operates much as a thermostat does to regulate temperature.
As we will see, malfunctioning of this negative feedback system has been implicated in various forms of psycho- pathology such as depression and posttraumatic stress disorder.
synthesized from a single amino acid (monoamine means “one amine”). Norepinephrine has been implicated as playing an important role in the emergency reactions our bodies show when we are exposed to an acutely stressful or dangerous situation, as well as in attention, orientation, and basic motives (see Chapters 5 and 6). Some of the functions of dopamine include pleasure and cognitive processing, and it has been implicated in schizophrenia (see Chapter 13) as well as in addictive disorders (see Chapter 11). Serotonin has been found to have important effects on the way we think and process information from our environment as well as on behaviors and moods. Not surprisingly, then, it seems to play an important role in emotional disorders such as anxiety and depression, as well as in suicide, as we will see in Chapters 6 and 7. In Chapter 13 we discuss the excitatory neurotransmitter glutamate, which has been implicated in schizophrenia. Finally, in Chapter 6, we discuss the neurotransmitter GABA, which is strongly implicated in reducing anxiety as well as other emotional states characterized by high levels of arousal. Each will be discussed at greater length when the relevant disorders are discussed.
Given that many forms of psychopathology have been associated with various abnormalities in neurotransmitter functioning and with altered sensitivities of receptor sites, it is not surprising that many of the medications used to treat various disorders have the synapse as their site of action. For example, certain medications act to increase or decrease the concentrations of pertinent neurotransmitters in the synaptic gap. They may do so by blocking the reup- take process, by altering the sensitivity of the receptor sites, or by affecting the actions of the enzymes that ordinarily break down the neurotransmitter substances. Medications that facilitate the effects of a neurotransmitter on the post- synaptic neuron are called agonists, and those that oppose or inhibit the effects of a neurotransmitter on a postsynap- tic neuron are called antagonists.
hormonaL imbaLanCES Some forms of psychopa- thology have also been linked to hormonal imbalances. hormones are chemical messengers secreted by a set of endocrine glands in our bodies. Each of the endocrine glands produces and releases its own set of hormones directly into our bloodstream. The hormones then travel and directly affect target cells in various parts of our brain and body, influencing diverse events such as fight-or- flight reactions, sexual responses, physical growth, and many other physical expressions of mental states. Our central nervous system is linked to the endocrine system (in what is known as the neuroendocrine system) by the effects of the hypothalamus on the pituitary gland, which is the master gland of the body, producing a variety of hormones that regulate or control the other endocrine glands (see Figure 3.5).
Hypothalamus Pituitary gland
Thyroid gland
Adrenal glands
Ovary (female)
Testis (male)
Gonads
Figure 3.5 Major Glands of the Endocrine System This figure illustrates some of the major glands of the endocrine sys- tem, which produce and release hormones into the bloodstream. The hypothalamic-pituitary-adrenal axis is also shown (red arrows). The hypothalamus and pituitary are closely connected, and the hypothalamus periodically sends hormone signals to the pituitary (the master gland), which in turn sends another hormone to the corti- cal part of the adrenal glands (above the kidneys) to release epi- nephrine and the stress hormone cortisol.
Causal Factors and Viewpoints 75
emotionality, (2) extraversion or positive emotionality, and (3) constraint (conscientiousness and agreeableness; Rothbart & Bates, 2006; Watson et al., 1994). The infant dimensions of fearfulness and irritability, which show few gender differences (Else-Quest et al., 2006), correspond to the adult dimension of neuroticism—the disposition to experience negative affect. The infant dimensions of posi- tive affect and possibly activity level seem related to the adult dimension of extraversion, and the infant dimension of attentional persistence and effortful control seems related to the adult dimension of constraint or control. One quanti- tative review concluded that, on average, boys show slightly higher levels of activity and intense pleasure than do girls, whereas girls, on average, seem to have greater control of their impulses and greater ability to regulate their attention (Else-Quest et al., 2006). At least some aspects of temperament show a moderate degree of stability from late in the first year of life through at least middle childhood, although temperament can also change (Kagan, 2003).
Just as we saw in the discussion of genotype– environment correlations, the temperament of an infant or young child has profound effects on a variety of important developmental processes. For example, a child with a fear- ful temperament has many opportunities for the classical conditioning of fear to situations in which fear is provoked; later the child may learn to avoid entering those feared sit- uations, and evidence suggests that he or she may be espe- cially likely to learn to fear social situations (Fox et al., 2010; Kagan, 2003). In addition, children with high levels of positive affect and activity are more likely to show high levels of mastery motivation, whereas children with high levels of fear and sadness are less likely to show mastery motivation (Posner & Rothbart, 2007).
Finally, children with high levels of negative emotion- ality are more difficult for parents to be supportive of, and different parents have different styles of parenting such children. This seems to be true especially in families with lower socioeconomic status, which are, on average, less supportive of difficult children than families of mid to high socioeconomic status. The latter families seem to be more resourceful in adapting their parenting styles when faced with such high negative emotionality in a child (Paulussen- Hoogeboom et al., 2007).
Not surprisingly, temperament may also set the stage for the development of various forms of psychopathology later in life. For example, children who are fearful and hypervigilant in many novel or unfamiliar situations have been labeled behaviorally inhibited by Kagan, Fox, and their colleagues. This trait has a significant heritable component (Kagan, 2003) and, when it is stable, is a risk factor for the development of anxiety disorders later in childhood and probably in adulthood (Fox et al., 2010; Kagan, 2003). Con- versely, 2-year-old children who are highly uninhibited, showing little fear of anything, may have difficulty learning
Sex hormones are produced by the gonadal glands, and imbalance in these (such as the male hormones, the androgens) can also contribute to maladaptive behavior. Moreover, gonadal hormonal influences on the developing nervous system also seem to contribute to some of the differences between behavior in men and in women (Hayward, 2003; Hines, 2004).
Temperament temperament refers to a child’s reactivity and characteristic ways of self-regulation, which is believed to be biologically programmed. When we say that babies differ in tempera- ment, we mean that they show differences in their character- istic emotional and arousal responses to various stimuli and in their tendency to approach, withdraw, or attend to vari- ous situations (Rothbart, Derryberry, & Hershey, 2000). Some babies naturally are startled by slight sounds or cry when sunlight hits their faces; others are seemingly insensi- tive to such stimulation. These behaviors are strongly influ- enced by genetic factors, but prenatal and postnatal environmental factors also play a role in their development (Goldsmith, 2003; Rothbart, Derryberry, & Hershey, 2000).
Our early temperament is thought to be the basis from which our personality develops. Starting at about 2 to 3 months of age, approximately five dimensions of tempera- ment can be identified: fearfulness, irritability/frustration, positive affect, activity level, and attentional persistence/ effortful control, although some of these emerge later than others. These seem to be related to the three important dimensions of adult personality: (1) neuroticism or negative
Temperament is consistent over time, causing us to have similar reactions in similar contexts.
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At a more general level, we must remind ourselves again that few, if any, mental disorders are independent of people’s personalities or of the problems they face in trying to live their lives. We will examine perspectives that emphasize these psychological and sociocultural consider- ations in the sections that follow, keeping in mind that the ultimate challenge will be to integrate these varying per- spectives into a theoretically consistent biopsychosocial perspective on psychopathology.
in review • What is the relationship between an individual’s genotype and
phenotype, and how can genotypes shape and interact with the environment?
• Describe at least two methods for studying genetic influences on abnormal behavior.
• What do we mean by “neural plasticity”?
• Describe the sequence of events involved in the transmission of nerve impulses.
• Explain how neurotransmitter and hormonal abnormalities might produce abnormal behavior.
• What is temperament, and why is it important for the origins of abnormal behavior?
The Psychological Perspective 3.4 Describe the most prominent psychological
perspectives on abnormal psychology.
There are many more psychological than biological inter- pretations of abnormal behavior, reflecting a wider range of opinions on how best to understand humans as people with motives, desires, perceptions, thoughts, and so on, rather than just as biological organisms. In this section we examine in some depth three perspectives on human nature and behavior that have been particularly influen- tial: psychodynamic, behavioral, and cognitive-behavioral.
moral standards for their behavior from parents or society (Frick, Cornell, Bodin, et al., 2003; Rothbart, Ahadi, & Evans, 2000), and they have been shown at age 13 to exhibit more aggressive and delinquent behavior (Schwartz et al., 1996). If these personality ingredients are combined with high levels of hostility, the stage also might be set for the development of conduct disorder and antisocial personal- ity disorder (Harpur et al., 1993).
The Impact of the Biological Viewpoint Biological discoveries have profoundly affected the way we think about human behavior. We now recognize the impor- tant role of biochemical factors and innate characteristics, many of which are genetically determined, in both normal and abnormal behavior. However, as Gorenstein (1992) and others argued two decades ago, there are several common errors in the way many people interpret the meaning of recent biological advances. It is incorrect to think—as some prominent biological researchers have—that establishing biological differences between, for example, individuals with schizophrenia and those without schizophrenia in and of itself substantiates that schizophrenia is an illness (e.g., Andreasen, 1984; Kety, 1974). All behavioral traits (introver- sion and extraversion, for example, or high and low sensa- tion seeking) have biological characteristics, yet we do not label these traits as illnesses. Thus, the decision about what constitutes a mental illness or disorder ultimately still rests on clinical judgment regarding the functional effects of the disordered behavior—specifically whether it leads to clini- cally significant distress or impairment in functioning. Establishing the biological substrate does not bear on this issue because all behavior—normal and abnormal—has a biological substrate.
As Gorenstein (1992) also pointed out, the effects of psychological events are always mediated through the activities of the central nervous system because all our thoughts, feelings, and behaviors occur as biological events in the brain. However, we must remember that biology alone does not shape our thoughts, feelings, and behav- iors; they instead occur via interaction with social events in our environment. As noted earlier, we must draw from multiple perspectives in order to fully understand abnor- mal (and normal) behavior.
Research Close-Up Mediator
A mediator (or mediating variable) lies between two other variables and helps explain the relationship between them. You can think of it as being like an intermediate variable, hence the name.
Causal Factors and Viewpoints 77
from eating to painting. The id operates on the pleasure principle, engaging in completely selfish and pleasure- oriented behavior, concerned only with the immediate gratification of instinctual needs without reference to real- ity or moral considerations. Although the id can generate mental images and wish-fulfilling fantasies, referred to as primary process thinking, it cannot undertake the realistic actions needed to meet instinctual demands.
According to Freud’s theory, a second part of the per- sonality that he called the ego develops after the first few months of life. The ego mediates between the demands of the id and the realities of the external world. For example, during toilet training the child learns to control a bodily function to meet parental and societal expectations, and it is the developing ego that assumes the role of mediating between the physical needs of the body/id and the need to find an appropriate place and time. One of the basic func- tions of the ego is to meet id demands, but in such a way as to ensure the well-being and survival of the individual. This role requires the use of reason and other intellectual resources in dealing with the external world, as well as the exercise of control over id demands. The ego’s adaptive measures are referred to as secondary process thinking, and the ego operates on the reality principle.
Freud viewed id demands, especially sexual and aggressive strivings, as inherently in conflict with the rules and prohibitions imposed by society. He postulated that as a child grows and gradually learns the rules of parents and society regarding right and wrong, a third part of the personality gradually emerges from the ego— the superego. The superego is the outgrowth of internal- izing the taboos and moral values of society concerning what is right and wrong. It is essentially what we refer to as the conscience. As the superego develops, it becomes an inner control system that deals with the uninhibited desires of the id. Because the ego mediates among the desires of the id, the demands of reality, and the moral constraints of the superego, it is often called the executive branch of the personality.
Freud believed that the interplay of id, ego, and super- ego is of crucial significance in determining behavior. Often inner mental conflicts arise because the three sub- systems are striving for different goals. If unresolved, these intrapsychic conflicts lead to mental disorder.
Anxiety, Defense Mechanisms, and the Unconscious The concept of anxiety—generalized feelings of fear and apprehension—is prominent in the psychoanalytic view- point because Freud believed that it plays a key causal role in most of the forms of psychopathology discussed in this text. He believed that the anxiety is sometimes overtly experienced, and at other times it is repressed and then transformed into and manifested in other overt symptoms such as conversion blindness or paralysis (see Chapter 8).
These three viewpoints represent distinct and sometimes conflicting orientations, but they are in many ways com- plementary. They all emphasize the importance of early experience and an awareness of psychological processes within an individual, as well as how these are influenced by social factors. The Developments in Thinking box later in this chapter presents a few of the major themes of two additional psychological perspectives: the humanistic and existential perspectives.
The Psychodynamic Perspective As we noted in Chapter 2, Sigmund Freud founded the psychoanalytic school, which emphasized the role of uncon- scious motives and thoughts and their dynamic interrela- tionships in the determination of both normal and abnormal behavior. A key concept here is the unconscious. According to Freud, the conscious part of the mind repre- sents a relatively small area, whereas the unconscious part, like the submerged part of an iceberg, is the much larger portion. In the depths of the unconscious are the hurtful memories, forbidden desires, and other experiences that have been repressed—that is, pushed out of consciousness. However, Freud believed that unconscious material con- tinues to seek expression and emerges in fantasies, dreams, slips of the tongue, and so forth. Until such unconscious material is brought to awareness and integrated into the conscious part of the mind—for example, through psycho- analysis (a form of psychotherapy Freud developed; see Chapter 16)—it may lead to irrational and maladaptive behavior. For our purposes, a general overview of the prin- ciples of classical psychoanalytic theory will suffice (see Luborsky & Barrett, 2006, or any of Freud’s original works for more information). We then discuss several of the newer psychodynamic perspectives, which were the second generation of theories that stemmed in some important ways out of Freud’s original psychoanalytic theory and yet also departed from it in significant ways.
funDamEntaLS of frEuD’S pSyChoanaLytiC thEory
The Structure of Personality: Id, Ego, and Superego In an effort to explain human behavior, Freud theorized that a person’s behavior results from the interaction of three key components of the personality or psyche: the id, ego, and superego. The id is the source of instinctual drives and is the first structure to appear in infancy. These drives are inherited and are considered to be of two opposing types: (1) life instincts, which are constructive drives primarily of a sexual nature and which constitute the libido, the basic emotional and psychic energy of life; and (2) death instincts, which are destructive drives that tend toward aggression, destruction, and eventual death. Freud used the term sex- ual in a broad sense to refer to almost anything pleasurable,
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Each stage is characterized by a dominant mode of achiev- ing libidinal (sexual) pleasure:
1. oral stage: During the first 2 years of life, the mouth is the principal erogenous zone: An infant’s greatest source of gratification is sucking, a process that is nec- essary for feeding.
2. anal stage: From ages 2 to 3, the anus provides the major source of pleasurable stimulation during the time when toilet training is often going on and there are urges both for retention and for elimination.
3. phallic stage: From ages 3 to 5 or 6, self-manipulation of the genitals provides the major source of pleasura- ble sensation.
4. Latency period: From ages 6 to 12, sexual motivations recede in importance as a child becomes preoccupied with developing skills and other activities.
5. Genital stage: After puberty, the deepest feelings of pleasure come from sexual relations.
Freud believed that appropriate gratification during each stage is important if a person is to avoid being stuck, or fixated, at that level. For example, he maintained that an infant who
Anxiety is almost universally experienced at some point. This woman shows her anxiety while awaiting news about the outcome of surgery on her sick child.
Table 3.1 Ego-Defense Mechanisms
Mechanism Example
Displacement. Discharging pent-up feelings, often of hostility, on objects less dangerous than those arousing the feelings.
A woman harassed by her boss at work initiates an argument with her husband.
Fixation. Attaching oneself in an unreasonable or exaggerated way to some person, or arresting emotional development on a childhood or adolescent level.
An unmarried, middle-aged man still depends on his mother to provide his basic needs.
Projection. Attributing one’s unacceptable motives or characteristics to others.
An expansionist-minded dictator of a totalitarian state is convinced that neighboring countries are planning to invade.
Rationalization. Using contrived explanations to conceal or disguise unworthy motives for one’s behavior.
A fanatical racist uses ambiguous passages from the scriptures to justify his hostile actions toward minorities.
Reaction formation. Preventing the awareness or expression of unacceptable desires by an exaggerated adoption of seemingly opposite behavior.
A man troubled by homosexual urges initiates a zealous community campaign to stamp out gay bars.
Regression. Retreating to an earlier developmental level involving less mature behavior and responsibility.
A man with shattered self-esteem reverts to childlike “showing off” and exhibits his genitals to young girls.
Repression. Preventing painful or dangerous thoughts from entering consciousness.
A mother’s occasional murderous impulses toward her hyperactive 2-year-old are denied access to awareness.
Sublimation. Channeling frustrated sexual energy into substitutive activities.
A sexually frustrated artist paints wildly erotic pictures.
SouRcE: Based on A. Freud (1946) and DSM-IV-TR (American Psychiatric Association, 2000). Anxiety is the body’s natural warning system that sig-
nals impending danger and the need to take corrective action. Indeed, it is the anxiety that humans experience when they see a fast-approaching tiger (or bus) that keeps us alive and allows us to procreate and pass this trait on. However, when it is extreme, persistent, and occurs outside the context of real danger, anxiety can be considered prob- lematic or even pathological. Freud believed that in many instances, the ego can cope with elevated anxiety through rational measures (i.e., we talk ourselves down). However, Freud suggested that when our anxiety exists only in our unconscious and we are not aware of it, it cannot be dealt with through rational measures. In these cases the ego resorts to irrational protective measures that are referred to as ego-defense mechanisms, some of which are described in Table 3.1. These defense mechanisms, Freud proposed, reduce anxiety by helping a person push painful ideas out of consciousness (such as when we “forget” a dental appointment) rather than by dealing directly with the prob- lem. These mechanisms result in a distorted view of reality, although some are clearly more adaptive than others.
Psychosexual Stages of Development In addition to his concept of the structure of personality, Freud also proposed that there are five psychosexual stages of development that we all pass through from infancy through puberty.
Causal Factors and Viewpoints 79
could be more like her father and brothers. She emerges from the complex when she comes to identify with her mother and settles for a promissory note: One day she will have a man of her own who can give her a baby—which unconsciously serves as a type of penis substitute.
Resolution of this conflict is considered essential if a young adult of either sex is to develop satisfactory hetero- sexual relationships. The psychoanalytic perspective holds that the best we can hope for is to reach a compromise among our warring inclinations—and to realize as much instinctual gratification as possible with minimal punish- ment and guilt. This perspective thus presents a determin- istic view of human behavior that minimizes rationality and freedom of self-determination. On a group level, it interprets violence, war, and related phenomena as the inevitable products of the aggressive and destructive instincts present in human nature.
nEwEr pSyChoDynamiC pErSpECtivES In seeking to understand his patients and develop his theories, Freud was chiefly concerned with the workings of the id, its nature as a source of energy, and the manner in which this id energy could be channeled or transformed. He also focused on the superego and the role of conscience but paid relatively little attention to the importance of the ego. Later theorists developed some of Freud’s basic ideas in three somewhat different directions.
Ego Psychology One new direction was that taken by his daughter Anna Freud (1895–1982), who was much more concerned with how the ego performs its central functions as the “executive” of personality. She and some of the other influential second-generation psychodynamic theorists refined and elaborated on the ego-defense mechanisms and put the ego in the foreground, giving it an important organizing role in personality development (e.g., Freud, 1946). According to this view, psychopathology develops when the ego does not function adequately to control or
does not receive adequate oral gratification may, in adult life, be prone to excessive eating or other forms of oral stimula- tion, such as biting fingernails, smoking, or drinking.
The demands of the id are evident in early childhood. According to Freud, babies pass through an oral stage, in which sucking is a dominant pleasure.
The Oedipus Complex and the Electra Complex In gen- eral, each psychosexual stage of development places demands on a child and arouses conflicts that Freud believed must be resolved in order to avoid later fixations. One of the most important conflicts occurs during the phal- lic stage, when the pleasures of self-stimulation and accom- panying fantasies pave the way for the oedipus complex. According to Greek mythology, Oedipus unknowingly killed his father and married his mother. Each young boy, Freud thought, symbolically relives the Oedipus drama. He longs for his mother sexually and views his father as a hated rival; however, each young boy also fears that his father will punish his son’s lust by cutting off his penis. This castration anxiety forces the boy to repress his sexual desire for his mother and his hostility toward his father. Eventually, if all goes well, the boy identifies with his father and comes to have only harmless affection for his mother, channeling his sexual impulses toward another woman.
The Electra complex is the female counterpart of the Oedipus complex and is also drawn from a Greek tragedy. It is based on the view that each girl desires to possess her father and to replace her mother. Freud also believed that each girl at this stage experiences penis envy, wishing she
Anna Freud (1895–1982) studied the important role of the ego in normal and abnormal development and elaborated the theory of ego-defense reactions.
80 Chapter 3
traits, they also perceive the external world in abrupt extremes. For example, a person may be “all good” one moment and “all bad” the next (Koenigsberg et al., 2000).
The Interpersonal Perspective A third set of second- generation psychodynamic theorists focused on social deter- minants of behavior. We are social beings, and much of what we are is a product of our relationships with others. It is logical to expect that much of psychopathology reflects this fact—that psychopathology is rooted in the unfortu- nate tendencies we have developed while dealing with our interpersonal environments. This is the focus of the inter- personal perspective, which began with the defection in 1911 of Alfred Adler (1870–1937) from the psychoanalytic viewpoint of his teacher, Sigmund Freud, and emphasizes social and cultural forces rather than inner instincts as determinants of behavior. In Adler’s view, people are inherently social beings motivated primarily by the desire to belong to and participate in a group.
Over time, a number of other psychodynamic theorists also took issue with psychoanalytic theory for its neglect of crucial social factors. Among the best known of these theorists are Erich Fromm (1900–1980) and Karen Horney (1885–1952). Fromm focused on the orientations, or dispositions (exploi- tive, for example), that people adopted in their interactions with others. He believed that when these orientations to the social environment were maladaptive, they served as the bases of much psychopathology. Horney independently developed a similar view and, in particular, vigorously rejected Freud’s demeaning psychoanalytic view of women (for instance, the idea that women experience penis envy).
delay impulse gratification or does not make adequate use of defense mechanisms when faced with internal conflicts. This school became known as ego psychology.
Object-Relations Theory A second new psychodynamic perspective was object-relations theory, developed by a number of prominent theorists including Melanie Klein, Margaret Mahler, W. R. D. Fairburn, and D. W. Winnicott, starting in the 1930s and 1940s. Although there are many variations on object-relations theory, they share a focus on individuals’ interactions with real and imagined other peo- ple (external and internal objects) and on the relationships that people experience between their external and internal objects. Object in this context refers to the symbolic repre- sentation of another person in the infant’s or child’s envi- ronment, most often a parent. Through a process of introjection, a child symbolically incorporates into his or her personality (through images and memories) important peo- ple in his or her life. For example, a child might internalize images of a punishing father; that image then becomes a harsh self-critic, influencing how the child behaves. The general notion is that internalized objects could have vari- ous conflicting properties—such as exciting or attractive versus hostile, frustrating, or rejecting—and also that these objects could split off from the central ego and maintain independent existences, thus giving rise to inner conflicts. An individual experiencing such splitting among internal- ized objects is, so to speak, “the servant of many masters” and cannot therefore lead an integrated, orderly life.
Margaret Mahler (1897–1985) elaborated the object-relations approach, which many see as the main focus of contemporary psychoanalysis.
For example, Otto Kernberg, an influential American psychoanalyst, has a theory that people with borderline per- sonality disorder, whose chief characteristic is instability (especially in personal relationships), are unable to achieve a full and stable personal identity (self) because of an inability to integrate and reconcile pathological internal- ized objects (Kernberg 1985, 1996; Kernberg & Michels, 2009). Because of their inability to structure their internal world in such a way that the people they know (including themselves) can have a mixture of both good and bad
Erich Fromm (1900–1980) focused on the orientations that people adopt in their interactions with others. He believed that these basic orientations to the social environment were the bases of much psychopathology.
Erik Erikson (1902–1994) also extended the interpersonal aspects of psychoanalytic theory. He elaborated and broad- ened Freud’s psychosexual stages into more socially oriented concepts, describing crises or conflicts that occurred at eight
Causal Factors and Viewpoints 81
Freud greatly advanced our understanding of both normal and abnormal behavior. Many of his original concepts have become fundamental to our thinking about human nature and behavior and have even had an impor- tant influence on the intellectual history of Western civili- zation. Two of Freud’s contributions stand out as particularly noteworthy:
1. He developed therapeutic techniques such as free asso- ciation and dream analysis for becoming acquainted with both the conscious and the unconscious aspects of mental life (see Chapter 16). Freud emphasized several points that have been incorporated (in modified forms) into current thinking: (a) there are psychological factors outside our conscious awareness that influence our behavior; (b) early childhood experiences can have an important and lasting impact on the development of both normal and abnormal personality; and (c) sexual factors can play a large role in human behavior and mental disorders. Although, as we have said, Freud used the term sexual in a much broader sense than usual, the idea struck a common chord, and the role of sexual factors in human behavior was finally brought out into the open as an appropriate topic for scientific investigation (see Chapter 12).
2. He demonstrated that certain abnormal mental phe- nomena occur in an attempt to cope with difficult problems and are simply exaggerations of normal ego- defense mechanisms. This realization that the same psychological principles apply to both normal and abnormal behavior dissipated much of the mystery and fear surrounding mental disorders.
After years of prominence, the psychoanalytic per- spective came under attack from many directions. Two important criticisms of traditional psychoanalytic theory center on its failure as a scientific theory to explain abnor- mal behavior. First, many believe that it fails to realize the scientific limits of personal reports of experience as the pri- mary mode of obtaining information. Second, there is a lack of scientific evidence to support many of its explana- tory assumptions or the effectiveness of traditional psycho- analysis. In addition, Freudian theory in particular has been criticized for an overemphasis on the sex drive, for its demeaning view of women, for pessimism about basic human nature, for exaggerating the role of unconscious processes, and for failing to consider motives toward per- sonal growth and fulfillment.
impaCt of nEwEr pSyChoDynamiC pErSpECtivES The second generation of psychodynamic theorists has done much to improve scientific efforts to measure concepts such as a person’s core (but unconscious) conflictual rela- tionships (e.g., Horowitz et al., 1991; Luborsky & Barrett, 2006). Some progress has also been made in understanding
stages, each of which could be resolved in a healthy or unhealthy way. For example, Erikson believed that during what Freud called the “oral stage,” when a child is preoccu- pied with oral gratification, a child’s real development centers on learning either “basic trust” or “basic mistrust” of her or his social world. Achieving a certain level of trust, for instance, is necessary for later competence in many areas of life.
Erik Erikson (1902–1994) elaborated and broadened Freud’s psychosexual stages into more socially oriented concepts. Erikson described conflicts that occurred at eight stages, each of which could be resolved in a healthy or unhealthy way.
Attachment Theory Finally, John Bowlby’s attachment theory, which can in many ways be seen as having its roots in the interpersonal and object-relations perspectives, has become an enormously influential theory in child psychol- ogy and child psychiatry as well as in adult psychopathol- ogy. Drawing on Freud and others from these perspectives, Bowlby’s theory (1969, 1973, 1980) emphasizes the impor- tance of early experience, especially early experience with attachment relationships, as laying the foundation for later functioning throughout childhood, adolescence, and adult- hood. He stresses the importance of the quality of parental care to the development of secure attachments, but he also sees the infant as playing a more active role in shaping the course of his or her own development than had most of the earlier theorists (Carlson & Sroufe, 1995; Rutter et al., 2009; Sroufe et al., 2000).
impaCt of thE pSyChoanaLytiC pErSpECtivE Freud’s psychoanalytic theory can be seen as the first sys- tematic approach to showing how human psychological processes can result in mental disorders. Much as the biological perspective had replaced superstition with organic pathology as the suspected cause of mental disor- ders for many psychiatrists and psychologists, the psycho- analytic perspective replaced brain pathology with intrapsychic conflict and exaggerated ego defenses as the suspected cause of at least some mental disorders.
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interpersonal psychotherapy for certain disorders such as depression, bulimia, and some personality disorders can be as effective, or nearly as effective, as cognitive-behavioral treatment—considered by many to be the treatment of choice for these disorders (Benjamin, 2004; Hollon et al., 2006; Wilson & Fairburn, 2007).
The Developments in Thinking box presents two fur- ther psychological perspectives that developed in the mid- dle of the twentieth century in part because their founders did not believe that psychodynamic theories acknowledged a person’s freedom of choice or the concept of free will.
how psychodynamic therapy works and in documenting its effectiveness for certain problems (e.g., Crits-Christoph et al., 2004; Shedler, 2010). In addition, Bowlby’s attachment theory has generated an enormous amount of research supporting many of its basic tenets about normal and abnormal child development and adult psychopathology (e.g., Grossman et al., 2005; Rutter et al., 2009).
The focus of interpersonal therapy is on alleviating problem-causing relationships and on helping people achieve more satisfactory relationships. In recent years, major progress has been made in documenting that
Developments in Thinking The Humanistic and Existential Perspectives
The Humanistic Perspective The humanistic perspective views human nature as basically “good.” Paying less attention to unconscious processes and past causes, it emphasizes present conscious processes and places strong emphasis on people’s inherent capacity for responsible self-direction. Humanistic psychologists think that much of the empirical research designed to investigate causal factors is too simplistic to uncover the complexities of human behavior. Instead, this perspective is concerned with processes such as love, hope, creativity, values, meaning, personal growth, and self-fulfillment. Although these abstract processes are not readily subject to empirical investigation, certain underlying themes and principles of humanistic psychology can be identified, including the self as a unifying theme and a focus on values and personal growth.
In using the concept of self as a unifying theme, humanistic psychologists emphasize the importance of individuality. Among humanistic psychologists, Carl Rogers (1902–1987) developed the most systematic formulation of the self-concept, based largely on his pioneering research into the nature of the psychotherapeu- tic process. Rogers (1951, 1959) stated his views in a series of propositions that may be summarized as follows:
• Each individual exists in a private world of experience of which
the I, me, or myself is the center.
• The most basic striving of an individual is toward the mainte- nance, enhancement, and actualization of the self, and his or her inner tendencies are toward health and wholeness under normal conditions.
• Perceived threat to the self is followed by a defense, including a tightening of perception and behavior and the introduction of self-defense mechanisms.
Humanistic psychologists emphasize that values and the process of choice are key in guiding our behavior and achieving meaningful and fulfilling lives. Each of us must develop values and a sense of our own identity based on our own experiences rather than blindly accepting the values of others; otherwise, we deny our own experiences and lose touch with our own feelings. Only in this way can we become self-actualizing, meaning that we are
achieving our full potential. According to this view, psychopathol- ogy is essentially the blocking or distortion of personal growth and the natural tendency toward physical and mental health. Chapter 16 presents the humanistic approach to psychotherapy.
The Existential Perspective The existential perspective resembles the humanistic view in its emphasis on the uniqueness of each individual, the quest for val- ues and meaning, and the existence of freedom for self-direction and self-fulfillment. However, it takes a less optimistic view of human beings and places more emphasis on their irrational ten- dencies and the difficulties inherent in self-fulfillment—particularly in a modern, bureaucratic, and dehumanizing mass society. In short, living is much more of a “confrontation” for the existential- ists than for the humanists. Existential thinkers are especially con- cerned with the inner experiences of an individual in his or her attempts to understand and deal with the deepest human prob- lems. Existentialism has several basic themes:
• Existence and essence. Our existence is a given, but what we
make of it—our essence—is up to us. Our essence is created
by our choices because our choices reflect the values on
which we base and order our lives.
• Meaning and value. The will-to-meaning is a basic human ten- dency to find satisfying values and guide one’s life by them.
• Existential anxiety and the encounter with nothingness. Non- being, or nothingness, which in its final form is death, is the inescapable fate of all human beings. The awareness of our inevitable death and its implications for our living can lead to existential anxiety, a deep concern over whether we are living meaningful and fulfilling lives.
Thus, existential psychologists focus on the importance of estab- lishing values and acquiring a level of spiritual maturity worthy of the freedom and dignity bestowed by one’s humanness. Avoiding such central issues creates corrupted, meaningless, and wasted lives. Much abnormal behavior, therefore, is seen as the product of a failure to deal constructively with existential despair and frustration.
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elicits salivation, a stimulus that reliably precedes and sig- nals the presentation of food will also come to elicit saliva- tion (Pavlov, 1927). In this case, food is the unconditioned stimulus (UCS) and salivation the unconditioned response (UCR). A stimulus that signals food delivery and eventu- ally elicits salivation is called a conditioned stimulus (CS). Conditioning has occurred when presentation of the condi- tioned stimulus alone elicits salivation—the conditioned response (CR). The same general process occurs when a neutral CS is paired with a painful or frightening stimulus such as a mild electric shock or loud noise, as illustrated in Figure 3.6, although in this case fear rather than salivation is conditioned.
The Behavioral Perspective The behavioral perspective arose in the early twentieth cen- tury in part as a reaction against the unscientific methods of psychoanalysis. Behavioral psychologists believed that the study of subjective experience (e.g., free association and dream analysis) did not provide acceptable scientific data because such observations were not open to verification by other investigators. In their view, only the study of directly observable behavior and of the stimuli and reinforcing con- ditions that control it could serve as a basis for understand- ing human behavior, normal and abnormal.
Importantly, this perspective was developed through laboratory research rather than clinical practice with patients; however, its implications for explaining and treat- ing maladaptive behavior soon became evident. As we noted in Chapter 2, the roots of the behavioral perspective are in Pavlov’s study of classical conditioning and in Thorn- dike’s study of instrumental conditioning (later renamed operant conditioning by Skinner; today both terms are used). The behavioral approach really came together with the 1924 publication of Watson’s book Behaviorism.
Learning—the modification of behavior as a conse- quence of experience—is the central theme of the behav- ioral approach. Because most human behavior is learned, the behaviorists addressed the question of how learning occurs. Behaviorists focus on the effects of environmental conditions (stimuli) on the acquisition, modification, and possible elimination of various types of response patterns, both adaptive and maladaptive.
CLaSSiCaL ConDitioninG A specific stimulus may come to elicit a specific response through the process of classical conditioning. For example, although food naturally
Orientation response to light
Unconditioned response (UCR) (pain and fear)
Conditioned response (fear) (CR)
Conditioned response (fear) (CR)
Classical Conditioning
Prior to conditioning: Conditioned stimulus (neutral) (CS) (light) Unconditioned stimulus (UCS) (painful stimulus)
During conditioning: Conditioned stimulus (light) (CS) + Unconditioned stimulus (UCS) (painful stimulus)
Following conditioning: Conditioned stimulus (alone) (CS)
Figure 3.6 Classical Conditioning Before conditioning, the CS is neutral and has no capacity to elicit fear. However, after being repeatedly followed by a painful or frightening UCS that elicits pain, fear, or distress, the CS gradually acquires the capacity to elicit a fear CR. If there are also interspersed trials in which the UCS occurs without being preceded by the CS, conditioning does not occur because in this case the CS is not a reliable predictor of the occurrence of the UCS.
The hallmark of classical conditioning is that a for- merly neutral stimulus—the CS—acquires the capacity to elicit biologically adaptive responses through repeated pairings with the UCS (e.g., Bouton, 2007; Domjan, 2009). However, we also now know that this process of classical conditioning is not as blind or automatic as was once thought. Rather, it seems that animals (and people) actively
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that instrumental conditioning consisted of simple strengthening of a stimulus–response connection every time that reinforcement occurred, it is now believed that the animal or person learns a response–outcome expectancy (e.g., Domjan, 2005)—that is, learns that a response will lead to a reward outcome. If sufficiently motivated for that outcome (e.g., being hungry), the person will make the response that he or she has learned produces the outcome (e.g., opening the refrigerator).
acquire information about what CSs allow them to predict, expect, or prepare for an upcoming biologically significant event (the UCS). That is, they learn what is often called a stimulus-stimulus expectancy. Indeed, only CSs that provide reliable and nonredundant information about the occur- rence of a UCS acquire the capacity to elicit CRs (Hall, 1994; Rescorla, 1988). For example, if UCSs occur as often without being preceded by a CS as they do with the CS, conditioning will not occur because the CS in this case does not provide reliable information about the occurrence of the UCS.
Classically conditioned responses are well maintained over time; that is, they are not simply forgotten (even over many years). However, if a CS is repeatedly presented without the UCS, the conditioned response gradually extinguishes. This gradual process, known as extinction, should not be confused with the idea of unlearning because we know that the response may return at some future point in time (a phenomenon Pavlov called spontaneous recovery). Moreover, a somewhat weaker CR may also still be elicited in different environmental contexts than in the one where the extinction process took place (Bouton, 1994, 2002; Bouton et al., 2006). Thus, any extinction of fear that has taken place in a therapist’s office may not necessarily generalize completely and automatically to other contexts outside the therapist’s office (see Craske & Mystkowski, 2006; Mystkowski & Mineka, 2007). As we shall see later, these principles of extinction and spontaneous recovery have important implications for many forms of behavioral treatment.
Classical conditioning is important in abnormal psy- chology because many physiological and emotional responses can be conditioned, including those related to fear, anxiety, or sexual arousal and those stimulated by drugs of abuse. Thus, for example, one can learn a fear of the dark if fear-producing stimuli (such as frightening dreams or fantasies) occur regularly in the dark, or one can acquire a fear of snakes if bitten by a snake (Mineka & — Sutton, 2006; Mineka & Zinbarg, 2006). In addition, a young man who has his first few powerful sexual experiences (UCR) with a very attractive woman (UCS) wearing some form of distinctive clothing (CS—such as black fishnet stock- ings) may find in the future that he becomes very sexually aroused (CR) simply upon seeing fishnet stockings.
opErant ConDitioninG In operant (or instrumental) conditioning, an individual learns how to achieve a desired goal. The goal in question may be to obtain some- thing that is rewarding or to escape from something that is unpleasant. Essential here is the concept of reinforcement, which refers either to the delivery of a reward or pleasant stimulus, or to the removal of or escape from an aversive stimulus. New responses are learned and tend to recur if they are reinforced. Although it was originally thought
Initially a high rate of reinforcement may be necessary to establish an instrumental response, but lesser rates are usually sufficient to maintain it. In fact, an instrumental response appears to be especially persistent when rein- forcement is intermittent—when the reinforcing stimulus does not invariably follow the response—as demonstrated in gambling, when occasional wins seem to maintain high rates of responding. However, when reinforcement is con- sistently withheld over time, the conditioned response— whether classical or instrumental—gradually extinguishes. In short, the subject eventually stops making the response.
A special problem arises in situations in which a sub- ject has been conditioned to anticipate an aversive event and so consistently avoids those situations. For example, a boy who has nearly drowned in a swimming pool may develop a fear of water and a conditioned avoidance response in which he consistently avoids all large bodies of water. According to one influential theory, when he sees a pond, lake, or swimming pool, he feels anxious; running away and avoiding contact lessens his anxiety and thus is rein- forcing. As a result, his avoidance response is highly resis- tant to extinction. It also prevents him from having experiences with water that could bring about extinction of his fear. In later discussions, we will see that conditioned avoidance responses play a role in many patterns of abnor- mal behavior.
As we grow up, instrumental learning becomes an important mechanism for discriminating between what will prove rewarding and what will prove unrewarding— and thus for acquiring the behaviors essential for coping with our world. Unfortunately, what we learn is not always
Causal Factors and Viewpoints 85
expand our opportunities for learning both adaptive and maladaptive behavior.
impaCt of thE bEhavioraL pErSpECtivE Because there was so much resistance from well-entrenched sup- porters of psychoanalysis, behavior therapy did not become well established as a powerful way of viewing and treating abnormal behavior until the 1960s and 1970s. By then, the behavioral assault on the prevailing psychody- namic doctrine of the time (Salter, 1949; Wolpe, 1958) was well under way and important evidence had been gath- ered on the power of behavior therapy techniques.
By means of a relatively few basic concepts, the behav- ioral perspective attempts to explain the acquisition, modi- fication, and extinction of nearly all types of behavior. Maladaptive behavior is viewed as essentially the result of (1) a failure to learn necessary adaptive behaviors or com- petencies, such as how to establish satisfying personal rela- tionships, and/or (2) the learning of ineffective or maladaptive responses. Maladaptive behavior is thus the result of learning that has gone awry and is defined in terms of specific, observable, undesirable responses.
For the behavior therapist, the focus of therapy is on changing specific behaviors and emotional responses— eliminating undesirable reactions and learning desirable ones. For example, fears and phobias can be successfully treated by prolonged exposure to the feared objects or situ- ations—an extinction procedure derived from principles of extinction of classical conditioning. Or an inappropriate sexual attraction to a deviant stimulus (such as prepubertal children) can be altered by pairing pictures of the deviant stimuli with a foul odor or another unpleasant stimulus. Classic work using the principles of instrumental condi- tioning also showed that institutionalized people with chronic mental illness can be retaught basic living skills such as clothing and feeding themselves through the use of tokens that are earned for appropriate behavior and that can be turned in for desirable rewards (candy, time watch- ing television, passes to go outside, etc.).
The behavioral approach is well known for its preci- sion and objectivity, for its wealth of research, and for its demonstrated effectiveness in changing specific behaviors. A behavior therapist specifies what behavior is to be changed and how it is to be changed. Later, the effective- ness of the therapy can be evaluated objectively by the degree to which the stated goals have been achieved. Nev- ertheless, the behavioral perspective has been criticized for several reasons. One early criticism was that behavior ther- apy was concerned only with symptoms, not underlying causes. However, this criticism has been considered unfair by many contemporary behavior therapists, given that successful symptom-focused treatment often has very pos- itive effects on other aspects of a person’s life (e.g., Borkovec et al., 1995; Lenz & Demal, 2000). Still others have argued
useful in the long run. We may learn to value things (such as cigarettes or alcohol) that seem attractive in the short run but that can actually hurt us in the long run, or we may learn coping patterns (such as helplessness, bullying, or other irresponsible behaviors) that are maladaptive rather than adaptive in the long run.
GEnEraLization anD DiSCrimination In both classical and instrumental conditioning, when a response is conditioned to one stimulus or set of stimuli, it can be evoked by other, similar stimuli; this process is called generalization. A person who fears bees, for example, may generalize that fear to all flying insects. A process comple- mentary to generalization is discrimination, which occurs when a person learns to distinguish between similar stim- uli and to respond differently to them based on which ones are followed by reinforcement. For example, because red strawberries taste good and green ones do not, a condi- tioned discrimination will occur if a person has experience with both.
The concepts of generalization and discrimination have many implications for the development of maladaptive behavior. Although generalization enables us to use past experiences in sizing up new situations, the possibility of making inappropriate generalizations always exists, as when a troubled adolescent fails to discriminate between friendly and hostile teasing from peers. In some instances, an important discrimination seems to be beyond an individ- ual’s capability (as when a bigoted person deals with others on the basis of stereotypes rather than as individuals) and may lead to inappropriate and maladaptive behavior.
obSErvationaL LEarninG Human and nonhuman primates are also capable of observational learning—that is, learning through observation alone, without directly experiencing an unconditioned stimulus (for classical con- ditioning) or a reinforcement (for instrumental condition- ing). For instance, children can acquire new fears by simply observing a parent or peer behaving fearfully with some object or situation that the child did not initially fear. In this case, they experience the fear of the parent or peer vicariously, and that fear becomes attached to the formerly neutral object (Mineka & Oehlberg, 2008; Mineka & Sutton, 2006). For observational instrumental learning, Bandura did a classic series of experiments in the 1960s on how children observationally learned various novel, aggres- sive responses toward a large Bobo doll after they had observed models being reinforced for these responses (see Bandura, 1969). Although the children themselves were never directly reinforced for showing these novel aggressive responses, they nonetheless showed them when given the opportunity to interact with the Bobo doll themselves. The possibilities for observational condition- ing of both classical and instrumental responses greatly
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for this perspective is the concept of a schema, which was adapted from cognitive psychology by Aaron Beck (b. 1921), another pioneering cognitive theorist (e.g., Beck, 1967; Neisser, 1967, 1982). A schema is an underlying rep- resentation of knowledge that guides the current process- ing of information and often leads to distortions in attention, memory, and comprehension. People develop different schemas based on their temperament, abilities, and experiences.
SChEmaS anD CoGnitivE DiStortionS Our schemas about the world around us and about ourselves (self-schemas) are our guides, one might say, through the complexities of living in the world as we understand it. We all have schemas about other people (for example, expectations that they are lazy or very career oriented). We also have schemas about social roles (for example, expecta- tions about what the appropriate behaviors for a widow are) and about events (for example, what sequences of events are appropriate for a particular situation such as someone coping with a loss; Bodenhausen & Morales, 2013;
that the behavioral approach oversimplifies human behav- ior and is unable to explain all of its complexities. This lat- ter criticism stems at least in part from misunderstandings about current developments in behavioral approaches (e.g., Bouton, 2007; Bouton et al., 2001; Mineka & Oehlberg, 2008; Mineka & Zinbarg, 2006). Whatever its limitations, the behavioral perspective has had a tremendous impact on contemporary views of human nature, behavior, and psychopathology.
The Cognitive-Behavioral Perspective Since the 1950s many psychologists, including some learn- ing theorists, focused on cognitive processes and their impact on behavior. Cognitive psychology involves the study of basic information-processing mechanisms such as attention and memory, as well as higher mental processes such as thinking, planning, and decision making. The cur- rent emphasis within psychology as a whole on under- standing all of these facets of normal human cognition originally began as a reaction against the relatively mecha- nistic nature of the traditional, radical behavioral view- point (espoused by Watson and Skinner), including its failure to attend to the importance of mental processes— both in their own right and for their influence on emotions and behavior.
Albert Bandura (b. 1925), a learning theorist who devel- oped an early cognitive-behavioral perspective, placed con- siderable emphasis on the cognitive aspects of learning. Bandura stressed that human beings regulate behavior by internal symbolic processes—thoughts. That is, we learn by internal reinforcement. According to Bandura, we prepare ourselves for difficult tasks, for example, by visualizing what the consequences would be if we did not perform them. Thus we take our automobiles to the garage in the fall and have the antifreeze checked because we can “see” our- selves stranded on a road in winter. We do not always require external reinforcement to alter our behavior pat- terns; our cognitive abilities allow us to solve many prob- lems internally. Bandura (1974) went so far as to say that human beings have “a capacity for self-direction” (p. 861). Bandura later developed a theory of self-efficacy, the belief that one can achieve desired goals (1986, 1997). He posited that cognitive-behavioral treatments work in large part by improving self-efficacy.
Other cognitive-behavioral theorists abandoned the learning theory framework more vigorously than did Bandura and focused almost exclusively on cognitive processes and their impact on behavior. Today the cogni- tive or cognitive-behavioral perspective on abnormal behavior generally focuses on how thoughts and infor- mation processing can become distorted and lead to mal- adaptive emotions and behavior. One central construct
Albert Bandura (b. 1925) stressed that people learn more by internal than external reinforcement. They can visualize the consequences of their actions rather than rely exclusively on environmental reinforcements.
Causal Factors and Viewpoints 87
This is in part because we are usually not completely con- scious of our schemas. In other words, although our daily decisions and behavior are largely shaped by these frames of reference, we may be unaware of the assumptions on which they are based—or even of making assumptions at all. We think that we are simply seeing things the way they are and often do not consider the fact that other views of the “real” world might be possible or that other rules for what is “right” might exist.
We tend to work new experiences into our existing cognitive frameworks, even if the new information has to be reinterpreted or distorted to make it fit—a process known as assimilation. In other words, we are likely to cling to existing assumptions and to reject or distort new infor- mation that contradicts them. Accommodation—changing our existing frameworks to make it possible to incorporate new information that doesn’t fit—is more difficult and threatening, especially when important assumptions are challenged. Accommodation is, of course, a basic goal of psychological therapies—explicitly in the case of the cogni- tive and cognitive-behavioral therapies, but deeply embed- ded in virtually all other approaches as well.
According to Beck (1967; Beck et al., 2005), different forms of psychopathology are characterized by different maladaptive schemas that have developed as a function of adverse early learning experiences. These maladaptive schemas lead to the distortions in thinking that are charac- teristic of certain disorders such as anxiety, depression, and personality disorders. In addition to studying the nature of dysfunctional schemas associated with different forms of psychopathology, researchers have also studied several dif- ferent patterns of distorted information processing exhib- ited by people with various forms of psychopathology. This
Clark, Beck, & Alford, 1999). Our self-schemas include our views on who we are, what we might become, and what is important to us. Other aspects of our self-schemas concern our notions of the various roles we occupy or might occupy in our social environment such as “woman,” “man,” “student,” “parent,” “physician,” “American,” and so on. Most people have clear ideas about at least some of their own personal attributes and less clear ideas about other attributes (Fiske & Taylor, 1991; Kunda, 1999).
Our self-schemas—our frames of reference for who we are, what we might become, and what is important to us—influence our choice of goals and our confidence in attaining them. Until his mid-30s, Ang Lee was an unemployed stay-at-home dad. He eventually pursued his dream of making movies, and soon thereafter went on to write and/or direct award-winning films such as Sense and Sensibility, Crouching Tiger, Hidden Dragon, and Life of Pi. It was likely a self- schema that he is a filmmaker that led him to continue to pursue his dream for so long.
Schemas about the world and self-schemas are vital to our ability to engage in effective and organized behavior because they enable us to focus on the most relevant and important bits of information among the amazingly com- plex array of information that is available to our senses. However, schemas are also sources of psychological vul- nerabilities because some of our schemas or certain aspects of our self-schemas may be distorted and inaccurate. In addition, we often hold some schemas—even distorted ones—with conviction, making them resistant to change.
Aaron Beck (b. 1921) pioneered the development of cognitive theories of depression, anxiety, and personality disorders. He also developed highly effective cognitive-behavioral treatments for these disorders.
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test because I’m stupid” as opposed to “I failed the test because the teacher was in a bad mood and graded it unfairly”). However inaccurate our attributions may be, they become important parts of our view of the world and can have significant effects on our emotional well-being (Abramson et al., 1978; Mineka et al., 2002). Interestingly, nondepressed people tend to have what is called a self-serving bias in which they are more likely to make internal, stable, and global attributions for positive rather than negative events (e.g., Mezulis et al., 2004).
research has illuminated the cognitive mechanisms that may be involved in causing or maintaining certain disor- ders. For example, individuals who are depressed show memory biases favoring negative information over posi- tive or neutral information. Such biases are likely to help reinforce or maintain one’s current depressed state (e.g., Joormann, 2009; Mathews & MacLeod, 2005).
Another important feature of information processing is that a great deal of information is processed noncon- sciously, or outside of our awareness. Note that the term nonconscious does not refer to Freud’s concept of the unconscious, in which primitive emotional conflicts are thought to simmer. Instead, the term nonconscious mental activity as studied by cognitive psychologists is simply a descriptive term for mental processes that are occurring without our being aware of them. One example relevant to psychopathology is that anxious people seem to have their attention drawn to threatening information even when that information is presented subliminally (that is, without the person’s awareness; e.g., Mathews & MacLeod, 2005). Another relevant example occurs in the well-known phenomenon of implicit memory, which is demonstrated when a person’s behavior reveals that she or he remembers a previously learned word or activity even though she or he cannot consciously remember it. For example, if someone asks you for your old home phone number from about 10 years ago, you may not be able to recall it (no explicit memory for it), but if you picked up a phone you might dial it correctly (intact implicit memory for it).
attributionS, attributionaL StyLE, anD pSyChopathoLoGy Attribution theory has also con- tributed significantly to the cognitive-behavioral approach (Fiske & Taylor, 1991; Gotlib & Abramson, 1999). attribution is simply the process of assigning causes to things that happen. We may attribute behavior to external events such as rewards or punishments (“He did it for the money”), or we may assume that the causes are internal and derive from traits within ourselves or others (“He did it because he is so generous”). Causal attributions help us explain our own or other people’s behaviors and make it possible to predict what we or others are likely to do in the future. A student who fails a test may attribute the failure to a lack of intelligence (a personal trait) or to ambiguous test questions or unclear directions (environmental causes).
Attribution theorists have been interested in whether different forms of psychopathology are associated with distinctive and dysfunctional attributional styles. Attribu- tional style is a characteristic way in which an individual tends to assign causes to bad events or good events. For example, people with depression tend to attribute bad events to internal, stable, and global causes (“I failed the
The cognitive perspective suggests that it is not events, but our attributions about events, that influence our feelings and behaviors. For instance, if you are home alone at night and hear a strange noise, you may believe it was caused by the wind and do nothing. But, if you believe it was caused by an intruder, you may grab a large knife (and a large phone), like Drew Barrymore in the classic movie Scream.
CoGnitivE thErapy Beck, who is generally consid- ered the founder of cognitive therapy, has been enormously influential in the development of cognitive-behavioral treatment approaches to various forms of psychopathol- ogy. Following Beck’s lead, cognitive-behavioral theorists and clinicians have simply shifted their focus from overt behavior itself to the underlying cognitions assumed to be producing the maladaptive emotions and behavior. Funda- mental to Beck’s perspective is the idea that the way we interpret events and experiences determines our emotional reactions to them. Suppose, for example, that you are
Causal Factors and Viewpoints 89
Skinner is gone, this debate will surely continue in some form. Indeed, Wolpe (1988, 1993), another founder of behavior therapy, also remained highly critical of the cog- nitive perspective until his death in 1997. However, these criticisms have seemed to be decreasing in recent years as more and more evidence accumulates for the efficacy of cognitive-behavioral treatments for various disorders ranging from schizophrenia to anxiety, depression, and personality disorders (e.g., Barlow, 2008; Butler et al., 2006; Tolin, 2010). This approach has also been greatly advanced by the accumulation of sophisticated information-processing studies of the effects of emotion on cognition and behavior (e.g., Joormann & Quinn, 2014; Ochsner et al., 2012). This is because such studies do not rely on the self-report tech- niques that were originally central to this approach, and which are especially open to the kinds of criticisms raised by Skinner and Wolpe.
What the Adoption of a Perspective Does and Does Not Do Each of the psychological perspectives on human behavior— psychodynamic, behavioral, and cognitive-behavioral— contributes to our understanding of psychopathology, but none alone can account for the complex variety of human maladaptive behaviors. Because different causal perspec- tives influence which components of maladaptive behavior the observer focuses on, each perspective depends on generalizations from limited observations and research. For example, in attempting to explain a complex disorder such as alcohol dependence, the more traditional psycho- dynamic viewpoint focuses on intrapsychic conflict and anxiety that the person attempts to reduce through the intake of alcohol. The more recent interpersonal variant on the psychodynamic perspective focuses on difficulties in a person’s past and present relationships that contribute to drinking. The behavioral viewpoint focuses on faulty learning of habits to reduce stress (drinking alcohol) and environmental conditions that may be exacerbating or maintaining the condition; and the cognitive-behavioral viewpoint focuses on maladaptive thinking including deficits in problem solving and information processing, such as irrational beliefs about the need for alcohol to reduce stress.
Thus, which perspective we adopt has important consequences: It influences our perception of maladaptive behavior, the types of evidence we look for, and the way in which we are likely to interpret data. A wide range of psy- chological causal factors have been implicated in the ori- gins of maladaptive behavior, and some of these different viewpoints provide contrasting (or sometimes comple- mentary) explanations for how the causal factors exert their effects. (See Figure 3.7.)
sitting in your living room and hear a crash in the adjacent dining room. You remember that you left the window open in the dining room and conclude that a gust of wind must have knocked over your favorite vase, which was sitting on the table. What would your emotional reaction be? Probably you would be annoyed or angry with your- self either for having left the window open or for having left the vase out (or both!). By contrast, suppose you con- clude that a burglar must have climbed in the open win- dow. What would your emotional reaction be then? In all likelihood, you would feel frightened. Thus, your inter- pretation of the crash you heard in the next room funda- mentally determines your emotional reaction to it. Moreover, certain individuals with prominent danger schemas may be especially prone to making the burglar assumption in this example, leaving them at risk for anx- iety and worry.
One central issue for cognitive therapy, then, is how best to alter distorted and maladaptive cognitions, includ- ing the underlying maladaptive schemas that lead to dif- ferent disorders and their associated emotions. For example, cognitive-behavioral clinicians are concerned with their clients’ self-statements—that is, with what their clients say to themselves by way of interpreting their experiences. People who interpret what happens in their lives as a negative reflection of their self-worth are likely to feel depressed; people who interpret the sensa- tion that their heart is racing as meaning that they may have a heart attack and die are likely to have a panic attack. Cognitive-behavioral clinicians use a variety of techniques designed to alter whatever negative cognitive biases the client harbors (e.g., see Barlow, 2008; Beck et al., 2004; Hollon & Beck, 1994; Hollon et al., 2006). This is in contrast to, for example, psychodynamic practice, which assumes that diverse problems are due to a limited array of intrapsychic conflicts (such as an unresolved Oedipus complex) and tends not to focus treatment directly on a person’s particular problems or complaints. Many widely used cognitive-behavioral therapies will be described in later chapters.
thE impaCt of thE CoGnitivE-bEhavioraL pErSpECtivE The cognitive-behavioral viewpoint has had a powerful impact on contemporary clinical psychol- ogy. Many researchers and clinicians have found support for the principle of altering human behavior through changing the way people think about themselves and oth- ers. Many traditional behaviorists, however, have remained skeptical of the cognitive-behavioral viewpoint. B. F. Skin- ner (1990), in his last major address, remained true to behaviorism. He questioned the move away from princi- ples of operant conditioning. He reminded his audience that cognitions are not observable phenomena and, as such, cannot be relied on as solid empirical data. Although
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in which the events in one child’s life may be vastly differ- ent from those in another child’s life is whether they are predictable or controllable. Exposure to multiple uncontrol- lable and unpredictable frightening events is likely to leave a person vulnerable to anxiety and negative affect, a cen- tral problem in a number of mental disorders such as anxi- ety and depression (Barlow, 2002; Mineka & Zinbarg, 2006). It is important to note that a person exposed to the same frequency and intensity of negative outcomes that are pre- dictable and/or controllable will experience less stress and be less likely to develop anxiety or depression.
In this section we examine the types of social factors that make people vulnerable to disorder or that may pre- cipitate disorder. Social factors are environmental influences—often unpredictable and uncontrollable negative events—that can negatively affect a person psy- chologically, making him or her less resourceful in coping with events. We will focus on several different types of social factors that can each have important detrimental effects on a child’s socioemotional development: (1) early deprivation or trauma, (2) problems in parenting style, (3) marital discord and divorce, (4) low socioeconomic sta- tus and unemployment, (5) maladaptive peer relation- ships, and (6) prejudice and discrimination.
Early Deprivation or Trauma Children who do not have the resources that are typically supplied by parents or parental surrogates may be left with deep and sometimes irreversible psychological scars. The needed resources range from food and shelter to love and attention. Deprivation of such resources can occur in sev- eral forms. The most severe manifestations of deprivation are usually seen among abandoned or orphaned children, who may be either institutionalized or placed in a succes- sion of unwholesome and inadequate foster homes. How- ever, it can also occur in intact families where, for one reason or another, parents are unable (for instance, because of mental disorder) or unwilling to provide close and fre- quent human attention and nurturing.
inStitutionaLization In some cases children are raised in an institution where, compared with an ordinary home, there is likely to be significantly less warmth and physical contact; less intellectual, emotional, and social stimulation; and a lack of encouragement and help in pos- itive learning. Current estimates are that worldwide up to 8 million children live in orphanages (Bos et al., 2011). Research done when institutionalization was more com- mon in the United States and the United Kingdom makes it clear that the long-range prognosis for most children who suffer early and prolonged environmental and social depri- vation through institutionalization is unfavorable, espe- cially if the institutionalization lasts longer than 6 months (Beckett et al., 2006; Kreppner et al., 2007; Wiik et al., 2011).
in review • Contrast the newer psychodynamic perspectives—ego psychol-
ogy, object-relations theory, and the interpersonal and attachment theory perspectives—with the earlier, Freudian perspective.
• What is the central theme of the behavioral perspective, and what has been its impact?
• How do classical and operant conditioning, generalization, dis- crimination, and observational learning contribute to the origins of abnormal behavior?
• What is the focus of the cognitive-behavioral perspective, and what has been its impact?
• Why are schemas and self-schemas so important for under- standing abnormal behavior and its treatment?
• What role do cognitive distortions and attributions have in psy- chopathology, according to the cognitive-behavioral perspective?
The Social Perspective 3.5 Describe three social factors known to contribute
to abnormal behavior.
We begin life with a great capacity to learn from experi- ence. What we learn from our experiences may help us face challenges resourcefully and may lead to resilience in the face of future stressors. Unfortunately, some of our experi- ences may be much less helpful in our later lives, and we may be deeply influenced by factors in early childhood over which we have no control. One good example of ways
Psychodynamic Viewpoint
“He’s reducing intrapsychic conflict and
anxiety.”
Cognitive-Behavioral Viewpoint
“He’s thinking about his problems
the wrong way, and he irrationally
believes that alcohol will reduce
his stress.”
“He’s learned the wrong habits
for reducing stress and he has a stressful job.”
Behavioral Viewpoint
Person Drinking Alcohol Excessively
Three Major Psychosocial Perspectives
Figure 3.7 Three Major Psychological Perspectives on Alcohol Dependence
Causal Factors and Viewpoints 91
countries and in some other parts of the world, where the plight of children in orphanages has often been deplor- able (Johnson, 2000). In general, early institutionalization is associated with long-lasting negative effects, and the earlier children are adopted out of orphanages the better they do (see Johnson, 2000, for a review).
Many children institutionalized in infancy and early child- hood show severe emotional, behavioral, and learning problems and are at risk for disturbed attachment relation- ships and psychopathology (e.g., Bos et al., 2011; Ellis et al., 2004; Smyke et al., 2007).
These problems seem to be mediated, at least in part, by reduced brain development (McLaughlin et al., 2010). Indeed, children raised in institutions from an early age show significant reductions in both gray and white matter volume. In one recent study, researchers compared children raised in Romanian orphanages to never-institutionalized Romanian children. Importantly, the children raised in orphanages were then randomly assigned to either remain in the orphanage or to participate in a foster care interven- tion. Interestingly, assignment to the foster care interven- tion was not associated with any significant changes in total gray matter—having been institutionalized was asso- ciated with lower total gray matter volume (Sheridan et al., 2012; Figure 3.8). However, the children in the foster care condition showed smaller decreases in white matter volume to the point where they were not significantly dif- ferent from the never-institutionalized children. This sug- gests that some effects of institutionalization are persistent, but that with intervention some of the effects of early depravation can be at least partially reversed.
These Romanian orphans spend most of their days in their cribs. The lack of physical contact and social stimulation and support causes many children who are often institutionalized starting in infancy and early childhood to show severe emotional, behavioral, and learning problems. They are also at elevated risk for psychopathology.
Fortunately, the results of this line of research have had a major impact on public policy in this and some other societies, which have recognized the need to place such children in foster or adoptive families rather than in institutions (Johnson, 2000). Accordingly, conducting research on the effects of institutionalization in Western societies is less urgent today—and less feasible—than it once was. Unfortunately, however, enlightened policies have not been implemented in some Eastern European
A ve
ra ge
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al g
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(c c)
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CAU FCG CAU B = –31.4* FCG B = –36.1*
Significant in model 3 (controlling for gender and age)
(a)
Total Cortical Gray Matter
NIG 400.00
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(b)
Total Cortical White Matter
NIG 350.00
400.00
425.00
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n.s.
Figure 3.8 Reduced Brain Development in Institutionalized Children (a) A study by Sheridan and colleagues (2012) showed that children raised in deprived environments (a Romanian orphanage in this case) have less total cortical gray matter than those in a never- institutionalized group, regardless of whether they were later placed in a more enriched foster care intervention (the “foster care group” or FCG) or not (the “care as usual group” or CAU). (b) The same study by Sheridan and colleagues showed that although the FCG intervention did not counteract the earlier effects of deprivation, it did seem to lessen the decrease in total cortical white matter associated with earlier deprivation, as shown in this figure.
(From Sheridan et al., 2012.)
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others to treat them in a similar negative manner and to not expect that they will fare well in such relationships. Consequently, they may selectively avoid new relation- ships and experiences that could correct their expectations (Shields et al., 2001).
These effects of early abuse may endure into adoles- cence and adulthood. For example, previously abused or neglected children have, on average, lower levels of edu- cation, employment, and earnings (Currie & Widom, 2010). Childhood physical abuse predicts both familial and nonfamilial violence in adolescence and adulthood, especially in abused men (Cicchetti & Toth, 1995b; Serbin & Karp, 2004). Thus, a significant proportion of parents who reject or abuse their children have themselves been the victims of parental rejection. Their early history of rejection or abuse would clearly have had damaging effects on their schemas and self-schemas, and they were probably unable to internalize good models of parenting (e.g., Serbin & Karp, 2004; Shields et al., 2001). Estimates suggest that there is about a 30 percent chance of this pat- tern of intergenerational transmission of abuse (Kaufman & Zigler, 1989).
It is important to remember that maltreated children— whether the maltreatment comes from abuse or from deprivation—can improve to at least some extent when the caregiving environment improves (Cicchetti & Toth, 1995a; Emery & Laumann-Billings, 1998). Moreover, there are always a range of effects, and those children who are least likely to show these negative outcomes tend to have one or more protective factors such as a good relationship with some adult during childhood, a higher IQ, positive school experiences, or physical attractiveness.
SEparation Bowlby (1960, 1973) first summarized the traumatic effects, for children from 2 to 5 years old, of being separated from their parents during prolonged periods of hospitalization. First, there are the short-term or acute effects of the separation, which can include significant despair during the separation as well as detachment from the parents upon reunion; Bowlby considered this to be a normal response to prolonged separation, even in infants with a secure attachment. However, he also found evidence that children who undergo a number of such separations may develop an insecure attachment. In addition, there can be longer-term effects of early separation from one or both parents. For example, such separations can cause an increased vulnerability to stressors in adulthood, making it more likely that the person will become depressed (Bowlby, 1980) or show other psychiatric symptoms (Canetti et al., 2000; Carlson et al., 2003). As with other early traumatic experiences, the long-term effects of separation depend heavily on whether support and reassurance are given a child by parents or other significant people, which is most likely if the child has a secure relationship with at least one
nEGLECt anD abuSE in thE homE Most infants subjected to parental deprivation are not separated from their parents and placed in institutions; rather, they suffer from maltreatment in their own home. In the United States, there are nearly 4 million reports of child maltreatment each year and approximately 20 percent are verified as actual, documented maltreatment. This means that 9 out of every 1,000 children are known to be victims of abuse or neglect, with countless numbers of other unreported cases. The majority (78 percent) of these cases are cases of neglect, with physical abuse (18 percent) and sexual abuse (9 per- cent) being less common (U.S. Department of Health and Human Services, 2013).
Outright parental abuse (physical or sexual or both) of children has been associated with many negative effects on their emotional, intellectual, and physical develop- ment, although some studies have suggested that, at least among infants, gross neglect may be worse than having an abusive relationship. Abused children often have a ten- dency to be overly aggressive (both verbally and physi- cally), even to the extent of bullying. Some even respond with anger and aggression to friendly overtures from peers (Cicchetti & Toth, 2005). Researchers also found that maltreated children often have difficulties in linguistic development and significant problems in behavioral, emo- tional, and social functioning, including conduct disorder, depression and anxiety, and impaired relationships with peers, who tend to avoid or reject them (Collishaw, Pickles, et al., 2007; Shonk & Cicchetti, 2001). Such adverse conse- quences are perhaps not surprising given the multitude of very long-lasting negative neurobiological effects that maltreatment has on the developing nervous system (Gunnar & Quevedo, 2007; Watts-English et al., 2006). For example, an important 30-year follow-up study of indi- viduals born on the Isle of Wight in the 1960s who reported having been physically or sexually abused as children found that about two-thirds of them had elevated rates of both adolescent and adult psychopathology compared to individuals who did not report such abuse. A recent quan- titative review also reported adverse effects of childhood abuse on numerous adult physical health outcomes (Wegman & Stetler, 2009).
Abused and maltreated infants and toddlers are also quite likely to develop atypical patterns of attachment— most often a disorganized and disoriented style of attachment (Barnett et al., 1999), characterized by insecure, disorga- nized, and inconsistent behavior with the primary care- giver. Such a child might at one point act dazed and show frozen behavior when reunited with his or her caregiver. However, at another point he or she might actually approach the caregiver but then immediately reject and avoid her. A significant portion of these children continue to show these confused patterns of relating to their care- giver up to at least age 13, after which they often expect
Causal Factors and Viewpoints 93
parEntaL pSyChopathoLoGy Parents who have various forms of psychopathology (including schizophre- nia, depression, antisocial personality disorder, and alcohol use problems) tend to have one or more children who are at heightened risk for a wide range of developmental difficul- ties (unless protective factors are also present; Brennan et al., 2003; Masten, 2007). The focus of most research in this area has been on mothers, but there is good evidence that fathers with mental disorders or others who are minimally involved in caretaking in infancy can also make significant contributions to child and adolescent psychopathology, especially to problems such as depression, conduct disor- der, delinquency, and attention-deficit disorder (Boyce et al., 2006; Phares et al., 2002). Although some of these effects undoubtedly have a genetic component, many researchers believe that genetic influences cannot account for all of the adverse effects that parental psychopathology can have on children (Hammen, 2009; Sher et al., 2005).
Consider some examples. Although many children of people with serious alcohol abuse problems do not have difficulties, others have elevated rates of truancy, sub- stance abuse, and a greater likelihood of dropping out of school, as well as higher levels of anxiety and depression and lower levels of self-esteem (Leonard & Eiden, 2007; Marmorstein et al., 2009). In addition, the children of par- ents who are seriously depressed are at enhanced risk for depression and other disorders themselves (Burt et al., 2005; Hammen, 2009), at least partly because depression makes for unskillful parenting—notably including either intrusive or withdrawn behavior (Field et al., 2006), exces- sive criticism, and ineffectiveness in managing and disci- plining the children (Rogosch et al., 2004). Not surprisingly, children of mothers with depression also are more likely than children of nondepressed mothers to live in environ- ments with high levels of stress (Hammen, 2009).
parEntinG StyLES: warmth anD ControL Researchers have been interested in how parenting styles— including their disciplinary styles—affect children’s behavior over the course of development. A parenting style reflects an attitude and values that are expressed toward a child across a wide range of settings (Williams et al., 2009). Four types of parenting styles have been identified that seem to be related to different developmental outcomes for children: (1) author- itative, (2) authoritarian, (3) permissive/indulgent, and (4) neglectful/uninvolved. These styles vary in the degree of parental warmth (amount of support, encouragement, and affection versus shame, rejection, and hostility) and in the degree of parental control (extent of discipline and monitoring versus leaving the children largely unsupervised; Manzeske & Stright, 2009; Morris, 2001). (See Figure 3.9.) Parental con- trol includes both behavioral control (rewards and punish- ments) and psychological control (e.g., expression of approval versus disapproval, or guilt induction).
parent (Canetti et al., 2000). Interestingly, many children who experience even a parent’s death do not exhibit dis- cernible long-term effects (Canetti et al., 2000).
Problems with parenting style can have profound effects on a child’s subsequent ability to cope with life’s challenges and thus create vulnerability to various forms of psychopathology.
Problems in Parenting Style Even in the absence of severe deprivation, neglect, or trauma, many kinds of deviations in parenting can have profound effects on a child’s subsequent ability to cope with life’s challenges and thus can create a child’s vulner- ability to various forms of psychopathology. Therefore, although their explanations vary considerably, the psycho- logical viewpoints on causes of psychopathology all focus on the behavioral tendencies a child acquires in the course of early social interaction with others—chiefly parents or parental surrogates (Parke, 2004; Sroufe et al., 2000).
It is important to note that a parent–child relationship is always bidirectional: As in any continuing relationship, the behavior of each person affects the behavior of the other. For instance, children who are anxious, irritable, and impulsive may be more difficult to care for, and can elicit anxiety, irritability, and impulsiveness in their parents. The parents’ behavior may in turn lead to worsening in the child’s behavior (Crouter & Booth, 2003; Rutter, 2006a).
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They tend to be attentive and sensitive to their children’s needs while still enforcing their limits. This style of parent- ing is associated with the most positive early social devel- opment; the children tend to be energetic and friendly and to show development of general competencies for dealing with others and with their environments (Baumrind, 1993; Simons et al., 2005). They also usually have secure attach- ment relationships and show high levels of overall well- being, as well as good school performance when followed into late adolescence (Berk, 2003; Slicker & Thornberry, 2002). Not surprisingly they also are less likely to exhibit either emotional disorders (e.g., anxiety and depression) or behavioral problems (e.g., conduct problems and delin- quency) (Williams et al., 2009). Authoritative parenting also seems to promote resilience in children living in highly stressful contexts (Salem-Pickartz & Donnelly, 2007).
Authoritarian Parenting Parents with an authoritarian style are high on control but low on warmth. They often appear quite cold and demanding, favoring punitive methods if their children disobey. Their children tend to be conflicted, irritable, and moody (Baumrind, 1993; Siegler et al., 2003). When followed into adolescence, these children tend to be lower in social and academic competence than children of authoritative parents, with boys doing particularly poorly in social and cognitive skills. Boys with authoritarian fathers—especially those high on hostility—are also at heightened risk of engaging in substance abuse and other delinquent activity (Bronte-Tinkew et al., 2006; Hoeve et al.,
Healthy parenting styles are those that reflect warmth and clear limits and restrictions regarding certain kinds of behaviors while allowing considerable freedom within certain boundaries. The children raised in these environments tend to be energetic and friendly and show general competencies for dealing with others.
Parents are high on warmth and moderate on control, very careful to set clear limits and restrictions regarding certain kinds of behaviors.
Research Shows: Children tend to be friendly and to show development of general competencies for dealing with others and with their environments.
Authoritative Permissive/ Indulgent
Parents are high on warmth and low on control and discipline.
Research Shows: Children tend to be impulsive and aggressive. Overly indulged children are characteristically spoiled, selfish, impatient, inconsiderate, and demanding.
Neglectful/ Uninvolved
Parents are low on warmth and low on control.
Research Shows: Children tend to be moody and to have low self-esteem and conduct problems later in childhood. They also have problems with peer relations and with academic performance.
Authoritarian
Parents are low on warmth and high on control and o�en cold and demanding.
Research Shows: Children tend to be conflicted, irritable, and moody. When followed into adolescence, these children have more negative outcomes, the boys doing particularly poorly in social and cognitive skills.
Figure 3.9 Parenting Styles
Authoritative Parenting The authoritative style is one in which the parents are both very warm and very careful to set clear standards and limits on certain kinds of behaviors while allowing considerable freedom within these limits.
Causal Factors and Viewpoints 95
parents than children from less conflictual marriages (Cummings et al., 2004; Du Rocher Schudlich, et al., 2004). College students who report high levels of marital conflict in their parents also show elevated conflict in their own romantic relationships, which in turn is linked to poorer quality of their own romantic relationships (Cui & Fincham, 2010). Interestingly, children can be buffered against many of the damaging effects of marital conflict if one or both parents have the following characteristics: warmth, prone- ness to giving praise and approval, and ability to inhibit rejecting behavior toward their children (Katz & Gottman, 1997). Longitudinal studies have documented that the damaging effects of serious marital discord on children continue into adulthood: The offspring’s own marriages are more likely to be marked by discord (whether or not the parents divorced). Some of this intergenerational transmission of marital discord may be the result of the offspring having learned negative interaction styles by observing their own parents’ marital interactions (Amato, 2006; Amato & Booth, 2001).
DivorCED famiLiES Nearly 20 percent of marriages end in divorce around the world, and the United States’ rate is among the highest at 40 percent (Breslau et al., 2011). Estimates suggest that approximately 20 percent of children under the age of 18 are living in a single-parent household—some with unwed parents and some with divorced parents.
Effects of Divorce on Parents Unhappy marriages are dif- ficult, but ending a marital relationship can also be enor- mously stressful for the adults, both mentally and physically. The negative effects are often temporary, with most people being able to adapt constructively within 2 to 3 years, but some adults never fully recover (Amato, 2000; Hetherington, 2003a). Divorced and separated persons are overrepresented among psychiatric patients, although the direction of the causal relationship is not always clear. It should also be recognized, however, that divorce actually benefits some individuals (Amato, 2000, 2010)—with some evidence that women are more likely to benefit than men (Hetherington, 2003a). There is also some evidence that individuals who were in high-distress marriages before divorce are more likely to show an increase in happiness than are individuals who were in low-distress marriages before divorce (Amato & Hohmann-Marriott, 2007). In addition, favorable adjustment after divorce is positively associated with higher income, dating someone steadily, remarriage, having had relatively favorable attitudes toward divorce before it happened, and being the partner who initiated the divorce (Amato, 2000).
Effects of Divorce on Children Divorce can have traumatic effects on children, too. Feelings of insecurity and rejection may be aggravated by conflicting loyalties. Delinquency
2009). If such authoritarian parents also use overly severe discipline in the form of physical punishment—as opposed to the withdrawal of approval and privileges—the result tends to be increased aggressive behavior on the part of the child (Berk, 2003).
Permissive/Indulgent Parenting Parents with a permissive/ indulgent style are high on warmth but low on discipline and control. This lenient style of parenting is associated with impulsive and aggressive behavior in childhood and adolescence (Baumrind, 1967; Hetherington & Parke, 1993). Overly indulged children are characteristically spoiled, selfish, impatient, inconsiderate, and demand- ing (Baumrind, 1971, 1975). In adolescence, they tend to do less well academically and to show more antisocial behaviors (Steinberg et al., 2006). Confusion and diffi- culties in adjustment may occur when “reality” forces them to reassess their assumptions about themselves and the world.
Neglectful/Uninvolved Parenting Finally, parents who are low both on warmth and on control exhibit the neglectful/ uninvolved style. They tend to be disengaged and not sup- portive of their children. This style of parental uninvolve- ment is associated with disruptions in attachment during early childhood (Egeland & Sroufe, 1981; Karavasilis et al., 2003) and with moodiness, low self-esteem, and conduct problems later in childhood. These children of uninvolved parents also have problems with peer relations and with academic performance (Hetherington & Parke, 1993; see also Berk, 2003).
Marital Discord and Divorce Disturbed parent–child patterns such as parental rejection are rarely found in severe form unless the total familial context is also abnormal. Thus, disturbed family structure is an overarching risk factor that increases an individual’s vulnerability to particular stressors. We will distinguish between intact families where there is significant marital discord and families that have been disrupted by divorce or separation.
maritaL DiSCorD All couples argue, but when taken to an extreme, marital discord can have damaging psycho- logical effects on both adults and their children (e.g., Amato, 2006; Amato & Booth, 2001; Parke, 2004). More severe cases of marital discord may expose children to one or more of the stressors we have already discussed: child abuse or neglect, the effects of living with a parent with a serious mental disorder, authoritarian or neglectful/ uninvolved parenting, and spouse abuse. But even less severe cases of marital discord also have negative effects on many children. For example, children of parents with high levels of overt conflict show a greater disposition to behave aggressively toward both their peers and their
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1991b). At one time it was thought that the detrimental effects of divorce might be minimized if a successful remar- riage provided an adequate environment for childrearing. Unfortunately, however, the Amato and Keith (1991b) review revealed that children living with a stepparent were often no better off than children living with a single parent, although this was truer for girls than for boys. Other studies have shown that children—especially very young children—living with a stepparent are at increased risk for physical abuse (injury and even death) by the stepparent relative to children living with two biological parents (Daly & Wilson, 1988, 1996).
Low Socioeconomic Status and Unemployment In our society the lower the socioeconomic class, the higher the incidence of mental and physical disorders (Caracci & Mezzich, 2001; Conger & Donnellan, 2007). The strength of this inverse correlation varies with different types of men- tal disorder, however. For example, antisocial personality disorder is strongly related to socioeconomic status (SES), occurring about 3 times as often in the lowest income cate- gory as in the highest income category, whereas depressive disorders occur only about 1.5 times as often in the lowest income category as in the highest income category (Kessler & Zhao, 1999; Monroe et al., 2009).
There are many reasons for this general inverse asso- ciation. One factor is that some people with mental disor- ders slide down to the lower rungs of the economic ladder and remain there, sometimes because they do not have the economic or personal resources to climb back up (Gottesman, 1991) and sometimes because of prejudice and stigma against those with mental illness (Caracci & Mezzich, 2001). Another factor is that, on average, people who live in poverty encounter more—and more severe— stressors in their lives, than do more affluent people, and they usually have fewer resources for dealing with them (Twenge & Campbell, 2002).
Children and adolescents from lower SES families also tend to have more psychological problems. One recent, large-scale study of U.S. adolescents examined different measures of low SES and found that adolescents’ percep- tions of their social status are most strongly linked to higher rates of mental disorders, more so than factors like family income (McLaughlin, Costello, et al., 2012). It is important to keep in mind that many children from lower SES homes do very well, especially those with higher IQs and those with adequate relationships at home, in school, and with peers (Felsman & Valliant, 1987; Long & Valliant, 1984; Masten & Coatsworth, 1995).
Studies have repeatedly found unemployment—with its financial hardships, self-devaluation, and emotional distress—to be associated with enhanced vulnerability to
and a wide range of other psychological problems such as anxiety and depression are much more frequent among children and adolescents from divorced families than among those from intact families, although it is likely that a contributing factor here is prior or continuing parental strife (Strohschein, 2005). However, findings also show that, on average, such children had shown these problems to some degree even before their parents divorced (Amato, 2010; Strohschein, 2005). In addition, the adverse effects of divorce on adaptive functioning may persist into adult- hood. On average, compared to young adults from families without divorce, young adults from divorced families have somewhat lower educational attainment, lower incomes, lower life satisfaction, and an increased probability of being on welfare and having children out of wedlock (Chase-Lansdale et al., 1995; Hetherington et al., 1998). Children from divorced families are also more likely to have their own marriages end in divorce (Amato & DeBoer, 2001; Hetherington, 2003b). There is evidence that these effects even occurred in a subsequent third generation. Specifically, in a study of nearly 700 grandparents and their grandchildren, Amato and Cheadle (2005) found that divorce in the grandparents was associated with lower education, more marital discord, and weaker parental ties in the grandchildren.
Research Close-Up Direction of the Causal Relationship
Recall that, in a correlational or observational study, an as- sociation between two variables does not allow us to make inferences about causal direction. For example, divorce could precipitate psychological problems. Alternatively, people with psychological disorders might be more likely to have problem- atic marriages and end up divorced.
Nevertheless, many children adjust quite well to the divorce of their parents. Indeed, a quantitative review of 92 studies on parental divorce and the well-being of chil- dren, conducted on 13,000 children from 1950 to 1990, con- cluded that the average negative effects of divorce on children are actually quite modest, as are the negative effects persisting into adulthood (Amato & Keith, 1991b). Amato and Keith (1991a, 1991b) also found that the negative effects of divorce seemed to decrease from the 1950s through the 1980s (particularly since 1970), perhaps because the stigma of divorce was decreasing. However, a follow-up review of 67 such studies published in the 1990s showed no further decreases in these negative effects since 1990 (Amato, 2001).
The effects of divorce on children are often more favor- able than the effects of remaining in a home torn by marital conflict and dissension (Amato, 2010; Amato & Keith,
Causal Factors and Viewpoints 97
the victim (and as many as 20 to 30 percent actually encour- age the bully; Salmivalli, 2010; Salmivalli & Voeten, 2004). A small percentage (approximately 20 percent), however, do take the side of the victim and may even help defend him or her. Victims who have one or more classmates defend them show less distress and higher self-esteem.
In recent years a new form of particularly insidious bullying has emerged as an enormous problem in many North American schools. Cyberbullying, as it is called, includes sending offensive, harassing, or intimidating mes- sages over the Internet, spreading ugly rumors on certain Internet sites, and spreading someone’s very personal information (Willard, 2007). Some estimate that as many as one-third of teenagers who use the Internet engage in cyberbullying (Li, 2007; Scharnberg, 2007). The psychologi- cal consequences of cyberbullying on the victims can be very serious—including anxiety, school phobia, lower self- esteem, suicidal ideation, and occasional cases of suicide (Thomas, 2006).
psychopathology (e.g., Dooley et al., 2000; Grzywacz & Dooley, 2003; Thomas et al., 2007). In particular, rates of depression, marital problems, and somatic (bodily) com- plaints increase during periods of unemployment but usu- ally normalize when employment rates recover (Jones, 1992; Murphy & Athanasou, 1999). These effects occur even when mental health status before unemployment is taken into account. Not surprisingly, the wives of unem- ployed men are also adversely affected, exhibiting higher levels of anxiety, depression, and hostility, which seem to be at least partially caused by the distress of the unem- ployed husband (Dew et al., 1987). Children too can be seriously affected. In the worst cases, unemployed fathers are much more likely to engage in child abuse (Cicchetti & Lynch, 1995; Dew et al., 1991).
Finally, economic crises since 1990 have centered not only on unemployment but also on the effects that corpo- rate restructuring and downsizing have had on upper- middle-class people, many of whom find themselves having to look for jobs requiring lower skills and paying much lower incomes than they earned in the past. In other cases people are forced to work only part time and often do not make enough to live on. Several large studies of people who were underemployed (or who had inadequate employment) found that rates of depression were compa- rable or nearly comparable to those seen in unemployed individuals (Dooley & Prause, 2004; Dooley et al., 2000; Grzywacz & Dooley, 2003).
Maladaptive Peer Relationships Learning how to navigate the world as a child can be a dif- ficult and confusing task. Learning how to successfully navigate relationships with your peers can be even harder. Many children and adolescents are able to develop healthy and adaptive peer relationships with no major disruptions. However, some will experience different types of prob- lems, such as becoming a bully or the victim of some form of intentional exclusion or aggression. Unfortunately, such problems in peer relationships are associated with an increased risk of psychological disorders.
Several studies have found bullies to show high levels of both proactive aggression (where they initiate the aggressive behavior) and reactive aggression (where they overreact when confronted; Salmivalli, 2010; Salmivalli & Nieminen, 2002). Although some bullies probably behave this way because of deficits in social skills, others have a more sophisticated understanding of social behavior, which enables them to manipulate and organize their peers (often driven by status goals) so that they can avoid being caught while making others suffer (Salmivalli, 2010). Most children report having negative attitudes toward bullying; however, studies suggest that when bullying actually occurs most students do nothing to intervene or support
Cyberbulling has emerged as a new and especially troublesome form of bullying. Amanda Todd, a 15-year-old high school student, was repeatedly bullied online, leading to problems with anxiety, depression, drug use, and ultimately to her suicide.
Fortunately, there is another side to this coin. Peer relations can be difficult, but they can also be sources of key learning experiences that stand an individual in good stead for many years. For a resourceful child, the winning and losing and the successes and failures of the school years provide excellent training in coming to grips with the real world and with her or his developing self—its capabilities and limitations, its attractive and unattractive qualities. The experience of intimacy with a friend has its beginning in this period of intense social involvement. If all goes well, a child emerges into adolescence with a con- siderable repertoire of social knowledge and skills that add up to social competence. Such resources can be strong protective factors against parental rejection, frustration, demoralization, despair, and mental disorder (Masten, 2007; Sentse et al., 2010).
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consistent with what they have experienced at home but is out of synch with the context they share with peers (Cicchetti & Toth, 2005; Shields et al., 2001). In addition, having a poor ability to understand a peer’s emotions (such as fear and sadness) in kindergarten also predicts aggressive behavior toward peers in the third grade (Dodge et al., 2002).
The second subset of children who may become chronic victims of rejection are not aggressive but, rather, are highly unassertive and quite submissive toward their peers, often because of social anxiety and fear of being scorned or attacked (Schwartz et al., 1993). Such isolation is likely to have serious consequences because it often leads to peer rejection, which in turn deprives a child of further opportunities to learn the rules of social behavior and interchange, rules that become more sophisticated and subtle with increasing age (Coie, 1990; Ladd, 2006). Repeated social failure or becoming the victim of bullies is the usual result, which has further damaging effects on self-confidence and self-esteem and sometimes leads to loneliness, depression, and anxiety, especially during the elementary school years (Burks et al., 1995; Ladd, 2006).
In summary, children who fail to establish satisfactory relationships with peers during the developmental years are deprived of a crucial set of background experiences and are at higher-than-average risk for a variety of nega- tive outcomes in adolescence and adulthood including depression, school dropout, suicidal ideation, and delin- quency (Heilbron & Prinstein, 2010). However, one should also remember that peer social problems may also be early markers of disorders that have a heritable component but do not become full blown until later in adolescence or adulthood. Peer social problems may reflect some heritable diathesis, but they also serve as stressors that make it more likely that the underlying vulnerability will lead to full- blown disorder later.
Prejudice and Discrimination in Race, Gender, and Ethnicity Many members of our society are repeatedly subjected to prejudice (prejudgment based on personal characteristics) and discrimination (unjust treatment of others based on perceived group membership) based on their gender, race (i.e., the category to which others assign a person based on their physical characteristics, such as skin color), and eth- nicity (i.e., a social group with a common culture, history, and homeland). Prejudice and discrimination can occur anywhere—on the street, on college campuses, in schools, or in the workplace. For example, two common types of discrimination that occur in the workplace are (1) access dis- crimination, wherein members of a certain group (e.g., women, people of a certain race or ethnicity) are not hired because of their personal characteristics, and (2) treatment discrimination, wherein certain types of people are given a
SourCES of popuLarity vErSuS rEjECtion What determines which children will be popular and which will be rejected? There seem to be two types of popular chil- dren—the prosocial and the antisocial types. Prosocial pop- ular children communicate with their peers in friendly and assertive yet cooperative ways. They tend to be good stu- dents relative to their less popular peers (Zettergreen, 2003). Antisocial popular children—usually boys—tend to be “tough boys” who may be athletically skilled but who do poorly academically. They tend to be highly aggressive and defiant of authority (Berk, 2003).
Juvenile socializing is a risky business in which a child’s hard-won prestige in a group is probably perceived as being constantly in jeopardy. Actually, reputation and status in a group tend to be stable, and a child who has been rejected by peers is likely to continue to have problems in peer relationships.
Much attention has been devoted to determining why some children are persistently rejected by their peers and the consequences of such rejection. There also appear to be two types of rejected children—those who are too aggres- sive and those who are very withdrawn (Ladd, 2006). The rejected children who are aggressive take an excessively demanding or aggressive approach when interacting with their peers. They often take offense too readily and attri- bute hostile intent to the teasing of their peers, thus escalat- ing confrontations to unintended levels (Dodge, 2006; Reijntjes et al., 2011). Indeed, the tendency to attribute hos- tile intent to others in grade 8 has been shown to predict levels of antisocial behavior in grade 11 (Lansford et al., 2006). Such children also tend to take a more punitive and less forgiving attitude toward such situations (Coie et al., 1991; Crick & Dodge, 1994). This may be especially likely in children who have been maltreated by their parents and have therefore developed maladaptive mental representa- tions of caregivers and expect maltreatment. Expecting mal- treatment, they may approach social situations with hyperarousal, anxiety, and angry reactivity, which may be
Causal Factors and Viewpoints 99
• What effects do low SES and unemployment have on adults and children?
• How can prejudice and discrimination have adverse effects on the development of abnormal behavior?
The Cultural Perspective 3.6 Explain how cultural differences can influence
perceptions of abnormal behavior.
Understanding the causes of abnormal behavior also requires taking into account the cultural context in which the behavior occurs. Indeed, what is considered to be normal and abnormal differs in different places around the world. Sociology and anthropology have shown that individual personality development reflects the larger society—its institutions, norms, values, and ideas—as well as the immediate family and other groups. Studies in these disciplines have illuminated the relationship between various sociocultural conditions and mental disorders (for example, the relationship between the par- ticular stressors in a given society and the types of men- tal disorders that typically occur in it). Further studies showed that the patterns of both physical and mental disorders within a given society could change over time as sociocultural conditions change. These discoveries have added important new dimensions to modern per- spectives on abnormal behavior (Fabrega, 2001; Tsai et al., 2001; Westermeyer & Janca, 1997).
The cultural perspective is concerned with the impact of culture on the definition and manifestation of mental disorders. The relationships are complex. However, cross- cultural research can enhance our knowledge about the range of variation that is possible in human behavioral and emotional development and can generate ideas about what causes normal and abnormal behavior—ideas that can later be tested more rigorously in the laboratory (Canino & Alegria, 2008).
Universal and Culture-Specific Symptoms of Disorders Research supports the view that many psychological dis- turbances—in both adults and children—are universal, appearing in most cultures studied (Butcher, 2005; Kessler & Ustun, 2008). Examining such issues is, of course, never easy because of the need to adapt psychological tests across barriers of language and culture and to validate their use in other cultures. One example of such research has shown that when some tests are translated into the language of different cultures, they need to be adapted so that they are appropriate for the new cultural context. In addition, care must be taken not to miss what may be culture-specific
job but are paid less and receive fewer opportunities for promotion (Eagly & Carli, 2007; Eagly & Karau, 2002). Beyond the obvious financial effects of such treatment, prejudice and discrimination can lead to higher levels of stress and can have negative downstream effects on a per- son’s physical and mental health.
Indeed, prejudice against minority groups may help to explain why these groups sometimes show increased prev- alence of certain mental disorders such as depression (Cohler et al., 1995; Kessler et al., 1994). One possible rea- son for this is that perceived discrimination may serve as a stressor that threatens self-esteem, which in turn increases psychological distress (e.g., Cassidy et al., 2004). A recent study of Arab and Muslim Americans 2 years after the bombing of the World Trade Center in New York found increased psychological distress, lower levels of happiness, and increased health problems in those who had experi- enced personal or familial prejudice, discrimination, or violence (Padela & Heisler, 2010).
Experimental laboratory studies have tested how prej- udice and discrimination may “get under the skin” to increase the likelihood of negative health outcomes. Such studies have shown that the experience or perception of racial discrimination leads to increases in anger and car- diovascular reactivity (Mendes et al., 2008). In addition, discrimination increases risk-taking behavior, an effect that is partially mediated (or explained) by increased cardio- vascular reactivity (Jamieson et al., 2013). Perceived dis- crimination also predicts lower levels of well-being for women (Ryff et al., 2003).
The Impact of the Social Perspective With our increased understanding of social influences on mental health, what was previously an almost exclusive concern with individuals’ minds has broadened to include a concern with how factors in peoples’ environment can influence the occurrence of mental disorders. Research in this area has led to programs designed to improve the social conditions that foster maladaptive behavior and mental disorder, and to community facilities for the early detection, treatment, and long-range prevention of mental disorder. In Chapter 17 we will examine some clinical facilities and other programs—both governmental and private—that have been established as a result of community efforts.
in review • What are the most important effects of a child’s being exposed to
early deprivation or abuse?
• What kinds of influences do different parenting styles tend to have on children’s development?
• What is the typical range of effects that divorce and marital dis- cord can have on children? What about effects on adults?
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In another example, Kleinman (1986, 1988) compared the ways in which Chinese people (in Taiwan and the Peo- ple’s Republic of China) and Westerners deal with stress. He found that in Western societies, depression was a fre- quent reaction to individual stress. In China, on the other hand, he noted a relatively low rate of reported depression (Kleinman, 2004). Instead, the effects of stress were more typically manifested in physical problems such as fatigue, weakness, and other complaints. Moreover, Kleinman and Good (1985) surveyed the experience of depression across cultures. Their data show that important elements of depression in Western societies—for example, the acute sense of guilt typically experienced—do not appear in many other cultures. They also point out that the symp- toms of depression, such as sadness, hopelessness, unhap- piness, and a lack of pleasure in the things of the world and in social relationships, have dramatically different mean- ings in different societies. For Buddhists, seeking pleasure from things of the world and social relationships is the basis of all suffering; a willful disengagement is thus the first step toward achieving enlightenment. For Shi’ite Mus- lims in Iran, grief is a religious experience associated with recognition of the tragic consequences of living justly in an unjust world; the ability to experience grief fully is thus a marker of depth of personality and understanding.
In addition to the influence of culture on the symp- toms experienced in different cultures, there are also entire patterns of symptoms in certain cultures that are unlike the patterns experienced in most other parts of the world. Although a variety of these culture-specific manifestations of mental disorders will be discussed in various parts of this text, the few discussed here serve to illustrate the gen- eral idea. In recent years, for example, a phenomenon known as hikikomori has emerged as quite common in Japan, affecting as many as 700,000 individuals. This is a disorder of acute social withdrawal in which young people just remain in their room in their parents’ house and refuse social interactions for at least 6 months, but often for many years. Hikikomori seems to be caused, at least in part, by a combination of shy temperament, parental rejection, poor parental attachment, and social exclusion by peers (Krieg & Dickie, 2013). These potential causal factors are univer- sal, but the outcome or manifestation of the resulting abnormal behavior can look different in different cultures. Other examples of culture-specific manifestations of men- tal disorders will be covered in subsequent chapters (such as koro and taijin kyofusho discussed in Chapter 6).
Culture and Over- and Undercontrolled Behavior Studies of the prevalence of different kinds of childhood psychopathology in different cultures raise some fascinat- ing issues. In cultures such as that of Thailand, adults are
elements of various disorders such as anxiety and depres- sion (Sue & Chang, 2003; Weisz, Weiss, et al., 2006).
Cultural factors influence the form and course of certain disorders. For example, in Western societies people suffering from stress frequently will become depressed. In China, stress is not manifested as depression but in physical problems such as fatigue and weakness.
The Minnesota Multiphasic Personality Inventory (MMPI-2; see Chapter 4) is the best validated and most widely used test that has been adapted for use in many cul- tures (e.g., Butcher, 2011). For example, the basic pattern of disturbed thoughts and behaviors that we call schizophre- nia can be found among nearly all peoples, although the prevalence and symptoms vary to some degree (Woo & Oei, 2007). Moreover, certain psychological symptoms, as measured, are consistently found among similarly diag- nosed clinical groups in many other countries. For exam- ple, Butcher (1996a) found that psychiatric patients from Italy, Switzerland, Chile, India, Greece, and the United States who were diagnosed with paranoid schizophrenia produced similar general personality and symptom pat- terns on the MMPI. The same MMPI-2 pattern was also found to occur among patients with schizophrenia in Japan (Hayama, 1999).
Nevertheless, although some universal symptoms and patterns of symptoms appear, sociocultural factors often influence which disorders develop, the forms they take, how prevalent they are, and their courses. For exam- ple, the prevalence of major depressive disorder varies widely across the cultures of the world. In one study con- ducted in 10 countries around the world, the prevalence ranged from 3 percent in Japan to nearly 17 percent in the United States (Andrade et al., 2004). Differences can also emerge in the prognosis or outcomes of several severe mental disorders in different countries. Several interna- tional studies have found a more favorable course of schizophrenia in developing countries than in developed countries (Kulhara & Chakrabarti, 2001).
Causal Factors and Viewpoints 101
Two cross-national studies (Weisz et al., 1987), con- firmed that Thai children and adolescents do indeed have a greater prevalence of overcontrolled problems than do American children. Although there were no differences in the rate of undercontrolled behavior problems between the two countries, there were differences in the kinds of under- controlled behavior problems reported. For example, Thai adolescents had higher scores than American adolescents on indirect and subtle forms of undercontrol not involving interpersonal aggression such as having difficulty concen- trating or being cruel to animals. American adolescents, on the other hand, had higher scores than Thai adolescents on behaviors like fighting, bullying, and disobeying at school (Weisz et al., 1993). In addition, these investigators found that Thai and American parents differ a good deal in which problems they will bring for treatment. In general, Thai par- ents seem less likely than American parents to refer their children for psychological treatment (Weisz & Weiss, 1991; Weisz et al., 1997). This may be in part because of their Bud- dhist belief in the transience of problems and their opti- mism that their child’s behavior will improve. Alternatively, Thai parents may not refer their children with undercon- trolled problems for treatment simply because these prob- lems are so unacceptable that the parents are embarrassed to go public with them (Weisz et al., 1997).
Cultural differences in psychopathology may also result from differences in what cultures consider to be the ideal kinds of parent–child attachment relationships. The World Around Us box discusses research on cultural differences in what Japanese and Western cultures believe to be the nature of ideal versus disordered attachment relationships.
in review • Give an example of universal and culture-specific symptoms of
disorders.
• What cultural factors help account for differences in problems involving overcontrolled and undercontrolled behavior in Thai ver- sus American children?
highly intolerant of undercontrolled behavior such as aggres- sion, disobedience, and disrespectful acts in their children (Weisz et al., 2003). Children are explicitly taught to be polite and deferential and to inhibit any expression of anger. This raises interesting questions about whether childhood problems stemming from undercontrolled behavior are lower in Thailand than in the United States, where such behavior seems to be tolerated to a greater extent. It also raises the question of whether problems related to overcontrolled behavior such as shyness, anxiety, and depression would be overrepresented in Thailand rel- ative to the United States.
In Thailand, children tend to exhibit overcontrolled behavior and are explicitly taught by their parents to be polite and deferential and to inhibit any expression of anger. This is in contrast to American children, whose parents tend to tolerate undercontrolled behavior to a greater extent.
The World Around Us Culture and Attachment Relationships
Recently, research has shown that there are significant cross- cultural differences in views of ideal parent–child attachment rela- tionships. Accordingly, there are different views of what consti- tutes disordered attachment relationships that can increase risk for psychopathology. Views on the function of good attachment relationships (and the nature of disordered attachment) in West- ern cultures have been found to differ rather dramatically from those seen in Japan (Rothbaum, Weisz, et al., 2000, 2001). In Western societies, secure attachment relationships are thought
to occur when a mother responds in a sensitive fashion to a child’s signals (e.g., signs of hunger or discomfort) yet gradually allows the child to explore the environment and develop some autonomy. In the United States one study found that teachers similarly prefer to respond to explicit expression of needs and to foster children’s independence and self-expression, which would also foster secure attachments (Rothbaum et al., 2006). Impor- tantly, securely attached children (relative to insecurely attached children) are thought to be less anxious and depressed, better
102 Chapter 3
able to cope with negative emotional states, and better able to form close relationships with peers.
However, in Japan, parents’ goals are to anticipate all the child’s needs and thereby avoid any exposure to stress such as hunger or discomfort and to foster dependency (Rothbaum, Weisz, et al., 2000, 2001). Japanese teachers also prefer to anticipate their students’ needs and to foster dependency on other tasks (Rothbaum et al., 2006). Accordingly, children who are considered securely attached in Japan are very dependent on their mothers (and teachers), and independent children are thought to have disturbed attachments. Moreover, because the Japanese value social harmony, children who are dependent and emotionally restrained and who express their feelings only indi- rectly are the ones viewed as competent; they also tend to be self-critical and self-effacing. This is very different from Western cultures, where children who show exploration and autonomy and are willing to express strong feelings and even disagreement
openly are considered to be socially competent. Such children in Western cultures also tend to have positive self-views (Rothbaum, Weisz, et al., 2000).
Given such differences, it is not surprising that different clinical interventions are viewed as appropriate for children with behavior problems in these two cultures. For example, American therapists often help their clients to develop their own separate identities and assume that expression of negative feelings toward others (including parents) may be necessary. By contrast, Japa- nese therapists are more likely to encourage clients to be grateful to others (especially their parents) and encourage devotion (see Rothbaum, Weisz, et al., 2000, 2001).
Mismatches between cultural expectations and children’s behavior can lead to that behavior being considered abnor- mal. Based on what you have learned so far, when would that behavior be considered a mental disorder?
Unresolved Issues Theoretical Perspectives and the Causes of Abnormal Behavior
The perspectives described in this chapter are theoretical constructions devised to orient psychologists in the study of abnormal behavior. As a set of hypothetical guidelines, each per- spective emphasizes the importance and integrity of its own position to the exclusion of other explanations. Most psychody- namically oriented clinicians, for example, value those traditional writings and beliefs consistent with Freudian or later psychody- namic theories, and they minimize or ignore the teachings of opposing viewpoints. They usually adhere to prescribed prac- tices of psychodynamic therapy and do not use other methods such as exposure therapy.
Advantages of Having a Theoretical Perspective Theoretical integrity and adherence to a systematic viewpoint have a key advantage: They ensure a consistent approach to one’s practice or research efforts. Once mastered, the methodol- ogy can guide a practitioner or researcher through the complex web of human problems. But such adherence to a theory has its disadvantages. By excluding other possible explanations, it can blind researchers to other factors that may be equally important. The fact is that none of the theories devised to date addresses the whole spectrum of abnormality—each is limited in some way in its focus.
Two general trends have occurred as a result. First, the original model or theory may be revised by expanding or modify- ing some elements of the system. The many examples of such modified interpretations include Adler’s and Erikson’s modifica- tions of Freudian theory and the more recent cognitive-behavioral approach’s modification of behavior therapy. But many of the early Freudian theorists did not accept the neo-Freudian addi- tions, and some classical behavior therapists today still do not
accept the revisions proposed by cognitive behaviorists. There- fore, the second trend has been for theoretical viewpoints to multiply and coexist—each with its own proponents—rather than being assimilated into previous views.
The Eclectic Approach Alternatively, aspects of two or more diverse approaches may be combined in a more general, eclectic approach. In practice, many psychologists have responded to the existence of many perspectives by adopting an eclectic stance; that is, they accept working ideas from several viewpoints and incorporate which- ever they find useful. For example, a psychologist using an eclectic approach might accept causal explanations from psy- chodynamic theory while applying techniques of anxiety reduc- tion from behavior therapy. Another psychologist might combine techniques from the cognitive-behavioral approach with those from the interpersonal approach. Purists in the field—those who advocate a single viewpoint—are skeptical about eclecticism, claiming that an eclectic approach tends to lack integrity and produces a “crazy quilt” of inconsistent practice with little ratio- nale. This criticism may be true, but the approach certainly seems to work for many psychotherapists.
Typically, those who use an eclectic approach to treatment make no attempt to synthesize the theoretical perspectives. Although this approach can work in practical settings, it is not successful at a theoretical level because the underlying prin- ciples of many of the theoretical perspectives are incompatible as they now stand. Thus, the eclectic approach still falls short of the final goal, which is to tackle the theoretical clutter and develop a single, comprehensive, internally consistent viewpoint that accurately reflects what we know empirically about abnor- mal behavior.
Causal Factors and Viewpoints 103
The Biopsychosocial Unified Approach At present, the only attempt at such a unified perspective that has been developing is called the biopsychosocial perspective. This viewpoint reflects the conviction that most disorders are the result of many causal factors—biological, psychological, and sociocul- tural—interacting with one another. Moreover, for any given per- son, the particular combination of causal factors may be unique, or at least not widely shared by large numbers of people with the
same disorder. For example, some children may become delin- quents primarily because of having a heavy genetic loading for antisocial behavior, whereas others may become delinquent pri- marily because of environmental influences such as living in an area with a large number of gangs. Therefore, we can still hope to achieve a scientific understanding of many of the causes of abnormal behavior even if we cannot predict such behavior with exact certainty in each individual case and are often left with some “unexplained” influences.
Summary 3.1 Distinguish between risk factors and causes of
abnormal behavior.
• In considering the causes of abnormal behavior, it is important to distinguish among necessary, sufficient, and contributory causal factors, as well as between relatively distal causal factors and those that are more proximal.
• Usually the occurrence of abnormal or maladaptive behavior is considered to be the joint product of a per- son’s predisposition or vulnerability (diathesis) to dis- order and of certain stressors that challenge his or her coping resources.
• The concept of protective factors is important for understanding why some people with both a diathesis and a stressor may remain resilient and not develop a disorder.
3.2 List the perspectives that psychologists take to understand the causes of abnormal behavior.
This chapter discusses biological, psychological, social, and cultural perspectives, each of which tends to emphasize the importance of causal factors of a characteristic type. Ultimately we strive for an integrative biopsychosocial viewpoint.
3.3 Explain what the biological perspective tells us about abnormal behavior and also explain the biological causal factors of abnormal behavior.
• In examining biologically based vulnerabilities, we must consider abnormalities in genetics, brain dys- function and neural plasticity, neurotransmitter and hormonal abnormalities in the brain or other parts of the central nervous system, and temperament.
• Genetic vulnerabilities can affect the development of mental disorders through multiple mechanisms, including ways in which the genotype may affect the
phenotype (genotype–environment correlations) and ways in which they affect an individual’s susceptibil- ity to environmental influences (genotype–environment interactions).
• Methods for studying the extent of genetic versus environmental influences include the family history method, the twin method, and the adoption method. More recently, linkage analysis and association studies are beginning to contribute knowledge about the exact location of genes contributing to mental disorders.
• Studies of neural plasticity have shown that genetic programs for brain development are not as fixed as once believed and that existing neural circuits can often be modified based on experience.
• Many different neurotransmitter and hormonal abnormalities contribute to the development of men- tal disorders because of the effects they exert on differ- ent relevant brain and body areas for different disorders.
• Temperament is strongly influenced by genetic fac- tors and refers to a baby’s characteristic ways of reacting to the environment and his or her ways of self-regulation. It forms the basis of our adult person- ality, which in turn influences our vulnerability to different disorders.
3.4 Describe the most prominent psychological perspectives on abnormal psychology.
• In examining psychologically based vulnerabilities, three primary perspectives have developed since the end of the nineteenth century: psychodynamic, behav- ioral, and cognitive-behavioral.
• The oldest psychological viewpoint on abnormal behavior is Freudian psychoanalytic theory. For many years this view was preoccupied with questions about libidinal (id) energies and their containment.
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• The cognitive-behavioral viewpoint attempts to incor- porate the complexities of human cognition, and how it can become distorted, into an understanding of the causes of psychopathology.
• People’s schemas and self-schemas play a central role in the way they process information, in how they attri- bute outcomes to causes, and in their values. The effi- ciency, accuracy, and coherence of a person’s schemas and self-schemas and attributions appear to provide an important protection against breakdown.
• Treatments developed from the cognitive-behavioral perspective attempt to alter maladaptive thinking and improve a person’s abilities to solve problems and to achieve goals.
3.5 Describe three social factors known to contribute to abnormal behavior.
• Sources of psychologically determined vulnerability include early deprivation or trauma, problems in par- enting style, marital discord and divorce, low socio- economic status and unemployment, maladaptive peer relationships, and prejudice and discrimination.
3.6 Explain how cultural differences can influence perceptions of abnormal behavior.
• The cultural perspective is concerned with the contri- bution of cultural variables to mental disorder.
• Although many serious mental disorders are fairly universal, the form that some disorders take and their prevalence vary widely among different cultures.
• The biopsychosocial approach is promising, but in many ways it is merely a descriptive acknowledgment of the complex interactions among biological, psycho- logical, and sociocultural risk factors rather than a clearly articulated theory of how they interact.
• More recently, four second-generation psychodynamic theories departed in significant ways from Freud’s original ideas.
• Anna Freud’s ego psychology focused on the important role of the ego in normal and abnormal behavior, with special attention focused on ego-defense reactions.
• Object-relations theorists focused on the role of the quality of very early (pre-Oedipal) mother–infant rela- tionships for normal development.
• The originators of the interpersonal perspective took exception to the Freudian emphasis on the internal determinants of motivation and behavior and instead emphasized the social and cultural forces that shape behavior.
• Attachment theory, which has roots in both the inter- personal and object-relations perspectives, emphasizes the importance of early experiences with attachment relationships for laying the foundation for later child, adolescent, and adult development.
• Psychoanalysis and closely related therapeutic approaches are termed psychodynamic in recognition of their attention to inner, often unconscious forces.
• The behavioral perspective focuses on the role of learning in human behavior and attributes maladap- tive behavior either to a failure to learn appropriate behaviors or to the learning of maladaptive behaviors.
• The primary forms of learning studied are classical conditioning and operant (instrumental) conditioning. The effects of each are modified by principles of gener- alization and discrimination. Observational learning is also important.
• Adherents of the behavioral viewpoint attempt to alter maladaptive behavior by extinguishing it or providing training in new, more adaptive behaviors.
adoption method, p. 70 association studies, p. 71 attachment theory, p. 81 attribution, p. 88 behavior genetics, p. 69 biopsychosocial viewpoint, p. 66 castration anxiety, p. 79 causal risk factor, p. 61 chromosomes, p. 67 classical conditioning, p. 83 cognitive-behavioral
perspective, p. 86 concordance rate, p. 69 contributory cause, p. 62 correlate, p. 61
cortisol, p. 74 developmental psychopathology, p. 65 developmental systems
approach, p. 72 diathesis, p. 63 diathesis–stress models, p. 63 discrimination, p. 85 ego, p. 77 ego-defense mechanisms, p. 78 ego psychology, p. 80 Electra complex, p. 79 etiology, p. 61 extinction, p. 84 family history method, p. 69 fixed marker, p. 61
generalization, p. 85 genes, p. 67 genotype, p. 68 genotype–environment
correlation, p. 68 genotype–environment
interaction, p. 68 hikikomori, p. 100 hormones, p. 74 hypothalamic-pituitary-adrenal
(HPA) axis, p. 74 id, p. 77 interpersonal perspective, p. 80 intrapsychic conflicts, p. 77 learning, p. 83
Key Terms
Causal Factors and Viewpoints 105
libido, p. 77 linkage analysis, p. 70 necessary cause, p. 61 neurotransmitters, p. 73 object-relations theory, p. 80 observational learning, p. 85 Oedipus complex, p. 79 operant (instrumental)
conditioning, p. 84 phenotype, p. 68 pituitary gland, p. 74
pleasure principle, p. 77 polygenic, p. 68 primary process thinking, p. 77 protective factors, p. 64 psychosexual stages of
development, p. 78 reality principle, p. 77 reinforcement, p. 84 resilience, p. 64 risk factor, p. 61 schema, p. 86
secondary process thinking, p. 77 self-schema, p. 87 spontaneous recovery, p. 84 stress, p. 63 sufficient cause, p. 61 superego, p. 77 synapse, p. 73 temperament, p. 75 twin method, p. 69 variable marker, p. 61 variable risk factor, p. 61
106
Learning Objectives
4.1 Identify the basic elements in assessment.
4.2 Describe the factors involved in the assessment of the physical organism.
4.3 Explain the interview process, clinical observation, and testing in psychosocial assessment.
4.4 Evaluate the case study of a woman who experienced violence in the workplace.
4.5 Discuss how practitioners integrate assessment data in treatment planning.
4.6 Explain the process for classifying abnormal behavior.
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and emotional risk children experience in schools as a means of ensuring adequate adjustment and performance later. Criteria based on these measurements may be estab- lished as part of the treatment plan such that the therapy is considered successful and is terminated only when the cli- ent’s behavior meets these predetermined criteria. Also, as we will see in later chapters, comparison of posttreatment with pretreatment assessment results is an essential feature of many research projects designed to evaluate the effec- tiveness of various therapies.
In this chapter, we review some of the more commonly used assessment procedures and show how the data obtained can be integrated into a coherent clinical picture for making decisions about referral and treatment. Our survey includes a discussion of physical, neurological, and neuropsychological assessment; the clinical interview; behavioral observation; and personality assessment through the use of projective and objective psychological tests. Later in the chapter we examine the process of arriv- ing at a clinical diagnosis using DSM-5.
Let us look first at what exactly a clinician is trying to learn during the psychological assessment of a client.
The Basic Elements in Assessment 4.1 Identify the basic elements in assessment.
What does a clinician need to know? First, of course, the presenting problem, or major symptoms and behavior the client is experiencing, must be identified. Is it a situational problem precipitated by some environmental stressor such as divorce or unemployment, a manifestation of a more pervasive and long-term disorder, or some combination of the two? Is there any evidence of recent deterioration in cognitive functioning? What is the duration of the current complaint, and how is the person dealing with the prob- lem? What, if any, prior help has been sought? Are there indications of self-defeating behavior and personality dete- rioration, or is the individual using available personal and environmental resources in a good effort to cope? How pervasively has the problem affected the person’s perfor- mance of important social roles? Does the individual’s symptomatic behavior fit any of the diagnostic patterns in the DSM-5?
The Relationship Between Assessment and Diagnosis It is important to have an adequate classification of the pre- senting problem for a number of reasons. Clinically, knowl- edge of a person’s type of disorder can help in planning
The assessment of the personality and motivation of others has been of interest to people since antiquity. Hathaway (1965) pointed out that one of the earliest descriptions of using behavioral observation in assessing personality can be found in the Old Testament. Gideon relied on observa- tions of his men who trembled with fear to consider whether they were fit for duty; Gideon also observed how soldiers chose to drink water from a stream as a means of selecting effective men for battle. In ancient Rome, Tacitus provided examples in which the appraisal of a person’s personality entered into their leader’s judgments about them. Tacitus (translated by Grant, 1956, p. 36) points out that Emperor Tiberius evaluated his subordinates in his meetings by often pretending to be hesitant in order to detect what the leading men were thinking.
Psychological assessment is one of the oldest and most widely developed branches of contemporary psy- chology, dating back to the work of Galton (1879) in the nineteenth century (Butcher, 2010; Weiner & Greene, 2008). In this chapter we focus on the initial clinical assessment and on arriving at a clinical diagnosis according to DSM-5. Psychological assessment refers to a procedure by which clinicians, using psychological tests, observation, and interviews, develop a summary of the client’s symptoms and problems. Clinical diagnosis is the process through which a clinician arrives at a general “summary classifica- tion” of the patient’s symptoms by following a clearly defined system such as DSM-5 or ICD-10 (International Classification of Diseases), the latter published by the World Health Organization (WHO).
Assessment is an ongoing process and may be impor- tant at various points during treatment, not just at the beginning—for example, to examine the client’s progress in treatment or to evaluate the outcome. In the initial clini- cal assessment, an attempt is usually made to identify the main dimensions of a client’s problem and to predict the probable course of events under various conditions. It is at this initial stage that crucial decisions have to be made— such as what (if any) treatment approach is to be offered, whether the problem will require hospitalization, to what extent family members will need to be included as co- clients, and so on. Sometimes these decisions must be made quickly, as in emergency conditions, and without critical information. As will be seen, various psychological measurement instruments are employed to maximize assessment efficiency in this type of pretreatment examina- tion process (Harwood & Beutler, 2009).
A less obvious, but equally important, function of pre- treatment assessment is establishing baselines for various psychological functions so that the effects of treatment can be measured. For example, Kamphaus, Reynolds, and Dever (2014) showed the importance of childhood assessment screening for determining the behavioral
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caretaker for a spouse suffering from Alzheimer’s disease is so challenging that it can result in significant psychologi- cal impairment, especially where outside supports are lacking.
The diverse and often conflicting bits of information about the individual’s personality traits, behavior patterns, environmental demands, and so on, must then be inte- grated into a consistent and meaningful picture. Some cli- nicians refer to this picture as a “dynamic formulation” because it not only describes the current situation but also includes hypotheses about what is driving the person to behave in maladaptive ways. At this point in the assess- ment, the clinician should have a plausible explanation for why a normally passive and mild-mannered man sud- denly flew into a rage and started breaking up furniture, for example. The formulation should allow the clinician to develop hypotheses about the client’s future behavior as well. What is the likelihood of improvement or deteriora- tion if the person’s problems are left untreated? Which behaviors should be the initial focus of change, and what treatment methods are likely to be most efficient in produc- ing this change? How much change might be expected from a particular type of treatment?
Where feasible, decisions about treatment are made collaboratively with the consent and approval of the indi- vidual. In cases of severe disorder, however, they may have to be made without the client’s participation or, in rare instances, even without consulting responsible family members. As has already been indicated, knowledge of the person’s strengths and resources is important; in short, what qualities does the client bring to treatment that can enhance the chances of improvement? Because a wide range of factors can play important roles in causing and maintaining maladaptive behavior, assessment may involve the coordinated use of physical, psychological, and environmental assessment procedures. Moreover, as we have indicated, the nature and comprehensiveness of clini- cal assessments vary with the problem and the treatment
and managing the appropriate treatment. Administra- tively, it is essential to know the range of diagnostic prob- lems that are represented in the client population and for which treatment facilities need to be available. If most cli- ents at a facility have been diagnosed as having personality disorders, for example, then the staffing, physical environ- ment, and treatment facilities should be arranged accord- ingly, with appropriate security and clearly established rules. In many cases, a formal diagnosis is necessary before insurance claims can be filed to cover a client’s treatment costs. Thus, the nature of the difficulty needs to be under- stood as clearly as possible, including a diagnostic catego- rization if appropriate (see the “Classifying Abnormal Behavior” section at the end of this chapter).
Taking a Social or Behavioral History For most clinical purposes, assigning a formal diagnostic classification per se is much less important than having a clear understanding of the individual’s behavioral history, intellectual functioning, personality characteristics, and environmental pressures and resources. That is, an ade- quate assessment includes much more than the diagnostic label. For example, it should include an objective descrip- tion of the person’s behavior. How does the person charac- teristically respond to other people? Are there excesses in behavior present, such as eating or drinking too much? Are there notable deficits, for example, in social skills? How appropriate is the person’s behavior? Is the person mani- festing behavior that is plainly unresponsive or uncoopera- tive? Excesses, deficits, and appropriateness are key dimensions to be noted if the clinician is to understand the particular disorder that has brought the individual to the clinic or hospital.
PERSONALITY FACTORS Assessment should include a description of any relevant long-term personality charac- teristics. Has the person typically responded in deviant ways to particular kinds of situations—for example, those requiring submission to legitimate authority? Are there personality traits or behavior patterns that predispose the individual to behave in maladaptive ways? Does the per- son tend to become enmeshed with others to the point of losing his or her identity, or is he or she so self-absorbed that intimate relationships are not possible? Is the person able to accept help from others? Is the person capable of genuine affection and of accepting appropriate responsibil- ity for the welfare of others? Such questions are at the heart of many assessment efforts.
THE SOCIAL CONTEXT It is also important to assess the social context in which the individual functions. What kinds of environmental demands are typically placed on the person, and what supports or special stressors exist in her or his life situation? For example, being the primary
Some patients with cognitive deterioration are difficult to evaluate and to provide health care for, often requiring special facilities.
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The challenges of understanding clients when per- forming multicultural assessments have been described (Butcher et al., 2006; Hays, 2008) and involve both test instrument characteristics and sociocultural factors such as the relationships among culture, behavior, and psychopa- thology. Psychologists need to ensure that the test proce- dures they employ are appropriate for the particular client. For example, the psychological equivalence of a test for use with a particular population should be determined. The meaning or cultural significance of test items should be similar across cultural groups (Butcher & Han, 1996), and the norms used to compare the client should be appropri- ate. In using Western-developed tests, users need to take into account the dominant language, socioeconomic status, ethnicity, and gender of their clients. For example, clients from non–English-speaking countries might have insuffi- cient English language skills, which will influence their test performance. When using a translated version of a test, interpreters need to be aware of the possible differences that can arise when using an adapted version. Thus, psy- chologists need to be aware of the available research on the instrument’s use with the target population in order to assess whether the adapted version measures the same variables in the new cultures. Finally, test users need to be concerned with the impact and fairness of the instruments they employ with clients from diverse groups—for exam- ple, whether there are any possible performance differ- ences on the scales between groups.
The most widely used personality measure, the Min- nesota Multiphasic Personality Inventory (MMPI-2) (dis- cussed later in this chapter), has been widely evaluated both in international applications with translated versions (Butcher & Williams, 2009) and in diverse subcultural groups in the United States (Butcher et al., 2007). Spanish- language versions of the test have been developed. Recent research has provided support for the use of the MMPI-2 with minorities (Robin et al., 2003), and the analyses pro- vided by Hall and colleagues (1999) support the use of the MMPI-2 with Hispanic clients.
The Influence of Professional Orientation How clinicians go about the assessment process often depends on their basic treatment orientations. For exam- ple, a biologically oriented clinician—typically a psychia- trist or other medical practitioner—is likely to focus on biological assessment methods aimed at determining any underlying organic malfunctioning that may be causing the maladaptive behavior. A psychodynamic or psychoan- alytically oriented clinician may choose unstructured per- sonality assessment techniques, such as the Rorschach inkblots or the Thematic Apperception Test (described later in this chapter), to identify intrapsychic conflicts or
agency’s facilities. Assessment by phone in a suicide pre- vention center (Stolberg & Bongar, 2009), for example, is quite different from assessment aimed at developing a treatment plan for a person who has come to a clinic for help (Perry, 2009).
Ensuring Culturally Sensitive Assessment Procedures Increasingly, practitioners are being asked to conduct psychological evaluations for clients from diverse ethnic and language backgrounds. In both clinical and court settings, for example, a psychologist might be referred a client who has limited English language skills and low exposure to American mores, values, and laws. It is criti- cal for the psychologist to be informed of the issues involved in multicultural assessment (often referred to as cultural competence) and to use testing procedures that have been adapted and validated for culturally diverse clients (Butcher et al., 2015).
Psychological assessment of clients from diverse eth- nic backgrounds has increased greatly in recent years. The growing number of minorities requiring a clinical or foren- sic evaluation comes about, in part, from the influx of immigrants or refugees, many of whom encounter adjust- ment difficulties. The U.S. Census Bureau (2014) reports that the Hispanic population now makes up 17 percent of the U.S. population. People of Hispanic origin are now the largest ethnic minority group in the United States. African Americans now represent 12.6 percent of the population, Asians 4.8 percent, Native Americans 0.9 percent, and Native Hawaiians/Pacific Islanders 0.2 percent. Many immigrants, especially those of color, become members of ethnic minorities when they relocate to North America. As such, they may experience racial discrimination or may be further viewed as inferior by the nonminority community due to their lack of political power or lack of adaptive skills arising from their difficulties in acculturation (Green, 2009; Hays, 2008).
To fairly and successfully treat such individuals, the ethics code of the American Psychological Association (2002) recommends that psychologists consider various test factors, test-taking abilities, and other characteristics of the person being assessed, such as situational, linguistic, and cultural differences, that might affect his or her judg- ments or reduce the accuracy of his or her interpretations. Thus, psychologists who use tests in a culturally compe- tent manner must bear in mind a range of issues and fac- tors involved with culturally and linguistically diverse clients. These issues involve the importance of ensuring that the characteristics of the test being employed are appropriate across cultures and that potential biasing fac- tors do not interfere with critical thinking in the overall assessment process.
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measure. In the context of testing or classification, valid- ity is the degree to which a measure accurately conveys to us something clinically important about the person whose behavior fits the category, such as helping to pre- dict the future course of the disorder. If, for example, a person is predicted to have or is diagnosed as having schizophrenia, we should be able to infer the presence of some fairly precise characteristics that differentiate the person from individuals who are considered normal or from those with other types of mental disorder. The clas- sification or diagnosis of schizophrenia, for example, implies a disorder of unusually stubborn persistence, with recurrent episodes being common.
Normally, the validity of a mental health measure or classification presupposes reliability. If clinicians can’t agree on the class to which a person with a disorder’s behavior belongs, then the question of the validity of the diagnostic classifications under consideration becomes irrelevant. To put it another way, if we can’t confidently pin down what the diagnosis is, then whatever useful informa- tion a given diagnosis might convey about the person being evaluated is lost. On the other hand, good reliability does not in itself guarantee validity. For example, handed- ness (left, right, ambidextrous) can be assessed with a high degree of reliability, but handedness accurately predicts neither mental health status nor countless other behavioral qualities on which people vary; that is, it is not a valid index of these qualities (although it may be a valid index for success in certain situations involving the game of base- ball, for example). In like manner, reliable assignment of a person’s behavior to a given class of mental disorder will prove useful only to the extent that the validity of that class has been established through research.
Standardization is a process by which a psychological test is administered, scored, and interpreted in a consistent or “standard” manner. Standardized tests are considered to be more fair than nonstandardized tests in that they are applied consistently and in the same manner to all persons taking them. Many psychological tests are standardized to allow the test user to compare a particular individual’s score on the test with a reference population, often referred to as a normative sample. For example, comparing a par- ticular individual’s test score on a distribution of test scores from a large normative population can enable the user to evaluate whether the individual’s score is low, average, or high along the distribution of scores (referred to as a T score distribution).
Trust and Rapport Between the Clinician and the Client In order for psychological assessment to proceed effec- tively and to provide a clear understanding of behavior and symptoms, the client being evaluated must feel
may simply proceed with therapy, expecting these con- flicts to emerge naturally as part of the treatment process. A behaviorally oriented clinician, in an effort to determine the functional relationships between environmental events or reinforcements and the abnormal behavior, will rely on such techniques as behavioral observation and self-monitoring to identify learned maladaptive patterns; for a cognitively oriented behaviorist, the focus would shift to the dysfunctional thoughts supposedly mediating those patterns.
The preceding examples represent general trends and are in no way meant to imply that clinicians of a particular orientation limit themselves to a particular assessment method or that each assessment technique is limited to a particular theoretical orientation. Such trends are instead a matter of emphasis and point to the fact that certain types of assessments are more conducive than others to uncovering particular causal factors or for eliciting infor- mation about symptomatic behavior central to under- standing and treating a disorder within a given conceptual framework.
As you will see in what follows, both physical and psychosocial data can be extremely important to under- standing a patient. In the sections that follow, we discuss several assessment instruments and examine in some detail an actual psychological study of a woman who expe- rienced a traumatic situation in the workplace that resulted in severe emotional adjustment problems.
Reliability, Validity, and Standardization Three measurement concepts that are important in under- standing clinical assessment and the utility of psychologi- cal tests are reliability, validity, and standardization. These concepts are briefly described here and then illustrated throughout the chapter. A psychological test or measure- ment construct needs to show reliability in order to be effective. Reliability is a term describing the degree to which an assessment measure produces the same result each time it is used to evaluate the same thing. If, for example, your scale showed a significantly different weight each time you stepped on it over a brief period of time, you would consider it a fairly unreliable measure of your body mass. In the context of assessment or classifica- tion, reliability is an index of the extent to which a mea- surement instrument can agree that a person’s behavior fits a given diagnostic class. If the observations are differ- ent, it may mean that the classification criteria are not pre- cise enough to determine whether the suspected disorder is present.
The psychological test or classification system must also be valid. Validity is the extent to which a measuring instrument actually measures what it is supposed to
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Assessment of the Physical Organism 4.2 Describe the factors involved in the assessment of
the physical organism.
In some situations and with certain psychological prob- lems, a medical evaluation is necessary to rule out the pos- sibility that physical abnormalities may be causing or contributing to the problem. The medical evaluation may include both a general physical examination and special examinations aimed at assessing the structural (anatomi- cal) and functional (physiological) integrity of the brain as a behaviorally significant physical system (Swartz, 2014).
The General Physical Examination In cases in which physical symptoms are part of the pre- senting clinical picture, a referral for a medical evaluation is recommended. A physical examination consists of the kinds of procedures most of us have experienced when getting a “medical checkup.” Typically, a medical history is obtained, and the major systems of the body are checked (LeBlond et al., 2004; Swartz, 2014). This part of the assess- ment procedure is of obvious importance for disorders that entail physical problems, such as a psychologically based physical condition, addictive disorders, and organic brain syndromes. In addition, a variety of organic conditions, including various hormonal irregularities, can produce behavioral symptoms that closely mimic those of mental disorders usually considered to have predominantly psy- chosocial origins. Although some long-lasting pain can be related to actual organic conditions, other such pain can result from strictly emotional factors. A case in point is chronic back pain, in which psychological factors may sometimes play an important part. A diagnostic error in this type of situation could result in costly and ineffective surgery; hence, in equivocal cases, most clinicians insist on a medical clearance before initiating psychosocially based interventions.
The Neurological Examination Because brain pathology is sometimes involved in some mental disorders (e.g., unusual memory deficits or motor impairments), a specialized neurological examination can be administered in addition to a general medical examina- tion. This may involve the client’s getting an electroen- cephalogram (EEG) to assess brain wave patterns in awake and sleeping states. An EEG is a graphical record of the brain’s electrical activity (Yamada & Meng, 2011). It is obtained by placing electrodes on the scalp and amplifying the minute brain wave impulses from various brain areas; these amplified impulses drive oscillating pens whose
comfortable with the clinician. In a clinical assessment situation, this means that a client must feel that the test- ing will help the practitioner gain a clear understanding of her or his problems and must understand how the tests will be used and how the psychologist will incor- porate them into the clinical evaluation. The clinician should explain what will happen during assessment and how the information gathered will help provide a clearer picture of the problems the client is facing.
Clients need to be assured that the feelings, beliefs, attitudes, and personal history that they are disclosing will be used appropriately, will be kept in strict confidence, and will be made available only to therapists or others involved in the case. An important aspect of confidentiality is that the test results are released to a third party only if the client signs an appropriate release form. In cases in which the person is being tested for a third party such as the court system, the client in effect is the referring source—for example, the judge ordering the evaluation—not the indi- vidual being tested. In these cases the testing relationship is likely to be strained and developing rapport is likely to be difficult. Of course, in a court-ordered evaluation, the person’s test-taking behavior is likely to be very different from what it would be otherwise, and interpretation of the test needs to reflect this different motivational set created by the person’s unwillingness to cooperate.
People being tested in a clinical situation are usually highly motivated to be evaluated and like to know the results of the testing. They generally are eager for some definition of their discomfort. Moreover, providing test feedback in a clinical setting can be an important element in the treatment process (Harwood & Beutler, 2009). Inter- estingly, when patients are given appropriate feedback on test results, they tend to improve—just from gaining a per- spective on their problems as a result of the testing. The test feedback process itself can be a powerful clinical inter- vention (Finn & Kamphuis, 2006). When persons who were not provided psychological test feedback were compared with those who were provided with feedback, the latter group showed a significant decline in reported symptoms and an increase in measured self-esteem as a result of hav- ing a clearer understanding of their own resources.
in review • What is the difference between clinical diagnosis and psycho-
logical assessment? What components must be integrated into a dynamic formulation?
• Describe the important elements in a social or behavioral history.
• What does it mean to use culturally fair assessments?
• What is the impact of professional orientation on the structure and form of a psychological evaluation?
• Does providing test feedback to clients aid them in their adjustment?
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Essentially, MRI involves the precise measurement of variations in magnetic fields that are caused by the vary- ing amounts of water content of various organs and parts of organs. In this manner the anatomical structure of a cross section at any given plane through an organ such as the brain can be computed and graphically depicted with astonishing structural differentiation and clarity. MRI thus makes possible, by noninvasive means, visualization of all but the most minute abnormalities of brain structure. It has been particularly useful in confirming degenerative brain processes as shown, for example, in enlarged areas of the brain. Therefore, MRI studies have considerable potential to illuminate the contribution of brain anomalies to nonorganic psychoses such as schizophrenia, and some progress in this area has already been made (Mathalondolf et al., 2001).
Still, the MRI can be problematic. For example, some patients have a claustrophobic reaction to being placed into the narrow cylinder of the MRI machine that is neces- sary to contain the magnetic field and block out external radio signals. In addition, an evaluation and critique of the MRI approach in medicine was published by Joyce (2008), who interviewed physicians and MRI technologists and also conducted ethnographic research at imaging sites and attended radiology conferences. In her critique, she dem- onstrated that current beliefs about MRI draw on cultural ideas about technology and are reinforced by health care policies and insurance reimbursement practices. How- ever, her review raises questions about the work practices of many physicians and technologists and suggests that MRI scans do not reveal the truth about the body that many medical practices often hold. For example, she con- cludes that MRI studies do not always lead to better out- comes for patients.
deviations are traced on a strip of paper moving at a con- stant speed. Much is known about the normal pattern of brain impulses in waking and sleeping states and under various conditions of sensory stimulation. Significant divergences from the normal pattern can thus reflect abnormalities of brain function such as might be caused by a brain tumor or other lesion. An EEG may reveal a dysrhythmia, or irregular pattern, in the brain’s electrical activity. For example, recent research has supported a link between resting frontal EEG asymmetry and depression (see Stewart et al., 2010) and anxiety (see Thibodeau et al., 2006). When an EEG reveals an irregular pattern, other specialized techniques may be used in an attempt to arrive at a more precise diagnosis of the problem.
An EEG is a graphical record of the brain’s electrical activity. Electrodes are placed on the scalp, and brain wave impulses are amplified. The amplified impulses drive oscillating pens whose deviations are traced on a strip of paper moving at a constant speed. Significant differences from the normal pattern can reflect abnormalities of brain function.
ANATOMICAL BRAIN SCANS Radiological technology, such as a computerized axial tomography (CAT) scan, is one of these specialized techniques (Mishra & Singh, 2010). Through the use of X-rays, a CAT scan reveals images of parts of the brain that might be diseased. This procedure has aided neurological study in recent years by providing rapid access, without surgery, to accurate information about the localization and extent of anomalies in the brain’s structural characteristics. The procedure involves the use of computer analysis applied to X-ray beams across sec- tions of a patient’s brain to produce images that a neurolo- gist can then interpret.
CAT scans have been increasingly replaced by magnetic resonance imaging (MRI). The images of the interior of the brain are frequently sharper with MRI because of its superior ability to differentiate subtle variations in soft tis- sue. In addition, the MRI procedure is normally far less complicated to administer than a CAT scan and does not subject the patient to ionizing radiation.
PET SCANS: A METABOLIC PORTRAIT Another scan- ning technique is the positron emission tomography (PET) scan. Whereas a CAT scan is limited to distinguish- ing anatomical features such as the shape of a particular internal structure, a PET scan allows for an appraisal of
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A number of studies have provided support for this optimism (MacDonald & Jones, 2009). Research using fMRI has explored the cortical functioning that underlies various psychological processes; for example, one study showed that psychological factors or environmental events can affect brain processes as measured by fMRI. Eisenberger, Lieberman, and Williams (2003) found that participants who were excluded from social participation showed a sim- ilar pattern of brain activation (in the right ventral prefron- tal cortex) as participants experiencing physical pain. Joseph and colleagues (2014) studied differences between alcohol users and problem drinkers and found that indi- viduals who report problematic drinking, but who are not alcohol dependent, may show patterns that are consistent with findings in individuals who are alcohol dependent; and Dager et al. (2014) reported that heavy drinkers dif- fered from light drinkers in the ways their brains compen- sated during memory tasks. Longe and colleagues (2010) found that fMRI was effective at detecting neural correlates for self-critical thinking. Some researchers have pointed out that fMRI has a high potential for contributing to a treat- ment approach in mental health care (Schneider et al., 2009). Although some research has suggested that fMRI can be an effective procedure for detecting malingering or lying (Langleben et al., 2005), one court has recently ruled against the use of fMRI as a lie detector (Couzin-Frankel, 2010).
Other studies have addressed problems in abnormal behavior. One study showed that the impaired time estima- tion found in people with schizophrenia might result from dysfunction in specific areas of the brain, thalamus, and prefrontal cortex (Suzuki et al., 2004), while others addressed cortical functioning in auditory hallucinations in schizophrenia (Shergill et al., 2000); effects of neuroleptic medication in people with schizophrenia (Braus et al., 1999); and the neuroanatomy of anxiety (Paulesu et al. 2010)
how an organ is functioning (Meyer et al., 2012). The PET scan provides metabolic portraits by tracking natural com- pounds, such as glucose, as they are metabolized by the brain or other organs. By revealing areas of differential metabolic activity, the PET scan enables a medical special- ist to obtain more clear-cut diagnoses of brain pathology by, for example, pinpointing sites responsible for epileptic seizures, trauma from head injury or stroke, and brain tumors. Thus, the PET scan may be able to reveal problems that are not immediately apparent anatomically. Moreover, the use of PET scans in research on brain pathology that occurs in abnormal conditions such as Alzheimer’s disease may lead to important discoveries about the organic pro- cesses underlying these disorders and aid in the treatment of dementia (Saykin et al., 2006). PET scans have, however, been of somewhat limited value thus far because of the low-fidelity pictures obtained (Fletcher, 2004) and their cost, since they require a very expensive instrument nearby to produce the short-lived radioactive atoms required for the procedure. Although PET scans are admitted into court cases to illustrate potential brain damage, some investiga- tors recommend questioning their use in forensic evalua- tions (Moriarty et al., 2013).
THE FUNCTIONAL MRI The technique known as functional MRI (fMRI) has been used in the study of psy- chopathology for a number of years. As originally devel- oped and employed, the MRI could reveal brain structure but not brain activity. For the latter, clinicians and investi- gators remained dependent on PET scans. Improving on these techniques, fMRI most often measures changes in local oxygenation (i.e., blood flow) of specific areas of brain tissue that in turn depend on neuronal activity in those specific regions (Bandettini, 2007; Ulmer & Jansen, 2010). Ongoing psychological activity, such as sensations, images, and thoughts, can thus be “mapped,” at least in principle, revealing the specific areas of the brain that appear to be involved in their neurophysiological processes. For exam- ple, one study (Wright & Jackson, 2007) examined the task of judgment of serve direction among tennis players and found that different patterns produce different responses in the brain.
Because the measurement of change in this context is critically time dependent, the emergence of fMRI required the development of high-speed devices for enhancing the recording process, as well as the computerized analysis of incoming data. These improvements are now widely avail- able and will likely lead to a marked increase in studying people with disorders using functional imaging. Optimism about the ultimate value of fMRI in mapping cognitive processes in mental disorders is still strong. The fMRI is thought by some to hold more promise for depicting brain abnormalities than currently used procedures such as the neuropsychological examination (see next section).
The functional MRI (fMRI), like the MRI, allows clinicians to “map” brain structure. The exciting breakthrough in fMRI technology gives clinicians the ability to measure brain activities underlying such things as sensations, images, and thoughts, revealing the specific areas of the brain involved.
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standardized tasks, particularly perceptual-motor tasks, can give valuable clues about any cognitive and intellec- tual impairment following brain damage (Horton, 2008; Lezak et al., 2004; Reitan & Wolfson, 1985). Such testing can even provide clues to the probable location of the brain damage, although PET scans, MRIs, and other physical tests may be more effective in determining the exact loca- tion of the injury.
Many neuropsychologists prefer to administer a highly individualized array of tests, depending on a patient’s case history and other available information. Oth- ers administer a standard set of tests that have been prese- lected to sample, in a systematic and comprehensive manner, a broad range of psychological competencies known to be adversely affected by various types of brain injury (Gass, 2009). The use of a constant set of tests has many research and clinical advantages, although it may compromise flexibility. Consider the components of one such standard procedure, the Halstead-Reitan neuropsy- chological test battery. The Halstead-Reitan battery is com- posed of several tests and variables from which an “index of impairment” can be computed (Preiss & Preiss, 2013; Reitan & Wolfson, 1985). In addition, it provides specific information about a subject’s functioning in several skill areas. The Halstead-Reitan battery for adults is made up of a group of tests such as the following:
1. Halstead category test: Measures a subject’s ability to learn and remember material and can provide clues as to his or her judgment and impulsivity. The subject is presented with a stimulus (on a screen) that suggests a number between 1 and 4. The subject presses a button indicating the number she or he believes was sug- gested. A correct choice is followed by the sound of a pleasant doorbell, an incorrect choice by a loud buzzer. The person is required to determine from the pattern of buzzers and bells what the underlying principle of the correct choice is.
2. Tactual performance test: Measures a subject’s motor speed, response to the unfamiliar, and ability to learn and use tactile and kinesthetic cues. The test surface is a board that has spaces for 10 blocks of varied shapes. The subject is blindfolded (never actually seeing the board) and asked to place the blocks into the correct grooves in the board. Later, the subject is asked to draw the blocks and the board from tactile memory.
3. Rhythm test: Measures attention and sustained con- centration through an auditory perception task. It includes 30 pairs of rhythmic beats that are presented on a tape recorder. The subject is asked whether the pairs are the same or different.
4. Speech sounds perception test: Determines whether an individual can identify spoken words. Nonsense words are presented on a tape recorder, and the subject
and depression (Brody et al., 2001). Finally, Whalley and colleagues (2004) found that the fMRI technique has the potential of adding to our understanding of the early development of psychological disorder. One study of treatment for aphasia, a disorder in which there is a loss of ability to communicate verbally (Meinzer et al., 2007), showed that changes in behavioral performance and the brain activation pattern were disclosed as affecting the brain’s reorganization.
There are some clear methodological limitations that can influence fMRI results. For example, both MRI and fMRI are quite sensitive to instrument errors or inaccurate observations as a result of slight movements of the person being evaluated (Davidson et al., 2003; Shulman, 2013). Additionally, the results of fMRI studies are often difficult to interpret. Even though group differences emerge between a cognitively impaired group and a control sam- ple, the results usually do not provide much specific infor- mation about the processes studied. Fletcher (2004) provides a somewhat sobering analysis of the current sta- tus of fMRI in contemporary psychiatry, noting that many professionals who had hoped for intricate and unambigu- ous results might be disappointed with the overall lack of effective, pragmatic methodology in fMRI assessment of cognitive processes. At this point the fMRI is not consid- ered to be a valid or useful diagnostic tool for mental disor- ders or for use in forensic evaluations (Buckholtz & Faigman, 2014); however, investigators are optimistic that this procedure shows great promise for understanding brain functioning (MacDonald & Jones, 2009). The primary value of this procedure continues to be research into corti- cal activity and cognitive processes.
The Neuropsychological Examination The techniques described so far have shown success in identifying brain abnormalities that are very often accom- panied by gross impairments in behavior and varied psy- chological deficits. However, behavioral and psychological impairments due to organic brain abnormalities may man- ifest before any organic brain lesion is detectable by scan- ning or other means. In these instances, reliable techniques are needed to measure any alteration in behavioral or psy- chological functioning that has occurred because of the organic brain pathology. This need is met by a growing cadre of psychologists specializing in neuropsychological assessment, which involves the use of various testing devices to measure a person’s cognitive, perceptual, and motor performance as clues to the extent and location of brain damage (Snyder et al., 2006).
In many instances of known or suspected organic brain involvement, a clinical neuropsychologist adminis- ters a test battery to a patient. The person’s performance on
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face-to-face interaction in which a clinician obtains infor- mation about various aspects of a client’s situation, behav- ior, and personality (Berthold & Ellinger, 2009; Craig, 2009; Sharp et al., 2013). The interview may vary from a simple set of questions or prompts to a more extended and detailed format (Kici & Westhoff, 2004). It may be relatively open in character, with an interviewer making moment-to- moment decisions about his or her next question on the basis of responses to previous ones, or it may be more tightly controlled and structured so as to ensure that a par- ticular set of questions is covered. In the latter case, the interviewer may choose from a number of highly struc- tured, standardized interview formats whose reliability has been established in prior research.
STRUCTURED AND UNSTRUCTURED INTERVIEWS Although many clinicians prefer the freedom to explore as they feel responses merit, research data show that the more controlled and structured assessment interview yields far more reliable results than the flexible format. There appears to be widespread overconfidence among clinicians in the accuracy of their own methods and judgments (Taylor & Meux, 1997). Every rule has exceptions, but in most instances, an assessor is wise to conduct an interview that is carefully structured in terms of goals, comprehensive symptom review, other content to be explored, and the type of relationship the interviewer attempts to establish with the person.
Structured interviews follow a predetermined set of questions throughout the interview, for example, “Have you ever had periods in which you could not sleep lately?” and “Have you experienced feeling very nervous about being in public?” The beginning statements and introduc- tion to the interview follow set procedures. The themes and questions are predetermined to obtain particular responses for all items. The interviewer cannot deviate from the question lists and procedures. All questions are asked of each client in a preset way. Each question is struc- tured in a manner so as to allow responses to be quantified or clearly determined. On the negative side, structured interviews typically take longer to administer than unstructured interviews and may include some seemingly tangential questions. Clients can sometimes be frustrated by the overly detailed questions in areas that are of no concern to them.
Unstructured assessment interviews are typically subjective and do not follow a predetermined set of ques- tions. The beginning statements in the interview are usu- ally general, and follow-up questions are tailored for each client. The content of the interview questions is influenced by the habits or theoretical views of the interviewer. The interviewer does not ask the same questions of all clients; rather, he or she subjectively decides what to ask based on the client’s response to previous questions. Because the
is asked to identify the presented word in a list of four printed words. This task measures the subject’s con- centration, attention, and comprehension.
5. Finger oscillation task: Measures the speed at which an individual can depress a lever with the index finger. Several trials are given for each hand.
In summary, the medical and neuropsychological sci- ences are developing many new procedures to assess brain functioning and behavioral manifestations of organic dis- order. Medical procedures to assess organic brain damage include EEGs and CAT, PET, and MRI scans. The new tech- nology holds great promise for detecting and evaluating organic brain dysfunction and increasing our understand- ing of brain function. Neuropsychological testing provides a clinician with important behavioral information on how organic brain damage is affecting a person’s present func- tioning. However, in cases where the psychological diffi- culty is thought to result from nonorganic causes, psychosocial assessment is used.
in review • Compare and contrast five important neurological procedures.
What makes each one particularly valuable?
• What is the difference between a PET scan and an fMRI?
• Describe the use of neuropsychological tests in evaluating the behavioral effects of organic brain disorders.
Psychosocial Assessment 4.3 Explain the interview process, clinical observation,
and testing in psychosocial assessment.
Psychosocial assessment attempts to provide a realistic pic- ture of an individual in interaction with his or her social environment. This picture includes relevant information about the individual’s personality makeup and present level of functioning, as well as information about the stressors and resources in her or his life situation. For example, early in the process, clinicians may act as puzzle solvers, absorbing as much information about the client as possible—present feelings, attitudes, memories, demo- graphic facts—and trying to fit the pieces together into a meaningful pattern. Clinicians typically formulate hypoth- eses and discard or confirm them as they proceed. Starting with a global technique such as a clinical interview, clini- cians may later select more specific assessment tasks or tests. The following are some of the psychosocial proce- dures that may be used.
Assessment Interviews An assessment interview, often considered the central element of the assessment process, usually involves a
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observable criteria for diagnosis and provides specific guidelines for making diagnostic judgments. “Winging it” has limited use in this type of assessment process. The operational approach leads to more reliable psychiatric diagnoses, perhaps at some cost in reduced interviewer flexibility. It is also important to consider racial or ethnic factors when conducting diagnostic interviews. Recent research indicates (Alcántara & Gone, 2014) that the inter- view process and outcome can be substantially influenced by the ethnicity of the interviewer and the client.
The Clinical Observation of Behavior One of the traditional and most useful assessment tools that a clinician has available is direct observation of a client’s characteristic behavior (Hartmann et al., 2004). The main purpose of direct observation is to learn more about the person’s psychological functioning by attending to his or her appearance and behavior in various contexts. In clinical observation the clinician provides an objective description of the person’s appearance and behavior—her or his per- sonal hygiene and emotional responses and any depres- sion, anxiety, aggression, hallucinations, or delusions she or he may manifest. Ideally, clinical observation takes place in a natural environment (such as observing a child’s behavior in a classroom or at home), but it is more likely to take place upon admission to a clinic or hospital (Leichtman, 2009). For example, a brief description is usually made of a sub- ject’s behavior upon hospital admission, and more detailed observations are made periodically on the ward.
Some practitioners and researchers use a more con- trolled, rather than a naturalistic, behavioral setting for conducting observations in contrived situations. These analogue situations, which are designed to yield information about the person’s adaptive strategies, might involve such tasks as staged role-playing, event reenactment, family interaction assignments, or think-aloud procedures (Haynes et al., 2009).
In addition to making their own observations, many clinicians enlist their clients’ help by providing them instruction in self-monitoring: self-observation and objec- tive reporting of behavior, thoughts, and feelings as they occur in various natural settings. This method can be a valuable aid in determining the kinds of situations in which maladaptive behavior is likely to be evoked, and numerous studies also show it to have therapeutic benefits in its own right. Alternatively, a client may be asked to fill out a more or less formal self-report or a checklist concern- ing problematic reactions experienced in various situa- tions. Many instruments have been published in the professional literature and are commercially available to clinicians. These approaches recognize that people are excellent sources of information about themselves. Assum- ing that the right questions are asked and that people are
questions are asked in an unplanned way, important crite- ria needed for a DSM-5 diagnosis might be skipped. Responses based on unstructured interviews are difficult to quantify or compare with responses of clients from other interviews. Thus, the use of unstructured interviews in mental health research is limited. On the positive side, cli- ents may view unstructured interviews as being more sen- sitive to their needs or problems than more structured procedures. Moreover, the spontaneous follow-up ques- tions that emerge in an unstructured interview can, at times, provide valuable information that would not emerge in a structured interview.
During an assessment interview, a clinician obtains information about various aspects of a patient’s situation, behavior, and personality makeup. The interview is usually conducted face to face and may have a relatively open structure or be more tightly controlled, depending on the goals and style of the clinician.
The reliability of an assessment interview may be enhanced by the use of rating scales that help focus inquiry and quantify the interview data. For example, an individ- ual may be rated on a 3-, 5-, or 7-point scale with respect to self-esteem, anxiety, and various other characteristics. Such a structured and preselected format is particularly effective in obtaining a comprehensive impression, or “profile,” of the subject and her or his life situation and in revealing specific problems or crises—such as marital difficulties, drug dependence, or suicidal fantasies—that may require immediate therapeutic intervention.
Clinical interviews can be subject to error because they rely on human judgment to choose the questions and pro- cess the information. Evidence of this unreliability includes the fact that different clinicians have often arrived at differ- ent formal diagnoses on the basis of the interview data they elicited from a particular client. It is chiefly for this reason that recent versions of the DSM have emphasized an “operational” assessment approach, one that specifies
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Rating scales based on contemporary diagnostic sys- tems, the ICD-10 and DSM-5, are available. The DSM-5 (American Psychiatric Association, 2013) provides several rating scales, called “Cross-Cutting Symptom Measures,” that clinicians can use to obtain the symptom experiences of clients and for follow-up evaluations of symptoms over time. The rating scales are completed by the client (or some by the practitioner) or by the parent/custodian if the patient is a child or adolescent. The WHO provides a widely used rating scale for mental health and health prob- lems, called the WHODAS 2.0 (WHO, 2014b).
Psychological Tests Interviews and behavioral observation are relatively direct attempts to determine a person’s beliefs, attitudes, and problems. Psychological tests are a more indirect means of assessing psychological characteristics. Scientifically devel- oped psychological tests (as opposed to the recreational ones sometimes appearing in magazines or on the Internet) are standardized sets of procedures or tasks for obtaining samples of behavior (see American Psychological Associa- tion, 2014; Kolen & Hendrickson, 2013). A subject’s responses to the standardized stimuli are compared with those of other people who have comparable demographic characteristics, usually determined through established
willing to disclose information about themselves, the results can have a crucial bearing on treatment planning.
RATING SCALES As in the case of interviews, the use of rating scales in clinical observation and in self-reports helps both to organize information and to encourage reliability and objectivity (Aiken, 1996; Garb, 2007). That is, the formal structure of a scale is likely to keep observer inferences to a minimum. The most useful rating scales are those that enable a rater to indicate not only the presence or absence of a trait or behavior but also its prominence or degree. The following item is an example from such a rating scale; the observer would check the most appropriate description.
Sexual Behavior
____ 1. Sexually assaultive: aggressively approaches males or females with sexual intent.
____ 2. Sexually soliciting: exposes genitals with sexual intent, makes overt sexual advances to other patients or staff, and masturbates openly.
____ 3. No overt sexual behavior: not preoccupied with discussion of sexual matters.
____ 4. Avoids sex topics: made uneasy by discussion of sex, becomes disturbed if approached sexually by others.
____ 5. Excessive prudishness about sex: considers sex filthy, condemns sexual behavior in others, becomes panic-stricken if approached sexually.
Ratings like these may be made not only as part of an initial evaluation but also to check on the course or outcome of treatment. One of the rating scales most widely used for recording observations in clinical practice and in psychiatric research is the Brief Psychiatric Rating Scale (BPRS) (Leucht, 2014; Overall & Hollister, 1982). The BPRS provides a structured and quantifiable format for rating clinical symp- toms such as overconcern with physical symptoms, anxiety, emotional withdrawal, guilt feelings, hostility, suspicious- ness, and unusual thought patterns. It contains 24 scales that are scored from ratings made by a clinician following an interview with a patient. The distinct patterns of behavior reflected in the BPRS ratings enable clinicians to make a stan- dardized comparison of their patients’ symptoms with the behavior of other patients in mental health settings. The BPRS has been found to be an extremely useful instrument in clinical research (e.g., see Davidson et al., 2004), especially for the purpose of assigning patients to treatment groups on the basis of similarity in symptoms. However, it is not widely used for making treatment or diagnostic decisions in clinical practice. The Hamilton Rating Scale for Depression (HRSD), a similar but more specifically targeted instrument, is one of the most widely used procedures for selecting research sub- jects who are clinically depressed and also for assessing the response of such subjects to various treatments (see Beevers & Miller, 2004; Brown et al., 2007).
A wide variety of psychological tests have been developed that measure the intellectual abilities of children. The researcher in this photo is measuring this child’s cognitive development by evaluating how she classifies and sorts the candy.
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INTELLIGENCE TESTS A clinician can choose from a wide range of intelligence tests. The Wechsler Intelligence Scale for Children–Revised (WISC-IV) (see Weiss et al., 2006) and the current edition of the Stanford-Binet Intelli- gence Scale (Kamphaus & Kroncke, 2004) are widely used in clinical settings for measuring the intellectual abilities of children (Wasserman, 2003). Probably the most commonly used test for measuring adult intelligence is the Wechsler Adult Intelligence Scale–Revised (WAIS-IV) (Lichtenberger & Kaufman, 2009; Weiss et al., 2013). It includes both ver- bal and performance material and consists of 15 subtests. A brief description of two of the subtests will serve to illus- trate the types of functions the WAIS-IV measures.
• Vocabulary (verbal): This subtest consists of a list of words to define that are presented orally to the indi- vidual. This task is designed to evaluate knowledge of vocabulary, which has been shown to be highly related to general intelligence.
• Digit span (performance): In this test of short-term memory, a sequence of numbers is administered orally. The individual is asked to repeat the digits in the order administered. Another task in this subtest involves the individual remembering the numbers, holding them in memory, and reversing the order sequence—that is, the individual is instructed to say them backward (Lichtenberger & Kaufman, 2009).
test norms or test score distributions. From these compari- sons, a clinician can then draw inferences about how much the person’s psychological qualities differ from those of a reference group, typically a psychologically normal one. Among the characteristics that these tests can measure are coping patterns, motive patterns, personality characteris- tics, role behaviors, values, levels of depression or anxiety, and intellectual functioning. Impressive advances in the technology of test development have made it possible to create instruments of acceptable reliability and validity to measure almost any conceivable psychological characteris- tic on which people may vary. Moreover, many procedures are available in a computer-administered and computer- interpreted format (see the Developments in Practice box).
Although psychological tests are more precise and often more reliable than interviews or some observational techniques, they are far from perfect tools. Their value often depends on the competence of the clinician who interprets them. In general, they are useful diagnostic tools for psychologists in much the same way that blood tests, X-ray films, and MRI scans are useful to physicians. In all these cases, pathology may be revealed in people who appear to be normal, or a general impression of “some- thing wrong” can be checked against more precise infor- mation. Two general categories of psychological tests for use in clinical practice are intelligence tests and personality tests (projective and objective).
Developments in Practice The Automated Practice: Use of the Computer in Psychological Testing
Perhaps the most dramatic innovation in clinical assessment dur- ing the past 40 years has been the increasing use of computers in individual assessment. Computers are effectively used in assessment both to gather information directly from an individual and to assemble and evaluate all the information that has been gathered previously through interviews, tests, and other assess- ment procedures. By comparing the incoming information with data previously stored in its memory banks, a computer can per- form a wide range of assessment tasks (Butcher et al., 2009; Butcher, 2013). It can supply a probable diagnosis, indicate the likelihood of certain kinds of behavior, suggest the most appro- priate form of treatment, predict the outcome, and print a sum- mary report concerning the subject. In many of these functions, a computer is actually superior to a clinician because it is more efficient and accurate in recalling stored material (Epstein & Klinkenberg, 2001; Olson, 2001).
With the increased efficiency and reliability of computers one might expect a nearly unanimous welcoming of them into clinical practice. Luxton, Pruitt, and Osenbach (2014) have noted a broad acceptance of automated assessment through “telehealth technologies” that can be used to conduct psycho- logical evaluations. However, new technologies are not always
accepted or readily applied; a few hold-outs continue to resist using such “modern” techniques as e-mail, fax machines, and computerized billing in their practices (McMinn et al., 1999). Some clinicians are reluctant to use computer-based test inter- pretations (Rabin et al., 2014) in spite of their demonstrated util- ity and low cost. Even though most clinics and independent practitioners use microcomputers for record keeping and billing purposes, a smaller number incorporate computer-based clini- cal assessment procedures into their practice. Possible reasons for the underutilization of computer-based assessment proce- dures include the following: (1) Practitioners who were trained before the widespread use of computers may feel uncomfort- able with them or may not have time to get acquainted with their use; (2) they may limit their practice to psychological treatment and do not use extensive pretreatment assessments in their practice; (3) they may have little interest in, or time for, the sys- tematic evaluation of treatment efficacy that periodic formal assessments facilitate; or (4) they may feel that the impersonal and mechanized look of the keyboard or booklets and answer sheets common to much computerized assessment is inconsis- tent with the image and style of warm and personal engagement they hope to convey to clients.
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PROJECTIVE PERSONALITY TESTS A great many tests have been designed to measure personal characteristics other than intellectual ability. It is customary to group these personality tests into projective and objective mea- sures. Projective personality tests are unstructured in that they rely on various ambiguous stimuli such as inkblots or vague pictures rather than on explicit verbal questions, and in that the person’s responses are not limited to the “true,” “false,” or “cannot say” variety. Through their interpretations of these ambiguous materials, people reveal a good deal about their personal preoccupations, conflicts, motives, coping techniques, and other personality charac- teristics. An assumption underlying the use of projective techniques is that in trying to make sense out of vague, unstructured stimuli, individuals “project” their own prob- lems, motives, and wishes into the situation. Such responses are akin to the childhood pastime of seeing objects or scenes in cloud formations, with the important exception that the stimuli are in this case fixed and largely the same for all subjects. It is the latter circumstance that permits determination of the normative range of responses to the test materials, which in turn can be used to identify objectively deviant responding. Thus, projective tests are aimed at discovering the ways in which an individual’s past learning and personality structure may lead him or her to organize and perceive ambiguous information from the environment. Prominent among the several projective tests in common use are the Rorschach Inkblot Test, the Thematic Apperception Test (TAT), and sentence comple- tion tests.
The Rorschach The Rorschach Inkblot Test is named after the Swiss psychiatrist Hermann Rorschach (1884–1922), who initiated the experimental use of inkblots in personality assessment in 1911. And, even though the Rorschach test was developed over a century ago, it is still widely used in evaluating people with mental health problems. The test uses 10 inkblot pictures, to which a subject responds in suc- cession after being instructed as follows (Exner, 1993):
People may see many different things in these inkblot pictures; now tell me what you see, what it makes you think of, what it means to you.
The following excerpts are taken from a subject’s responses to one of the actual blots:
This looks like two men with genital organs exposed. They have had a terrible fight and blood has splashed up against the wall. They have knives or sharp instruments in their hands and have just cut up a body. They have already taken out the lungs and other organs. The body is dismembered . . . nothing remains but a shell . . . the pel- vic region. They were fighting as to who will complete the final dismemberment . . . like two vultures swooping down . . . .
Individually administered intelligence tests—such as the WISC-IV, the WAIS-IV, and the Stanford-Binet— typically require 2 to 3 hours to administer, score, and interpret. In many clinical situations, there is not enough time or funding to use these tests. In cases where intellec- tual impairment or organic brain damage is thought to be central to a patient’s problem, however, intelligence testing may be the most crucial diagnostic procedure in the test battery. Moreover, information about cognitive functioning or deterioration can provide valuable clues to a person’s intellectual resources in dealing with problems (Kihlstrom, 2002). Yet in many clinical settings and for many clinical cases, gaining a thorough understanding of a client’s prob- lems and initiating a treatment program do not require knowing the kind of detailed information about intellec- tual functioning that these instruments provide. In these cases, intelligence testing is not recommended.
David Wechsler (1896–1981) served in the military, testing army recruits during World War I. He came to believe that the ways in which psychologists viewed and measured “intelligence” was inadequate. In 1934 he began construction of the most widely used adult intelligence test battery, the Wechsler Adult Intelligence Scale (WAIS), which set the standard for practical measurement of intelligence.
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Meyer, 2009), the Rorschach test has also been widely crit- icized as an instrument with low or negligible validity (Garb et al., 1998; Hunsley & Bailey, 1999). A new inter- pretive system has recently been developed in an effort to provide a more effective system than the Exner Rorschach Comprehensive System (see Meyer et al., 2011).
The use of the Rorschach in clinical assessment has diminished somewhat (Butcher et al., 2013; Piotrowski et al., 1998), in part because insurance companies do not pay for the considerable amount of time needed to administer, score, and interpret the test. However, the Rorschach remains one of the most frequently used instruments in personality assessment (see Choca, 2012, for an introduction).
The Thematic Apperception Test The Thematic Apper- ception Test (TAT) was introduced in 1935 by its authors, C. D. Morgan and Henry Murray of the Harvard Psycho- logical Clinic. It still is widely used in clinical practice (Rossini & Moretti, 1997) and personality research (Teglasi, 2010). The TAT uses a series of simple pictures, some highly representational and others quite abstract, about which a subject is instructed to make up stories. The con- tent of the pictures, much of them depicting people in var- ious contexts, is highly ambiguous as to actions and motives, so subjects tend to project their own conflicts and worries onto it (see Morgan, 2002, for a historical descrip- tion of the test stimuli).
Several scoring and interpretation systems have been developed to focus on different aspects of a subject’s stories such as expressions of needs (Atkinson, 1992), the person’s perception of reality (Arnold, 1962), and the person’s fanta- sies (Klinger, 1979). It is time consuming to apply these sys- tems, and there is little evidence that they make a clinically significant contribution. Hence, most often a clinician sim- ply makes a qualitative and subjective determination of how the story content reflects the person’s underlying traits, motives, and preoccupations. Such interpretations often depend as much on “art” as on “science,” and there is much room for error in such an informal procedure.
An example of the way a subject’s problems may be reflected in TAT stories is shown in the following case, which is based on Card 1 (a picture of a boy staring at a violin on a table in front of him). The client, David, was a 15-year-old boy who had been referred to the clinic by his parents because of their concern about his withdrawal and poor work at school.
David’s TAT Response
David was generally cooperative during the testing, although he remained rather unemotional and unenthusiastic throughout. When he was given Card 1 of the TAT, he paused for over a minute, care- fully scrutinizing the card.
The extremely violent content of this response was not common for this particular blot or for any other blot in the series. Although no responsible examiner would base con- clusions on a single instance, such content was consistent with other data from this subject, who was diagnosed as an antisocial personality with strong hostility.
Use of the Rorschach in clinical assessment is compli- cated and requires considerable training (Exner & Erdberg, 2002; Weiner & Meyer, 2009). Methods of administering the test vary; some approaches can take several hours and hence must compete for time with other essential clinical services. Furthermore, the results of the Rorschach can be unreliable because of the subjective nature of test interpre- tations. For example, interpreters might disagree on the symbolic significance of the response “a house in flames.” One person might interpret this particular response as sug- gesting great feelings of anxiety, whereas another inter- preter might see it as suggesting a desire on the part of the patient to set fires. One reason for the diminished use of the Rorschach in projective testing today comes from the fact that many clinical treatments used in today’s mental health facilities generally require specific behavioral descriptions rather than descriptions of deep-seated per- sonality dynamics, such as those that typically result from interpretation of the Rorschach test.
In the hands of a skilled interpreter, however, the Rorschach can be useful in uncovering certain psychody- namic issues, such as the impact of unconscious motiva- tions on current perceptions of others (Weiner, 2013). Furthermore, attempts have been made to objectify Ror- schach interpretations by clearly specifying test variables and empirically exploring their relationship to external cri- teria such as clinical diagnoses (Exner, 1995). The Ror- schach, although generally considered an open-ended, subjective instrument, has been adapted for computer interpretation (Exner, 1987). In a study of the reliability of conclusions drawn from the computer interpretation sys- tem, Meyer and colleagues (2005) found that clinicians tended to draw the same conclusions from Rorschach responses as the computer system did.
Some researchers, however, have raised questions about the norms on which the Exner Rorschach Compre- hensive System, a scoring and interpretation system, is based (Shaffer et al., 1999; Wood et al., 2001) or on the validity of some of the measures (Wood et al., 2015). The Rorschach was shown to “overpathologize” persons tak- ing the test—that is, the test appears to show psychopa- thology even when the person is a “normal” person randomly drawn from the community. The extent to which the Rorschach provides valid information beyond what is available from other, more economical instru- ments has not been demonstrated. Although some researchers have rallied support for the comprehensive system (Hibbard, 2003; Mihura et al., 2013, 2015; Weiner &
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sentences that an adult might be asked to complete, as in these examples:
1. I wish _________________________________________
2. My mother _____________________________________
3. Sex ____________________________________________
4. I hate __________________________________________
5. People ________________________________________
Sentence completion tests, which are related to the free-association method, a procedure in which a client is asked to respond freely, are somewhat more structured than the Rorschach and most other projective tests. They help examiners pinpoint important clues to an individual’s problems, attitudes, and symptoms through the content of her or his responses. Interpretation of the item responses, however, is generally subjective and unreliable. Despite the fact that the test stimuli (the sentence stems) are stan- dard, interpretation is usually done in an ad hoc manner and without benefit of normative comparisons.
In sum, projective tests have an important place in many clinical settings, particularly those that attempt to obtain a comprehensive picture of a person’s psychody- namic functioning and those that have the necessary trained staff to conduct extensive individual psychological evaluations. The great strengths of projective techniques— their unstructured nature and their focus on the unique aspects of personality—are at the same time their weak- nesses because they make interpretation subjective, unreli- able, and difficult to validate. Moreover, projective tests typically require a great deal of time to administer and advanced skill to interpret—both scarce quantities in many clinical settings.
OBJECTIVE PERSONALITY TESTS Objective personality tests are structured—that is, they typically use question- naires, self-report inventories, or rating scales in which questions or items are carefully phrased and alternative responses are specified as choices. They therefore involve a far more controlled format than projective devices and thus are more amenable to objectively based quantifica- tion. One virtue of such quantification is its precision, which in turn enhances the reliability of test outcomes.
A large number of personality assessment measures are available for use in personality and clinical assessment. For example, the NEO-PI (Neuroticism-Extroversion- Openness Personality Inventory) provides information on the major dimensions in personality and is widely used in evaluating personality factors in normal-range populations (Costa & Widiger, 2002). In addition, many objective assessment instruments have been developed to assess focused clinical problems. For example, the Millon Clinical Multiaxial Inventory (MCMI-III; see Choca, 2004) was developed to evaluate the underlying personality
“I think this is a . . . uh . . . machine gun . . . yeah, it’s a machine gun. The guy is staring at it. Maybe he got it for his birthday or stole it or something.” [Pause. The examiner reminded him that he was to make up a story about the picture.]
“OK. This boy, I’ll call him Karl, found this machine gun . . . a Browning automatic rifle . . . in his garage. He kept it in his room for protection. One day he decided to take it to school to quiet down the jocks that lord it over everyone. When he walked into the locker hall, he cut loose on the top jock, Amos, and wasted him. Nobody bothered him after that because they knew he kept the BAR in his locker.”
It was inferred from this story that David was experiencing a high level of frustration and anger in his life. The extent of this anger was reflected in his perception of the violin in the picture as a machine gun—an instrument of violence. The clinician concluded that David was feeling threatened not only by people at school but even in his own home, where he needed “protection.”
This example shows how stories based on TAT cards may provide a clinician with information about a person’s conflicts and worries as well as clues as to how the person is handling these problems.
The TAT has been criticized on several grounds (Lilienfeld et al., 2001). There is a “dated” quality to the test stimuli: The pictures, developed in the 1930s, appear quaint to many contemporary subjects, who have diffi- culty identifying with the characters in the pictures. Subjects often preface their stories with statements like “This is something from a movie I saw on the late-night movies.” Additionally, the TAT can require a great deal of time to administer and interpret. As with the Ror- schach, interpretation of responses to the TAT is gener- ally subjective, which limits the reliability and validity of the test.
A review (Rossini & Moretti, 1997) pointed out an interesting paradox: Even though the TAT remains popu- lar among practicing clinicians, clinical training programs have reduced the amount of time devoted to teaching graduate students about the TAT, and relatively few con- temporary training resources (such as books and manuals) exist. Again, we must note that some examiners, notably those who have long experience in the instrument’s use, are capable of making astonishingly accurate interpreta- tions with TAT stories. Typically, however, they have dif- ficulty teaching these skills to others. On reflection, such an observation should not be unduly surprising, but it does point to the essentially “artistic” element involved at this skill level.
Sentence Completion Test Another projective procedure that has proved useful in personality assessment is the sentence completion test (Fernald & Fernald, 2010). A number of such tests have been designed for children, ado- lescents, and adults. Such tests consist of the beginnings of
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150 times and used in over 46 countries; Butcher, 2010.) International use of the revised inventory is increasing rapidly; over 32 translations have been made since it was published in 1989 (Butcher & Williams, 2009).
The Validity and Clinical Scales of the MMPI The original MMPI, a self-report questionnaire, consisted of 550 items covering topics ranging from physical condition and psy- chological states to moral and social attitudes. Typically, cli- ents are encouraged to answer all of the items either “true” or “false.” The pool of items was originally administered to a large group of normal individuals (affectionately called the “Minnesota normals”) and several quite homogeneous groups of patients with particular psychiatric diagnoses. Answers to all the items were then item-analyzed to see which ones differentiated the various groups. On the basis of the findings, the 10 clinical scales were constructed, each consisting of the items that were answered by one of the patient groups in the direction opposite to the predominant response of the normal group. This rather ingenious method of selecting scorable items, known as “empirical keying,” originated with the MMPI and doubtless accounts for much of the instrument’s power. Note that it involves no subjec- tive prejudgment about the “meaning” of a true or false answer to any item; that meaning resides entirely in whether the answer is the same as the answer deviantly
given by patients of varying diagnoses. Should an examinee’s pattern of true and false responses closely approximate that of a particular pathological group, it is a reasonable inference that he or she shares other psychiatrically significant characteristics with that group—and may in fact “psychologically” be a mem- ber of that group. (See the MMPI-2 pro- file in Table 4.1.)
Each of these 10 clinical scales thus measures tendencies to respond in psy- chologically deviant ways. Raw scores on these scales are compared with the corresponding scores of the normal population, many of whom did (and do) answer a few items in the critical direction (suggesting psychological problems), and the results are plotted on the standard MMPI profile form. By drawing a line connecting the scores for the different scales, a clinician can con- struct a profile that shows how far from normal a patient’s performance is on each of the scales. To reiterate the basic
strategy with an example, the Schizophrenia scale is made up of the items that patients diagnosed with schizophre- nia consistently answered in a way that differentiated
dimensions among clients in psychological treatment or prior to the beginning of therapy. In this chapter, we focus primarily on the most widely used personality assessment instrument, the MMPI-2.
The MMPI One of the major structured inventories for personality assessment is the Minnesota Multiphasic Personality Inventory (MMPI), now called the MMPI-2 for adults after a revision in 1989 (Butcher, 2011; Friedman et al., 2015). We focus on it here because in many ways it is the prototype and the standard for this class of instruments.
Several years in development, the MMPI was intro- duced for general use in 1943 by Starke Hathaway and J. C. McKinley; it is today the most widely used personal- ity test for clinical and forensic (court-related) assessment and for psychopathology research in the United States (Archer et al., 2006; Lally, 2003). (For a comprehensive dis- cussion of the use of the MMPI-2 in court testimony, see Butcher et al., 2015.) The MMPI-2 is also the personality assessment instrument most frequently taught in graduate clinical psychology programs (Ready & Veague, 2014). Over 19,000 books and articles on the MMPI instruments have been published since the test was introduced. More- over, translated versions of the inventory are widely used internationally. (The original MMPI was translated over
Starke R. Hathaway (1903–1984), clinical psychologist, was a pioneer in physiological psychology and personality assessment. In 1940, he and J. C. McKinley published the Minnesota Multiphasic Personality Inventory for evaluating the symptoms and behavior of psychiatric and medical patients. The MMPI became the most widely used personality assessment instrument in use, and its revised version (MMPI-2) is the most frequently used personality measure today.
J. C. McKinley (1891–1950), a neuropsychiatrist at the University of Minnesota Hospital, coauthored the MMPI with Starke Hathaway and conducted research on the MMPI with both medical and psychiatric populations.
Clinical Assessment and Diagnosis 123
insights. In addition to the validity scales and the 10 clini- cal scales, a number of additional scales have been devised—for example, to detect substance abuse, marital distress, and posttraumatic stress disorder.
Clinically, the MMPI is used in several ways to evalu- ate a patient’s personality characteristics and clinical prob- lems. Perhaps the most typical use of the MMPI is as a diagnostic standard. As we have seen, the individual’s profile pattern is compared with profiles of known patient groups. If the profile matches a group, information about patients in this group can suggest a broad descriptive diag- nosis for the patient under study.
Revision of the Original MMPI The original MMPI, in spite of being the most widely used personality measure, has not been without its critics. Some psychodynamically
them from normal individuals. People who score high (relative to norms) on this scale, though not necessarily schizophrenic, often show characteristics typical of that clinical population. For instance, high scorers on this scale may be socially inept, may be withdrawn, and may have peculiar thought processes; they may have diminished contact with reality and, in severe cases, may have delu- sions and hallucinations.
The MMPI also includes a number of validity scales to detect whether a patient has answered the questions in a straightforward, honest manner. For example, there is one scale that detects lying by one’s claiming of extreme virtue and several scales that detect possible malingering or fak- ing of symptoms. Extreme endorsement of the items on any of these scales may invalidate the test, whereas lesser endorsements frequently contribute important interpretive
Table 4.1 The Scales of the MMPI-2
Validity Scales
Cannot say score (?) Measures the total number of unanswered items
Infrequency scale (F) Measures the tendency to falsely claim or exaggerate psychological problems in the first part of the booklet; alternatively, detects random responding
Infrequency scale (FB) Measures the tendency to falsely claim or exaggerate psychological problems on items toward the end of the booklet
Infrequency scale (Fp) Measures the tendency to exaggerate psychological problems among psychiatric inpatients
Lie scale (L) Measures the tendency to claim excessive virtue or to try to present an overall favorable image
Defensiveness scale (K) Measures the tendency to see oneself in an unrealistically positive way
Superlative Self-Presentation scale (S) Measures the tendency for some people to present themselves in a highly positive manner or superlative manner. The S scale contains five subscales that address ways in which the person presents in an overly positive manner
Response Inconsistency scale (VRIN) Measures the tendency to endorse items in an inconsistent or random manner
Response Inconsistency scale (TRIN) Measures the tendency to endorse items in an inconsistently true or false manner
Clinical Scales
Scale 1 Hypochondriasis (Hs) Measures excessive somatic concern and physical complaints
Scale 2 Depression (D) Measures symptomatic depression
Scale 3 Hysteria (Hy) Measures hysteroid personality features such as a “rose-colored glasses” view of the world and the ten- dency to develop physical problems under stress
Scale 4 Psychopathic deviate (Pd) Measures antisocial tendencies
Scale 5 Masculinity-femininity (Mf) Measures gender-role reversal
Scale 6 Paranoia (Pa) Measures suspicious, paranoid ideation
Scale 7 Psychasthenia (Pt) Measures anxiety and obsessive, worrying behavior
Scale 8 Schizophrenia (Sc) Measures peculiarities in thinking, feeling, and social behavior
Scale 9 Hypomania (Ma) Measures unrealistically elated mood state and tendencies to yield to impulses
Scale 0 Social introversion (Si) Measures social anxiety, withdrawal, and overcontrol
Special Scales
Scale APS Addiction Proneness scale Assesses the extent to which the person matches personality features of people in substance use treatment
Scale AAS Addiction Acknowledgment scale Assesses the extent to which the person has acknowledged substance abuse problems
Scale MAC-R MacAndrew Addiction scale An empirical scale measuring proneness to become addicted to various substances
Scale MDS Marital Distress scale Assesses perceived marital relationship problems
Hostility scale (Ho) Addresses hostility or anger control problems
Posttraumatic Stress scale (Pk) Assesses a number of symptoms and attitudes that are found among people who are experiencing post- traumatic stress problems
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involved the MMPI. Over 50 years ago, psychologists at the Mayo Clinic programmed a computer to score and interpret clinical profiles. Computerized personality assessment has evolved substantially during the past few years, and other highly sophisticated MMPI and MMPI-2 interpretation systems have been developed (Butcher et al., 2004). Computer-based MMPI interpretation systems typi- cally employ powerful actuarial procedures (Grove et al., 2000). In such systems, descriptions of the actual behavior or other established characteristics of many subjects with particular patterns of test scores have been stored in the computer. Whenever a person has one of these test score patterns, the appropriate description is printed out in the computer’s evaluation. Such descriptions have been writ- ten and stored for a number of different test score patterns, most of them based on MMPI-2 scores.
The accumulation of precise actuarial data for an instrument like the MMPI-2 is difficult, time consuming, and expensive. This is in part because of the complexity of the instrument itself; the potential number of signifi- cantly different MMPI-2 profile patterns is legion. The profiles of many subjects therefore do not “fit” the profile types for which actuarial data are available. Problems of actuarial data acquisition also arise at the other end: the behaviors or problems that are to be detected or predicted by the instrument. Many conditions that are of vital clini- cal importance are relatively rare (for example, suicide) or are psychologically complex (for example, possible psy- chogenic components in a patient’s physical illness). Thus, it is difficult to accumulate enough cases to serve as an adequate actuarial database. In these situations, the interpretive program writer is forced to fall back on gen- eral clinical lore and practical experience to formulate clinical descriptions appropriate to the types of profiles actually obtained.
Sometimes the different paragraphs generated by the computer have inconsistencies resulting from the fact that different parts of a subject’s test pattern call up different paragraphs from the computer. The computer simply prints out blindly what has been found to be typical for people making similar scores on the various clinical scales and cannot integrate the descriptions it picks up. At this point the human element comes in: In the clinical use of computers, it is always essential that a trained profes- sional further interpret and monitor the assessment data (Atlis et al., 2006).
Computerized personality assessment is no longer a novelty but an important, dependable adjunct to clinical assessment. Computerized psychological evaluations are a quick and efficient means of providing a clinician with needed information early in the decision-making process. Examples of computer-generated descriptions for the case of Andrea C., presented in the next section, appear in the evaluations reprinted in the Developments in Practice box.
oriented clinicians felt that the MMPI (like other struc- tured, objective tests) was superficial and did not ade- quately reflect the complexities of an individual taking the test. Some behaviorally oriented critics, on the other hand, criticized the MMPI (and in fact, the entire genre of personality tests) as being too oriented toward measur- ing unobservable “mentalistic” constructs such as traits. A more specific criticism was leveled at the datedness of the MMPI.
In response to these criticisms, the publisher of the MMPI sponsored a revision of the instrument. The scales listed on the standard original MMPI-2 profile form are described in Table 4.1. This revised MMPI, designated “MMPI-2” for adults, became available for general profes- sional use in mid-1989 (Butcher, 2011; Butcher et al., 2001), and the MMPI-A for adolescents (see Williams & Butcher, 2011) was published in 1992. The original 10 clinical scales were kept on the revised version. The revised versions of the MMPI have been validated in many clinical studies (Greene, 2011).
Research has provided strong support for the revised versions of the MMPI (Friedman et al., 2015; Greene et al., 2003). The clinical scales, which, apart from minimal item deletion or rewording, have been retained in their original form, seem to measure the same properties of personality organization and functioning as they always have. A com- parable stability of meaning is observed for the standard validity scales (also essentially unchanged), which have been reinforced with three additional scales to detect ten- dencies to respond untruthfully to some items.
Advantages and Limitations of Objective Personality Tests Self-report inventories such as the MMPI have a number of advantages over other types of personality tests. They are cost effective, highly reliable, and objective; they also can be scored and interpreted (and, if desired, even administered) by computer. A number of general criticisms, however, have been leveled against the use of self-report inventories. As we have seen, some clinicians consider them too mechanistic to portray the complexity of human beings and their problems accurately. Also, because these tests require the subject to read, compre- hend, and answer verbal material, patients who are illiter- ate or confused cannot take the tests. Furthermore, the individual’s cooperation is required in self-report invento- ries, and it is possible that the person might distort his or her answers to create a particular impression. The validity scales of the MMPI-2 are a direct attempt to deal with this last criticism.
Because of their scoring formats and emphasis on test validation, scientifically constructed objective personality inventories lend themselves particularly well to automated interpretation. The earliest practical applications of com- puter technology to test scoring and interpretation
Clinical Assessment and Diagnosis 125
Andrea suffered a number of physical injuries and recurring symptoms from the assault and was hospitalized for 8 days following the attack. Her symptoms included a fractured skull, fractured nose, multiple stab wounds on her body, facial injuries, dizziness, impaired balance, wrist pain, residual cognitive symptoms from being uncon- scious, poor memory, intense anxiety, and symptoms of posttraumatic stress. After recovery from the physical inju- ries she was fearful to return to work, and she applied for disability as a result of her injuries. The company for which she worked rejected her request, and she filed a lawsuit for personal injury disability.
A psychological evaluation was requested by the company’s insurer to determine the legitimacy of Andrea’s disability claim. As a central part of the evalua- tion, the MMPI-2 was administered by the psychologist hired by the defense to appraise Andrea’s personality and symptoms (see the validity, clinical, and supplementary profiles shown in Figures 4.1 and 4.2). The MMPI-2 clini- cal scale pattern shows clear mental health problems. Her clinical scale pattern with the high scores on the D (Depression), Hs (Hypochondriasis), and Pt (Anxiety)
The Case of Andrea C.: Experiencing Violence in the Workplace 4.4 Evaluate the case study of a woman who
experienced violence in the workplace.
Andrea C., a 49-year-old divorced woman, was employed as a manager in a firm whose office was located in a somewhat isolated section of the community. Her respon- sibilities included opening the office building at 6:00 a.m. and preparing the office activities for the day. She felt somewhat unsafe in opening up the office alone and had complained to upper management about the lack of secu- rity in the building. One morning, as she was opening the office door, she was accosted by a stranger who hit her on the head, knocking her unconscious, breaking her nose, and cutting her face and neck. The assailant stabbed her several times in her leg and attempted to sexually assault her, but ran away with her purse as car lights came on the street.
MMPI-2 VALIDITY PATTERN
Raw Score: 10 10 12 8 1 4 13 20
T Score: 70 58T 79 74 49 52 46 43
Response %: 100 100 100 100 100 100 100 100
VRIN
30
Cannot Say (Raw): 0
Percent True: 50
Percent False: 50
Raw Score T Score Resp.%
S1 - Beliefs in Human Goodness 4 40 100 S2 - Serenity 1 33 100 S3 - Contentment with Life 4 52 100 S4 - Patience/Denial of Irritability 5 53 100 S5 - Denial of Moral Flaws 5 61 100
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MMPI®-2 Outpatient Mental Health Interpretive Report 08/01/2008, Page 2
ID: AC
Figure 4.1 Profile of the MMPI-2 validity scales for Andrea C.
(Excerpted from The Minnesota Report™: Adult Clinical System-Revised, 4th Edition, by James N. Butcher.)
MMPI®-2 Outpatient Mental Health Interpretive Report 08/01/2008, Page 3
ID: AC
Raw Score: 25 41 39 24 31 13 36 39 20 48 19 26 3 26 30 *
K Correction: 7 5 13 13 3
T Score: 90 94 89 66 62 59 90 90 59 72 50 58 56 77 66 *
Response %: 100 100 100 100 100 100 100 100 100 100 100 100 100 100 100 *
Welsh Code: 2178*3”0’4+5-69/F’+-L/K:
Profile Elevation: 79.6
*MDS scores are reported only for clients who indicate that they are married or separated.
MMPI-2 CLINICAL AND SUPPLEMENTARY SCALES PROFILE
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D HyHs Pd Mf Pa Pt Sc Ma Si MAC-R APS AAS PK Ho MDS
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Figure 4.2 Profile of the MMPI-2 clinical scales and supplementary scales for Andrea C.
(Excerpted from The Minnesota Report™: Adult Clinical System-Revised, 4th Edition, by James N. Butcher.)
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EVALUATING ANDREA’S COMPUTER-GENERATED MMPI-2 REPORT The narrative report of the computer- based MMPI-2 interpretation contains technical test infor- mation to assist the assessment psychologist in interpreting the test results. The report is considered a professional-to- professional consultation and is not recommended for release to patients. The computer report for Andrea con- tains detailed data about the relative frequency of the test pattern’s occurrence in relevant clinical settings and in the normative or standardized population. For example, the report provides information as to how Andrea’s elevated clinical scale scores compare with persons being evaluated in an outpatient clinical setting as well as the frequency of the score in the MMPI-2 general normative sample of women. Her test results indicated that her highest score, the Depression scale score, typically occurs in 18.7 percent of the outpatient women. Moreover, only 4.4 percent of women in the normative sample obtain this high elevation on the Depression scale. Thus, this high Depression scale elevation is considered to be a relatively common symptom among women seeking outpatient mental health services.
scales, along with the high score obtained on the PTSD scale, indicate that she is experiencing mental health symptoms related to stressful life events. A full descrip- tion of this symptom picture is presented in the computer- based interpretive report shown in the Developments in Practice box.
Interestingly, the insurance company’s psychological expert recommended against Andrea’s receiving compen- sation based on his interpretation of a controversial psy- chological scale (referred to as the Fake Bad Scale, or FBS) that was designed to assess “malingering.” After an initial hearing to examine the validity and acceptability of the FBS, the judge in the case prohibited the use of the scale as a measure of effort, malingering, or overreporting of symp- toms to bolster his opinion.
The case went to trial, and Andrea’s attorneys relied on the medical evidence and results of the MMPI-2 to sup- port her claim of physical damages and posttraumatic adjustment problems. The jury awarded Andrea substan- tial damages as a result of the injuries and the trauma that she experienced from the assault.
Developments in Practice Computer-Based MMPI-2 Report for Andrea C.
Profile Validity This client endorsed a number of psychological problems, sug- gesting that she is experiencing a high degree of stress. Although the MMPI-2 clinical scale profile is probably valid, it may show some exaggeration of symptoms. In addition, please note that the client’s approach to the MMPI-2 items was somewhat inconsis- tent. She endorsed items in a pattern that suggests some care- lessness or inattention to content.
Symptomatic Patterns Her profile configuration, which incorporates correlates of Hs and D, is not as clearly defined as those of many other clients from this clinical setting. In interpreting the profile, the practitioner should also consider any prominent clinical scale elevations that are close in elevation to the prototype. This client’s profile presents a broad and mixed picture in which physical complaints and depressed affect are likely to be salient features. The client is exhibiting much somatic distress and may be experiencing a problem with her psychological adjustment. Her physical com- plaints are probably extreme, possibly reflecting a general lack of effectiveness in life. There are likely to be long-standing personal- ity problems predisposing her to develop physical symptoms under stress. She is probably feeling quite tense and nervous, and she may be feeling that she cannot get by without help for her physical problems. She is likely to be reporting a great deal of pain, and she feels that others do not understand how sick she is feeling. She may be quite irritable and may become hostile if her symptoms are not given “proper” attention.
Many individuals with this profile have a history of psycho- physiological disorders. They tend to overreact to minor problems with physical symptoms. Ulcers and gastrointestinal distress are common. The possibility of actual organic problems, therefore, should be carefully evaluated. Individuals with this profile report a great deal of tension and a depressed mood. They tend to be pessimistic and gloomy in their outlook.
In addition, the following description is suggested by the cli- ent’s scores on the content scales. She endorsed a number of items suggesting that she is experiencing low morale and a depressed mood. She reports a preoccupation with feeling guilty and unworthy. She feels that she deserves to be punished for wrongs she has committed. She feels regretful and unhappy about life, and she seems plagued by anxiety and worry about the future. She feels hopeless at times and feels that she is a con- demned person. She has difficulty managing routine affairs, and the items she endorsed suggest a poor memory, concentration problems, and an inability to make decisions. She appears to be immobilized and withdrawn and has no energy for life. She views her physical health as failing and reports numerous somatic con- cerns. She feels that life is no longer worthwhile and that she is losing control of her thought processes.
According to her response content, there is a strong possibil- ity that she has seriously contemplated suicide. She feels some- what self-alienated and expresses some personal misgivings or a vague sense of remorse about past acts. She feels that life is unre- warding and dull, and she finds it hard to settle down. The client’s response content suggests that she feels intensely fearful about a large number of objects and activities. This hypersensitivity and
Clinical Assessment and Diagnosis 127
fearfulness appear to be generalized at this point and may be debilitating to her in social and work situations.
Long-term personality factors identified by other scale eleva- tions may help provide a clinical context for the symptoms she is presently experiencing. She apparently holds some unusual beliefs that appear to be disconnected from reality. Her high score on one MMPI-2 scale, the PSYC (Psychoticism) scale, suggests that she often feels alienated from others and might experience unusual symptoms such as delusional beliefs, circumstantial and tangential thinking, and loose associations. She also shows a meager capacity to experience pleasure in life. Persons with high scores on another MMPI-2 scale, the INTR (Introversion/Low Positive Emotionality), tend to be pessimistic.
Profile Frequency Profile interpretation can be greatly facilitated by examining the relative frequency of clinical scale patterns in various settings. The client’s high-point clinical scale score (D) occurred in 7.0 percent of the MMPI-2 normative sample of women. However, only 4.4 per- cent of the women had D scale peak scores at or above a T score of 65, and only 2.1 percent had well-defined D spikes. Her ele- vated MMPI-2 profile configuration (1-2/2-1) is rare in samples of normals, occurring in 1.0 percent of the MMPI-2 normative sample of women.
This high-point MMPI-2 score is the most frequent clinical scale score in various samples of outpatient women. In the Pearson outpatient sample, the high-point clinical scale score on D occurred in 18.7 percent of the women. Moreover, 17.1 percent of the out- patient women had the D scale spike at or above a T score of 65, and 9.0 percent had well-defined D spikes. Her elevated MMPI-2 profile configuration (1-2/2-1) occurred in 2.9 percent of the women in the Pearson outpatient sample.
Profile Stability The relative elevation of her clinical scale scores suggests that her profile is not as well defined as many other profiles. There was no difference between the profile type used to develop the present report (involving Hs and D) and the next highest scale in the profile code. Therefore, behavioral elements related to elevations on Pt should be considered as well. For example, intensification of anx- iety, negative self-image, and unproductive rumination could be important in her symptom pattern.
Interpersonal Relations She appears to be somewhat passive-dependent in relationships. She may manipulate others through her physical symptoms, and she may become hostile if sufficient attention is not paid to her complaints.
She is a very introverted person who has difficulty meeting and interacting with other people. She is shy and emotionally dis- tant. She tends to be very uneasy, rigid, and overcontrolled in social situations. Her shyness is probably symptomatic of a broader pattern of social withdrawal. Personality characteristics related to social introversion tend to be stable over time. Her gen- erally reclusive behavior, introverted lifestyle, and tendency toward interpersonal avoidance may be prominent in any future test results.
The client’s scores on the content scales suggest the follow- ing additional information concerning her interpersonal relations. She appears to be an individual who has rather cynical views about life. Any efforts to initiate new behaviors may be colored by her negativism. She may view relationships with others as threat- ening and harmful.
Diagnostic Considerations Individuals with this profile type are often seen as neurotic and may receive a diagnosis of somatoform disorder. Actual organic problems such as ulcers or hypertension might be part of the clinical picture. Some individuals with this profile have problems with abuse of pain medication or other prescription drugs.
Treatment Considerations Her view of herself as physically disabled needs to be considered in any treatment planning. She tends to somatize her difficulties and to seek medical solutions rather than deal with them psycho- logically. She seems to tolerate a high level of psychological con- flict and may not be motivated to deal with her problems directly. She is probably not a strong candidate for psychotherapy treat- ment approaches that require self-scrutiny, insight development, and high motivation for change. Psychological treatment may progress more rapidly if her symptoms are dealt with through behavior modification techniques. However, with her generally pessimistic attitude and low energy resources, she seems to have little hope of getting better.
The client’s scores on the content scales seem to indicate low potential for change. She may feel that her problems are not addressable through therapy and that she is not likely to benefit much from psychological treatment at this time. Her apparently negative treatment attitudes may need to be explored early in therapy if treatment is to be successful.
She harbors many negative work attitudes that could limit her adaptability in the workplace. Her low morale and lack of interest in work could impair future adjustment to employment, a factor that should be taken into consideration in treatment.
Source: Excerpted from The Minnesota Report™: Adult Clinical System- Revised, 4th Edition, by James N. Butcher.
The reader should also note that some of the scales mentioned in the computer narrative report for Andrea are not listed in Table 4.1. There are a number of other MMPI-2 scales in the literature and in common use with the MMPI-2 that are not listed due to space restrictions in this book. For example, the MMPI-2 has 15 content-based
scales, that is, scales that are comprised of homogeneous content themes (such as Negative Work Attitudes, Family Problems, and Type-A Behavior). These scales address specific problem themes in patients with mental health challenges. Five additional scales, referred to as the Psy- chopathology Five (PSY-5) scales, address the personality
128 Chapter 4
with the decisions to be made regarding treatment. By put- ting together all the information they have gathered, they can see whether the findings complement each other and form a definitive clinical picture or whether gaps or dis- crepancies exist that necessitate further investigation.
This integration of all the data gathered at the time of an original assessment may lead to agreement on a tenta- tive diagnostic classification for a patient. In any case, the findings of each member of the team, as well as the recom- mendations for treatment, are entered into the case record so that it will always be possible to check back and see why a certain course of therapy was undertaken, how accurate the clinical assessment was, and how valid the treatment decision turned out to be.
New assessment data collected during the course of therapy provide feedback on the therapy’s effectiveness and serve as a basis for making needed modifications in an ongoing treatment program. As we have noted, clinical assessment data are also commonly used in evaluating the progress of therapy and in comparing the effectiveness of different therapeutic and preventive approaches.
Ethical Issues in Assessment The decisions made on the basis of assessment data may have far-reaching implications for the people involved. A staff decision may determine whether a person with severe depression will be hospitalized or remain with her or his family, or whether an accused person will be declared com- petent to stand trial. Thus, a valid decision, based on accu- rate assessment data, is of far more than theoretical importance. Because of the impact that assessment can have on the lives of others, it is important that those involved keep several factors in mind when evaluating test results:
1. Potential cultural bias of the instrument or the clinician: Some psychological tests may not elicit valid informa- tion for a patient from a minority group (Gray-Little, 2009; Wen-Shing & Streltzer, 2008). A clinician from one sociocultural background may have trouble assessing objectively the behavior of someone from another back- ground. It is important to ensure—as Greene and col- leagues (2003) and Zapata-Sola and colleagues (2009) have shown with the MMPI-2—that the instrument can be confidently used with persons from minority groups.
2. Theoretical orientation of the clinician: Assessment is inevitably influenced by a clinician’s assumptions, per- ceptions, and theoretical orientation. For example, a psychoanalyst and a behaviorist might assess the same behaviors quite differently. The psychoanalytically ori- ented professional is likely to view behaviors as reflect- ing underlying motives, whereas the behavioral clini- cian is likely to view the behaviors in the context of the immediate or preceding stimulus situations. Different treatment recommendations are likely to result.
disorder content domains that are referred to as the “Big 5” personality dimensions. These personality dimensions include Aggressiveness, Psychoticism, Disconstraint, Negative Emotionality/Neuroticism, and Introversion/ Low Positive Emotionality.
in review • Distinguish between structured and unstructured clinical assess-
ment interviews.
• What are the assumptions behind the use of projective personal- ity tests? How do they differ from objective tests?
• What advantages do objective personality tests offer over less structured tests?
• What is the Minnesota Multiphasic Personality Inventory (MMPI-2)? Describe how the MMPI-2 scales work.
The Integration of Assessment Data 4.5 Discuss how practitioners integrate assessment
data in treatment planning.
As assessment data are collected, their significance must be interpreted so that they can be integrated into a coherent working model for use in planning. Clinicians in individ- ual private practice normally assume this complicated task on their own. In a clinic or hospital setting, assessment data are often evaluated in a staff conference attended by members of an interdisciplinary team (perhaps consisting of a clinical psychologist, a psychiatrist, a social worker, and other mental health personnel) who are concerned
In a clinic or hospital setting, assessment data are usually evaluated in a staff conference attended by members of an interdisciplinary team—including, for example, a clinical psychologist, a psychiatrist, a social worker, and a psychiatric nurse. A staff decision may determine whether a person with severe depression will be hospitalized or remain with his or her family or whether an accused person will be declared competent to stand trial. Because these decisions can have such great impact on the lives of the clients, it is critical that clinicians be well aware of the limitations of assessment.
Clinical Assessment and Diagnosis 129
difficulty in recognizing the essential features of “dog- ness.” “Dogness” is an example of what psychologists refer to as a “cognitive prototype” or “pattern.”
In abnormal psychology, classification involves the attempt to delineate meaningful subvarieties of maladap- tive behavior. Like defining abnormal behavior, classifica- tion of some kind is a necessary first step toward introducing order into our discussion of the nature, causes, and treatment of such behavior. Classification makes it possible to communicate about particular clusters of abnormal behavior in agreed-on and relatively precise ways. For example, we cannot conduct research on what might cause eating disorders unless we begin with a more or less clear definition of the behavior under examination; otherwise, we would be unable to select, for intensive study, persons whose behavior displays the aberrant eat- ing patterns we hope to understand. There are other rea- sons for diagnostic classifications, too, such as gathering statistics on how common the various types of disorders are and meeting the needs of medical insurance companies (which insist on having formal diagnoses before they will authorize payment of claims).
Keep in mind that, just as with the process of defining abnormality itself, all classification is the product of human invention—it is, in essence, a matter of making generaliza- tions based on what has been observed. Even when obser- vations are precise and carefully made, the generalizations we arrive at go beyond those observations and enable us to make inferences about underlying similarities and differ- ences. For example, it is common for people experiencing episodes of panic to feel they are about to die. When “panic” is carefully delineated, we find that it is not in fact associated with any enhanced risk of death but, rather, that the people experiencing such episodes tend to share cer- tain other characteristics, such as recent exposure to highly stressful events.
It is not unusual for a classification system to be an ongoing work in progress as new knowledge demonstrates an earlier generalization to be incomplete or flawed. It is important to bear in mind, too, that formal classification is successfully accomplished only through precise techniques of psychological, or clinical, assessment—techniques that have been increasingly refined over the years.
Differing Models of Classification Three basic approaches are currently used to classify abnormal behavior: the categorical, the dimensional, and the prototypal (Widiger & Boyd, 2009).
THE CATEGORICAL APPROACH The categorical approach, like the diagnostic system of general medical diseases, assumes (1) that all human behavior can be divided into the categories of “healthy” and “disordered,” and (2) that within the latter there exist discrete, nonoverlapping
3. Underemphasis on the external situation: Many clini- cians overemphasize personality traits as the cause of patients’ problems without paying enough attention to the possible role of stressors and other circumstances in the patients’ life situations. An undue focus on a patient’s personality, which some assessment tech- niques encourage, can divert attention from poten- tially critical environmental factors.
4. Insufficient validation: Some psychological assess- ment procedures in use today have not been suffi- ciently validated. For example, unlike many of the per- sonality scales, widely used procedures for behavioral observation and behavioral self-report and the projec- tive techniques have not been subjected to strict psy- chometric validation.
5. Inaccurate data or premature evaluation: There is always the possibility that some assessment data— and any diagnostic label or treatment based on them— may be inaccurate or that the team leader (usually a psychiatrist) might choose to ignore test data in favor of other information. Some risk is always involved in making predictions for an individual on the basis of group data or averages. Inaccurate data or premature conclusions may not only lead to a misunderstanding of a patient’s problem but also close off attempts to get further information, with possibly grave consequences for the patient.
in review • What are some ethical issues that clinicians should be aware of
when evaluating a patient’s test results?
• Are there concerns over cultural biases in some psychological tests?
• What is test validity?
Classifying Abnormal Behavior 4.6 Explain the process for classifying abnormal
behavior.
Classification is important in any science, whether we are studying chemical elements, plants, planets, or people. With an agreed-on classification system we can be confi- dent that we are communicating clearly. If someone says to you, “I saw a dog running down the street,” you can prob- ably produce a mental image broadly approximating the appearance of that dog—not from seeing it but rather from your knowledge of animal classifications. There are of course many breeds of dogs, which vary widely in size, color, muzzle length, and so on, and yet we have little
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prototypical case of each personality disorder rather than having a listing of diagnostic criteria as it now has. The diagnostician could indicate on a 5-point scale the extent to which a patient matches this description. The clinician would simply rate the overall similarity or “match” between a patient and the prototype.
As we shall see, the official diagnostic criteria defining the various recognized classes of mental disorder, although explicitly intended to create categorical entities, more often than not result in prototypal ones. The central features of the various identified disorders are often somewhat vague, as are the boundaries purporting to separate one disorder from another. Much evidence suggests that a strict categor- ical approach to identifying differences among types of human behavior, whether normal or abnormal, may well be an unattainable goal. Bearing this in mind as we pro- ceed may help you avoid some confusion. For example, we commonly find that two or more identified disorders regu- larly occur together in the same individual—a situation known as comorbidity. Does this really mean that such a person has two or more entirely separate and distinct dis- orders? In the typical instance, probably not.
Formal Diagnostic Classification of Mental Disorders Today, two major psychiatric classification systems are in use: the International Classification of Diseases (ICD-10) system, pub- lished by the WHO, and the Diagnostic and Statistical Manual of Mental Disorders (DSM-5), published by the American Psy- chiatric Association. The ICD-10 system is widely used in Europe and many other countries, whereas the DSM system is the standard guide for the United States. Both systems are similar in many respects, such as in using symptoms as the focus of classification and in dividing problems into different facets (to be described in the section that follows).
Certain differences in the way symptoms are grouped in these two systems can sometimes result in a different classification on the DSM than on the ICD-10. We will focus on the DSM system in our discussion of what is to be con- sidered a mental disorder. The DSM specifies what sub- types of mental disorders are currently officially recognized and provides, for each, a set of defining criteria in the United States and some other countries. As already noted, the system purports to be a categorical one with sharp boundaries separating the various disorders from one another, but it is in fact a prototypal one with much fuzzi- ness of boundaries and considerable interpenetration, or overlap, of the various “categories” of disorder it identifies.
The criteria that define the recognized categories of dis- order consist for the most part of symptoms and signs. The term symptoms generally refers to the patient’s subjective description, the complaints she or he presents about what is wrong. Signs, on the other hand, are objective observations
classes or types of disorder that have a high degree of within-class homogeneity in both symptoms displayed and the underlying organization of the disorder identified.
THE DIMENSIONAL APPROACH The dimensional and prototypal approaches differ fundamentally in the assump- tions they make, particularly with respect to the require- ment of discrete and internally homogeneous classes of behavior. In the dimensional approach, it is assumed that a person’s typical behavior is the product of differing strengths or intensities of behavior along several definable dimen- sions such as mood, emotional stability, aggressiveness, gen- der identity, anxiousness, interpersonal trust, clarity of thinking and communication, social introversion, and so on. The important dimensions, once established, are the same for everyone. People are assumed to differ from one another in their configuration or profile of these dimensional traits (each ranging from very low to very high), not in terms of behavioral indications of a corresponding “dysfunctional” entity presumed to underlie and give rise to the disordered pattern of behavior (Miller et al., 2004; Widiger et al., 2012). “Normal” is discriminated from “abnormal,” then, in terms of precise statistical criteria derived from dimensional inten- sities among unselected people in general, most of whom may be presumed to be close to average, or mentally “nor- mal.” We could decide, for example, that anything above the 97th normative percentile on aggressiveness and anything below the 3rd normative percentile on sociability would be considered “abnormal” findings.
Dimensionally based diagnosis has the incidental ben- efit of directly addressing treatment options. Because the patient’s profile of psychological characteristics will nor- mally consist of deviantly high and low points, therapies can be designed to moderate those of excessive intensity (e.g., anxiety) and to enhance those that constitute deficit status (e.g., inhibited self-assertiveness).
Of course, in taking a dimensional approach, it would be possible (perhaps even probable) to discover that such profiles tend to cluster together in types—and even that some of these types are correlated, though imperfectly, with recognizable sorts of gross behavioral malfunctions such as anxiety disorders or depression. It is highly unlikely, however, that any individual’s profile will exactly fit a narrowly defined type or that the types identified will not have some overlapping features. This brings us to the prototypal approach.
THE PROTOTYPAL APPROACH A prototype (as the term is used here) is a conceptual entity (e.g., personality disor- der) depicting an idealized combination of characteristics that more or less regularly occur together in a less-than- perfect or standard way at the level of actual observation. Westen, Shedler, and Bradley (2006), for example, suggest that the DSM should provide a narrative description of a
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The number of recognized mental disorders has increased enormously from DSM-I to DSM-5 due both to the addition of new diagnoses and to the elaborate subdi- vision of older ones. Because it is unlikely that the nature of the American psyche has changed much in the interim period, it seems more reasonable to assume that mental health professionals view their field in a different light than they did 50 years ago. The DSM system is now both more comprehensive and more finely differentiated into subsets of disorders. Most diagnostic categories in DSM-5 contain a listing of subtypes and specifiers that allow the diagnostician to further refine the diagnosis in order to provide more specific subgroupings of patients.
GENDER DIFFERENCES IN DIAGNOSIS In the origin and manifestation of mental health symptoms, gender dif- ferences have long been noted for some disorders. Some disorders show a higher prevalence rate for male patients (such as antisocial personality) than females; other disor- ders (such as anorexia) are more prominently found in females. Moreover, males and females who are diagnosed with the same disorder (such as conduct disorder) often show different symptom patterns. Males have a higher rate of fighting and aggression, and females have a greater ten- dency to lie and be truant from school and they tend to run away from home. The DSM-5 allows for gender-related differences to be incorporated into the diagnosis.
APPRAISAL OF CULTURAL BACKGROUND IN DSM-5 The United States is a highly diverse society that is com- prised of people from multiple language and cultural back- grounds. Increasingly today, mental health practitioners find themselves engaged in a diagnostic evaluation of a cli- ent from a diverse background and with marginal or lim- ited English language skills. The client’s ethnicity and cultural background, level of English language compre- hension, religious background, and extent of their acclima- tion to the United States can result in incorrect appraisal of mental health symptoms. People who have not been accul- turated to the environment in which they live can appear more psychologically disturbed on tests and interviews than they actually are (Okazaki et al., 2009). It is extremely important for the clinician to carefully appraise the client’s background, including the values and attitudes they might bring to the interview, in order to reduce negative impact on the decision-making process.
The DSM-5 provides a structured interview that focuses on the patient’s approach to problems. The Cul- tural Formulation Interview (CFI) contains 16 questions that the practitioner can use to obtain information during a mental health assessment about the potential impact the client’s culture can have on mental health care. The interview questions inquire about patients’ perspectives on their present problems, how they perceive the influence of others
that the diagnostician may make either directly (such as the patient’s inability to look another person in the eye) or indi- rectly (such as the results of pertinent tests administered by a psychological examiner). To make any given diagnosis, the diagnostician must observe the particular criteria—the symptoms and signs that the DSM indicates must be met (see Black & Andreasen, 2014).
THE EVOLUTION OF THE DSM The DSM is currently in its fifth edition (DSM-5), published in 2013 after consider- able debate and controversy. This system is the product of more than a six-decade evolution involving increasing refinement and precision in the identification and descrip- tion of mental disorders. The first edition of the manual (DSM-I) appeared in 1952 and was largely an outgrowth of attempts to standardize diagnostic practices in use among military personnel during World War II. The 1968 DSM-II reflected the additional insights gleaned from a markedly expanded postwar research effort in mental health spon- sored by the federal government. Over time, practitioners recognized a defect in both these early efforts: The various types of disorders identified were described in narrative and jargon-laden terms that proved too vague for mental health professionals to agree on their meaning. The result was a serious limitation of diagnostic reliability; that is, two professionals examining the same patient might very well come up with completely different impressions of what disorder(s) the patient had. DSM-III (1980) and DSM-IV-TR (2000) provided further modification and elaboration of disorders with efforts to make the diagnostic classification clearer. DSM-5 incorporated more theoretical shifts in diag- nostic thinking for many years and has been the most con- troversial alteration to diagnostic thinking to date. (See the Unresolved Issues at the end of this chapter.)
To address this clinical and scientific impasse, the DSM-III of 1980 introduced a radically different approach, one intended to remove, as much as possible, the element of sub- jective judgment from the diagnostic process. It did so by adopting an “operational” method of defining the various disorders that would officially be recognized. This innova- tion meant that the DSM system would now specify the exact observations that must be made for a given diagnostic label to be applied. In a typical case, a specific number of signs or symptoms from a designated list must be present before a diagnosis can properly be assigned. The new approach, continued in the DSM-III’s revised version of 1987 (DSM-III-R) and in the 1994 DSM-IV, clearly enhanced diagnostic reliability and made efforts to incorporate cul- tural and ethnic considerations. As an example of the opera- tional approach to diagnosis in DSM-5, see the diagnostic criteria for Persistent Depressive Disorder (Dysthemia) in Chapter 7. Note that the revised diagnostic system combines diagnostic criteria from two diagnoses from DSM-IV: Chronic Major Depression and Dysthymic Disorder.
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change has developed during the past 50 years: For years the traditional term for a person who goes to see a mental health professional was patient, a term that is closely asso- ciated with medical sickness and a passive stance, waiting (patiently) for the doctor’s cure. Today many mental health professionals, especially those trained in nonmedical set- tings, prefer the term client because it implies greater par- ticipation on the part of an individual and more responsibility for bringing about his or her own recovery. We use these terms interchangeably in this text.
LIMITED USEFULNESS OF DIAGNOSIS Keep in mind that a DSM diagnosis per se may be of limited usefulness. Arriving at a diagnosis is usually required, at least in the form of a “diagnostic impression,” before the commence- ment of clinical services. This is necessitated, perhaps unwisely, by medical insurance requirements and long- standing clinical administrative tradition. The additional information required for adequate clinical assessment may be extensive and extremely difficult to unearth. For the most part, in keeping with psychiatric tradition, that pro- cess is interview based. That is, the examiner engages the patient (or perhaps a family member of the patient) in a conversation designed to elicit the information necessary to place the patient in one or more DSM diagnostic catego- ries. The interviewer introduces various questions and probes, typically becoming increasingly specific as she or he develops diagnostic hypotheses and checks them out with additional probes related to the criteria for particular DSM diagnoses. Physicians in general medical practice do something similar in the course of an examination.
UNSTRUCTURED DIAGNOSTIC INTERVIEWS Like the assessment interviews described earlier, diagnostic inter- views are of two general types: unstructured and struc- tured. In the unstructured interview, the examiner follows no preexisting plan with respect to content and sequence of the probes introduced. Unstructured interviews, as their name implies, are somewhat freewheeling. The therapist/ clinician asks questions as they occur to him or her, in part on the basis of the responses to previous questions. For example, if the patient/client mentions a father who trav- eled a lot when he or she was a child, the clinician is free to ask, “Did you miss your father?” or (pursuing a different tack), “How did your mother handle that?” rather than being required to ask the next question in a predetermined list. Many clinical examiners prefer this unfettered approach because it enables them to follow perhaps idiosyncratic “leads.” In the preceding example, the clinician might have chosen to ask about the mother’s reaction on the basis of a developing suspicion that the mother may have been depressed during the client’s childhood years. There is one serious drawback to the freewheeling style, however: The information that an interview yields is limited to the content
in influencing their problems, and ways in which their cul- tural background can influence their adjustment. More- over, the interview inquires about patients’ previous expe- riences when seeking treatment for their problems. The interview questions attempt to obtain clients’ perspectives without typecasting their problems.
THE PROBLEM OF LABELING The psychiatric diagno- ses of the sort typified by the DSM system are not uni- formly revered among mental health professionals (e.g., MacCulloch, 2010; Sarbin, 1997). One important criticism is that a psychiatric diagnosis is little more than a label applied to a defined category of socially disapproved or otherwise problematic behavior.
The diagnostic label describes neither a person nor any underlying pathological condition (“dysfunction”) the per- son necessarily harbors but, rather, some behavioral pattern associated with that person’s current level of functioning. Yet once a label has been assigned, it may close off further inquiry. It is all too easy—even for professionals—to accept a label as an accurate and complete description of an individual rather than of that person’s current behavior. When a person is labeled “depressed” or “schizophrenic,” others are more likely to make certain assumptions about that person that may or may not be accurate. In fact, a diagnostic label can make it hard to look at the person’s behavior objectively, without preconceptions about how he or she will act. These expectations can influence even clinically important interac- tions and treatment choices. For example, arrival at the diag- nosis “persistent depressive disorder” may cut off any further inquiry about the patient’s life situation and lead abruptly to a prescription for antidepressant medication (Tucker, 1998), or the application of a label such as “borderline personality” might cause the mental health treatment staff to be less opti- mistic about the patient’s prognosis (Markham, 2003).
Once an individual is labeled, he or she may accept a redefined identity and play out the expectations of that role. (“I’m nothing but a substance abuser. I might as well do drugs—everyone expects me to anyway. Also, this is a condition deemed out of my control, so it is pointless for me to be an active participant in my treatment.”) This acquisition of a new social identity can be harmful for a variety of reasons. The pejorative and stigmatizing implica- tions of many psychiatric labels can mark people as second- class citizens with severe limitations that are often presumed to be permanent (Link, 2001; Slovenko, 2001). They can also have devastating effects on a person’s morale, self-esteem, and relationships with others. The person so labeled may decide that he or she “is” the diag- nosis and may thus adopt it as a life “career.”
Clearly, it is in the person with the disorder’s best interests for mental health professionals to be circumspect in the diagnostic process, in their use of labels, and in ensuring confidentiality with respect to both. A related
Clinical Assessment and Diagnosis 133
enormously from these developments. A number of struc- tured diagnostic interviews have been developed that can be used in various contexts. In clinical and research situa- tions, a popular instrument has been the Schedules for Clinical Assessment in Neuropsychiatry (SCAN), pub- lished by the WHO (1994), which enables the diagnostician to arrive at an ICD-10 diagnosis.
in review • Why is a classification system needed in abnormal psychology?
• What is the meaning of reliability and validity in the context of such a classification system?
• What is the difference between dimensional and prototypal clas- sification strategies?
• Describe the differences between structured and unstructured diagnostic interviews.
of that interview. Should another clinician conduct another unstructured interview of the same patient, he or she might come up with a different clinical picture.
STRUCTURED DIAGNOSTIC INTERVIEWS The struc- tured interview probes the client in a manner that is highly controlled (Daniel & Gurczynski, 2010; Mestre et al., 2013). Guided by a sort of master plan (sometimes to the extent of specifying the examiner’s exact wording), the clinician using a structured interview typically seeks to discover whether the person’s symptoms and signs “fit” diagnostic criteria that are more precise and “operational” than in the past. The use of more precise criteria and of highly struc- tured diagnostic interviewing has substantially improved diagnostic reliability, but the structured interview format is still used only sporadically in routine clinical work. Never- theless, the precision of clinical research, including epide- miological research to be discussed later, has profited
Unresolved Issues The DSM-5: Issues in Acceptance of Changed Diagnostic Criteria
Change is a part of life, and complex criteria such as those con- tained in the Diagnostic and Statistical Manual can become obso- lete or inadequate as a result of new research developments or changes in clinical practice requirements. As noted in Chapter 1, periodic updating of the diagnostic criteria is required to make them more effective and acceptable to the professional commu- nity. The revision of the diagnostic system that resulted in DSM-5 was an arduous task that was initiated in 2007 by the American Psychiatric Association. The revision program involved obtaining substantial input from numerous mental health professionals, both practitioners and researchers, before it was completed. Although many aspects of the DSM-IV-TR version were continued in the DSM-5 because of their clarity and broad acceptance, some cat- egories were modified, moved to different locations in the system, or even dropped. Moreover, a number of new diagnostic criteria were added. The revision process for the DSM generated sub- stantial controversy, and a number of critics have expressed their concerns over various changes (see the Thinking Critically box in Chapter 1 as well as discussions by Alarcón et al., 2009; Batstra & Frances, 2012a, 2012b; Jones, 2012; Kornstein, 2010).
One of the most widely discussed problems with the earlier diagnostic manuals was the manner in which personality disor- ders were classified, that is, in a categorical rather than dimen- sional system. Earlier in this chapter, we described the differing approaches to categorizing personality disorders from the dimen- sional versus the prototypal perspective. (This topic will be con- sidered in greater detail in Chapter 10.) The debates between the proponents of each classification are likely to continue (see also the comprehensive discussion provided by O’Donohue et al., 2007). The DSM-5 system will likely require substantial time and effort to overcome issues and various viewpoints on conceptual- izing personality disorders in order to produce a model that will be useful both in clinical diagnosis and in guiding research.
Personality disorders are not the only diagnostic catego- ries that required significant rethinking. Other categories, such as posttraumatic stress disorder (PTSD), have been found to be unclear in many respects and limited or overly narrow in others (see Chapter 5). The earlier diagnostic manuals required direct involvement in an experienced trauma in order for the PTSD diag- nosis to be applied. However, as a result of experiences following the World Trade Center terrorist attack in 2001, many people who were “traumatized” by the unfolding saga through the constant media coverage of the events also experienced PTSD as a result of indirect exposure. Under the DSM-IV-TR, these circumstances would not apply, so the diagnostic classification of PTSD would be considered inappropriate. This requirement resulted in many authorities proposing a modification of the criteria to reduce this limitation (Marshall et al., 2007), while others remain concerned that such changes could result in a problematic expansion of the diagnosis of PTSD. For example, there is concern that the broad- ened classification would label people who might be experiencing “normal” grief as having a major depressive disorder (Frances, 2010b). This could result from a “medicalization of normal emo- tion” and could prompt some drug companies to “quickly and greedily” pounce on the opportunity to mount a marketing cam- paign for people who are bereaved (Frances, 2010b).
The diagnostic criteria for mental disorders in the DSM are not viewed by most mental health professionals as fixed-component systems but as workable criteria that evolve and develop to accom- modate new research and practical developments. The periodic remaking of the DSM is never a smooth transition, but the resulting system is, nevertheless, a valuable conceptual guide that provides an agreed-on language that students, practitioners, and research- ers can employ to enable clear communication about mental disor- ders. Frances and Widiger (2012) pointed out that the DSM system is “imperfect, but it is indispensable” (p. 111).
Summary 4.1 Identify the basic elements in assessment.
• Clinical assessment is one of the most important and complex responsibilities of mental health profession- als. The extent to which a person’s problems are understood and appropriately treated depends largely on the adequacy of the psychological assessment.
• The goals of psychological assessment include identi- fying and describing the individual’s symptoms; determining the chronicity and severity of the prob- lems; evaluating the potential causal factors in the per- son’s background; and exploring the individual’s personal resources that might be an asset in his or her treatment program.
4.2 Describe the factors involved in the assessment of the physical organism.
• Because many psychological problems have physical components, either as underlying causal factors or as symptom patterns, it is often important to include a medical examination in the psychological assessment.
• In cases where organic brain damage is suspected, it is important to conduct neurological tests—such as an EEG; a CAT, PET, or MRI scan; or an fMRI—to help determine the site and extent of organic brain disorder.
• For someone with suspected organic brain damage, a battery of neuropsychological tests might be recom- mended to determine whether or in what manner the underlying brain disorder is affecting her or his mental and behavioral capabilities.
4.3 Explain the interview process, clinical observation, and testing in psychosocial assessment.
• The most widely used and flexible psychosocial assess- ment methods are the clinical interview and behavior observation. There are two basic strategies in assess- ment by interview: structured and unstructured inter- view procedures. Clinical observation involves the clinician’s development of an objective description of the person’s appearance and behavior including emo- tional responses and mental health symptoms he or she may manifest.
• Psychological tests include standardized stimuli for collecting behavior samples that can be compared with other individuals’ behavior via test norms. Examples include intelligence and personality tests.
• Two different personality-testing approaches have evolved: (1) projective tests, such as the Rorschach or
the TAT, in which unstructured stimuli are presented to a subject, who then “projects” meaning or structure onto the stimulus, thereby revealing “hidden” motives, feelings, and so on; and (2) objective tests, or personal- ity inventories, in which a subject is required to read and respond to itemized statements or questions.
• Objectively scored personality tests, such as the MMPI-2 and MMPI-A, provide a cost-effective means of collect- ing a great deal of personality information rapidly.
4.4 Evaluate the case study of a woman who experienced violence in the workplace.
• Andrea C.’s case, involving a computer interpretation of the MMPI-2, illustrates the use of psychological assessment in describing mental health problems.
4.5 Discuss how practitioners integrate assessment data in treatment planning.
• Clinicians in individual private practice normally interpret assessment data and integrate it into a work- ing model for use in planning on their own.
• In a clinic or hospital setting, assessment data are often evaluated in a staff conference attended by members of an interdisciplinary team. By putting together all the information that has been gathered, the team can see whether the findings complement each other and form a clinical picture along with recommendations for treatment. Because of the impact such an assess- ment can have on the lives of others, it is important for those involved to keep several ethical factors in mind when evaluating test results.
4.6 Explain the process for classifying abnormal behavior.
• Three basic approaches are currently used for classify- ing abnormal behavior: the categorical, the dimen- sional, and the prototypal.
• Two major psychiatric classification systems are in use: the International Classification of Diseases (ICD-10) system, published by the WHO, and the Diagnostic and Statistical Manual of Mental Disorders (DSM-5), published by the American Psychiatric Association.
• The client’s gender, ethnicity, and cultural background are taken into consideration in the appraisal of mental health symptoms for a DSM diagnosis. Arriving at a diagnosis is usually required in mental health settings, at least in the form of a “diagnostic impression,” before the commencement of clinical services.
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Clinical Assessment and Diagnosis 135
actuarial procedures, p. 124 aphasia, p. 114 Brief Psychiatric Rating Scale
(BPRS), p. 117 clinical diagnosis, p. 107 comorbidity, p. 130 computerized axial tomography
(CAT) scan, p. 112 cultural competence, p. 109 dysrhythmia, p. 112 electroencephalogram (EEG), p. 111 forensic, p. 122 functional MRI (fMRI), p. 113 intelligence test, p. 118
magnetic resonance imaging (MRI), p. 112
Minnesota Multiphasic Personality Inventory (MMPI), p. 122
neuropsychological assessment, p. 114 objective personality tests, p. 121 personality tests, p. 119 positron emission tomography (PET)
scan, p. 112 presenting problem, p. 107 projective personality tests, p. 119 psychological assessment, p. 114 rating scales, p. 116 reliability, p. 110
role-playing, p. 116 Rorschach Inkblot Test, p. 119 self-monitoring, p. 116 sentence completion test, p. 121 signs, p. 130 standardization, p. 110 structured assessment
interview, p. 115 symptoms, p. 130 T score distribution, p. 110 Thematic Apperception Test (TAT), p. 120 unstructured assessment
interviews, p. 115 validity, p. 110
Key Terms
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Learning Objectives
5.1 Explain the factors that make people more stress sensitive and the characteristics of stressors that make them hardest to cope with.
5.2 Summarize how the body responds to stress.
5.3 Discuss how stress causes dysregulation in the immune system.
5.4 Describe the role that emotions play in physical health and identify helpful and harmful emotions.
5.5 Explain the psychological interventions that can be used to reduce stress and treat stress-related disorders.
5.6 Identify the similarities and differences between adjustment disorder, posttraumatic stress disorder, and acute stress disorder.
5.7 Describe the clinical features of and risk factors for posttraumatic stress disorder.
5.8 Explain the treatment approaches that are used to help people with PTSD.
Chapter 5
Stress and Physical and Mental Health
Stress and Physical and Mental Health 137
Day in and day out there was a never-ending flow of mangled bodies of young soldiers. Jennifer recalled one especially traumatic event:
I was working one evening. We received information that a vehicle, on a routine convoy mission, had been hit by an improvised explo- sive device (IED). Three wounded men and one dead soldier were on their way to our hospital. Two medics in the back room were processing the dead soldier for Mortuary Affairs. The dead soldier was lying on a cot. The air was strong with the smell of burned flesh. I was staring at the body and trying to grasp what was differ- ent about this particular body. After a while I realized. The upper chest and head of the dead soldier were completely missing. We received his head about an hour later. (Based on Feczer & Bjorklund, 2009).
With its deadlines, interpersonal tensions, financial pres- sures, and everyday hassles, daily life places many demands on us. We are all exposed to stress, and this expo- sure affects our physical and our psychological well-being. Sometimes even leisure activities can be stressful. For example, a loss in the Superbowl is followed by an increase in heart attacks and deaths over the following 2 weeks in the losing team’s city (Kloner et al., 2011). And watching a stressful soccer match more than doubles the risk of having acute cardiovascular problems (Wilbert-Lampen et al., 2008). How are you affected by stress? Does it make you anxious? Does it give you migraines?
After a Superbowl loss, heart attacks and deaths increase in the losing team’s city.
The field of health psychology is concerned with the effects of stress and other psychological factors in the development and maintenance of physical problems. Health psychology is a subspecialty within behavioral medicine. A behavioral medicine approach to physical ill- ness is concerned with psychological factors that may pre- dispose an individual to medical problems. These may include such factors as stressful life events, certain person- ality traits, particular coping styles, and lack of social sup- port. Within behavioral medicine there is also a focus on the effects of stress on the body, including the immune, endocrine, gastrointestinal, and cardiovascular systems.
But stress affects the mind as well as the body. As we discussed in Chapter 3, the role that stress can play in trigger- ing the onset of mental disorders in vulnerable people is explicitly acknowledged in the diathesis-stress model. More- over, exposure to extreme and traumatic stress may over- whelm the coping resources of otherwise apparently healthy people, leading to mental disorders such as posttraumatic stress disorder (PTSD), as in the following example.
Posttraumatic Stress in a Military Nurse
Jennifer developed PTSD after she served as a nurse in Iraq. During her deployment she worked 12- to 14-hour shifts in 120-degree temperatures. Sleep was hard to come by and disaster was routine.
In this chapter we consider the role that stress plays in the development of physical and mental disorders. We dis- cuss both physical and mental problems because the mind and the body are powerfully connected and because stress takes its toll on both. Although the problems that are linked to stress are many, we focus particularly on the most severe stress-related physical and mental disorders. In the physi- cal realm, we place an emphasis on heart disease. For men- tal disorders, we concern ourselves primarily with PTSD.
What Is Stress? 5.1 Explain the factors that make people more stress
sensitive and the characteristics of stressors that make them hardest to cope with.
Life would be very simple if all of our needs were auto- matically satisfied. In reality, however, many obstacles, both personal and environmental, get in the way. A prom- ising athletic career may be brought to an end by injury; we may have less money than we need; we may be rejected by the person we love. The demands of life require that we adjust. When we experience or perceive challenges to our physical or emotional well-being that exceed our coping resources and abilities, the psychological condition that results is typically referred to as stress (see Shalev, 2009). To avoid confusion, we will refer to external demands as stressors, to the effects they create within the organism as stress, and to efforts to deal with stress as coping strategies. It is also important to note that stress is fundamentally an interactive and dynamic construct because it reflects the interaction between the organism and the environment over time (Monroe, 2008).
All situations that require adjustment can be regarded as potentially stressful. Prior to the influential work of Canadian physician and endocrinologist Hans Selye (1956, 1976), stress was a term used by engineers. Selye took the word and used it to describe the difficulties and strains experienced by living organisms as they struggled to cope with and adapt to changing environmental conditions. His
138 Chapter 5
others. This may be linked, in part, to coping skills and the presence—or absence—of particular resources. Chil- dren, for example, are particularly vulnerable to severe stressors such as war and terrorism (Petrovic, 2004). Research also suggests that adolescents with parents who are depressed are more sensitive to stressful events; these adolescents are also more likely to have problems with depression themselves after experiencing stressful life events than those who do not have parents with depression (Bouma et al., 2008).
Individual characteristics that have been identified as improving a person’s ability to handle life stress include higher levels of optimism, greater psychological control or mastery, increased self-esteem, and better social support (Declercq et al., 2007; Taylor & Stanton, 2007). These stable factors are linked to reduced levels of distress in the face of life events as well as more favorable health outcomes. There is also some evidence from twin studies that differ- ences in coping styles may be linked to underlying genetic differences (Jang et al., 2007).
More generally, it is now widely accepted that our genetic makeup can render us more or less “stress sensi- tive.” Researchers are exploring genes that may play a role in determining how reactive to stress we are (Alexander et al., 2009; Armbruster et al., 2012). A major development in stress research was the discovery that a particular form of a particular gene (the 5HTTLPR gene) was linked to how likely it was that people would become depressed in the face of life stress. Caspi and colleagues (2003) found that people who had two “short” forms of this gene (the s/s gen- otype) were more likely to develop depression when they experienced four or more stressful life events than were people who had two “long” forms of this gene (the l/l gen- otype). Although this specific finding was controversial for a while, there is now clear support for the original result (Karg et al., 2011). Even more recent research has clarified that the interaction between the s carrier genotype (one or two s alleles) and life events is most marked for interper- sonal events (such as those involving loss or rejection) rather than for noninterpersonal life events that do not involve relationships (Vrshek-Schallhorn et al., 2013).
The amount of stress we experience early in life may also make us more sensitive to stress later on (Gillespie & Nemeroff, 2007; Lupien et al., 2009). The effects of stress may be cumulative, with each stressful experience serving to make the system more reactive. Evidence from animal studies shows that being exposed to a single stressful expe- rience can enhance responsiveness to stressful events that occur later (Johnson, O’Connor, et al., 2002). Rats that were exposed to stressful tail shocks produced more of the stress hormone cortisol when they were later exposed to another stressful experience (being placed on a platform). Other biological changes associated with stress were also more pronounced in these rats. These results suggest that prior
Stress and the DSM The relationship between stress and psychopathology is considered so important that the role of stress is recognized in diagnostic formulations. Nowhere is this more apparent than in the diagnosis of PTSD—a severe disorder that we will discuss in detail later. PTSD was classified as an anxi- ety disorder in DSM-IV-TR. However, DSM-5 introduced a new diagnostic category called trauma- and stressor- related disorders. PTSD is now included there. Some other disorders in this new category are adjustment disorder and acute stress disorder. These disorders involve patterns of psychological and behavioral disturbances that occur in response to identifiable stressors. The key differences among them lie not only in the severity of the disturbances but also in the nature of the stressors and the time frame during which the disorders occur.
Factors Predisposing a Person to Stress Everyone faces a unique pattern of demands to which he or she must adjust. This is because people perceive and interpret similar situations differently and also because, objectively, no two people are faced with exactly the same pattern of stressors. Some individuals are also more likely to develop long-term problems under stress than
Stress can result from both negative and positive events. Both types of stress can tax a person’s resources and coping skills, although distress (negative stress) typically has the potential to do more damage.
work provided the foundation for current stress research. Selye also noted that stress could occur not only in nega- tive situations (such as taking an examination) but also in positive situations (such as a wedding). Both kinds of stress can tax a person’s resources and coping skills, although bad stress (distress) typically has the potential to do more damage. Stress can also occur in more than one form—not just as a simple catastrophe but also as a continuous force that exceeds a person’s ability to manage it.
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which anyone has learned to cope. Likewise, recovery from the stress created by major surgery can be improved when a patient is given realistic expectations beforehand; know- ing what to expect adds predictability to the situation. In one study, patients who were about to undergo hip replace- ment surgery watched a 12-minute film the evening before they had the operation. The film described the entire proce- dure from the patient’s perspective. Compared to controls who did not see the film, patients who saw the video were less anxious on the morning of the surgery, were less anx- ious after the surgery, and needed less pain medication (Doering et al., 2000).
stressful experiences may sensitize us biologically, making us more reactive to later stressful experiences. The term stress tolerance refers to a person’s ability to withstand stress without becoming seriously impaired.
Stressful experiences may also create a self-perpetuating cycle by changing how we think about, or appraise, the things that happen to us. Studies have shown that stressful situations may be related to or intensified by a person’s cognitions (Nixon & Bryant, 2005). This may explain why people with a history of depression tend to experience negative events as more stressful than other people do (Havermans et al., 2007). For example, if you’re feeling depressed or anxious already, you may perceive a friend’s canceling a movie date as an indication that she doesn’t want to spend time with you. Even though the reality may be that a demand in her own life has kept her from keeping your date, when you feel bad you will be much more inclined to come to a negative conclusion about what just happened rather than see the situation in a more balanced or more optimistic way. Can you think of an example in your own life when something like this has happened to you?
Characteristics of Stressors Why is misplacing our keys so much less stressful than being in an unhappy marriage or being fired from a job? At some level we all intuitively understand what makes one stressor more serious than another. The key factors involve (1) the severity of the stressor, (2) its chronicity (i.e., how long it lasts), (3) its timing, (4) how closely it affects our own lives, (5) how expected it is, and (6) how controllable it is.
Stressors that involve the more important aspects of a person’s life—such as the death of a loved one, a divorce, a job loss, a serious illness, or negative social exchanges— tend to be highly stressful for most people (Aldwin, 2007; Newsom et al., 2008). Furthermore, the longer a stressor operates, such as might be the case with abuse and emo- tional neglect, or with living in poverty, the more severe its effects. Encountering a number of stressors at the same time also makes a difference. If a man loses his job, learns that his wife is seriously ill, and receives news that his son has been arrested for selling drugs, all at the same time, the resulting stress will be more severe than if these events had occurred separately over an extended period. Symptoms of stress also intensify when a person is more closely involved in an immediately traumatic situation. Learning that the uncle of a close friend was injured in a car accident is not as stressful as being in an accident oneself.
Extensive research has shown that events that are unpredictable and unanticipated (and for which no previ- ously developed coping strategies are available) are likely to place a person under severe stress. A devastating house fire and the damage it brings are not occurrences with
A devastating house fire is not an event we can anticipate. It is almost impossible to be psychologically prepared to experience a stressor such as this.
Unpredictable and uncontrollable events cause the greatest stress. These people are reacting to the collapse of the World Trade Center towers after the terrorist attacks of September 11, 2001.
Finally, with an uncontrollable stressor, there is no way to reduce its impact, such as by escape or avoidance. In general, both people and animals are more stressed by unpredictable and uncontrollable stressors than by stress- ors that are of equal physical magnitude but are either pre- dictable or controllable or both (e.g., Evans & Stecker, 2004; Maier & Watkins, 2010).
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Most of us experience occasional periods of especially acute (sudden and intense) stress. The term crisis is used to refer to times when a stressful situation threatens to exceed or exceeds the adaptive capacities of a person or a group. Crises are often especially stressful, because the stressors are so potent that the coping techniques we typically use do not work. Stress can be distinguished from crisis in this way: A traumatic situation or crisis overwhelms a person’s ability to cope, whereas stress does not necessarily over- whelm the person.
Measuring Life Stress Life changes, even positive ones such as being promoted or getting married, place new demands on us and may there- fore be stressful. And the faster life changes occur, the greater the stress that is experienced.
A major focus of research on life changes has con- cerned the measurement of life stress. Years ago, Holmes and Rahe (1967) developed the Social Readjustment Rat- ing Scale. This is a self-report checklist of fairly common, stressful life experiences (see also Chung et al., 2010; Cooper & Dewe, 2007). A version of this scale, developed specifically to assess life stress in college students, is shown in Figure 5.1.
Although easy to use, limitations of the checklist method later led to the development of interview-based approaches such as the Life Events and Difficulties Sched- ule (LEDS; Brown & Harris, 1978). One advantage of the LEDS is that it includes an extensive manual that pro- vides rules for rating both acute and chronic forms of stress. The LEDS system also allows raters to consider the context in which a life event occurs and take into account a person’s unique circumstances when rating each life event. For example, if a woman who is happily married and in good financial circumstances learns that she is going to have a baby, she may experience this news in a way that is quite different from that of an unmarried teen- ager who is faced with the prospect of having to tell her parents that she is pregnant. Although interview-based approaches are more time consuming and costly to administer, they are considered more reliable than check- list methods and are preferred for research in this area (see Monroe, 2008).
Resilience After experiencing a potentially traumatic event, some people function well and experience very few symptoms in the following weeks and months. This kind of healthy psy- chological and physical functioning after a potentially traumatic event is called resilience. You might be surprised to learn that resilience is not rare. In fact, resilience is the most common reaction following loss or trauma (Bonanno et al., 2011; Quale & Schanke, 2010).
Figure 5.1 How Stressed Are You? Sum all your ratings to get a total score of your life stress in the past year. In a large sample of undergraduates, the average score was 1,247, with a range from 182 to 2,571 (Renner & Mackin, 1998). Where does your stress score fall?
College Life Stress Inventory
Copy the “stress rating” number into the last column for any item that has happened to you in the last year, then add these.
Event Stress Ratings Your Items
Being raped 100 Finding out that you are HIV-positive 100 Being accused of rape 98 Death of a close friend 97 Death of a close family member 96 Contracting a sexually transmitted disease
(other than AIDS) 94
Concerns about being pregnant 91 Finals week 90 Concerns about your partner being
pregnant 90
Oversleeping for an exam 89 Flunking a class 89 Having a boyfriend or girlfriend cheat on you 85 Ending a steady dating relationship 85 Serious illness in a close friend or family
member 85
Financial difficulties 84 Writing a major term paper 83 Being caught cheating on a test 83 Drunk driving 82 Sense of overload in school or work 82 Two exams in one day 80 Cheating on your boyfriend or girlfriend 77 Getting married 76 Negative consequences of drinking
or drug use 75
Depression or crisis in your best friend 73 Difficulties with parents 73 Talking in front of a class 72 Lack of sleep 69 Change in housing situation (hassles, moves) 69 Competing or performing in public 69 Getting in a physical fight 66 Difficulties with a roommate 66 Job changes (applying, new job, work
hassles) 65
Declaring a major or concerns about future plans
65
A class you hate 62 Drinking or use of drugs 61 Confrontations with professors 60 Starting a new semester 58 Going on a first date 57 Registration 55 Maintaining a steady dating relationship 55 Commuting to campus or work, or both 54 Peer pressures 53 Being away from home for the first time 53 Getting sick 52 Concerns about your appearance 52 Getting straight A’s 51 A difficult class that you love 48 Making new friends; getting along with friends 47 Fraternity or Sorority rush 47 Falling asleep in class 40 Attending an athletic event (e.g., football
game) 20
Total
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of trauma. Although people with this kind of self-enhanc- ing style are sometimes unpleasant to interact with, such a style may serve them well in times of crisis. For example, in a prospective study, Gupta and Bonanno (2010) showed that college students with this self-enhancing style coped much better over a 4-year period than people who did not.
in review • What factors play a role in determining a person’s stress tolerance?
• What characteristics of stressors make them more serious and more difficult to adapt to?
• Describe two methods that can be used to measure life stress.
• What is resilience? Describe three factors that increase resilience and three factors that are associated with reduced resilience.
Stress and Physical Health 5.2 Summarize how the body responds to stress.
The biological cost of adapting to stress is called the allostatic load (Oken et al., 2015). When we are relaxed and not experi- encing stress, our allostatic load is low. When we are stressed and feeling pressured, our allostatic load is higher. Although efforts to relate specific stressors to specific medical problems have not generally been successful, stress is becoming a key underlying theme in our understanding of the development and course of virtually all physical illness. For example, a person with allergies may find his or her resistance further lowered by emotional tension. Similarly, when a virus has already entered a person’s body—as is thought to be the case in multiple sclerosis—emotional stress may interfere with the body’s normal defensive forces or immune system. In like manner, any stress may tend to aggravate and maintain certain disorders, such as migraine headaches (Milde-Busch et al., 2011) and rheumatoid arthritis (Cutolo & Straub, 2006).
But why are some people more resilient than others? Research suggests that no single factor predicts resilience. Rather, resilience is linked to a variety of different charac- teristics and resources. Factors that increase resilience include being male, being older, and being well educated. Having more economic resources is also beneficial. Some earlier studies suggested that, after the 9/11 attacks in New York, African Americans and members of some Latino groups fared more poorly and showed lower levels of resil- ience compared to whites. However, race and ethnicity are often confounded with social class. Importantly, when social class is controlled for, statistics show that race and ethnicity are no longer predictive of reduced resiliency.
It also helps to be a positive person. Research shows that people who can still show genuine positive emotions when talking about their recent loss also tend to adjust better after bereavement (see Bonanno et al., 2011). In contrast, having more negative affect, being more inclined to ruminate, and trying to find meaning in what has happened is associated with people doing less well after a traumatic event.
Resilience is the most common response to a potentially traumatic event. Optimism, positive emotions, and having more economic resources are all predictive of resilience.
The importance of positive and negative emotions is nicely illustrated in a study of 80 people who were being treated in a specialized rehabilitation hospital (Quale & Schanke, 2010). All had multiple traumatic injuries or severe spinal cord injuries, usually caused by accidents. The people who showed most resilience in the months after their injuries were those who, when interviewed shortly after arriving in the hospital, reported that they generally had an optimistic approach to life. In addition to optimism, being generally high on positive affect and low on negative affect also predicted having a more resilient trajectory (as opposed to a distress trajectory) over the period of rehabilitation treatment.
Finally, it is interesting to note that people who are very self-confident and who view themselves in an overly positive light also tend to cope remarkably well in the face When we are relaxed and calm, our allostatic load is low.
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Everyday forms of stress can also elevate risk for heart disease and death (Matthews & Gump, 2002; Smith & Ruiz, 2002). A good example is work-related stress. Here the key factors appear to be having a highly demanding job and having little control over decision making. Both of these types of job stress increase risk for future heart disease. Moreover, this association still holds when other negative health behaviors (such as smoking) are controlled (see Peter & Siegrist, 2000). It is also inter- esting to note that, in people who work, most heart attacks occur on a Monday. The stress of returning to work after the weekend is thought to play a role in this (Kloner, 2006).
Finally, simply being asked to give a 5-minute speech about an assigned topic to a small (but evaluative) audi- ence was enough to produce detectable changes in car- diac function in about 20 percent of patients with existing coronary artery disease (see Sheps et al., 2002). Further- more, those patients who were most reactive to this form of mental stress were almost three times more likely (compared to the less reactive patients) to die in the next 5 to 6 years. Mental stress is known to raise blood pres- sure and also to cause an elevation in epinephrine. Men- tal stress may also reduce the oxygen supply to the heart muscle (Yeung et al., 1991). What the results of the Sheps study illustrate, however, is that stress does not have to be extreme or severe to be associated with lethal conse- quences later.
The Stress Response To understand why stress can lead to physical and psy- chological problems, we need to know what happens to our bodies when we experience stress. Faced with the threat of a perceived stressor, the body undergoes a cas- cade of biological changes. Two distinct systems are involved here. The sympathetic-adrenomedullary (SAM) system (see Gunnar & Quevedo, 2007) is designed to mobilize resources and prepare for a fight-or-flight response. The stress response begins in the hypothalamus, which stimulates the sympathetic nervous system (SNS). This, in turn, causes the inner portion of the adrenal glands (the adrenal medulla) to secrete adrenaline (also known as epinephrine) and noradrenaline (norepinephrine). As these circulate through the blood, they cause an increase in heart rate (familiar to all of us). They also get the body to metabolize glucose more rapidly. The second system involved in the stress response is called the hypothalamus- pituitary-adrenal (HPA) system (which we introduced in Chapter 3; also see Figure 5.3). In addition to stimulating the SNS, the hypothalamus releases a hormone called cor- ticotropin-releasing hormone (CRH). Traveling in the blood, this hormone stimulates the pituitary gland. The pituitary then secretes adrenocorticotropic hormone (ACTH). This
At the less severe end of the physical health spectrum, stress increases our susceptibility to catching a cold (Cohen, 2005). More dangerously, stress also increases the risk of having a heart attack. Several researchers have docu- mented that deaths from coronary heart disease (CHD) rise in the days and weeks following a severe earthquake (see Leor et al., 1996). As Figure 5.2 shows, after the Northridge earthquake in Los Angeles in 1994, the number of sudden deaths due to CHD rose from an average of 4.6 (in the days preceding the earthquake) to 24 on the day of the earth- quake (Kloner et al., 1997). There was also an increase in sudden death from cardiac events after the Hanshin-Awaji earthquake in Japan (Kario & Ohashi, 1997).
When our allostatic load is high, we experience the biological signs of stress including high heart rate and increased levels of cortisol.
11 14 17 20 23
N um
be r
of d
ea th
s
January 1994
30
20
10
0
Figure 5.2 Cardiac Deaths and Earthquakes On the day of the Northridge earthquake in California (January 17, 1994), cardiac deaths showed a sharp increase.
(Adapted from Leor et al., 1996. The New England Journal of Medicine, 334(7), February 15, 1996, p. 415.)
Stress and Physical and Mental Health 143
has survival value if you need to run away from a bear that has just attacked you. It also explains why cortisone injections are sometimes used to reduce inflammation in damaged joints.
But there is also a downside to cortisol. If the cortisol response is not shut off, cortisol can damage brain cells, especially in the hippocampus (see Sapolsky, 2000). At a very fundamental level, stress is bad for your brain. It may even stunt growth (babies who are stressed don’t gain weight in the normal way and “fail to thrive”). Accord- ingly, the brain has receptors to detect cortisol. When these are activated, they send a feedback message that is designed to dampen the activity of the glands involved in the stress response. But if the stressor remains, the HPA axis stays active and cortisol release continues. Although short-term cortisol production is highly adaptive, a chroni- cally overactive HPA axis, with high levels of circulating cortisol, may be problematic.
The Mind–Body Connection The link between stress and physical illness involves dis- eases (like colds) that are not directly related to nervous sys- tem activity. This suggests that stress may cause an overall vulnerability to disease by compromising immune function- ing. Psychoneuroimmunology is the study of the interac- tions between the nervous system and the immune system. Although it was once thought that the immune system was essentially “closed” and responsive only to challenges from foreign substances, we now know that this is not the case. The nervous system and the immune system communicate in ways that we are now beginning to understand.
Evidence continues to grow that the brain influences the immune system and that the immune system influ- ences the brain. In other words, a person’s behavior and psychological state can affect immune functioning. The status of the immune system also influences current men- tal states and behavioral dispositions by affecting the blood levels of circulating neurochemicals; these, in turn, modify brain states. For example, we have already seen that gluco- corticoids can cause stress-induced immunosuppression. In the short term, this can be adaptive (escape first, heal later). However, it makes sense that longer-term stress might create problems for the immune system. To appreci- ate why this might be, we need to describe briefly the basics of immune functioning.
Understanding the Immune System The word immune comes from the Latin immunis, which means “exempt.” The immune system protects the body from such things as viruses and bacteria. In many ways it can be likened to a police force. If it is too weak, it cannot function effectively, and the body succumbs to damage from invading viruses and bacteria. Conversely, if the
induces the adrenal cortex (the outer portion of the adre- nal gland) to produce the stress hormones called glucocor- ticoids. In humans, the stress glucocorticoid that is produced is called cortisol. Figure 5.3 illustrates this sequence of events.
Anterior pituitary
Hypothalamus
Adrenal cortex
ACTH (through
bloodstream)
Cortisol
CRH (through bloodstream)
Figure 5.3 The Hypothalamic-Pituitary-Adrenal (HPA) Axis Prolonged stress leads to secretion of the adrenal hormone cortisol, which elevates blood sugar and increases metabolism. These changes help the body sustain prolonged activity but at the expense of decreased immune system activity.
Cortisol is a good hormone to have around in an emer- gency. It prepares the body for fight or flight. It also inhib- its the innate immune response. This means that if an injury does occur, the body’s inflammatory response to it is delayed. In other words, escape has priority over healing, and tissue repair is secondary to staying alive. This obviously
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a chemical known as interleukin-1. With the help of the mac- rophages, the T-cells become activated and are able to begin to destroy antigens (Maier et al., 1994).
B-cells are different in structure from T-cells. When a B-cell recognizes an antigen, it begins to divide and to pro- duce antibodies that circulate in the blood. This process is facilitated by cytokines (like interleukin-1) that are released by the T-cells. We will tell you more about cytokines shortly. Production of antibodies takes 5 days or more (Maier et al., 1994). However, the response of the immune system will be much more rapid if the antigen ever appears in the future because the immune system has a “memory” of the invader.
The protective activity of the B- and T-cells is sup- ported and reinforced by other specialized components of the system, most notably natural killer cells, macrophages (which we have already mentioned), and granulocytes. The immune system’s response to antigen invasion is intri- cately orchestrated, requiring the intact functioning of numerous components.
in review • What is the evidence that stress is linked to physical health
problems?
• What is meant by the term allostatic load?
• What is cortisol? Is cortisol beneficial or harmful?
• Describe the biological changes that occur when we are under stress.
immune system is too strong and unselective, it can turn on the body’s own healthy cells. This is what may happen in the case of autoimmune diseases such as rheumatoid arthritis and lupus.
The front line of defense in the immune system is the white blood cells. These leukocytes (or lymphocytes) are produced in the bone marrow and then stored in various places throughout the body, such as the spleen and the lymph nodes. There are two important types of leukocytes. One type, called a B-cell (because it matures in the bone marrow), produces specific antibodies that are designed to respond to specific antigens. Antigens (the word is a con- traction of antibody generator) are foreign bodies such as viruses and bacteria, as well as internal invaders such as tumors and cancer cells. The second important type of leu- kocyte is the T-cell (so named because it matures in the thymus, which is an important endocrine gland). When the immune system is stimulated, B-cells and T-cells become activated and multiply rapidly, mounting various forms of counterattack (see Figure 5.4). If this did not happen, you would inevitably die of infection.
T-cells circulate through the blood and lymph systems in an inactive form. Each T-cell has receptors on its surface that recognize one specific type of antigen. However, the T-cells are unable to recognize antigens by themselves. They become activated when immune cells called macrophages (the word means “big eater”) detect antigens and start to engulf and digest them. To activate the T-cells, the macrophages release
Helper T-cell
B-cell
B-cell
Virgin B-cell binds
Bacteria enter through punctured skin
Antigen
Antigen
Macrophage envelops the antigen
Macrophage displays the antigen portion of the bacteria
B memory cell
Some B-cell progeny di�erentiate into memory cells that prepare an early defense in case the antigen returns
B-cells produce antibodies
Figure 5.4 Immune System Responses to a Bacterial Infection (Adapted from J. W. Kalat, 2001, Biological Psychology, 7th ed. Belmont, CA: Wadsworth.)
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Stress and Cytokines You now know that stress causes a dysregulation in the immune system, slowing down healing and making us more susceptible to illness. But how does this happen? To understand more, you need to know a little about cytokines. Cytokines are small protein molecules and they are an important component of the immune system. Cytokines serve as chemical messengers and allow immune cells to communicate with each other. One cytokine that you may have heard about is interferon, which is given to patients with cancer, multiple sclerosis, and hepatitis C.
What makes cytokines especially interesting is that in addition to communicating with the immune system, they also have broader effects. Importantly, they influence the brain. Researchers used to believe that the immune system was a self-contained entity. We now know this is not the case. Instead, the brain and the body work together to
Stress and Immune System Functioning 5.3 Explain how stress causes dysregulation in the
immune system.
Would you be surprised to learn that stress slows the heal- ing of wounds by as much as 24 to 40 percent (Gouin & Kiecolt-Glaser, 2011)? This is because stress is linked to suppression of the immune system (Segerstrom & Miller, 2004). In one study, 11 dental student volunteers had a punch biopsy wound performed on their hard palate (roof of the mouth) on two separate occasions. The first biopsy was performed in mid-August when the students were on summer vacation. The second occurred 6 weeks later, just 3 days before a major examination. On average, the wounds healed 40 percent more slowly during the stressful period before the examination than they did when the students were on vacation (Marucha et al., 1998). Indeed, for every person in this study, healing time was longer when the wound occurred during the time of high versus low stress (see Figure 5. 5).
Although short-term stress (such as occurs when we take an examination) compromises the immune system, it is the more enduring stressors such as unemployment or interpersonal problems with family or friends that are associated with the most global immunosuppression. Peo- ple who are unemployed have lower levels of immune functioning than people who are employed. The good news, however, is that immune functioning returns to nor- mal again once people find another job (Cohen et al., 2007).
D ay
s to
h ea
l
16
14
12
10
8
6
4
2
0
Low stress High stress
Figure 5.5 Wound Healing and Stress Healing time is shown for each of the 11 subjects for the two time periods, summer vacation (low stress) and examinations (high stress).
(Adapted from P. T. Marucha et al., Psychosomatic Medicine, 60:362–365 (1998).)
Stress causes our immune system to function less efficiently.
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Remick, 2000, for a review). They can be divided into two main categories: proinflammatory cytokines and anti- inflammatory cytokines. Proinflammatory cytokines such as interleukin-1 (IL-1), IL-6, or tumor necrosis factor (TNF) help us deal with challenges to our immune system by augmenting the immune response. In contrast, anti- inflammatory cytokines such as IL-4, IL-10, and IL-13 decrease or dampen the response that the immune system makes. Sometimes they accomplish this by blocking the synthesis of other cytokines.
Under conditions of stress, the production of proin- flammatory cytokines is disrupted. This affects the heal- ing of wounds. In a compelling demonstration of this, Kiecolt-Glaser and her colleagues (2005) recruited a sam- ple of married couples and admitted them for 24 hours to a hospital research unit. In the pursuit of science, the researchers then gave each member of the couple a blister wound to the arm. Following this, each couple was asked to engage in a supportive discussion. At various point after the discussion, fluid was taken from the blisters and analyzed for the presence of cytokines. Then, approxi- mately 2 months later, the couples came back, went through exactly the same procedures, but this time the discussion they were asked to have was designed to pro- voke marital conflict.
What were the findings? One result was that the blister wounds took 1 day longer to heal when couples had engaged in the conflict discussion compared to the sup- portive discussion. In other words, the stress of the conflict slowed down the healing process. This is similar to the findings of the study involving the dental students that we told you about earlier. What Kiecolt-Glaser and her col- leagues were also able to shed light on, however, was why wound healing was delayed. Although proinflammatory cytokine production (IL-1, IL-6, and TNF) increased in the blisters regardless of the nature of the discussion the cou- ple had had (reflecting the start of the healing process), cytokine production was lower overall after the conflict discussion than it was after the supportive exchange. So, even though you might not have wanted to be a partici- pant in this study, the results make a very important point. They tell us that the stress of marital conflict, like the stress of examinations, can disrupt the immune system and slow down wound healing.
Chronic Stress and Inflammation If short-term stress (like taking an examination) is bad, is long-term or chronic stress even worse? The answer here is yes. Evidence is growing that inflammation—increased levels of proinflammatory cytokines—is increased in peo- ple who are under prolonged stress. This is because long- term stress seems to interfere with the body’s ability to turn off cytokine production.
coordinate a response to sickness. For example, when you are ill you tend to feel tired, to sleep more, and to have very little appetite. This is classic sickness behavior and it is familiar to us all. What you may not know, how- ever, is that these symptoms of illness result, at least in part, from the effects of specific cytokines. These cyto- kines act on the brain and this is the reason we feel so unwell (Dantzer & Kelley, 2007). Although unpleasant, feeling this way is highly adaptive, causing us to with- draw from our usual routines, rest, and take care of our- selves until we get better.
Cytokines, which are produced by the immune system, have effects on the brain, making us feel unwell.
Not only is the brain influenced by products of the immune system (such as cytokines), but the close commu- nication between the brain and the immune system also means that the brain is capable of influencing immune pro- cesses. With this in mind, some of the findings discussed later in this chapter (the link between depression and physical disease, for example, and the health benefits of optimism and social support) make much more sense.
In the opposite direction, chronic problems at the level of the immune system may lead to behavioral changes or even to psychiatric problems. For example, as we mentioned earlier, patients who have cancer are some- times treated with cytokines to activate their immune sys- tems. One unfortunate consequence of this is that almost all patients experience fatigue, as well as sleep and appe- tite problems. In addition, somewhere between 30 and 50 percent of patients also experience depressed mood, anxi- ety, and cognitive problems—problems that are alleviated by antidepressant medications (Dantzer & Kelley, 2007; Musselman et al., 2001). In short, cytokines have great potential for helping us understand the links between physical and mental well-being that are at the heart of behavioral medicine.
Cytokines play an important role in mediating the inflammatory and immune response (see Kronfol &
Stress and Physical and Mental Health 147
Under ordinary conditions, IL-1 and other cytokines stimulate the HPA axis (refer back to Figure 5.3), leading to an increase in cortisol. Cortisol (which you will recall is a stress hormone) is supposed to regulate (turn off) cytokine production. In other words, cytokine production sets off a negative feedback loop that is designed to prevent an excessive or exaggerated immune or inflammatory response. Chronic stress, however, seems to impair the body’s ability to respond to the signals that will terminate immune system reactivity. The result is inflammation.
Chronic inflammation is a risk factor for a wide range of health problems and diseases. These include cardiovas- cular disease, type 2 diabetes, asthma, osteoporosis, rheu- matoid arthritis, and many others (Ershler & Keller, 2000; Jaremka et al., 2013). This is why doctors now test for the presence of C-reactive protein (CRP)—a molecule pro- duced by the liver in response to IL-6—when they want to assess a person’s risk for heart disease.
Chronic stress can take many forms. One correlational research study showed that women who were caring for a family member with Alzheimer’s disease had higher levels of IL-6 than women who were either anticipating the stress of relocation or who were experiencing neither of these stressors (Lutgendorf et al., 1999). This difference was found even though the women who were caregivers were 6 to 9 years younger than the women in the other two groups and even though IL-6 levels are known to increase with age. Other research links discrimination—another
Research Close-Up Correlational Research
In contrast to experimental research (which involves manipu- lating variables in some way and seeing what happens), in correlational research the researcher observes or assesses the characteristics of different groups, learning much about them without manipulating the conditions to which they are exposed.
The World Around Us Racial Discrimination and Cardiovascular Health in African Americans
Experiences of discrimination have been linked to a number of bad health outcomes, including increased blood pressure and signs of cardiovascular disease. But how might this association arise? An important mediator in this relationship may be C-reactive protein, or CRP.
CRP is a protein synthesized in the liver. High levels of CRP signal widespread inflammation in the body. In an interesting study, Lewis and colleagues (2010) measured levels of CRP in blood samples taken from 296 older African Americans, whose average age was 73. These research participants also completed a questionnaire that asked about their experiences of everyday discrimination. Items on the questionnaire included being treated with disrespect, getting poorer service in restaurants or stores, as well as experiences of being insulted or harassed.
The findings revealed a significant correlation between everyday discrimination and CRP, where more experiences of discrimination were associated with higher levels of CRP. The association also remained even after factors such as smoking, high blood pressure, depression, and other health problems were considered. Although much more remains to be learned, these preliminary findings are very exciting. They provide a clue about a
potential pathway through which experiences of racial bias might ultimately play a role in the poor cardiovascular health of older African Americans.
What is stressful about discrimination? Is this something you have experienced? If so, how did it affect you?
form of chronic stress—to elevated levels of CRP in African Americans (see the World Around Us box).
Stress and Premature Aging Much of our discussion so far has concerned fairly common forms of acute (e.g., examinations, disagreements) and chronic (discrimination, unemployment, caring for a spouse with dementia) forms of stress. But what about chronic and severe stress that occurs early in life? Researchers have begun to explore this issue and the results are very worri- some. Traumatic stressors that are experienced during child- hood seem to increase risk of premature death in later life.
In the first study of this kind, Brown and colleagues (2009) collected information about adverse childhood experiences from over 17,000 adults who attended a primary
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Telomeres (from the Greek words telos, meaning “end,” and meros, meaning “part”) are the protective end parts of chromosomes. You can think of them as being rather like the ends of shoelaces in this respect. Unfortunately, telo- meres shorten with age. And if they get too short, cells do not function correctly and the risk of disease is increased.
The reason all of this is so important is that stress shortens the length of telomeres. In the first study of this kind, Epel and her colleagues (2004) compared telomere lengths in the blood cells of two groups of mothers: mothers caring for a child with a chronic illness and mothers of children who were healthy. The longer the mothers had been caring for their ill child the shorter their telomeres were. And in both groups of mothers, telomere length was also related to how much stress the mothers reported being under. The differences were also not trivial. The reduction in telomere length in the mothers who felt most stressed was equiva- lent to 10 years of aging!
Research in this exciting area is now expanding rapidly and we have already learned a lot. We know that telomere length is maintained by an enzyme called telomerase and that the stress hormone cortisol can reduce the activity of this enzyme (Price et al., 2013). In other words, we are begin- ning to understand how experiencing stress can start to bring about an array of changes that, if left unchecked, can compromise the immune system, create conditions of chronic inflammation, and shorten the length of our telo- meres. We are also learning that drinking too much sugar- sweetened soda might shorten telomeres (Leung et al., 2014),
care clinic from 1995 to 1997. Adverse childhood experi- ences included such things as emotional, physical, or sex- ual abuse, domestic violence, having a family member incarcerated, and parental separation or divorce during the person’s first 18 years of life. Then, approximately 10 years later, the researchers identified people who had died in the intervening period. The findings were sobering. People who had reported six or more adverse events during their childhood died much earlier (in fact, almost 20 years ear- lier) than would have been expected based on estimates of standard life expectancy. The top two leading causes of death were heart disease (or stroke) and cancer.
Of course, interpreting data from a study such as this is complicated. However, a more recent study, using a pro- spective longitudinal design has reported that the risk of death was 57 percent higher in men who experienced two or more adverse childhood experiences compared to men who had not experienced any childhood adversity. For women, the corresponding figure was 80 percent increased risk. Moreover, lifestyle factors in adulthood did not pro- vide a very satisfactory explanation of the premature mor- tality that was found (Kelly-Irving et al., 2013).
What might this mean? Although we cannot yet be certain, there is reason to suspect that early life stress may have biological consequences that advance aging, making it more likely that people will die earlier from the kinds of diseases (cancer, heart disease) that are associated with increased age. But how could this come about? Telomeres may be part of the answer.
Telomere
Telomere
Chromosome
Cell
Telomeres are the protective end parts of chromosomes. Telomeres shorten with age, increasing the risk of disease. Stress also shortens telomeres. Telomere length is maintained by an enzyme called telomerase and the activity of telomerase is reduced by the stress hormone cortisol. If you needed a reason to reduce the amount of stress in your life, you have a good one now!
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hostility component of the Type A construct (including anger, contempt, scorn, cynicism, and mistrust) that is most closely correlated with coronary artery deterioration (Chida & Steptoe, 2009; Wong et al., 2013).
A more recent development is the identification of the “distressed” or Type D personality type (Denollet et al., 2000). People with Type D personality have a tendency to experience negative emotions and also to feel insecure and anxious. Men with CHD who scored high on measures of chronic emotional distress were more likely to have fatal and nonfatal heart attacks over the 5-year follow-up period than were men who did not have these Type D personality traits (Denollet et al., 2000). People with higher scores on the negative affectivity component of Type D personality (see Figure 5.6) are also at increased risk of having more problems after cardiac surgery (Tully et al., 2011).
pessimism may accelerate the rate of telomere shortening (O’Donovan et al., 2009), and meditation may promote telomerase activity (Jacobs et al., 2011). And just in case you are inclined to blow off the gym, you should also know that exercise seems to act as a buffer against the bad effects of stress on telomeres (Puterman et al., 2010). In essence, sci- ence is now explaining exactly why we should be striving to live in a happy, healthy, and more relaxed manner.
in review • How can acute stress lead to immunosuppression?
• How can chronic stress lead to inflammation?
• In what way might chronic stress lead to premature aging and disease?
• What is the difference between a cytokine and a telomere?
• How might racial bias play a role in the development of cardio- vascular disease?
Emotions and Health 5.4 Describe the role that emotions play in physical
health and identify helpful and harmful emotions.
We have already described how stress can result in the immune system going out of balance in ways that may compromise health. But stress is not the whole story. The same also seems to be true for negative emotions. Because the brain influences the immune system, psychological fac- tors are of great importance to our health and well-being. How you view problems and cope with challenges, and even your temperament, may directly affect your underly- ing physical health.
Personality Attempts to explore the psychological contribution to the development of heart disease date back to the identification of the Type A behavior pattern (Friedman & Rosenman, 1959). Type A behavior is characterized by excessive com- petitive drive, extreme commitment to work, impatience or time urgency, and hostility. Many of us know people who are like this, and the term Type A is commonly used in everyday language.
Early findings suggested that Type A personality in oth- erwise healthy men ages 35 to 59 was associated with a two- fold increased risk for coronary artery disease and an eightfold increased risk of having a heart attack over the course of an 8.5-year follow-up (Rosenman et al., 1975). A subsequent major study called the Framingham Heart Study not only confirmed the findings of the earlier (Western Col- laborative Group) study but extended them to women as well (see Kannel et al., 1987). However, as research with the construct has continued, it has become clear that it is the
TEST: ARE YOU A TYPE D?
The social and emotional problems associated with Type D personality can increase your chances of developing heart disease. Read each statement and circle the appropriate number to indicate your answer. There are no right or wrong answers: your own impression is the only thing that matters.
1. I make contact easily when I meet people
2. I o�en make a fuss about unimportant things
3. I o�en talk to strangers
4. I o�en feel unhappy
5. I am o�en irritated
6. I o�en feel inhibited in social interactions
7. I take a gloomy view of things
8. I find it hard to start a conversation
9. I am o�en in a bad mood
10. I am a closed kind of person
11. I would rather keep people at a distance
12. I o�en find myself worrying about something
13. I am o�en down in the dumps
14. When socializing, I don't find the right things to talk about
4 3 2 1 0
0 1 2 3 4
4 3 2 1 0
0 1 2 3 4
0 1 2 3 4
0 1 2 3 4
0 1 2 3 4
0 1 2 3 4
0 1 2 3 4
0 1 2 3 4
0 1 2 3 4
0 1 2 3 4
0 1 2 3 4
0 1 2 3 4
Fa ls
e
Le ss
fa ls
e
N eu
tr al
Le ss
t ru
e
Tr ueTAKE THE TEST
Circle your answers: 1
2 ADD YOUR ANSWERS Negative A�ectivity: Add scores for questions 2, 4, 5, 7, 9, 12 and 13
Social Inhibition: Add scores for questions 1, 3, 6, 8, 10, 11, and 14
3 SCORE THE RESULTS You qualify as a Type D personality if your Negative A�ectivity is 10 or higher and your Social Inhibition is 10 or higher.
Figure 5.6 Characteristics of the Type D Personality (Adapted from Johan Denollet, 1998,Personality and coronary heart disease: The type-D Scale-16 (DS16). Annals of Behavioral Medicine, 20(3) 209–215, and N. Kupper and J. Denollet, 2007. Type D Personality as a prognostic factor in heart disease: Assessment and mediating mechanisms. Journal of Personality Assessment, 89(3) 265–276.)
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Why are depression and heart disease so closely linked? Current thinking is that this is another example of the mind–body connection. As mentioned earlier, stress is
thought to activate the immune system, trig- gering the production of proinflammatory cytokines such as IL-1, IL-6, and tumor necro- sis factor by the white blood cells. Long-term exposure to these proinflammatory cytokines is thought to lead to changes in the brain that manifest themselves as symptoms of depres- sion. Depression may then interact with stress to further enhance the inflammatory responses that are naturally triggered by stress exposure, rather like putting gasoline on a fire (Fagundes et al., 2013). Proinflam- matory cytokines also trigger the growth of plaques in the blood vessels as well as mak- ing it more likely that those plaques will rup- ture and cause a heart attack. In other words, as illustrated in Figure 5.7, the link between heart disease and depression is due to inflam- mation and the presence of inflammatory cytokines (see Miller & Blackwell, 2006; Robles et al., 2005).
New findings also suggest that people who are depressed have shorter telomeres
Depression Like stress, depression is associated with disrupted immune function (Kiecolt-Glaser et al., 2002). Moreover, the relationship between depression and suppression of the immune system is at least partially independent of spe- cific situations or events that may have provoked depressed feelings. In other words, the state of being depressed adds something beyond any negative effects of the stressors pre- cipitating the depressed mood.
Depression is also a factor in heart disease. People with heart disease are approximately three times more likely than healthy people to be depressed (Chesney, 1996; Shapiro, 1996). This may not strike you as especially sur- prising. If you had heart disease, perhaps you would be depressed too. However, depression is much more com- monly found in people who have heart disease than it is in people who have other serious medical problems, like can- cer (Miller & Blackwell, 2006). Furthermore, heart attack patients with high levels of depressive symptoms after having a heart attack are three times more likely to die dur- ing the next 5 years than patients who do not show high lev- els of depression (Glassman, 2007; Lesperance et al., 2002). Research also suggests that anhedonia (which is a symptom of depression characterized by profound loss of interest or pleasure) may be especially predictive of increased mortality after a heart attack (Davidson et al., 2010).
Depression also appears to be a risk factor for the devel- opment of CHD. A recent meta-analysis of prospective studies involving almost 900,000 participants has shown that depression is associated with a 30 percent increased risk for developing heart disease or having a heart attack in
Research Close-Up Risk Factor
A risk factor is a variable that increases the likelihood of a spe- cific (and usually negative) outcome occurring at a later time. For example, obesity is a risk factor for heart disease; perfec- tionism is a risk factor for eating disorders.
Chronic Stressors
Excessive Inflammation
Depressive Symptoms
Cardiac Disease
Figure 5.7 Stress, Inflammation, Depression, and Heart Disease Model of how inflammatory processes mediate the relations among chronic stress- ors, depressive symptoms, and cardiac disease. Stressors activate the immune sys- tem in a way that leads to persistent inflammation. With long-term exposure to the molecular products of inflammation, people are expected to develop symptoms of depression and experience progression of cardiac disease.
(Adapted from Miller & Blackwell, 2006. Turning up the heat: Inflammation as a mechanism linking chronic stress, depression and heart disease. Current Directions in Psychological Science, 15(6), 269–272(4). Copyright © 2006. Reproduced with permission of Blackwell Publishing Ltd.)
the future (Gan et al., 2014). The link between depression and future heart problems also remained even when other potential confounding variables such as lifestyle were taken into account.
Stress and Physical and Mental Health 151
more likely to develop heart disease in the subsequent years. This association also held when other variables such as age, smoking, physical activity, and depression were accounted for statistically. Interestingly, no association between loneliness and depression was found for men (Thurston & Kubzansky, 2009). This may be because women were much more likely to report feelings of loneli- ness than men were.
than never depressed controls, even after controlling for other health and lifestyle variables (Verhoeven et al., 2014). In the study by Verhoeven and colleagues, the reduction in telomere length in the participants with depression was equivalent to 4 to 6 years of accelerated aging (that is, the depressed people had telomeres about the length of people 4 to 6 years older). There was also a dose–response relation- ship, meaning that the more chronic and severe the depres- sion, the shorter people’s telomeres were. Of course, one limitation of this study is that it was cross sectional. With- out longitudinal data we cannot say conclusively that depression causes a reduction in telomere length. Nonethe- less, the results give us pause for thought. One implication of these findings is that depression is an emotionally stress- ful condition that may have an impact on how much physi- cal wear and tear can be detected in the body. And the older our bodies are, the more liable we are to have the kinds of serious health problems that often accompany aging.
Anxiety Depression is not the only form of negative affect that is linked to CHD. Research has also demonstrated a relation- ship between phobic anxiety and increased risk for sudden cardiac death. In a classic early study, Kawachi, Colditz, and colleagues (1994) examined nearly 34,000 male profes- sionals who had been assessed for panic disorder, agora- phobia, and generalized anxiety. Over the course of the 2-year follow-up study, sudden cardiac death was six times higher in the men with the highest levels of anxiety. The findings were replicated in a second study of nearly 2,300 men who were participating in a normative aging study (Kawachi, Sparrow, et al., 1994, 1995). Prospective studies of women who were free of cardiac disease at the start of the study have also linked phobic anxiety with a higher risk of sudden cardiac death (Albert et al., 2005).
Social Isolation and Lack of Social Support How we live—and our feelings of social isolation—also make a difference. Studies point to the strong link between social factors and the development of CHD. Monkeys housed alone have four times more atherosclerosis (fatty deposits in blood vessels that eventually create a blockage) than monkeys housed in social groups (Shively et al., 1989). Lonely people are also at increased risk of developing heart disease. Loneliness is a different construct from social sup- port or depression, and it is not closely related to any objec- tive measures of a person’s social network size. In one study, 3,000 men and women who were free of cardiovas- cular problems were followed up for a period of more than 19 years. Women who reported higher levels of loneliness on two separate assessment occasions were 76 percent
Loneliness is a risk factor for the development of later heart disease in women.
For people who already have CHD, there is similar evidence that feelings of being emotionally supported make a difference. In one study of people who had already suffered a heart attack, those who reported that they had low levels of emotional support were almost three times more likely to experience another cardiac event (Berkman et al., 1992). In another study, death in patients with CHD was three times more likely during the next 5 years if they were unmarried or had no one to confide in (Williams et al., 1992). Echoing these findings, Coyne and colleagues (2001) have shown that the qual- ity of the marital relationship predicts 4-year survival rates in patients with congestive heart failure. Although uncertain at this time, it may be that the stress that comes from marital tension or from a lack of social sup- port triggers an inflammatory response in the immune system, causing depression and heart problems as a result. It may also be that depression, which is linked to relationship problems, could trigger an inflammatory response in its own right.
Positive Emotions Negative emotions such as depression, anxiety, and anger may be especially important to avoid because they are associated with poor health (see Kiecolt-Glaser et al., 2002). On the other hand, an optimistic outlook on life, as well as an absence of negative emotions, may have some beneficial health consequences (see Rasmussen et al., 2009).
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their heart rates went up, their blood pressures increased, and their skin conductance (a measure of SNS arousal) revealed more arousal. Even more striking was the find- ing that even after the grudge-harboring imagery was over and the subjects were told to relax, they were unable to do so. In other words, the high state of physiological arousal that had been triggered by dwelling on the past hurt could not easily be turned off.
What are the implications of these findings? Although fleeting feelings of anger probably do us no real harm, people who have a tendency to brood about the wrongs that other people have done to them may be doing themselves a major disservice. To the extent that perpetuating feelings of anger and increasing cardiovas- cular reactivity have consequences for heart disease and immune system functioning, harboring grudges may be hazardous to our health. Indeed, recent research shows that college-age adults who score high on a measure of forgivingness have fewer symptoms of both physical and mental health problems (Toussaint et al., 2015). Being forgiving also acts as a buffer against the effects of stress on mental health, although no similar association was found for physical health. Although the study just described was a cross-sectional one, longitudinal research has shown that more forgiveness predicts fewer health symptoms, but that having fewer health symp- toms does not predict being more forgiving (Seawell et al., 2014). In other words, it is most likely that it is for- giveness that is making a difference to health, rather than healthy people being more forgiving. If this is true, there is an important take-home message. Although it is not always easy, forgiving those who have offended us may lower our stress levels and enhance our physical and emotional well-being.
Now that you understand the importance of positive and negative emotions in physical health, consider the case of Dr. M.
The Angry Physician
Dr. M was a 44-year-old physician. The middle son of parents who had emigrated from Italy, he was ambitious and determined to make a successful life for himself and his family. He worked long hours helping patients with cancer, and he was caring and compas- sionate. His patients loved him. But his job was also very stressful. Added to the many demands of maintaining a busy medical prac- tice was the great sadness that he felt when (inevitably) many of his terminally ill patients died.
At home Dr. M was a loyal husband and devoted father to his three children. But he was not an easy person to live with. He found it hard to relax, and he had a very volatile disposition. He was frequently angry and would shout at everyone whenever he had had a bad day. Often his moods were caused by his feeling that he was not fully appreciated by the other doctors with whom
Perhaps you are familiar with the term positive psychology. This school of psychology focuses on human traits and resources such as humor, gratitude, and com- passion that might have direct implications for our phys- ical and mental well-being. An illustration of this comes from a study by Witvliet and colleagues (2001). These researchers asked college students to select a real-life interpersonal offense (such as rejection, betrayals of trust, and personal insults) that they had experienced in the past. The researchers then collected self-reports as well as heart rate, blood pressure, and facial muscle tension data from the students while they were imagining responding to the real-life transgression in a way that was either forgiving or unforgiving. In the forgiving con- dition, the students were asked to think about granting forgiveness or developing feelings of empathy for the perpetrator. In the unforgiving condition, they were asked to stay in the victim role, to go over the hurt in their minds, and to nurse a grudge.
The findings showed that when they were asked to be forgiving, participants did indeed report more feelings of empathy and forgiveness. And, when asked to ruminate and be unforgiving, participants reported that they felt more negative, angry, sad, aroused, and out of control. They also showed greater tension in their brows. Importantly,
Forgiving those who have wronged us may lower our stress levels and enhance overall well-being.
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Treatment of Stress-Related Physical Disorders 5.5 Explain the psychological interventions that can be
used to reduce stress and treat stress-related disorders.
As you have learned, environmental stressors are often closely linked to the development of a physical illness. Unfortunately, once an illness has developed and physical changes have taken place, removal of the stressor may not be enough to bring about recovery and restore health. This emphasizes the value of prevention and highlights the importance of stress management.
Biological Interventions People who have serious physical diseases obviously require medical treatment for their problems. For patients with CHD, such treatments might include surgical procedures as well as medications to lower cholesterol or reduce the risk of blood clots. However, in light of the strong associations between depression and risk for CHD, treating depression is also of the utmost importance. Unfortunately, most people with clinical depression go untreated, resulting in an unnec- essary added risk for CHD. Moreover, even though there is no medical risk factor that is more important in predicting mortality for patients who have already had a heart attack (Welin et al., 2000), physicians often fail to treat depression in their cardiac patients. Instead, they dismiss it as an under- standable consequence of having had a life-threatening medical scare (Glassman, 2005). Of those with major depres- sion at the time of a heart attack, approximately one-half of those who have gone without treatment remain depressed or else have relapsed again 1 year later (Hance et al., 1996). However, research shows that thousands of lives can be saved each year by giving antidepressant medications to patients who have suffered a myocardial infarction and who are depressed. In one study, patients treated with selective serotonin reuptake inhibitors (SSRIs) were much less likely to die or have another heart attack than patients who were not taking antidepressant medications (Taylor et al., 2005). It is also worth noting that, in this study, treatment with cognitive-behavior therapy (CBT; see Chapter 16 for more about this approach) was not associated with reduced mortality in the patients, although CBT treatment did help alleviate depression (see Berkman et al., 2003; Glassman, 2005).
Psychological Interventions How can we help ourselves stay healthy in the face of stress? As we have already mentioned, developing effective emotion regulation skills is probably beneficial. Evidence suggests that the following approaches are also helpful.
he worked. Although his wife realized that he “just needed to vent,” his moods took a toll on the family. His children distanced them- selves from him much of the time, and his wife became less and less happy in the marriage.
One day at work, Dr. M started to feel unwell. He began to sweat and experienced a heavy pressure in his chest. It was difficult for him to breathe. Dr. M recognized the severity of his symptoms and called out for medical help. He had a sudden and severe heart attack and survived only because he was working in a hospital at the time of the attack. If he had not received prompt medical attention, he almost certainly would have died.
After his heart attack Dr. M became very depressed. It was almost as though he could not accept that he, a physician, had a severe medical problem. Although he lived in fear of having another heart attack, his efforts to lose weight (which his doctor had told him to do) were sabotaged by his unwillingness to follow any diet. He would try and then give up, coming back from the Italian bakery with bags of pastries. Making the problem worse was the fact that because he was a doctor, his own doctors were somewhat reticent about telling him what he had to do to manage his illness. He went back to work, and his family walked on eggshells, afraid to do or say anything that might stress him. His wife tried to encourage him to follow the doctors’ recommendations. However, Dr. M’s attitude was that if he was going to die anyway, he might as well enjoy him- self until he did.
The Importance of Emotion Regulation If hostility, depression, and anxiety are all predictive of developing coronary heart disease, is it beneficial to be able to regulate one’s emotions? Research suggests that it is. In one study of men and women without a history of heart disease, it was found that it was the people who were least able to control their anger who developed more heart prob- lems during the next 10 to 15 years (Haukkala et al., 2010). In another study of 1,122 men who were followed for an average of 13 years, it was again those with the best emo- tion regulation skills who were the least likely to develop cardiac disease (Kubzansky et al., 2011). Taken together these findings suggest that self-regulation skills may be very important—not only for our psychological well-being but for our physical health as well. Although regulating our emotions is not easy, learning how to stay in emotional control is well worth the effort.
in review • What emotional risk factors are associated with coronary heart
disease?
• What is Type A personality?
• What is Type D personality?
• How might positive emotions be beneficial for our physical health?
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about the factors that determine whether or not expressive writing is helpful (moderator variables) as well as the mechanisms (mediating variables) through which expres- sive writing might work.
BIOFEEDBACK Biofeedback procedures aim to make patients more aware of such things as their heart rate, level of muscle tension, or blood pressure. This is done by con- necting the patient to monitoring equipment and then pro- viding a cue (for example, an audible tone) to the patient when he or she is successful at making a desired response (e.g., lowering blood pressure or decreasing tension in a facial muscle). Over time, patients become more con- sciously aware of their internal responses and are able to modify them when necessary.
Biofeedback seems to be helpful in treating some conditions, such as headaches (Nestoriuc et al., 2008). After an average of 11 sessions, patients report improve- ment in their symptoms and a decrease in the frequency of their headaches. Moreover, these treatment effects tend to be stable over time. Although it is especially helpful for children and adolescents, adults who have experienced headaches for a long time are also helped by biofeedback.
RELAXATION AND MEDITATION Researchers have examined the effects of various behavioral relaxation techniques on selected stress-related illnesses. The results have been variable, though generally encouraging. For example, evidence suggests that relaxation techniques can help patients with essential hypertension (see Blumenthal et al., 2002). Relaxation training can also help patients who experience tension headaches (Holroyd, 2002). How- ever, in general, people with headaches who are treated with biofeedback appear to do better than those treated only with relaxation, and the best clinical results occur when these two treatments are combined (Nestoriuc et al., 2008).
A current focus of interest is meditation. Schneider and colleagues (2005) have shown that the daily practice of Transcendental Meditation may be helpful in reducing blood pressure. In this study, 194 African American
EMOTIONAL DISCLOSURE “Opening up” and writing expressively about life problems in a systematic way does seem to be an effective therapy for many people with ill- nesses (Frattaroli, 2006; Pennebaker, 1997). It may also speed up wound healing. In one recent study, healthy older adults (average age 79 years) were asked to write for 20 minutes each day over a period of 3 consecutive days. One group wrote about their most traumatically stressful life experience, delving into their most private and deep thoughts and emotions. Another group simply wrote about their planned activities for the following day. Two weeks later, all participants were given a punch biopsy wound on their arm. Wound healing was significantly faster in the participants who had been asked to write about upsetting life events (Koschwanez et al., 2013). This is potentially very important because wound healing slows down as we get older. Simple interventions of this kind could therefore have great practical importance for seniors about to undergo surgery, for example.
Expressive writing also seems to provide some modest benefits (reduced fatigue at a 3-month follow-up assess- ment) for people who have been diagnosed with autoim- mune illnesses such as lupus and rheumatoid arthritis (Danoff-Burg et al., 2006). However, findings suggest that expressive writing does not seem to improve sleep prob- lems, depression, or overall quality of life in people being treated for cancer (Lepore et al., 2015). There is also some evidence that expressive writing may even get in the way of emotional recovery in people who have experienced a marital separation (Sbarra et al., 2013). In other words, the findings are often mixed and expressive writing is far from a cure-all.
In studies that involve emotional disclosure, patients often experience initial increases in emotional distress during the writing phase but then show improvement in their medical status over follow-up. Why emotional dis- closure provides clinical benefits for some patients is still not clear, however. One reason could be that patients are given an opportunity for emotional catharsis, or “blowing off steam.” Another possibility is that writing gives people an opportunity to rethink their problems or reduce how threatening these problems seem. This is known as refram- ing. But depending on the problem and the timing of when it occurred, there is perhaps the risk that expressive writing could sometimes lead to rumination (“Why did he leave me?”) rather than reframing (“That was a bad rela- tionship and I am better off on my own”). If this is the case, expressive writing too soon after an upsetting life event may make things worse rather than better. For events that are more in the past, however, it is not unrea- sonable to speculate that both emotional catharsis and rethinking problems could help improve immune func- tion or perhaps decrease levels of circulating stress hor- mones. As research progresses we will understand more
Stress and Physical and Mental Health 155
in review • Why is it so important to screen people with heart disease for
depression?
• What clinical approaches have been used to treat stress-related disorders?
Stress and Mental Health 5.6 Identify the similarities and differences between
adjustment disorder, posttraumatic stress disorder, and acute stress disorder.
Our focus thus far has been on describing the nature of stress, highlighting the role it plays in physical disorders. But, as we have noted repeatedly throughout this chapter, when we experience stress, we pay a price not only in our bodies but also in our minds. In the sections that follow, we discuss the psychological consequences of experiencing the kind of stress that overwhelms our abilities to adjust and to cope. More specifically, we focus on three DSM dis- orders, adjustment disorder, acute stress disorder, and PTSD. All of these are precipitated by exposure to stress. There are important differences between them, however. In adjustment disorder, the stressor is something that is com- monly experienced, and the nature of the psychological reaction is much less severe. In contrast, both acute stress disorder and PTSD involve exposure to a more traumatic stressor. This can lead to short term problems (acute stress disorder) or more long-term and intense difficulties that can be debilitating (PTSD).
Adjustment Disorder An adjustment disorder is a psychological response to a common stressor (e.g., divorce, death of a loved one, loss of a job) that results in clinically significant behavioral or emotional symptoms. The stressor can be a single event, such as going away to college, or involve multiple stress- ors, such as a business failure and marital problems. Peo- ple undergoing severe stress that exceeds their coping resources may warrant the diagnosis of adjustment disor- der (Strain & Newcorn, 2007). For the diagnosis to be given, symptoms must begin within 3 months of the onset of the stressor. In addition, the person must experience more distress than would be expected given the circum- stances or be unable to function as usual.
In adjustment disorder, the person’s symptoms lessen or disappear when the stressor ends or when the person learns to adapt to the stressor. In cases where the symp- toms continue beyond 6 months, the diagnosis is usually changed to some other mental disorder. Adjustment disor- der is probably the least stigmatizing and mildest diagno- sis a therapist can assign to a client.
patients with chronic hypertension were randomly assigned to receive training in either Transcendental Meditation or progressive muscle relaxation (which involves tensing and relaxing various muscle groups in a systematic way) or else to receive general information about lifestyle changes that would be helpful to them. Patients who practiced Transcendental Meditation for 20 minutes twice a day reduced their diastolic blood pres- sure significantly more than did patients who practiced muscle relaxation or who received sound health care advice.
COGNITIVE-BEHAVIOR THERAPY CBT has been shown to be an effective intervention for headache (Martin, Forsyth, & Reece, 2007), as well as for other types of pain. CBT-oriented family therapy was markedly more success- ful than routine pediatric care in alleviating children’s complaints of recurrent abdominal pain (Robins et al., 2005). Some CBT techniques have also been used for patients with rheumatoid arthritis. Compared to those receiving standard medical care, patients who received CBT showed better physical, social, and psychological functioning (Evers et al., 2002).
Finally, we note that making a conscious effort to slow down and enjoy life seems to be a prescription for better health. Meyer Friedman, who was the co-discoverer of the link between Type A behavior and heart disease, had a heart attack at age 55. A self-described Type-A personality, he made a conscious choice to change his ways in accor- dance with his own discoveries. To get more in touch with his slow, patient, and creative side, he read Proust’s lan- guid seven-volume opus Remembrance of Things Past three times. In short, he trained himself to relax and to enjoy life. He had the last laugh at stress by living to the ripe old age of 90 (Wargo, 2007).
Making an effort to slow down and relax may provide many health benefits.
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we have just discussed, and acute stress disorder (see next section) are also part of this new diagnostic category. This is because the experience of major stress is central to the development of all of these conditions.
Adjustment Disorder Caused by Unemployment Work-related problems can produce great stress in employ- ees (Lennon & Limonic, 2010). But being unemployed can be even more stressful. As a result of the recent recession, millions of Americans have had to cope with chronic unemployment. Tony is one of them.
Maybe Today Will Be the Day
Tony wakes up at 5:30 every morning and makes coffee. He arranges his laptop, phone, and notepad on the kitchen table. And then he waits for the phone to ring. Unemployed for the last 16 months after losing his job as a transportation sales manager, Tony spends the day sending out resumes and cover letters. But most days nothing happens. “The worst moment is at the end of the day when it’s 4:30 and you did everything you could, and the phone hasn’t rung, the emails haven’t come through,” says Tony. He asks himself what he is doing wrong. Tony misses his old routine of getting dressed in the morning and going out to work. But he tries to stay optimistic. “You always have to hope that that morning when you get up, it’s going to be the day.” (Based on Kwoh, 2010)
During the recent recession, unemployment reached a peak of 10.6 percent of the labor force in January 2010. Although things have improved since then, in almost every community, one can find workers who have been laid off from jobs they had held for many years and who are facing the end of their unemployment compensation. Unemploy- ment is an especially severe problem for young minority males, many of whom live in a permanent economic depression with few job prospects. Rates of unemployment for blacks are twice as high as they are for whites (Bureau of Labor Statistics, 2013).
Managing the stress associated with unemployment requires great coping strength, especially for people who have previously earned an adequate living. Some people (like Tony in the case example above) find ways to stay focused and motivated, even though this can be very diffi- cult at times. For others, however, unemployment can have serious long-term effects. One of the most disturbing find- ings is that unemployment, especially if it is prolonged, increases the risk of suicide (Borges et al., 2010; Classen & Dunn, 2011). Unemployment also takes its toll on other family members, especially children. When children live in families where a parent has lost a job, they are 15 percent more likely to have to repeat a grade at school (Stevens & Schaller, 2009).
Posttraumatic Stress Disorder In DSM-5 posttraumatic stress disorder is grouped with other disorders in a new diagnostic category called trauma- and stressor-related disorders. Adjustment disorder, which
The diagnosis of PTSD first entered the DSM in 1980 (see the Criteria for Posttraumatic Stress Disorder box later in this chapter for current clinical criteria). At this time, psychiatry began to realize that many veterans were emo- tionally scarred and unable to return to normal civilian life after their military service in Vietnam. The proposal to include PTSD in the diagnostic system was initially opposed, not least because including a disorder that had a clear and explicit cause (trauma) was inconsistent with the atheoretical nature of the DSM. Nonetheless, a consensus emerged that any extreme, terrifying, and stressful event
Traumatic stressors include combat, rape, and experiencing a natural disaster such as an earthquake, flood, tornado, or hurricane.
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met the symptom criteria for PTSD within 2 weeks of the assault. One month after the rape, this figure had declined to 63.3 percent of women, and after 3 months, 45.9 percent of the women were diagnosed with PTSD. Natural recov- ery with time is therefore a common pattern.
In the case of PTSD, however, the stress symptoms fail to abate even when the traumatic event has passed and the danger is over. Instead, what becomes established is a memory of the traumatic event that results in the trau- matic event being reexperienced involuntarily and with the same full emotional force that characterized the origi- nal experience (McNally, 2015). Although being able to remember potentially life-threatening experiences is highly adaptive for our overall survival, having prolonged, intense, and intrusive memories that cause extreme stress symptoms is not. This is why PTSD is considered to be a mental disorder.
that was life threatening and outside the ordinary bounds of everyday experience could lead to psychological symp- toms similar to those experienced by the Vietnam veterans. In other words, at the time of its entry into the DSM (which is after all a manual of mental disorders), PTSD was viewed as a normal response to an abnormal stressor (see McNally, 2008). In the Thinking Critically about DSM-5 box we describe how changes to the diagnostic criteria for PTSD have changed over time.
Traumatic stressors include combat, rape, being con- fined in a concentration camp, and experiencing a natural disaster such as a tsunami, earthquake, or tornado. These are all terrible experiences and, as would be expected, stress symptoms are very common in the immediate after- math of a traumatic event. However, for most people, these symptoms decrease with time. Rothbaum and Foa (1993) reported that 95 percent of women who had been raped
DSM-5 Thinking Critically about DSM-5 Changes to the Diagnostic Criteria for PTSD
When PTSD was first introduced into the DSM, the diagnostic
criteria required exposure to a traumatic event that was “outside
the range of usual human experience” and that would cause
“significant symptoms of distress in almost anyone.” The exem-
plars provided included rape, earthquakes, torture, and military
combat. In other words, the emphasis was on the nature of the
stressor itself and not on the emotional response of the victim
(Breslau & Kessler, 2001; McNally, 2008; Shalev, 2009).
A major change occurred with DSM-IV. Not only was there
a broadening of the range of experiences that could now be used
to diagnose PTSD, but it was also required that the person’s
response involve “intense fear, helplessness or horror.” Qualifying
events could now include learning about the death of a close
friend or relative (as long as the death was sudden and unex-
pected), being diagnosed with a life-threatening illness, or learn-
ing about traumatic events experienced by others. In short, there
was a change in emphasis from the characteristics of the stressor
to the experience of the victim. Rather than conceptualizing
PTSD as a normal response to an abnormal stressor, in DSM-IV,
PTSD was viewed as a pathological response to an extreme form
of stress (McNally, 2008).
The implications of these changes were not trivial. Using the
wider variety of stressors permitted in DSM-IV, a survey of com-
munity residents revealed that the vast majority (89.6 percent)
reported that they had been exposed to a traumatic event that
(given also the required level of emotional response and pres-
ence of other symptoms) would potentially qualify them for
PTSD diagnosis (Breslau & Kessler, 2001). In most cases, the
traumatic event was learning of the sudden and unexpected
death of a loved one. Moreover, females who reported
traumatic events were much more likely than males to also
report that they had had an emotional reaction that was
severe enough for them to qualify for the PTSD diagnosis. So
not only was the definition of a traumatic event broadened,
but the kind of emotional response that qualifies for PTSD was
much more likely to be reported by women than by men
(Pratchett et al., 2010).
In DSM-5, the diagnostic criteria for PTSD have been tight-
ened. The traumatic event must now be experienced by the per-
son directly, either because the event happens to you or because
you witness, in person, something traumatic happening to
someone else. No longer is it possible to experience trauma indi-
rectly through electronic media (which could occur when some-
one watches television footage of a terrible event). As before,
there is also a provision for experiencing trauma by learning of
the death of another person. However, the person must be a
close friend or relative and their death must have been violent or
accidental. Yet another change is the removal of the requirement
that the person respond in a particular way (i.e., with fear, help-
lessness, or horror) because this confounds the response with
the event itself (McNally, 2009) and also makes it more likely that
women will receive the diagnosis. Defining trauma exposure is
difficult to do. Nonetheless, we believe that the modifications that
have been made to the DSM criteria are good overall. Tightening
the diagnostic criteria in these ways means that PTSD is more
likely to remain a distinct diagnosis reserved for people who have
experienced devastating life events. No longer will it be possible
to diagnose PTSD in people who merely watch traumatic events
on their computer or television screens and are very distressed
by what they see.
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moment with the largest emotional impact (e.g., “Perpetra- tor standing at the window with the knife”; Hackmann et al., 2004). The clinical symptoms of PTSD are shown in the Criteria for Posttraumatic Stress Disorder box. Note that these symptoms are grouped into four main areas and con- cern the following:
1. Intrusion: Recurrent reexperiencing of the traumatic event through nightmares, intrusive images, and phys- iological reactivity to reminders of the trauma. (In DSM-IV ruminative thoughts about the trauma were also considered to reflect intrusion. This is not the case in DSM-5.)
2. Avoidance: Efforts to avoid thoughts, feelings, or reminders of the trauma.
3. Negative alterations in cognitions and mood: This includes such symptoms as feelings of detachment as well as negative emotional states such as shame or anger, or distorted blame of oneself or others.
4. Arousal and reactivity: Hypervigilance, excessive response when startled, aggression, and reckless behavior.
The symptoms are illustrated in the following case.
Abducted and Terrorized
Mr. A. was a married accountant, the father of two, in his early 30s. One night, while out running an errand, he was attacked by a group of young men. They forced him into their car and took him to a deserted country road. There they pulled him from the car and began beating and kicking him. They took his wallet, began taunting him about its contents (they had learned his name, his occupation, and the names of his wife and children), and threatened to go to his home and harm his family. Finally, after brutalizing him for several hours, they tied him to a tree. One man held a gun to his head. Mr. A. begged and pleaded for his life; then the armed assailant pulled the trigger. The gun was empty, but at the moment the trigger was pulled, Mr. A. defecated and urinated in his pants. Then the men untied him and left him on the road.
Mr. A. slowly made his way to a gas station and called the police. [One of the authors] was called to examine him and did so at intervals for the next 2 years. The diagnosis was PTSD. Mr. A. had clearly experienced an event outside the range of normal human experience and was reexperiencing the event in various ways: intrusive recollections, nightmares, flashbacks, and extreme fear upon seeing groups of tough-looking young men. He was initially remarkably numb in other respects: He felt estranged and detached. He withdrew from his family, lost interest in his job, and expected to die in the near future. Mr. A. also showed symptoms of increased physiological arousal. His sleep was poor, he had difficulty concentrating, and he was easily startled. When Mr. A. first spoke about his abduction in detail he actually soiled himself at the moment he described doing so during the original traumatic experience.
Mr. A. received treatment from a psychiatrist for the next 2 years. This consisted of twice-weekly individual psychotherapy as
Acute Stress Disorder The diagnosis of PTSD requires that symptoms must last for at least 1 month. What this means is that, in the study just described, the women who had symptoms within 2 weeks of the assault would not be diagnosed with PTSD. Instead, the diagnosis would be acute stress disorder. Acute stress disorder is a diagnostic category that can be used when symptoms develop shortly after experiencing a traumatic event and last for at least 2 days. The existence of this diagnosis means that people with symptoms do not have to wait a whole month to be diagnosed with PTSD. Instead they can receive treatment as soon as they experi- ence symptoms (Cardeña & Carlson, 2011). Moreover, if symptoms persist beyond 4 weeks, the diagnosis can be changed from acute stress disorder to posttraumatic stress disorder. Studies show that people who develop an acute stress disorder shortly after traumatic event are indeed at increased risk of developing PTSD (Kleim et al., 2007). This highlights the importance of early intervention.
Of course, PTSD is not the only disorder that can develop after a traumatic experience. Bryant and col- leagues (2010) conducted a prospective study of a large sample of people who were injured in accidents. They were assessed at the time of their injury and then fol- lowed up 3 and 12 months later. The investigators found that, 12 months after injury, 31 percent of patients reported a psychiatric disorder, and 22 percent of them had a disor- der they had never experienced before. The most common disorders were depression (9 percent), generalized anxiety disorder (9 percent), and PTSD (6 percent).
in review • What is an adjustment disorder?
• What kinds of stressors are potential triggers for the develop- ment of an adjustment disorder?
• What is the main difference between acute stress disorder and PTSD?
Posttraumatic Stress Disorder: Causes and Risk Factors 5.7 Describe the clinical features of and risk factors for
posttraumatic stress disorder.
In PTSD a traumatic event is thought to cause a pathological memory that is at the center of the characteristic clinical symptoms associated with the disorder (McNally, 2013). These memories are often brief fragments of the experience and typically concern events that happened just before the
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DSM-5 Criteria for. . . Posttraumatic Stress Disorder
Note: The following criteria apply to adults, adolescents, and chil- dren 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 threat- ened 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 memo- ries 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 indi- vidual feels or acts as if the traumatic event(s) were recur- ring. (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 trau- matic 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 trau- matic event(s).
D. Negative alterations in cognitions and mood associated with the traumatic event(s), beginning or worsening after the trau- matic event(s) occurred, as evidenced by two (or more) of the following:
1. Inability to remember an important aspect of the trau- matic 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 expec- tations 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 con- sequences of the traumatic event(s) that lead the indi- vidual 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 trau- matic 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.
Source: Reprinted with permission from the Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition (Copyright 2013). American Psychiatric Association.
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Estimates of the prevalence of PTSD vary widely across different studies (Sundin et al., 2010). One reason for this is that rates of PTSD seem to differ according to the type of trauma that is experienced. More specifically, trau- matic events that result from human intent (such as rape, as noted above) are more likely to cause PTSD than are traumatic events (such as accidents and natural disasters) that are not personal in nature (see Charuvastra & Cloitre, 2008). For example, Shalev and Freedman (2005) compared rates of PTSD after car accidents and after terrorist attacks in the same community in the Middle East. Interviews were conducted 1 week and 4 months after the traumatic event had occurred. Although there were no differences in the symptoms that people reported at the 1-week interview, at 4 months, rates of PTSD were much higher in the terrorist attack survivors than in those who had survived the car accidents. Traumatic events involving humans who do terri- ble things are perhaps even more difficult to come to terms with because they can destroy the sense of safety we often assume comes from being a member of a rule-abiding and lawful social group.
Another factor that is crucially important with respect to the development of PTSD is the degree of direct expo- sure to the traumatic event. After reviewing all published disaster research over a 25-year period, Neria, Nandi, and Galea (2008) have estimated that rates of PTSD range between 30 and 40 percent for adults who are directly exposed to disasters. The prevalence of PTSD in rescue workers, on the other hand, tends to be lower (5–10 per- cent), probably because they are not directly exposed to the traumatic event when it is happening. Nonetheless, these figures highlight the risk of PTSD in rescue workers. They also show that disasters leave large numbers of trauma- tized people in their wakes.
Finally, we should point out that differences in rates of PTSD across different studies may sometimes be linked to the way that PTSD is defined and the manner in which it is assessed. Estimates based on questionnaires tend to be higher than those based on clinical interviews. For exam- ple, in a study of Dutch veterans of the Iraq War, question- naire assessments yielded rates of PTSD of 21 percent. However, when structured diagnostic interviews were used, only 4 percent of veterans met the criteria for PTSD (Engelhard et al., 2007). Reasons for the overestimates when questionnaire measures are used include misunder- standing the meaning of items on the questionnaire, pres- ence of symptoms that cause little impairment in functioning, and inclusion of symptoms that began at times other than during or after a traumatic event.
THE TRAUMA OF MILITARY COMBAT In a combat sit- uation, with the continual threat of injury or death and repeated narrow escapes, a person’s ordinary coping meth- ods are relatively useless. The adequacy and security the
well as antidepressant medications. A focus of the therapy was the sense of shame and guilt Mr. A. felt over his behavior during his abduction. He wished he had been more stoic and had not pleaded for his life. With the help of his therapist, Mr. A. came to see that his murderous rage at his abductors was understandable, as was his desire for revenge. He was also able to accept that his response to his experience was likely similar to how others might have responded if faced with the same circumstances. By the end of treatment Mr. A. was almost without symptoms, although he still became somewhat anxious when he saw some groups of young men. Most important, his relationship with his wife and children was warm and close, and he was again interested in his work.
Prevalence of PTSD in the General Population Estimates from the National Comorbidity Survey Repli- cation (NCS-R) suggest that the lifetime prevalence of PTSD in the United States is 6.8 percent (Kessler, Berglund, Demler, et al., 2005). However, this figure obscures the gender difference in the prevalence of PTSD. The NCS-R data show that the lifetime prevalence of PTSD is higher in women. Over the course of their lives, 9.7 percent of women and 3.6 percent of men will develop this disorder.
The difference in the prevalence of PTSD in men and women is interesting, not least because studies show that men are much more likely to be exposed to traumatic events (Tolin & Foa, 2006). Some have suggested that the gender difference reflects the fact that women are more likely to be exposed to certain kinds of traumatic experi- ences, such as rape, that may be inherently more traumatic (Cortina & Kubiak, 2006). However, even when the type of traumatic event is controlled for, women still show higher rates of PTSD and tend to have more severe symptoms (Tolin & Foa, 2006). This suggests that there are differences between men and women that may determine their risk of developing PTSD after experiencing trauma.
Rates of PTSD after Traumatic Experiences Disasters, both naturally occurring and human caused, are far from rare occurrences. In a typical year countless people are exposed to the kinds of traumatic events that can cause PTSD. For example, more than 900 earthquakes with a magnitude between 5 and 8 on the Richter scale occur annually throughout the world (Naeem et al., 2011). Tsunamis also devastate coastal villages, and hurricanes, tornadoes, and floods destroy lives and livelihoods. Of course, some places are safer than others. Not surpris- ingly, rates of PTSD throughout the world tend to be lower in areas where people experience fewer natural disasters and where wars and organized violence are less common.
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surprisingly, this has taken a toll on the mental health of those team members.
The high prevalence of postdeployment mental disor- ders in these military personnel continues to be a major source of concern. A recent meta-analysis has reported rates of PTSD of 12.9 percent in military personnel follow- ing deployment to Iraq and a rate of 7.1 percent for those who served in Afghanistan (Hines et al., 2014). The figures for Iraq veterans are comparable to the rates of PTSD reported for veterans of the Vietnam War (12–16 percent; Thompson et al., 2006) and Gulf War (12 percent; Kang et al., 2003), but higher than rates of PTSD in U.K. military personnel following deployment to Iraq or Afghanistan (4.8 percent; see Iversen et al., 2009). In addition to PTSD, rates of depression, aggression, and problems with postde- ployment alcohol misuse are also elevated (Seal et al., 2009; Thomas et al., 2010).
As might be expected, rates of PTSD tend to be higher in military personnel who were deployed into a combat role versus a support role (12.4 versus 4.9 percent). Reflect- ing this, army and marine personnel had higher rates of PTSD (13 and 10 percent, respectively) than those who had served in the navy (7 percent) or air force (3 percent; Hines et al., 2014). There is also evidence that theater-specific duties may shape some of the symptoms that veterans have. In addition to PTSD, clinicians are seeing veterans with compulsive checking behaviors.
The military is also trying to cope with another serious problem—soldier suicide. During 2013, according to the most recent figures, 259 members of the armed forces took their own lives and many more made suicide attempts (U.S. Department of Defense, 2014). Most of these suicides resulted from self-inflicted gunshot wounds. Suicide rates in the U.S. Army are especially high. Clay’s story serves as a tragic reminder of how destructive and invisible some of the wounds of war can be.
A Warrior Takes His Own Life
Clay was a handsome and friendly 28-year-old. A former Marine cor- poral, he received a Purple Heart after taking a bullet in Iraq and later returned to combat in Afghanistan. After his deployment was over Clay became involved in humanitarian work in Chile and Haiti. He lob- bied in Washington to improve the disability claims process for veter- ans and was chosen to appear in a public service announcement to remind veterans that they were not alone. But Clay’s smiles and boundless energy were masks covering the emotional pain he lived with every day. Clay suffered from PTSD and depression. He also experienced survivor guilt, asking himself why he had survived when many people he had served with had died. One day in the early spring, Clay locked the door of his apartment and shot himself. His death leaves a void in the lives of his family and friends. It also highlights the need for continued efforts within the military to address the problem of suicide by members of the armed forces. (Based on Helfling, 2011)
person has known in the relatively safe and dependable civilian world are completely undermined. Combat brings with it constant fear, unpredictability, many uncontrollable circumstances, and the necessity of killing. Other factors may further contribute to the overall stress experienced by soldiers. These include separation from loved ones, reduc- tions in personal freedom, sleep deprivation, extreme and harsh climate conditions, and increased risk for disease.
Many people who have been involved in the turmoil of war experience devastating psychological problems for months or even years afterward (Garakani et al., 2004). During World War I, traumatic reactions to combat condi- tions were called “shell shock,” a term coined by a British pathologist, Col. Frederick Mott (1919), who regarded these reactions as organic conditions produced by minute brain hemorrhages. It was gradually realized, however, that only a small percentage of such cases represented physical injury. Most victims were suffering instead from the general combat situation, with its physical fatigue, ever-present threat of death or mutilation, and severe psy- chological shocks. During World War II, traumatic reac- tions to combat were known as operational fatigue and war neuroses, before finally being termed combat fatigue or com- bat exhaustion in the Korean and Vietnam Wars. Even the latter terms were none too aptly chosen because they implied that physical exhaustion played a more important role than was usually the case.
It has been estimated that in World War II, 10 percent of Americans in combat developed combat exhaustion. However, the actual incidence is not known because many soldiers received supportive therapy at their battalion aid stations and were returned to combat within a few hours. Recent evaluations of World War II psychiatric casualty files concluded that this practice of “forward psychiatry” was not effective at returning soldiers with shell shock to combat, but their improved mood and adjustment allowed them to be reassigned to noncombat roles, resulting in reduced manpower losses overall (Jones et al., 2007). In World War II, combat exhaustion was the greatest single cause of loss of personnel (Bloch, 1969).
MENTAL HEALTH CONSEQUENCES OF DEPLOYMENT TO IRAQ AND AFGHANISTAN Around 2.5 million members of the armed forces were deployed for operations in Iraq and Afghanistan according to U.S. Department of Defense figures. During these deployments these veterans were exposed to many traumatic experiences and had to function under conditions of sustained threat. In one study, the overwhelming majority (92 percent) of Army soldiers and Marines in Iraq reported that they had been attacked or ambushed, and 86 percent reported knowing someone who was killed or seriously injured (Hoge et al., 2004). We should also keep in mind that some brigade combat teams were deployed multiple times (Thomas et al., 2010). Not
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Given that someone has been exposed to a traumatic event, what factors increase risk for developing PTSD? As we have already noted, being female is a risk factor. Other individual risk factors that have been identified by researchers include higher levels of neuroticism (having a tendency to experience negative affect), having preexisting problems with depression and anxiety, and having a fam- ily history of depression, anxiety, and substance abuse (see McNally, 2015; Wilk et al., 2010). Reflecting this, a prospec- tive longitudinal study of military personnel has confirmed that psychiatric problems measured predeployment sig- nificantly increase the risk of developing PTSD postde- ployment (Sandweiss et al., 2011). This highlights the importance of mental health screening prior to deployment and the need to provide additional resources and support for soldiers who may be most vulnerable.
Low levels of social support have also been noted as a risk factor. One problem here, however, is that social sup- port is typically assessed after people have developed PTSD. This makes it difficult to separate cause from conse- quence. Do the emerging symptoms of PTSD alienate peo- ple and so reduce the available level of social support? Or is a lack of adequate social support causally implicated in the development of PTSD? It is also possible that both pro- cesses are operating. Also relevant are the appraisals peo- ple make of their own stress symptoms shortly after the trauma. If people believe that their symptoms are a sign of personal weakness or if they believe that others will be ashamed of them because they are experiencing symp- toms, they are at increased risk for developing PTSD, even when the level of initial symptoms is statistically controlled (Dunmore et al., 2001).
There is even some very new evidence suggesting that people who have disturbing thoughts or images about traumatic events that could happen in the future may be at elevated risk of developing PTSD later. Bertsen and Rubin (2015) asked Danish soldiers who were about to be deployed to Afghanistan to complete a measure of what
Causal Factors in Posttraumatic Stress Disorder The study of causal risk factors that might be involved in the development of PTSD has been a controversial area (McNally, 2008). There are two major reasons for this. First, the very notion of PTSD makes it explicit that PTSD is caused by experiencing trauma. So why should we look any further if we wish to know what causes PTSD? The second concern is that, if some people are more likely to develop PTSD in the face of severe stress than other people are, might this not lead to double victimization, with vic- tims of trauma also being stigmatized and being blamed for the troubles that they have?
On the other side of the issue, we know that not every- one who is exposed to a traumatic event will develop PTSD. This suggests that some people may be more vulnerable to developing PTSD than others. To prevent and better treat this disorder, we therefore need to understand more about the factors that are involved in its development.
As we have already noted, the nature of the trau- matic stressor and how directly it was experienced can account for much of the differences in stress response (see Dohrenwend et al., 2013). For example, there is a close relationship between the total number of people killed and wounded and the number of psychiatric casualties in war (Jones & Wessely, 2002). Soldiers who report killing or being responsible for killing during their deployment are also more vulnerable to developing PTSD (Maguen et al., 2010).
If the level of stress is high enough, then, the average person can be expected to develop some psychological dif- ficulties (which may be either short lived or long term) fol- lowing a traumatic event. But why is the breaking point of one person different from the breaking point of another? In the sections below, we highlight some areas that appear to be important.
Individual Risk Factors When it comes to risk for PTSD, we need to keep two things in mind: As has been noted by researchers in this field, there is risk for experiencing trauma and there is also risk for PTSD given that there has been exposure to trauma (see McNally, 2013). Not everyone is at equal risk when it comes to the like- lihood that she or he will experience a traumatic event. Cer- tain occupations, such as being a soldier or a firefighter, carry more risk than others, such as being a librarian. Risk factors that increase the likelihood of being exposed to trauma include being male, having less than a college education, having had conduct problems in childhood, having a family history of psychiatric disorder, and scoring high on mea- sures of extraversion and neuroticism (Breslau et al., 1991, 1995). Rates of exposure to traumatic events are also higher for black Americans than they are for white Americans.
Certain occupations place people at higher risk of experiencing a traumatic event.
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Biological Factors Given that PTSD is a stress disorder, you might expect that people with this disorder would have high levels of stress hormones such as cortisol. However, this does not seem to be the case (Pittman et al., 2012; Young & Breslau, 2004). Under conditions of imposed experimental stress (trauma reminders, cognitive challenges), people with PTSD do seem to show an exaggerated cortisol response (de Kloet et al., 2006). However, baseline levels of cortisol are often very similar in people with PTSD when they are compared to those of healthy controls (Meewisse et al., 2007).
Gender may be an important factor here, however. Women with PTSD do seem to have higher levels of base- line cortisol than women without PTSD. This is not so for men with and without PTSD. Another interesting finding is that levels of cortisol tend to be lower in people with PTSD who have experienced physical or sexual abuse. In other words, the type of trauma may be an important fac- tor (Meewisse et al., 2007). Although many of the findings in this area are confusing, researchers are still exploring biological dysregulations in PTSD.
Another focus of research interest is gene–environment interactions. Earlier we discussed how people with a particular form of a particular gene (the 5HTTLPR, or sero- tonin transporter gene) seem to be more at risk for devel- oping depression in the face of four or more life events. Data now suggest that this gene may also be a risk factor for the development of PTSD. Kilpatrick and colleagues (2007) collected DNA data and interviewed 589 adults from Florida 6 to 9 months after the 2004 hurricane season. The prevalence of post-hurricane PTSD in the sample over- all was 3.2 percent. Risk factors for developing PTSD were a high level of exposure to the hurricanes and low levels of social support. However, people who had the high-risk (s/s) genotype of the serotonin-transporter gene were at especially high risk for the development of PTSD if they also had high hurricane exposure and low social support. For those in this group, the rate of PTSD was 14.8 percent— 4.5 times higher. People with the s/s genotype were also more likely to develop depression if they had high hurri- cane exposure and low social support. These findings sug- gest that having the s/s form of the serotonin-transporter gene makes a bad situation worse. People with this geno- type may be especially susceptible to the effects of trau- matic stress, particularly if they also have low levels of social support.
A recent study sheds some light on why this might be. Disner and colleagues (2013) have reported that soldiers with two short alleles of the serotonin transporter gene (s/s genotype) were more likely to develop a bias toward look- ing longer at fearful facial stimuli after they had been deployed to Iraq versus before deployment. This gaze bias was found, even after other relevant factors (such as PTSD
they called pretraumatic stress reactions. This asked about how much people had been bothered by thoughts or images of possible future stressful experiences, or whether they had strong physical reactions when something reminded them of a stressful event they might experience at a later time. The measure of pretraumatic stress that the soldiers completed before deployment predicted their level of PTSD symptoms both during and after their ser- vice in Afghanistan, even after such factors as combat exposure and baseline PTSD symptoms were accounted for. This finding is potentially very important. It chal- lenges our understanding of PTSD as a disorder that is solely related to past experiences. Instead the results appear to highlight the importance of mental imagery, suggesting that pre- and posttraumatic stress reactions might have much in common.
On the other side of the coin, are there factors that may be protective and buffer against PTSD? Good cogni- tive ability seems to be important here. Breslau, Lucia, and Alvarado (2006) collected IQ data from 6-year-old chil- dren who lived in and around Detroit. When these chil- dren reached the age of 17, they were interviewed and assessed both for exposure to trauma and for PTSD. The children who at age 6 had IQ scores above 115 were less likely to have experienced a traumatic event by age 17; furthermore, if they had been exposed to trauma, they were at lower risk for developing PTSD. These findings suggest that having a higher IQ may be protective against experiencing trauma and developing PTSD because chil- dren who had average or below-average IQ scores were at similar risk for PTSD.
Similar findings have also been reported for Vietnam veterans. Kremen and colleagues (2007) collected informa- tion from a large sample of twins and also obtained infor- mation about the twins’ cognitive ability scores before they went to serve in Vietnam. All of the men involved in the study were subsequently exposed to traumatic events dur- ing their military service. Compared with men who had scored in the lowest quartile on the Armed Forces Qualifi- cation Test (a measure of cognitive ability), men who had scored in the highest quartile had a 48 percent lower risk of developing PTSD.
Why might higher pretrauma cognitive abilities pro- vide protection against PTSD? One possibility is that individuals with more intellectual resources might be better able to create some meaning from their traumatic experiences and translate them into a personal narrative of some kind. Earlier in this chapter, we discussed the therapeutic benefits of systematically writing about dis- tressing events (Pennebaker, 1997). Perhaps people with higher cognitive abilities are more naturally able to incorporate their traumatic experiences into their life narratives in ways that are ultimately adaptive and emo- tionally protective.
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glucocorticoids) has a negative impact on brain areas (like the hippocampus) that are important for healthy emotional functioning. Why then should we not expect to see some commonalities when we look at people who have disor- ders in which stress is implicated?
Sociocultural Factors Being a member of a minority group seems to place people at higher risk for developing PTSD. DiGrande and col- leagues (2011) studied 3,271 civilians who were evacuated from the World Trade Center towers on September 11, 2001. Two to three years after the attacks, 15 percent of peo- ple were assessed as having PTSD. Compared with whites, African American and Hispanic survivors were more likely to have PTSD. Echoing the discussion of resilience earlier in this chapter, being more educated and having a higher annual income were also factors associated with lower rates of PTSD overall.
Returning to a negative and unsupportive social envi- ronment can also increase vulnerability to posttraumatic stress (Charuvastra & Cloitre, 2008). For example, in a 1-year follow-up of Israeli men who had been psychiatric war casualties during the Yom Kippur War, Merbaum (1977) found that not only did these men continue to show extreme anxiety, depression, and extensive physical com- plaints, but (in many instances) they also appeared to become more disturbed over time. Merbaum hypothesized that the men’s further psychological deterioration was due to the negative attitudes of the community. In a country so reliant on the strength of its army for its survival, consider- able stigma is attached to psychological breakdown in combat. Because of this stigma, many of the men were experiencing not only isolation within their communities but also self-recrimination about what they perceived as their own failure. These feelings exacerbated the soldiers’ already stressful situations.
Sociocultural variables also appear to play a role in determining a person’s adjustment to combat. Important
symptoms and depression) had been controlled. What these findings suggest is that people with the s/s form of the serotonin-transporter gene may be especially sensitive to certain environmental experiences such as war zone stress, and that one consequence of this is that they become more attentive to negative stimuli. In other words, the interaction between certain genes and certain environmen- tal experiences may prime the attentional system to develop cognitive biases toward negative stimuli. Although this might possibly be adaptive in combat set- tings, it could contribute to the development of psychopa- thology at a later time.
What do we know about the brains of people with PTSD? Studies show that a brain area called the hippocam- pus seems to be reduced in size in people with PTSD (Pitt- man et al., 2012). The hippocampus is a brain area known to be involved in memory. It is also a brain area known to be responsive to stress. In a landmark study, Gilbertson and colleagues (2002) measured the volume of the hippocam- pus in combat veterans with and without PTSD. The results showed that the veterans with PTSD had smaller hippo- campal volumes than did the veterans without PTSD. The reason this study is so important, however, is that all the men were MZ (identical) twins. And when Gilbertson and colleagues looked at the volume of the hippocampus in the healthy co-twins of the combat veterans with PTSD, they found that these men also had small hippocampal volumes, just like their brothers. In contrast, the combat veterans who did not have PTSD, as well as their twins (who had not been involved in combat), had similar (and larger) hippocampal volumes. What these findings suggest, then, is that for rea- sons we do not yet understand, small hippocampal volume may be a vulnerability factor for developing PTSD in peo- ple who are exposed to trauma. There is also a possibility that trauma reduces the size of the hippocampus to some extent. A meta-analysis shows that people who have been exposed to trauma (but who do not have PTSD) have smaller hippocampi than people who have not been exposed to trauma (Woon et al., 2010). In other words, reduced hippocampal size could be both a risk factor for PTSD and also be a consequence of trauma exposure.
A major problem with research in this area is that many of the brain abnormalities associated with PTSD (including reduced hippocampal size) are also found in people who are depressed. Because PTSD and depression are highly comorbid and co-occurring disorders, it is there- fore hard for researchers to be sure which brain abnormali- ties are specific to PTSD and which might stem from depression (Kroes et al., 2011). But perhaps it is a bit naïve to expect that PTSD would be associated with brain abnor- malities that are completely unique and distinct and that are not shared with any other disorders. We know that stress plays a role in the development of depression and the development of PTSD. We also know that stress (via
Group cohesiveness and good leadership can help soldiers cope better with the inevitable stress of combat.
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The nature and extent of PTSD are somewhat controver- sial, however (McNally, 2015). The delayed version of PTSD is less well defined and more difficult to diagnose than dis- orders that emerge shortly after the precipitating incident (Andrews et al., 2007). Moreover, with the exception of Viet- nam veterans, cases of delayed-onset PTSD are exceedingly rare, with only one case of delayed PTSD being reported in a civilian study (Breslau et al., 1991). Reports of delayed stress syndrome among Vietnam combat veterans are often diffi- cult to relate explicitly to combat stress because these people may also have other significant adjustment problems. Some authorities have questioned whether a delayed reaction should be diagnosed as PTSD at all; instead, some would categorize such a reaction as another type of disorder. For example, people with adjustment difficulties may errone- ously attribute their present problems to specific incidents from their past, such as experiences in combat.
Also troubling are findings that show that 7 percent of men seeking treatment for combat-related PTSD had either never served in Vietnam or had not been in the military at all (Frueh et al., 2005). The wide publicity given to delayed PTSD and the potential for receiving service-connected disability payments may be relevant factors here. Based on their analysis of a large federal database, a group of labor economists has concluded that the enormous increase in PTSD disability claims made by Vietnam veterans results more from financial need than it does from psychiatric dis- order (Agrist et al., 2010).
in review • What risk factors are associated with experiencing trauma?
• What risk factors are implicated in the development of PTSD?
• Why might high IQ be protective against PTSD?
• How might genetic factors play a role in the development of PTSD?
• What is controversial about the diagnosis of delayed PTSD?
Prevention and Treatment of Stress Disorders 5.8 Explain the treatment approaches that are used to
help people with PTSD.
Prevention One way to prevent PTSD is to reduce the frequency of traumatic events. Although natural disasters are inevita- ble, efforts could be made to lessen the access that adoles- cents have to firearms. This could reduce the frequency of school violence and shootings. Other changes in the law and in social policy might also yield beneficial effects.
It is also worth considering whether it is possible to pre- vent maladaptive responses to stress by preparing people in
factors include justification for the combat and how clear and acceptable the war’s goals are to the person whose life is being put in harm’s way (Hoge et al., 2004). Identifica- tion with the combat unit and the quality of leadership also make a difference (Jones & Wessely, 2007).
Today, military psychiatrists apply techniques that have been learned during the past century to help reduce psychological casualties. Interventions that promote morale and encourage cohesion that were developed dur- ing World War II and the Korean and Vietnam Wars have proved effective at reducing psychological casualties occurring among U.S. troops during their deployments to the Afghanistan and Iraqi war zones (Ritchie, 2007). Stra- tegically placed combat stress control teams deploy as soon as is practical after combat engagements to provide timely counseling to troops. To improve the morale of troops, the military also makes an effort to provide breaks from long engagements by providing “safe” zones that include such improvements as air conditioning, regular mail delivery, and good food. One of the most effective morale builders among troops has been the availability of the Internet at most established facilities in both Iraq and Afghanistan.
Having access to the Internet improves the morale of soldiers during long deployments.
Long-Term Effects of Posttraumatic Stress As we have already noted, soldiers who have experienced combat exhaustion may show symptoms of posttraumatic stress for sustained periods of time (Shalev, 2009; Solomon & Mikulincer, 2007). If it develops, PTSD can be a severe and chronic condition. Moreover, in some cases, soldiers who stood up exceptionally well during their deployments have experienced delayed PTSD on their return home. The difficulties readjusting to life as a civilian after extended periods away from home cannot be underestimated. Feel- ings of responsibility associated with killing, as well as feelings of guilt for having survived when friends and unit peers did not, may also play a role here.
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The use of cognitive-behavioral techniques to help people manage potentially stressful situations or difficult events has been widely explored (Brewin & Holmes, 2003). This preventive strategy, often referred to as stress- inoculation training, prepares people to tolerate an antic- ipated threat by changing the things they say to themselves before or during a stressful event. As helpful as these approaches are, however, it is almost impossible to be prepared psychologically for most disasters or trau- matic situations, which by their nature are often unpre- dictable and uncontrollable.
Given this, what might be done to help people who have just experienced a traumatic event? How might we reduce risk for PTSD? Strange as it may seem, there is rea- son to believe that playing Tetris might have some benefits (see the World Around Us box).
advance and providing them with information and coping skills. As we noted earlier, this approach has been helpful for people experiencing the stress of major surgery. Other research further supports the idea that psychological pre- paredness can foster resilience in political activists who are arrested and tortured (Basoglu et al., 1997). Adequate train- ing and preparation for extreme stressors may also help sol- diers, firefighters, and others for whom exposure to traumatic events is highly likely. Findings from a study that examined PTSD in rescue and recovery workers at the World Trade Center site are consistent with this (Perrin, DiGrande, et al., 2007). Rates of PTSD differed markedly across occupations, with lower rates being reported in police (6.2 percent) and the highest rates being found in volunteers (21.2 percent) who had occupations that were completely unrelated to res- cue and recovery work (e.g., finance or real estate).
The World Around Us Does Playing Tetris After a Traumatic Event Reduce Flashbacks?
“Flashbacks,” or intrusive memories, are a hallmark feature of PTSD. They often involve visual experiences where the person reexperiences the traumatic event. Because of this flashbacks can be very frightening. But can flashbacks be prevented?
In a clever and creative study, Holmes and colleagues (2009) exposed a group of research participants to 12 minutes of graphic film footage depicting scenes of injury and death. Thirty minutes after seeing the footage, some participants played Tetris for 10 min- utes while others (control condition) sat quietly for the same period of time. All participants then used a diary to record the number of flashbacks they experienced over the course of the following week. Compared to the participants in the control condition, those people who played Tetris after viewing the trauma film reported significantly fewer involuntary flashbacks (4.6 versus 12.8 for controls).
But why should this be? Forming a memory involves a neuro- biological process. But in the early stages of this process (within the first 6 hours), the memory consolidation process can be disrupted. The brain also has a limited capacity. Because Tetris is a visuospatial task, playing Tetris shortly after the traumatic experience may dis- rupt the consolidation of traumatic visual memories. In other words, the new images of Tetris compete with the earlier visual images from the film, making the visual memories of the film less strong.
In other work, this same group of researchers has shown that simply being distracted after viewing the traumatic film does not reduce the frequency of later flashbacks (Holmes et al., 2010). In fact, participants who were assigned to a verbal task condition (playing Pub Quiz—a general knowledge, verbal computer game) showed an increased number of flashbacks compared to both the group that played Tetris and the group that did nothing.
Taken together, the results of these interesting studies sup- port the possibility that simple visuospatial tasks such as Tetris might have promise as a “cognitive vaccine” if they can be admin- istered early enough. Importantly, although they experienced fewer intrusive flashbacks, people who played Tetris were still
able to recall as many details from the film as people in the control group. In other words, their factual memories of the film remained intact. This is obviously important from the perspective of legal proceedings, where victims of trauma might need to testify about the events that they had experienced.
The researchers conducted a second study where the con- trol condition was playing Pub Quiz, a verbal computer game. Why was it important for the researchers to conduct a second study and why was using a verbal game a good choice for the control condition?
People who played Tetris after viewing a traumatic film reported fewer involuntary flashbacks the following week.
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or been exposed to other traumatic situations (Day, 2007). As a central strategy, traumatized victims are provided with emotional support and encouraged to talk about their experiences during the crisis (Dattilio & Freeman, 2007). The discussion is usually quite structured, and com- mon reactions to the trauma are normalized. Some believe that this form of counseling (much of which is conducted by people who are not mental health professionals) should be mandated for disaster victims in order to prevent PTSD (Conlon & Fahy, 2001). Indeed, a small industry has sprung up to provide debriefing services, and disaster scenes are often swarmed by well-intentioned service providers—many of whom have little or no mental health training.
One form of psychological debriefing is Critical Inci- dent Stress Debriefing (CISD; see McNally et al., 2003). A single session of CISD lasts between 3 and 4 hours and is conducted in a group format, usually 2 to 10 days after a “critical incident” or trauma.
Psychological debriefing is currently quite controver- sial. Reviews of the literature have generally failed to sup- port the clinical effectiveness of the approach (Bisson et al., 2009; Devilly et al., 2006; McNally et al., 2003). Although those who experience the debriefing sessions often report satisfaction with the procedure and with the organization’s desire to provide assistance, no well-controlled study has shown that it reduces symptoms of PTSD or hastens recov- ery in civilians (see Adler et al., 2008).
Clearly, trauma survivors should not be left alone to pick up the pieces of their lives. As we noted earlier, lack of social support is a risk factor for the development of PTSD. Moreover, providing the right kind of social sup- port may facilitate recovery. The most appropriate crisis intervention methods may not be those that follow an explicit protocol and urge emotional expression even when the trauma survivor is not ready. Rather, the most beneficial interventions may be those that focus explicitly on the needs of the individual and time their approaches accordingly. As Foa (cited in McNally et al., 2003) has wisely suggested, in the aftermath of a trauma, survivors should follow their own natural inclination and talk (or not talk) with the people they want to talk to. In a related vein, therapists should take their lead from the trauma survivor, engaging in active listening, being supportive, but not directing or pushing for more information than the survivor wishes to provide. Caring, kindness, and com- mon sense can go a long way to helping trauma survivors along the path to healing.
MEDICATIONS As we have seen, persons experiencing traumatic situations usually report intense feelings of anxiety or depression, numbing, intrusive thoughts, and sleep disturbance. To help with these problems, patients are often treated with antidepressants. Antipsychotic
Treatment for Stress Disorders As we have already discussed, many people who are exposed to a traumatic stressor will experience symptoms and then gradually begin to recover without any profes- sional help. After the terrorist attacks at the World Trade Center, grief and crisis counselors flocked to New York City because it was expected that countless numbers of people would be seeking psychological assistance. Rela- tively few people sought professional help, however, and millions of dollars that had been allocated to cover the costs of providing free counseling went unspent (McNally et al., 2003). With time, and with the help of friends and family, it is quite typical for traumatized people to recover naturally.
TELEPHONE HOTLINES National and local telephone hotlines provide help for people under severe stress and for people who are suicidal. In addition, there are specific hotlines for victims of rape and sexual assault and for run- aways who need help. Many of these hotlines are staffed by volunteers. How skilled and knowledgeable the volun- teer is plays an important role in how satisfied users are with the hotline (Finn et al., 2010). Studies also suggest that the most positive outcomes are seen when helpers show empathy and respect for callers (Mishara et al., 2007).
CRISIS INTERVENTION Crisis intervention has emerged in response to especially stressful situations, be they disas- ters or family situations that have become intolerable (Brown et al., 2013; Callahan, 2009; Krippner et al., 2012). Short-term crisis therapy is of brief duration and focuses on the immediate problem with which an individual or family is having difficulty (Scott & Stradling, 2006). Although med- ical problems may also require emergency treatment, thera- pists are concerned here with problems of an emotional nature. A central assumption in crisis-oriented therapy is that the individual was functioning well psychologically before the trauma. Thus therapy is focused only on helping the person through the immediate crisis, not on “remaking” her or his personality.
In such crisis situations, a therapist is usually very active, helping to clarify the problem, suggesting plans of action, providing reassurance, and otherwise providing needed information and support. A single-session behav- ioral treatment has been shown to lower fears and provide an increased sense of control among earthquake trauma victims (Basoglu et al., 2007). Although people are far from better after this single session, they receive knowledge and learn skills that will help them gain better control over their lives in the ensuing weeks and months.
PSYCHOLOGICAL DEBRIEFING Psychological debrief- ing approaches are designed to help and speed up the healing process in people who have experienced disasters
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effects of the prolonged exposure treatment were less robust than expected.
Recognizing the need for improvements in the treat- ment of PTSD, other approaches are now being devel- oped and refined. Ehlers and colleagues (2005) have developed a treatment for PTSD that is based on a cogni- tive model of the disorder. More specifically, it is thought that PTSD becomes persistent when people who have experienced trauma make excessively negative and idio- syncratic appraisals of what has happened to them in a way that creates a sense of a serious, current threat. For example, a bus driver who was assaulted by one of his passengers believed he was a terrible father who had failed his children because he had asked the passenger to buy a ticket before the passenger attacked him (Ehlers & Clark, 2008). Cognitive therapy for PTSD is designed to modify excessively negative appraisals of the trauma or its consequences, decrease the threat that patients experience when they have memories of the traumatic event, and remove problematic cognitive and behavioral strategies.
Evidence suggests that this treatment approach is very effective. In three different studies comparing patients who received cognitive therapy with patients assigned to a waiting list control group, rates of recov- ery were significantly higher in the cognitive therapy group and ranged from 71 to 89 percent. The drop-out rate was also very low. In fact, the only patient who dropped out of the treatment was a woman who moved abroad (Ehlers & Clark, 2008). Moreover, these treat- ment gains appear to continue after treatment has ended. Evidence further suggests that improvements in symptoms come as a result of changes in negative appraisals, just as predicted by the cognitive model (Kleim et al., 2013).
Another exciting treatment development that seems to be well received by clients is virtual reality exposure therapy (see the World Around Us box). There is also pre- liminary evidence that expressive writing, which we described earlier, may be beneficial (Sloan et al., 2013).
Trauma and Physical Health If stress is linked to problems with physical health, what role does psychological trauma play in our physical well- being? In asking this question we come full circle, again recognizing the importance of the mind–body connec- tion. Although questions like this have only recently begun to attract empirical attention, the findings give cause for concern. For example, in a sample of men and women who were HIV positive, previous trauma (occur- ring years before the study and usually during child- hood) was highly predictive of death from HIV and also
medications like those used to treat disorders such as schizophrenia are also sometimes used (Bartzokis et al., 2005; David et al., 2004). Unfortunately, evidence for the effectiveness many of these medications is slim. Antide- pressants (particularly SSRIs such as fluoxetine [Prozac], paroxetine [Paxil], and venlafaxine [Effexor]) provide modest benefits compared to placebo. However, there is little evidence that most other medications provide sig- nificant benefits (Hoskins et al., 2015).
COGNITIVE-BEHAVIORAL TREATMENTS If you watch a scary movie over and over again what happens? Over time, the fear decreases and the movie becomes less fright- ening to you. One behaviorally oriented treatment strategy that is now being used for PTSD is prolonged exposure (Cloitre, 2009). It operates on exactly the same principle. The patient is asked to vividly recount the traumatic event over and over until there is a decrease in his or her emotional responses. This procedure also involves repeated or extended exposure, either in vivo or in the imagination, to feared (but objectively harmless) stimuli that the patient is avoiding because of trauma-related fear (Foa & Rauch, 2004; Powers et al., 2010). Prolonged expo- sure can also be supplemented by other behavioral tech- niques (Taylor, 2010). For example, relaxation training might also be used to help the person manage anxiety fol- lowing a traumatic event.
Because prolonged exposure therapy involves per- suading clients to confront the traumatic memories they fear, the therapeutic relationship may be of great impor- tance in this kind of clinical intervention (Charuvastra & Cloitre, 2008). The client has to trust in the therapist enough to engage in the exposure treatment. In all clini- cal work, the therapist needs to provide a safe, warm, and supportive environment that can facilitate clinical change. For those who have been traumatized, and who may have extreme issues with trust, having a capable, understanding, and caring therapist may be especially necessary.
Prolonged exposure is an effective treatment for PTSD (Doane et al., 2010; Powers et al., 2010). In a recent study involving women who had served in the military, ten 90-minute treatment sessions led to a reduction of symp- toms and a decrease in the number of women meeting diagnostic criteria for PTSD compared to a sample of women who had received a form of treatment that focused on their current life problems (Schnurr et al., 2007). How- ever, one problem with prolonged exposure therapy is that it tends to have a higher dropout rate than other approaches. This no doubt is because it is difficult for peo- ple with PTSD to be exposed to their traumatic memories. Another current issue of concern is how long the treatment effects last. In the study just described, the longer-term
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from other causes (Leserman et al., 2007). In a more recent study, female political prisoners who had experi- enced torture during their detentions had high rates of both PTSD and cardiovascular problems when assessed one or two decades after their release (Ghaddar et al., 2014). In other words, traumatic events are not only bad for the mind, they also damage the body. Although the mechanisms for this are still being explored (recall the research on stress and telomeres we described earlier), these findings again highlight the role that stress and trauma play in both physical health and psychological well-being. So now that you have finished this chapter, go and relax!
in review • What strategies are useful for preventing or reducing maladaptive
responses to stress?
• Describe crisis intervention therapy. How is this treatment approach different from psychotherapy for other mental health conditions?
• In what ways are medications used to treat individuals in crisis?
• Describe the controversy surrounding the use of “debriefing interventions.”
• What forms of cognitive-behavioral treatments are effective for patients with PTSD?
• Why is the therapeutic relationship so important in the treatment of chronic PTSD?
The World Around Us Virtual Reality Exposure Treatment for PTSD in Military Personnel
Large numbers of military personnel begin showing signs of PTSD within 6 months of deploying (Milliken et al., 2007). However, because of stigma, many soldiers are reluctant to seek help. As one marine explained, “I didn’t want it put on my military record that I was crazy” (Halpern, 2008).
A much-needed development in this regard is the use of computer sim- ulations and virtual reality to provide a form of exposure therapy. Although such approaches are not new, tech- nological advances now allow for the virtual reality programs to be custom- ized to reflect the individual soldier’s traumatic experience as closely as possible. With the click of a mouse, the therapist can add such trauma- related cues as vibrations of the ground, the smell of smoke, and the sound of AK-47 fire. Treatment is typi- cally short term (4 weeks), consisting of four to six 90-minute individual sessions. The first session is devoted to obtaining sufficient details of the trauma (time of day, weather conditions, location, sounds, smells, etc.) to make the virtual reality experi- ence as realistic as possible. As the therapy progresses, new cues may be added to the program to provide further exposure experiences.
Early reports suggest that virtual reality exposure treatment is associated with substantial decreases in PTSD symptoms and improvements in overall functioning (Gerardi et al., 2008; Reger & Gahm, 2008). Importantly, virtual reality treatment approaches are also well received by soldiers and preferred over traditional
Virtual reality treatment is well received by soldiers.
talk therapy (Wilson et al., 2008). As one soldier put it, virtual reality “sounded pretty cool” (see Halpern, 2008). Given the growing numbers of veterans now being diagnosed with PTSD, any form of treatment that is well received by soldiers and pro- vides relief from debilitating symptoms cannot come a moment too soon.
What makes virtual reality therapy an acceptable form of treatment for many military personnel? And why do you think this approach is successful in helping reduce symptoms? How might it work?
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Unresolved Issues Why Is the Study of Trauma So Contentious?
Unlike other research topics, the field of traumatic stress study is characterized by passionate and highly divisive argument. For example, although researchers routinely seek to identify risk fac- tors for the development of various disorders such as depression or eating disorders, the idea that there could be individual risk factors for PTSD (apart from exposure to the traumatic event itself) was a taboo topic for many years. The reason it was unac- ceptable was because it was viewed as “blaming the victim.” There were also concerns that the study of vulnerability factors might provide the federal government with an excuse to deny treatment and benefits to Vietnam veterans. In other words, advocacy—rather than science—was the priority.
Now, of course, the study of individual vulnerability factors for PTSD is an active area of research. Nonetheless, individual scien- tists in this area are still subjected to attacks when they present findings that some in the trauma field do not want to hear (Satel, 2007). A case in point is the reanalysis of data from the National Vietnam Veterans Readjustment Study. This suggested that the originally reported estimates of PTSD might have been too high. Rather than engage in discourse about the methodology of the study or the statistical analysis used, prominent members of the
audience instead chose to attack the presenter, coming close to accusing him of lying (Satel, 2007).
This is not an isolated example. After scholars published a meta-analysis that revealed that there was only a weak associa- tion between childhood sexual abuse and later psychopathol- ogy (Rind et al., 1998) there was a huge outcry from experts in the trauma field. The American Psychological Association made efforts to distance itself from the conclusions made by the authors and eventually Congress weighed in, issuing a formal condemna- tion of the article (see Lilienfeld, 2002). In another case, some scholars were accused of “minimization or outright denial of human suffering” (Marshall, 2006, p. 629) after they referred to the transient rise in stress reactions following the 9/11 terrorist attacks as normal emotional responses (see McNally, 2013).
Science searches for truth. And, as McNally (2013) notes, advocacy for victims of trauma is best served by scientific inquiry that is free of ideology. If certain assumptions are off-limits to investigation or critique, no one is well served. Advocates for trauma victims are no doubt well intentioned. But when advocacy determines what scientific findings are or are not acceptable, do we not all lose?
Summary 5.1 Explain the factors that make people more stress
sensitive and the characteristics of stressors that make them hardest to cope with.
• When challenges to our physical or emotional well- being exceed our coping abilities or resources, we experience stress. Stress can result from negative or positive situations.
• How we deal with stress is linked to our coping skills and resources. For this reason children may be espe- cially vulnerable. People with the s/s genotype of the serotonin promoter (5HTTLPR) gene also seem to be more stress sensitive. Past experiences of stress may also make us more sensitive to stress later on. In con- trast, people who are optimistic, have higher self- esteem, better social support, and a greater sense of control or mastery in their own lives tend to handle life stress better overall.
• Key factors involved in making one situation more stressful than another include how severe the stressor is, how long it lasts, when it occurs, how much it
impacts our lives, how expected it is, and how much control we have over the situation.
5.2 Summarize how the body responds to stress.
• Stress takes its toll on our physical and psychological well-being.
• When we are stressed, the autonomic nervous system responds in a variety of ways. The hypothalamus stim- ulates the sympathetic nervous system, and hormones such as adrenaline (epinephrine) and noradrenaline (norepinephrine) are released from the adrenal medulla. These hormones circulate in the bloodstream and prepare the body for fight or flight. Heart rate increases, and the body metabolizes glucose more rap- idly to provide energy.
• Stress also activates the hypothalamus-pituitary- adrenal (HPA) system. A hormone called cortisol- releasing hormone is released from the hypothalamus, stimulating the pituitary gland and causing it to secrete ACTH. This stimulates the adrenal cortex to produce
Stress and Physical and Mental Health 171
rate, muscle tension, or blood pressure, is another approach for some stress-related problems such as headaches.
• Another widely used treatment is relaxation training. This can be combined with other approaches such as biofeedback.
• Meditation and other stress-reducing approaches that facilitate nonjudgmental awareness are now an active focus of research interest.
• Cognitive-behavioral therapy is also widely used. CBT can be helpful in reducing pain from headaches or stomach problems as well as providing techniques to help people cope with stress.
5.6 Identify the similarities and differences between adjustment disorder, posttraumatic stress disorder, and acute stress disorder.
• An adjustment disorder is a much less severe disorder than PTSD or acute stress disorder. Although all of these disorders result from stress, adjustment disorder is a response to a more common stressor such as unem- ployment or marital problems. In the case of PTSD and acute stress disorder, the stressor is much more severe and traumatic.
• Both PTSD and acute stress disorder have similar symptoms. The key difference between them involves the duration of symptoms. PTSD is diagnosed when symptoms have lasted for more than 1 month. If symptoms have only recently developed and have not lasted more than a month, the diagnosis is acute stress disorder. Also, because natural recovery with time is a common pattern, not everyone diagnosed with an acute stress disorder will go on to be diag- nosed with PTSD.
5.7 Describe the clinical features of and risk factors for posttraumatic stress disorder.
• In PTSD, experiencing a traumatic event is thought to create a pathological memory. This memory does not abate over time. When it intrudes, the person reexperi- ences the traumatic event with full emotional force even when there is no longer any danger.
• PTSD can involve a variety of symptoms, including intrusive memories or recurrent and distressing dreams about the event, avoidance of stimuli associ- ated with the trauma, negative cognitions or impaired memory about aspects of the traumatic event, and increased arousal or reactivity.
• Many factors influence a person’s response to stress- ful situations. The impact of stress depends not only on its severity but also on the person’s preexisting vulnerabilities. Resilience is the most common long- term trajectory.
stress hormones such as cortisol. High levels of cortisol may be beneficial in the short term but problematic over the longer term.
5.3 Discuss how stress causes dysregulation in the immune system.
• Stress compromises immune functioning, slowing down wound healing. Psychoneuroimmunology is a developing field concerned with the interactions between the nervous system and the immune system.
• In the immune system, specialized white blood cells called B-cells and T-cells respond to antigens such as viruses and bacteria. They are assisted by natural killer cells, granulocytes, and macrophages.
• Activation of the immune system stimulates the pro- duction of cytokines. Cytokines are chemical messen- gers that allow the brain and the immune system to communicate with each other. Some cytokines respond to a challenge to the immune system by causing an inflammatory response. Other cytokines, called anti- inflammatory cytokines, dampen the response that the immune system makes when it is challenged.
• Long-term stress seems to interfere with the body’s ability to turn off cytokine production, leading to inflammation.
5.4 Describe the role that emotions play in physical health and identify helpful and harmful emotions.
• Because the brain can influence the immune system, psychological factors are important to our physical well-being.
• Negative emotional states, such as depression, hostil- ity, anger, anxiety, or feelings of loneliness, have all been linked to the development of cardiovascular dis- ease. This may be because negative emotions function as a source of stress.
• In contrast, having a more optimistic attitude toward life, or being more forgiving, may have beneficial health consequences.
5.5 Explain the psychological interventions that can be used to reduce stress and treat stress-related disorders.
• Expressive writing, in which people write down their innermost thoughts about their most traumatically stressful experiences, speeds up wound healing and may be a valuable approach for individuals with some stress-related illnesses. This approach may work because it allows people to vent and/or because it also permits them to think about their problems in a differ- ent way (reframing).
• Biofeedback, in which people are helped via monitor- ing equipment to become more aware of their heart
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• Women with PTSD have higher baseline cortisol levels than women who do not have PTSD. This is not the case for men with PTSD. Under conditions of stress, people with PTSD show an exaggerated cortisol response.
• Having the s/s genotype of the serotonin-transporter gene may increase vulnerability to PTSD in the face of trauma exposure. Smaller hippocampal volume is also a biological vulnerability factor.
5.8 Explain the treatment approaches that are used to help people with PTSD.
• Medications are sometimes used in the treatment of PTSD, although they are not especially effective. Some SSRIs provide modest benefits.
• Psychological treatments include prolonged exposure therapy and cognitive therapy. A new approach that appears promising is the use of virtual reality expo- sure therapy.
• Although it is very common to experience psychologi- cal symptoms after a traumatic event, these often fade with time. Most people exposed to traumatic events do not develop PTSD. The prevalence of PTSD in the general population is 6.8 percent.
• Factors that increase a person’s risk of experiencing traumatic events include certain occupations (e.g., fire- fighter), being male, not having a college education, conduct problems in childhood, high levels of extra- version and neuroticism, as well as a family history of psychiatric problems.
• Factors that increase the risk of developing PTSD include being female and having low levels of social support; higher levels of neuroticism; a family history of depression, anxiety, and substance abuse; as well as preexisting problems with anxiety and depression. A tendency to have thoughts or images about traumatic events that could happen in the future has also been identified as a risk factor.
acute stress disorder, p. 158 adjustment disorder, p. 158 allostatic load, p. 141 antigens, p. 144 B-cell, p. 144 behavioral medicine, p. 137 coping strategies, p. 137 correlational research, p. 147 cortisol, p. 143 crisis, p. 140 crisis intervention, p. 167 cytokines, p. 145 debriefing sessions, p. 167
distress, p. 138 health psychology, p. 137 hypothalamus-pituitary-adrenal
(HPA) system, p. 142 immune system, p. 143 immunosuppression, p. 143 leukocytes, p. 144 lymphocytes, p. 144 positive psychology, p. 152 posttraumatic stress disorder
(PTSD), p. 137 prolonged exposure, p. 168 psychoneuroimmunology, p. 143
resilience, p. 140 stress, p. 137 stress-inoculation
training, p. 166 stress tolerance, p. 139 stressors, p. 137 sympathetic-adrenomedullary
(SAM) system, p. 142 T-cell, p. 144 telomere, p. 148 Type A behavior pattern, p. 149 Type D personality, p. 149
Key Terms
173
Learning Objectives
6.1 Distinguish between fear and anxiety.
6.2 Describe the essential features of anxiety disorders.
6.3 Explain the clinical features of specific phobias.
6.4 Discuss the clinical features of social phobia.
6.5 Describe the clinical features of panic disorder.
6.6 Explain the clinical aspects of generalized anxiety disorder.
6.7 Describe the clinical features of obsessive- compulsive disorder and how it is treated.
6.8 Summarize some examples of cultural differences in sources of worry.
Chapter 6
Panic, Anxiety, Obsessions, and Their Disorders
174 Chapter 6
others, if psychological defense mechanisms were able to deflect or mask it. The term neurosis was dropped from the DSM in 1980. In addition, in DSM-III, some disorders that did not involve obvious anxiety symptoms were reclassified as either dissociative or somatoform disorders. (Some neu- rotic disorders were absorbed into the mood disorders cate- gory as well—see Chapters 7 and 8.) In DSM-5 this trend has gone a step further. Obsessive-compulsive disorder (OCD) is no longer classified as an anxiety disorder. Instead, it is now listed in its own category of obsessive-compulsive and related disorders (see the Thinking Critically about DSM-5 box later in this chapter).
We begin by discussing the nature of fear and anxiety as emotional and cognitive states and patterns of responding, each of which has an extremely important adaptive value but to which humans at times seem all too vulnerable. We will then move to a discussion of the anxiety disorders. Finally, we consider OCD and other disorders from the new obsessive-compulsive and related disorders category.
The Fear and Anxiety Response Patterns 6.1 Distinguish between fear and anxiety.
There has never been complete agreement about how dis- tinct the two emotions of fear and anxiety are from each other. Historically, the most common way of distinguishing between the fear and anxiety response patterns has been to determine whether a clear and obvious source of danger is present that would be regarded as real by most people. When the source of danger is obvious, the experienced emo- tion has been called fear (e.g., “I’m afraid of snakes”). With anxiety, however, we frequently cannot specify clearly what the danger is (e.g., “I’m anxious about my parents’ health”).
Fear In recent years, many prominent researchers have pro- posed a more fundamental distinction between the fear and anxiety response patterns (e.g., Barlow, 2002; Bouton, 2005; McNaughton, 2008). According to these theorists, fear is a basic emotion (shared by many animals) that involves activation of the “fight-or-flight” response of the autonomic nervous system. This is an almost instanta- neous reaction to any imminent threat such as a dangerous predator or someone pointing a loaded gun.
Its adaptive value as a primitive alarm response to imminent danger is that it allows us to escape. When the fear response occurs in the absence of any obvious external danger, we say the person has had a spontaneous or uncued panic attack. The symptoms of a panic attack are nearly identical to those experienced during a state of fear
Jeni: Worried about Worrying So Much Jeni is a 21-year-old college student. Although she is doing excep- tionally well in school, for the past year she has worried constantly that she will fail and be thrown out. When her fellow students and professors try to reassure her, Jeni worries that they are just pre- tending to be nice to her because she is such a weak student. Jeni also worries about her mother becoming ill and about whether she is really liked by her friends. Although Jeni is able to acknowledge that her fears are excessive (she has supportive friends, her mother is in good health, and, based on her grades, Jeni is one of the top students in her school), she still struggles to control her worrying. Jeni has difficulty sleeping, often feels nervous and on edge, and experiences a great deal of muscle tension. When her friends sug- gested she take a yoga class to try and relax, Jeni even began to worry about that, fearing that she would be the worst student in the class. “I know it makes no sense,” she says, “But that’s how I am. I’ve always been a worrier. I even worry about worrying so much!”
Anxiety involves a general feeling of apprehension about possible future danger, whereas fear is an alarm reaction that occurs in response to immediate danger. The DSM has iden- tified a group of disorders—known as the anxiety disor- ders—that share symptoms of clinically significant anxiety or fear. Anxiety disorders affect approximately 29 percent of the U.S. population at some point in their lives and are the most common category of disorders for women and the second most common for men (Kessler, Berglund, Delmar, et al., 2005). In any 12-month period, about 18 percent of the adult population suffers from at least one anxiety dis- order (Kessler, Chiu, et al., 2005). Anxiety disorders create enormous personal, economic, and health care problems for those affected and for society more generally. Anxiety dis- orders have the earliest age of onset of all mental disorders (Kessler, Aguilar-Gaxiola, et al., 2009) and are associated with an increased prevalence of a number of medical condi- tions including asthma, chronic pain, hypertension, arthri- tis, cardiovascular disease, and irritable bowel syndrome (Roy-Byrne et al., 2008). People with anxiety disorders are very high users of medical services (Chavira et al., 2009).
Historically, anxiety disorders were considered to be classic neurotic disorders. Although individuals with neu- rotic disorders show maladaptive and self-defeating behav- iors, they are not incoherent, dangerous, or out of touch with reality. To Freud, these neurotic disorders developed when intrapsychic conflict produced significant anxiety. Anxiety was, in Freud’s formulation, a sign of an inner battle or con- flict between some primitive desire (from the id) and prohi- bitions against its expression (from the ego and superego). Sometimes this anxiety was overtly expressed (as in those disorders known today as the anxiety disorders). In certain other neurotic disorders, however, he believed that the anxi- ety might not be obvious, either to the person involved or to
Panic, Anxiety, Obsessions, and Their Disorders 175
except that panic attacks are often accompanied by a sub- jective sense of impending doom, including fears of dying, going crazy, or losing control. These latter cognitive symp- toms do not generally occur during fear states. Thus, fear and panic have three components:
1. cognitive/subjective components (e.g., “I’m going to die”)
2. physiological components (e.g., increased heart rate and heavy breathing)
3. behavioral components (e.g., a strong urge to escape or flee).
These components are only “loosely coupled” (Lang, 1985), which means that someone might show, for example, physiological and behavioral indications of fear or panic without much of the subjective component, or vice versa.
Fear or panic is a basic emotion that is shared by many animals, including humans, and may activate the fight-or-flight response of the sympathetic nervous system. This allows us to respond rapidly when faced with a dangerous situation, such as being threatened by a predator. In humans who are having a panic attack, there is no external threat; panic occurs because of some misfiring of this response system.
Anxiety In contrast to fear and panic, the anxiety response pattern is a complex blend of unpleasant emotions and cognitions that is both more oriented to the future and much more diffuse than fear (Barlow, 2002). But like fear, it has not only cognitive/subjective components but also physio- logical and behavioral components. At the cognitive/ subjective level, anxiety involves negative mood, worry about possible future threats or danger, self-preoccupation, and a sense of being unable to predict the future threat or to control it if it occurs. At a physiological level, anxiety often creates a state of tension and chronic overarousal, which may reflect risk assessment and readiness for deal- ing with danger should it occur (“Something awful may happen, and I had better be ready for it if it does”). Although there is no activation of the fight-or-flight response as there is with fear, anxiety does prepare or prime a person for the fight-or-flight response should the
Table 6.1 Components of Fear and Anxiety
Component Fear Anxiety
1. Cognitive/subjective “I am in danger!” “I am worried about what might happen.”
2. Physiological Increased heart rate, sweating
Tension, chronic overarousal
3. Behavioral Desire to escape or run General avoidance
anticipated danger occur. At a behavioral level, anxiety may create a strong tendency to avoid situations where danger might be encountered, but the immediate behav- ioral urge to flee is not present with anxiety as it is with fear (Barlow, 2002). Support for the idea that anxiety is descriptively and functionally distinct from fear or panic comes both from statistical analyses of subjective reports of panic and anxiety and from a great deal of neurobio- logical evidence (e.g., Bouton, 2005; Davis, 2006; Grillon, 2008). Table 6.1 compares and contrasts the components of fear and anxiety.
The adaptive value of anxiety may be that it helps us plan and prepare for a possible threat. In mild to moderate degrees, anxiety actually enhances learning and perfor- mance. For example, a mild amount of anxiety about how you are going to do on your next exam, or in your next ten- nis match, can actually be helpful. But, although anxiety is often adaptive in mild or moderate degrees, it is maladap- tive when it becomes chronic and severe, as we see in peo- ple diagnosed with anxiety disorders.
Although many threatening situations can occur that provoke fear or anxiety unconditionally, many of our sources of fear and anxiety are learned. Years of human and nonhuman animal experimentation have established that the basic fear and anxiety response patterns are highly conditionable (Fanselow & Ponnusamy, 2008; Lipp, 2006). That is, previously neutral and novel stimuli (conditioned stimuli) that are repeatedly paired with, and reliably pre- dict, frightening or unpleasant events such as various kinds of physical or psychological trauma (unconditioned stimulus) can acquire the capacity to elicit fear or anxiety themselves (conditioned response). Such conditioning is a completely normal and adaptive process that allows all of us to learn to anticipate upcoming frightening events if they are reliably preceded by a signal. Yet this normal and adaptive process can also lead in some cases to the devel- opment of clinically significant fears and anxieties, as we will see.
For example, a girl named Angela sometimes saw and heard her father physically abuse her mother in the eve- ning. After this happened four or five times, Angela started to become anxious as soon as she heard her father’s car arrive in the driveway at the end of the day. In such situations a wide variety of initially neutral stimuli may accidentally
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come to serve as cues that something threatening and unpleasant is about to happen—and thereby come to elicit fear or anxiety themselves. Our thoughts and images can also serve as conditioned stimuli capable of eliciting the fear or anxiety response pattern. For example, Angela came to feel anxious even when thinking about her father.
in review • Compare and contrast fear or panic with anxiety, making sure to
note that both emotions involve three response systems.
• Explain the significance of the fact that both fear and anxiety can be classically conditioned.
Overview of the Anxiety Disorders and Their Commonalities 6.2 Describe the essential features of anxiety disorders.
Anxiety disorders are characterized by unrealistic, irratio- nal fears or anxieties that cause significant distress and/or impairments in functioning. Among the disorders recog- nized in DSM-5 are:
1. specific phobia
2. social anxiety disorder (social phobia)
3. panic disorder
4. agoraphobia
5. generalized anxiety disorder.
People with these varied disorders differ from one another both in terms of the amount of fear or panic versus anxiety symptoms that they experience and in the kinds of objects or situations that most concern them. For example, people with specific or social phobias experience a fear or panic response not only when they encounter the object or situation that they fear, but also in response to even the possibility of encountering their phobic situation. People with panic disorder experience both frequent panic attacks and intense anxiety focused on the possibility of having another one. People with agoraphobia go to great lengths to avoid a variety of feared sit- uations, ranging from open streets and bridges to crowded public places. By contrast, people with generalized anxiety dis- order (like Jeni in the case study that opened this chapter) mostly experience a general sense of diffuse anxiety and worry about many potentially bad things that may happen; some may also experience an occasional panic attack, but it is not a focus of their anxiety. It is also important to note that many people with one anxiety disorder will experience at least one more anxiety disorder and/or depression either concurrently or at a different point in their lives (Brown & Barlow, 2009; Kessler, Berglund, Demler, et al., 2005).
Given these commonalities across the anxiety disorders, it should come as no surprise that there are some important similarities in the basic causes of these disorders (as well as many differences). Among biological causal factors, we will see that genetics contributes to each of these disorders and that at least part of the genetic vulnerability may be nonspe- cific, or common across the disorders (Shimada-Sugimoto et al., 2015). In adults, the common genetic vulnerability is manifested at a psychological level at least in part by the important personality trait called neuroticism—a proneness or disposition to experience negative mood states that is a common risk factor for both anxiety and mood disorders (Klein et al., 2009). The brain structures most centrally involved in most disorders are generally in the limbic sys- tem (often known as the “emotional brain”) and certain parts of the cortex, and the neurotransmitter substances that are most centrally involved are gamma aminobutyric acid (GABA), norepinephrine, and serotonin (see Chapter 3).
Among common psychological causal factors, we will see that classical conditioning of fear, panic, or anxiety to a range of stimuli plays an important role in many of these disorders (Mineka & Oehlberg, 2008; Mineka & Zinbarg, 2006). In addition, people who have perceptions of a lack of control over either their environments or their own emo- tions (or both) seem more vulnerable to developing anxiety disorders. The development of such perceptions of uncon- trollability depends heavily on the social environment peo- ple are raised in, including parenting styles (Hudson & Rapee, 2009; Mineka & Zinbarg, 2006). For certain disor- ders, faulty or distorted patterns of cognition also may play an important role. Finally, the sociocultural environ- ment in which people are raised also has prominent effects on the kinds of objects and experiences people become anxious about or come to fear. As with the other disorders described in this book, a biopsychosocial approach is best suited for understanding how all different types of causal factors interact with one another in the development of these disorders.
Finally, as we will see, many commonalities are seen across the effective treatments for the various anxiety
Panic, Anxiety, Obsessions, and Their Disorders 177
disorders (Barlow, 2004; Campbell-Sills & Barlow, 2007). For each disorder, graduated exposure to feared cues, objects, and situations—until fear or anxiety begins to habituate— constitutes the single most powerful thera- peutic ingredient. For certain disorders the addition of cognitive restructuring techniques can provide added benefit by helping the individual to understand his or her distorted patterns of thinking about anxiety-related situations and how these patterns can be changed. Medi- cations also can be useful in treating all disorders except specific phobias, and nearly all tend to fall into two pri- mary medication categories: antianxiety medications (anxiolytics) and antidepressant medications.
We now turn to a more detailed discussion of each dis- order, highlighting their common and their distinct fea- tures as well as what is known about their causes. We start with phobic disorders—the most common anxiety disorders. A phobia is a persistent and disproportionate fear of some specific object or situation that presents little or no actual danger and yet leads to a great deal of avoid- ance of these feared situations. As we will see, the three main categories of phobias are (1) specific phobia, (2) social phobia, and (3) agoraphobia.
in review • What is the central feature of all anxiety disorders? That is, what
do they have in common?
• What differentiates the anxiety disorders from one another?
• What are some common kinds of biological and psychosocial causes of the different anxiety disorders?
• What is the most important ingredient across effective psychoso- cial treatments for the anxiety disorders?
Specific Phobias 6.3 Explain the clinical features of specific phobias.
We all have things that we are afraid of: scary movies, tigers, clowns, scary movies about tiger-riding clowns. Having such fears is normal. However, a specific phobia is said to be present if a person shows strong and persistent fear that is triggered by the presence of a specific object or situation and leads to significant distress and/or impair- ment in a person’s ability to function (see DSM-5 box for diagnostic criteria). When people with specific phobias encounter a phobic stimulus, they often show an immedi- ate fear response that often resembles a panic attack except for the existence of a clear external trigger (APA, 2013). Not surprisingly, such individuals also experience anxiety if they anticipate they may encounter a phobic object or situ- ation and so go to great lengths to avoid encounters with their phobic stimulus. Indeed, they often even avoid seem- ingly harmless representations of it such as photographs or television images. For example, claustrophobic persons may go to great lengths to avoid entering a closet or an elevator, even if this means climbing many flights of stairs or turning down jobs that might require them to take an elevator. Generally, people with specific phobias recognize that their fear is somewhat excessive or unreasonable although occasionally they may not have this insight.
This avoidance is a cardinal characteristic of phobias; it occurs both because the phobic response itself is so unpleasant and because of the phobic person’s irrational appraisal of the likelihood that something terrible will hap- pen. Table 6.2 lists the five subtypes of specific phobias rec- ognized in DSM-5.
DSM-5 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 imme- diate 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 sociocul- tural 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 dis- tress 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 avoid- ance 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); reminders of traumatic events (as in posttraumatic stress disorder); separation from home or attachment figures (as in separation anxiety disorder); or social situations (as in social anxiety disorder).
Source: Reprinted with permission from the Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition (Copyright 2013). American Psychiatric Association.
178 Chapter 6
The following case is typical of specific phobia.
A Mother’s Fears
Mary, a married mother of three, was 47 at the time she first sought treatment for anxiety. She reported being intensely afraid of enclosed spaces (claustrophobia) and of heights (acrophobia) since her teens. She said that as a child, her older siblings used to lock her in closets and hold her down under blankets while saying things to scare her. She traced the onset of her claustro- phobia to those traumatic incidents, but she had no idea why she was afraid of heights. While her children had been growing up, she had been a housewife and had managed to live a fairly normal life in spite of her two specific phobias. However, her chil- dren were now grown, and she wanted to find a job outside her home. This was proving to be very difficult because she could not take elevators and was terrified of being any higher than the first floor of an office building. Moreover, her husband had for some years been working for an airline, which entitled him to free airline tickets. The fact that Mary could not fly (due to her phobias) had become a sore point in her marriage because they both wanted to be able to take advantage of these free tickets to travel to dis- tant places. Thus, although she had had these phobias for many years, they had become truly disabling only in recent years as her life circumstances had changed and she could no longer easily avoid heights or enclosed spaces.
If people who suffer from phobias attempt to approach the object of their phobia, they are overcome with fear or anxiety, which may vary from mild feelings of apprehen- sion and distress (usually while still at some distance) to full-fledged activation of the fight-or-flight response. Regardless of how it begins, phobic behavior tends to be reinforced because every time the person with a phobia avoids a feared situation, his or her anxiety decreases. In addition, the secondary benefits derived from being dis- abled, such as increased attention, sympathy, and some control over the behavior of others, can also sometimes reinforce a phobia.
One category of specific phobias that has a number of interesting and unique characteristics is blood-injection- injury phobia. It occurs in approximately 3 to 4 percent of the population (Ayala et al., 2009). People afflicted with
this phobia typically experience at least as much (if not more) disgust as fear (Teachman & Saporito, 2009). They also show a unique physiological response when confronted with the sight of blood or injury. Rather than showing the simple increase in heart rate and blood pressure seen when most people with phobias encounter their phobic object, these people show an initial acceleration, followed by a
People with acrophobia (fear of heights) are so frightened of being in high places like airplanes, tall buildings, or even upper levels of shopping malls that they go through great lengths to avoid them. If for some reason they must be in a high place, people with acrophobia will be extremely frightened and may have thoughts about falling or being injured in some way. We are pretty sure that this climber does not suffer from acrophobia.
In blood-injection-injury phobia, the afflicted person experiences disgust and fear at the sight of someone receiving an injection. When confronted with the sight of blood or injury, people with this phobic disorder often experience nausea, dizziness, or fainting.
Table 6.2 Subtypes of Specific Phobias in DSM-5
Phobia Type Examples
Animal Snakes, spiders, dogs, insects, birds
Natural environment Storms, heights, water
Blood-injection-injury Seeing blood or an injury, receiving an injection, seeing a person in a wheelchair
Situational Public transportation, tunnels, bridges, elevators, flying, driving, enclosed spaces
Other Choking, vomiting, “space phobia” (fear of falling down if away from walls or other support)
Data from the Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition, (Copyright 2013). American Psychiatric Association.
Panic, Anxiety, Obsessions, and Their Disorders 179
which sought to explain the development of phobic behav- ior through classical conditioning. The fear response can readily be conditioned to previously neutral stimuli when these stimuli are paired with traumatic or painful events. We would also expect that, once acquired, phobic fears would generalize to other, similar objects or situations. Recall, for example, that Mary’s claustrophobia had prob- ably been caused by multiple incidents as a child when her siblings locked her in closets and confined her under blan- kets to scare her. But as an adult, Mary feared elevators and caves as well as other enclosed places.
dramatic drop in both heart rate and blood pressure. This is very frequently accompanied by nausea, dizziness, or fainting, which does not occur with other specific phobias (Öst & Hellström, 1997; Page & Tan, 2009).
Interestingly, people with this phobia demonstrate this unique physiological response pattern only in the presence of blood and injury stimuli; they exhibit the more typical physiological response pattern characteristic of the fight-or- flight response to their other feared objects (Dahllöf & Öst, 1998). From an evolutionary and functional standpoint, this unique physiological response pattern may have evolved for a specific purpose: By fainting, the person being attacked might inhibit further attack, and if an attack did occur, the drop in blood pressure would minimize blood loss (Craske, 1999; Marks & Nesse, 1991). This type of phobia appears to be highly heritable (Czajkowski et al., 2011).
Prevalence, Age of Onset, and Gender Differences Specific phobias are common, occurring in about 12 per- cent of people at some point in their lifetime (Kessler, Chiu, et al., 2005). Phobias are much more common in women than in men, although the gender ratio varies by type of phobia. For example, about 90 to 95 percent of people with animal phobias are women, but the gender ratio is less than 2:1 for blood-injection-injury phobia. Animal phobias usually begin in childhood, as do blood-injection-injury phobias and dental phobias. However, other phobias such as claustrophobia and driving phobia tend to begin in ado- lescence or early adulthood (Barlow, 2002; Öst, 1987).
Psychological Causal Factors A variety of psychological causal factors have been impli- cated in the origins of specific phobias, ranging from deep- seated psychodynamic conflicts to relatively straightforward traumatic conditioning of fear and a multitude of individ- ual differences in who is at risk for such conditioning.
PSYCHOANALYTIC VIEWPOINT According to the psy- choanalytic view, phobias represent a defense against anxiety that stems from repressed impulses from the id. Because it is too dangerous to “know” the repressed id impulse, the anxiety is displaced onto some external object or situation that has some symbolic relationship to the real object of the anxiety (Freud, 1909). However, this prototypical psychodynamic account of how phobias are acquired was long criticized as being far too speculative, and an alterna- tive, simpler account from learning theory was first pro- posed by Wolpe and Rachman (1960), which has now been further refined and expanded as discussed below.
PHOBIAS AS LEARNED BEHAVIOR Wolpe and Rachman (1960) developed an account based on learning theory,
Monkeys who watch a model monkey (such as the one illustrated here) behaving fearfully with a live boa constrictor will rapidly acquire an intense fear of snakes themselves. Fears can thus be learned vicariously without any direct traumatic experience.
Vicarious Conditioning Direct traumatic conditioning in which a person has a terrifying experience in the presence of a neutral object or situation is not the only way that peo- ple can learn irrational, phobic fears. Simply watching a phobic person behaving fearfully with his or her phobic object can be distressing to the observer and can result in fear being transmitted from one person to another through vicarious or observational classical conditioning. In addi- tion, watching a nonfearful person undergoing a frighten- ing experience can also lead to vicarious conditioning. For example, one man, as a boy, had witnessed his grandfather vomit while dying. Shortly after this traumatic event (his grandfather’s distress while dying) the boy had developed a strong and persistent vomiting phobia. Indeed, when this man was in middle age he even contemplated suicide one time when he was nauseated and feared vomiting (Mineka & Zinbarg, 2006). Related experimental findings have been observed in laboratory analogue studies of human chil- dren. For example, two studies showed that 7- to 9-year- old children who saw pictures of an unfamiliar animal (an
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or to some extent controllable (e.g., by running away after the attack; Mineka, 1985; Mineka & Zinbarg, 1996, 2006). It has also been shown that our cognitions, or thoughts, can help maintain our phobias once they have been acquired. For example, people with phobias are constantly on the alert for their phobic objects or situations and for other stimuli relevant to their phobia (McNally & Reese, 2009). Nonphobic persons, by contrast, tend to direct their atten- tion away from threatening stimuli (Mineka et al., 2003). In addition, phobics also markedly overestimate the probabil- ity that feared objects have been, or will be, followed by frightening events. This cognitive bias may help maintain or strengthen phobic fears with the passage of time (Muhlberger et al., 2006; Öhman & Mineka, 2001).
Evolutionary Preparedness for Learning Certain Fears and Phobias Have you noticed that people are much more likely to have phobias of snakes, water, heights, and enclosed spaces than of motorcycles, guns, and chainsaws even though the latter objects may be at least as likely to be associated with trauma? This is because our evolutionary history has affected which stimuli we are most likely to come to fear. Primates and humans seem to be evolution- arily prepared to rapidly associate certain objects—such as snakes, spiders, water, and enclosed spaces—with fright- ening or unpleasant events (Mineka & Öhman, 2002; Öhman, 1996; Seligman, 1971). This prepared learning occurs because, over the course of evolution, those pri- mates and humans who rapidly acquired fears of certain objects or situations that posed real threats to our early ancestors may have enjoyed a selective advantage (mean- ing, they survived more often than those who had no fear of such things). Thus, “prepared” fears are not inborn or innate but rather are easily acquired or especially resistant to extinction. Guns, motorcycles, and chainsaws, by con- trast, were not present in our early evolutionary history and so did not convey any such selective advantage.
Experimental evidence strongly supports the prepared- ness theory of phobias. In one important series of experi- ments using human subjects, Öhman and his colleagues (see Öhman, 1996, 2009; Öhman & Mineka, 2001, for reviews) found that fear is conditioned more effectively to fear-relevant stimuli (slides of snakes and spiders) than to fear-irrelevant stimuli (slides of flowers and mushrooms). Moreover, once the individuals acquired the conditioned responses to fear-relevant stimuli, these responses (includ- ing activation of the relevant brain area, the amygdala) could be elicited even when the fear- relevant stimuli (but not the fear-irrelevant stimuli) were presented subliminally (i.e., presentation was so brief that the stimuli were not con- sciously perceived; e.g., Carlsson et al., 2004; Öhman et al., 2007). This subliminal activation of responses to phobic stimuli may help to account for certain aspects of the irra- tionality of phobias. That is, people with phobias may not
Australian marsupial) paired 10 times with fearful facial expressions showed increased fear beliefs and behavioral avoidance of this conditioned stimulus (CS) relative to chil- dren who saw the unfamiliar animal paired with happy facial expressions. These effects persisted for at least 1 week (Askew & Field, 2007; 2008).
Individual Differences in Learning Given all the traumas that people undergo and watch others experience, why don’t more people develop phobias (Mineka & Oehlberg, 2008)? One reason is that individual differences in life experiences strongly affect whether conditioned fears or phobias actually develop. Importantly, some life experi- ences may serve as risk factors and make certain people more vulnerable to phobias than others, whereas others experiences may serve as protective factors for the develop- ment of phobias (Mineka & Sutton, 2006). For example, children who have had more previous nontraumatic expe- riences with a dentist are less likely to develop dental anxi- ety after a bad and painful experience than are children with fewer previous nontraumatic experiences (Ten Berge et al., 2002). This is true for vicarious learning as well. For instance, toddlers who watch their mothers reacting posi- tively to a snake or spider later show less fear in response to snake or spider exposure than toddlers who didn’t see their mothers having positive experiences with the snake or spider (Egliston & Rapee, 2007). Results like these illus- trate how parents and others close to a child can help to influence the child’s later experience of fear and anxiety.
A person who has had good experiences with a potentially phobic stimulus, such as the little girl playing here with her dog, is likely to be immunized from later acquiring a fear of dogs even if she has a traumatic encounter with one.
Certain aspects of the conditioning experience, and our response to it, also are important in determining the level of fear that is conditioned. For example, experiencing an ines- capable and uncontrollable event, such as being attacked by a dog that one cannot escape from after being bitten, is expected to condition fear much more powerfully than experiencing the same intensity of trauma that is escapable
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Treatments An enormous body of literature has shown that the most effective treatment for specific phobias is exposure therapy— a form of behavior therapy that involves controlled expo- sure to the stimuli or situations that elicit phobic fear (Choy et al., 2007; Craske & Mystkowski, 2006). In exposure ther- apy, clients are encouraged to gradually expose themselves (either alone or with the aid of a clinician or friend) to their feared situations for long enough periods of time so that their fear begins to subside. One variant on this procedure, known as participant modeling, is often more effective than exposure alone. Here the therapist calmly models ways of interacting with the phobic stimulus or situation (Bandura, 1977, 1997). These techniques enable clients to learn that these situations are not as frightening as they had thought and that their anxiety, while unpleasant, is not harmful and will gradually dissipate (Craske & Mystkowski, 2006; Craske & Rowe, 1997). The new learning is believed to be mediated by changes in brain activation in the amygdala, which is centrally involved in the emotion of fear.
For certain phobias such as small-animal phobias, fly- ing phobia, claustrophobia, and blood-injury phobia, expo- sure therapy is often highly effective when administered in a single long session (of up to 3 hours) (Öst, 1997; Öst et al., 2001). This can be an advantage because some people are more likely to seek treatment if they have to go only once. This treatment has also been shown to be highly effective in youth with specific phobias (Ollendick et al., 2009).
An example of the use of exposure therapy comes from the treatment of Mary, the housewife whose acropho- bia and claustrophobia we described earlier.
Mary’s Treatment
Mary participated in 13 sessions of graduated exposure exercises in which her clinician accompanied Mary first into mildly fear-provoking situations and then gradually into more and more fear-provoking situ- ations. Mary also engaged in homework, doing these exposure exer- cises by herself. The prolonged in vivo (“real-life”) exposure sessions lasted as long as necessary for her anxiety to subside. Initial sessions focused on Mary’s claustrophobia and on getting her to be able to ride for a few floors in an elevator, first with the therapist and then alone. Later she took longer elevator rides in taller buildings. Expo- sure for the acrophobia consisted of walking around the periphery of the inner atrium on the top floor of a tall hotel and, later, spending time at a mountain vista overlook spot. The top step of Mary’s claustro- phobia hierarchy consisted of taking a tour of an underground cave. After 13 sessions, Mary successfully took a flight with her husband to Europe and climbed to the top of many tall tourist attractions there.
Several recent advances have boosted the feasibility and effectiveness of exposure therapy even further. Expo- sure to things like height and airplanes is not always feasible (e.g., for clients or clinicians who don’t live near
be able to control their fear because the fear may arise from cognitive structures that are not under conscious control (Öhman & Mineka, 2001; Öhman & Soares, 1993).
Another series of experiments showed that lab-reared monkeys in a vicarious conditioning paradigm can easily acquire fears of fear-relevant stimuli such as toy snakes and toy crocodiles but not of fear-irrelevant stimuli such as flowers and a toy rabbit (Cook & Mineka, 1989, 1990). Thus, both monkeys and humans seem selectively to asso- ciate certain fear-relevant stimuli with threat or danger. Importantly, these lab-reared monkeys had no prior expo- sure to any of the stimuli involved (e.g., snakes or flowers), supporting the evolutionarily based preparedness hypoth- esis even more strongly than the human experiments. For example, human subjects (unlike the lab-reared monkeys) might show superior conditioning to snakes or spiders because of preexisting negative associations to snakes or spiders rather than because of evolutionary factors (Mineka & Öhman, 2002).
Biological Causal Factors Genetic and temperamental variables also affect the speed and strength of conditioning of fear (Gray, 1987; Hettema et al., 2003; Oehlberg & Mineka, 2011). For example, Lonsdorf and colleagues (2009) found that individuals who are carriers of one of the two variants of the serotonin- transporter gene (the s allele, which has been linked to heightened neuroticism) show superior fear conditioning than those without the s allele. However, those with one of two variants of a different gene (the COMT met/met geno- type) did not show superior conditioning but did show enhanced resistance to extinction (see also Lonsdorf & Kalisch, 2011). Relatedly, Kagan and his colleagues (2001) found that behaviorally inhibited toddlers (who are exces- sively timid, shy, easily distressed, etc.) at 21 months of age were at higher risk of developing multiple specific phobias by 7 to 8 years of age than were uninhibited chil- dren (32 versus 5 percent).
Several behavior genetic studies also suggest a modest genetic contribution to the development of specific pho- bias. For example, large twin studies show that monozy- gotic (identical) twins are more likely to share animal phobias and situational phobias (such as of heights or water) than were dizygotic (nonidentical) twins (Hettema, Prescott, et al., 2005; Kendler et al., 1999b). However, the same studies also found that nonshared environmental factors (i.e., individual specific experiences not shared by twins) play a substantial role in the origins of specific pho- bias, a result that supports the idea that phobias are learned behaviors. Another study found that the heritabil- ity of animal phobias was separate from the heritability of complex phobias such as social phobia and agoraphobia (Czajkowski et al., 2011).
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an airport). To address this problem, psychologists have begun to use virtual reality to simulate different kinds of phobic situations. Controlled studies have yielded very promising results and show results comparable to those seen with live exposure (Choy et al., 2007; Parsons & Rizzo, 2008; Rothbaum et al., 2006).
One variation on exposure therapy is called participant modeling. Here the therapist models how to touch and pick up a live tarantula and encourages the spider-phobic client to imitate her behavior. This treatment is graduated, with the client’s first task being simply to touch the tarantula from the outside of the cage, then to touch the tarantula with a stick, then with a gloved hand, then with a bare hand, and finally to let the tarantula crawl over his hand. This is a highly effective treatment, with the most spider-phobic clients being able to reach the top of the hierarchy within 60 to 90 minutes.
New treatments using virtual reality environments allow therapists to simulate certain kinds of phobic situations, such as standing at heights or sitting in airplanes, in a contrived setting.
restructuring techniques alone has not produced results as good as those using exposure-based techniques, and the addition of cognitive techniques to exposure therapy has generally not added much (Craske & Mystkowski, 2006; Wolitzky-Taylor et al., 2008). Similarly, medication treat- ments are ineffective by themselves, and there is even some evidence that antianxiety medications may interfere with the beneficial effects of exposure therapy (Antony & Barlow, 2002; Choy et al., 2007). Recently, however, stud- ies have shown that a drug called d-cycloserine, which is known to facilitate extinction of conditioned fear in ani- mals (e.g., Davis et al., 2005, 2006), can enhance the effec- tiveness of exposure therapy for fear of heights in a virtual reality environment (Norberg et al., 2008, Ressler et al., 2004). d-Cycloserine by itself, however, has no effect.
in review • What are the five subtypes of specific phobias?
• Describe the original classical conditioning explanation for the origins of specific phobias as well as how vicarious conditioning may be involved.
• Explain several sources of individual differences in learning that have improved and expanded the basic conditioning hypothesis of phobia acquisition.
Researchers have tried several other ways of increasing the effectiveness of exposure therapy. The use of cognitive
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• Explain how evolutionary factors have influenced which objects and situations we are most likely to learn to fear.
• Describe the most effective treatment for specific phobias.
Social Phobia 6.4 Discuss the clinical features of social phobia.
Social phobia (or social anxiety disorder) is characterized by disabling fears of one or more specific social situations (such as public speaking, urinating in a public bathroom, or eating or writing in public; see the DSM-5 box). In these situations, a person fears that she or he may be exposed to the scrutiny and potential negative evaluation of others or that she or he may act in an embarrassing or humiliating manner. Because of their fears, people with social phobia either avoid these situations or endure them with great distress. Intense fear of public speaking is the single most common type of social phobia. DSM-5 also identifies two subtypes of social phobia, one of which centers on performance situations such as pub- lic speaking and one of which is more general and includes nonperformance situations (such as eating in public). People with the more general subtype of social phobia often have significant fears of most social situations (rather than simply a few) and often also have a diagnosis of avoidant personal- ity disorder (see Chapter 10; Stein & Stein, 2008).
Prevalence, Age of Onset, and Gender Differences Approximately 12 percent of the population meets the diagnostic criteria for social phobia at some point in their lives (Kessler, Berglund, Demler, et al., 2005; Ruscio et al., 2008). Social phobia is more common among women (about 60 percent of sufferers are women), and it typically begins during adolescence or early adulthood (Bruce et al., 2005; Ruscio et al., 2008). Nearly two-thirds of people with social phobia suffer from one or more additional anxiety disorders at some point in their lives, and about 50 percent also suffer from a depressive disorder at the same time (Kessler, Chiu, et al., 2005; Ruscio et al., 2008). Approximately one-third abuse alcohol to reduce their anxiety and help them face the situations they fear (for example, drinking before going to a party; Magee et al., 1996). Moreover, because of their distress and avoidance of social situations, people with social phobia, on aver- age, have lower employment rates and lower socioeco- nomic status, and approximately one-third have severe impairment in one or more domains of their life (Harvey et al., 2005; Ruscio et al., 2008). Finally, the disorder is remarkably persistent, with one study finding that only about a third recover spontaneously over a 12-year period (Bruce et al., 2005).
The case of Paul is typical of social phobia.
A Surgeon’s Social Phobia
Paul was a single, white male in his mid-30s when he first presented for treatment. He was a surgeon who reported a 13-year history of social phobia. He had very few social outlets because of his persis- tent concerns that people would notice how nervous he was in social situations, and he had not dated in many years. Convinced that peo- ple would perceive him as foolish or crazy, he particularly worried that people would notice how his jaw tensed up when around other people. Paul frequently chewed gum in public situations, believing that this kept his face from looking distorted. Notably, he had no particular problems talking with people in professional situations. For example, he was quite calm talking with patients before and after surgery. During surgery, when his face was covered with a mask, he also had no trouble carrying out surgical tasks or interacting with the other surgeons and nurses in the room. The trouble began when he left the operating room and had to make small talk—and eye con- tact—with the other doctors and nurses or with the patient’s family. He frequently had panic attacks in these social situations. During the panic attacks he experienced heart palpitations, fears of “going crazy,” and a sense of his mind “shutting down.” Because the panic attacks occurred only in social situations, he was diagnosed as hav- ing social phobia rather than panic disorder.
Paul’s social phobia and panic had begun about 13 years ear- lier when he was under a great deal of stress. His family’s business had failed, his parents had divorced, and his mother had had a heart attack. It was in this context of multiple stressors that a personally Intense fear of public speaking is the single most common social phobia.
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Psychological Causal Factors Like specific phobias, social phobia generally involves learned behaviors that have been shaped by evolutionary factors. Such learning is most likely to occur in people who are genetically or temperamentally at risk.
SOCIAL PHOBIA AS LEARNED BEHAVIOR As with specific phobias, social phobia often seems to originate from simple instances of direct or vicarious classical con- ditioning such as experiencing or witnessing a perceived social defeat or humiliation, or being or witnessing the target of anger or criticism (Harvey et al., 2005; Mineka & Zinbarg, 1995, 2006; Tillfors, 2004). In two studies, 56 to 58 percent of people with social phobia recalled and iden- tified direct traumatic experiences as having been involved in the origin of their social phobias (Öst & Hug- dahl, 1981; Townsley et al., 1995). Another study reported that 92 percent of an adult sample of people with social phobia reported a history of severe teasing in childhood, compared to only 35 percent in a group of people with obsessive-compulsive disorder (McCabe et al., 2003). Moreover, a laboratory study of people with social pho- bia revealed that they showed especially robust condi- tioning of fear when the unconditioned stimulus was
socially relevant (critical facial expressions and verbal insults) as opposed to more nonspecifically negative stimuli (such as unpleasant odors and painful pressure) (Lissek et al., 2008).
Öst and Hugdahl (1981) reported that another 13 per- cent of their subjects recalled vicarious conditioning expe- riences of some sort. One study interviewed a group of people with social phobia about their images of themselves in socially phobic situations and asked where those images had originated (Hackmann et al., 2000). Ninety-six percent of these people remembered some socially traumatic expe- rience that was linked to their own current image of them- selves in socially phobic situations. The themes of these memories included having been “criticized for having an anxiety symptom” (e.g., being red or blushing), and having felt “self-conscious and uncomfortable in public as a conse- quence of past criticism” such as “having previously been bullied and called a ‘nothing’” (Hackmann et al., 2000, p. 606). It is important to keep in mind that, as with specific phobias, not everyone who experiences direct or vicarious conditioning in social situations develops social phobia. Individual differences in experiences play an important role in who develops social phobia, as is the case with specific phobias.
SOCIAL FEARS AND PHOBIA IN AN EVOLUTIONARY CONTEXT Social fears and phobia by definition involve fears of members of one’s own species. By contrast, animal fears and phobias usually involve fear of potential preda- tors. Although animal fears probably evolved to trigger
DSM-5 Criteria for. . . Social Anxiety Disorder (Social Phobia)
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 conversa- tion, 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 failing 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 dis- tress or impairment in social, occupational, or other important areas of functioning.
H. The fear, anxiety, or avoidance is not attributable to the physio- logical effects of a substance (e.g., a drug of abuse, a medi- cation) 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, obe- sity, disfigurement from burns or injury) is present, the fear, anxiety, or avoidance is clearly unrelated or is excessive.
Source: Reprinted with permission from the Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition (Copyright 2013). American Psychiatric Association.
traumatic incident probably triggered the onset of his social phobia. One day he had come home from medical school to find his best friend in bed with his fiancée. About a month later he had his first panic attack and started avoiding social situations.
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uncontrollability and unpredictability often lead to sub- missive and unassertive behavior, which is characteristic of people who are socially anxious or phobic. This kind of behavior is especially likely if the perceptions of uncon- trollability stem from an actual social defeat, which is known in animals to lead to both increased submissive behavior and increased fear (Mineka & Zinbarg, 1995, 2006). Consistent with this, people with social phobia have a diminished sense of personal control over events in their lives (Leung & Heimberg, 1996). This diminished expectation of personal control may develop, at least in part, as a function of having been raised in families with somewhat overprotective (and sometimes rejecting) par- ents (Lieb et al., 2000).
COGNITIVE BIASES Cognitive factors also play a role in the onset and maintenance of social phobia. Beck and col- leagues (1985) suggested that people with social phobia tend to expect that other people will reject or negatively evaluate them. They argued that this leads to a sense of vulnerability when they are around people who might pose a threat. Clark and Wells (1995; Wells & Clark, 1997) later further pro- posed that these danger schemas of socially anxious people lead them to expect that they will behave in an awkward and unacceptable fashion, resulting in rejection and loss of status. Such negative expectations lead to their being preoc- cupied with bodily responses and with stereotyped, nega- tive self-images in social situations; to their overestimating how easily others will detect their anxiety; and to their mis- understanding how well they come across to others (Hirsch et al., 2004). Such intense self-preoccupation during social situations, even to the point of attending to their own heart rate, interferes with their ability to interact skillfully (Hirsch et al., 2003; Pineles & Mineka, 2005). A vicious cycle may evolve: The inward attention and potentially awkward interactions of someone with social phobia may lead others to react to them in a less friendly fashion, confirming their expectations (D. M. Clark, 1997; Clark & McManus, 2002).
Another cognitive bias seen in social phobia is a ten- dency to interpret ambiguous social information in a nega- tive rather than a benign manner (e.g., when someone smiles at you, does it mean they like you or that they think you’re foolish?). Moreover, it is the negatively biased inter- pretations that socially anxious people make that are remembered (Hertel et al., 2008). It has also been suggested that these biased cognitive processes combine to maintain social phobia and possibly even contribute to its develop- ment (Hirsch et al., 2006).
Biological Causal Factors The most important temperamental variable is behavioral inhibition, which shares characteristics with both neuroti- cism and introversion (Bienvenu et al., 2007). Behaviorally inhibited infants who are easily distressed by unfamiliar
activation of the fight-or-flight response to potential preda- tors, it has been proposed that social fears and phobia evolved as a by-product of dominance hierarchies that are a common social arrangement among animals such as pri- mates (Dimberg & Öhman, 1996; Öhman et al., 1985). Dominance hierarchies are established through aggressive encounters between members of a social group, and a defeated individual typically displays fear and submissive behavior but only rarely attempts to escape the situation completely. Thus, these investigators argued, it is not sur- prising that people with social phobia endure being in their feared situations rather than running away and escap- ing them, as people with animal phobias often do (Longin et al., 2010; Öhman, 2009).
If social phobia evolved as a by-product of dominance hierarchies, it is not surprising that humans have an evolu- tionarily based predisposition to acquire fears of social stimuli that signal dominance and aggression from other humans. These social stimuli include facial expressions of anger or contempt, which on average all humans seem to process more quickly and readily than happy or neutral facial expressions (Öhman, 2009; Schupp et al., 2004). In a series of experiments that paralleled ones for specific pho- bias, Öhman and colleagues demonstrated that subjects develop stronger conditioned responses when slides of angry faces are paired with mild electric shocks than when happy or neutral faces are paired with the same shocks (Dimberg & Öhman, 1996). Indeed, even very brief sublim- inal (not consciously perceived) presentations of the angry face that had been paired with shock were sufficient to acti- vate the conditioned responses (Parra et al., 1997), proba- bly because even these subliminal angry faces activate the amygdala—the central structure involved in fear learning (Öhman et al., 2007). Relatedly, people who have social phobia show greater activation of the amygdala (and other brain areas involved in emotion processing) in response to negative facial expressions (such as angry faces) than do normal controls (Goldin et al., 2009; Phan et al., 2006). Such results may help explain the seemingly irrational quality of social phobia, in that the angry faces are processed very quickly and an emotional reaction can be activated without a person’s awareness of any threat. The hyperactivity to negative facial expressions is paralleled by heightened neural responses to criticism (Blair et al., 2008; Shin & Liberzon, 2009).
PERCEPTIONS OF UNCONTROLLABILITY AND UNPREDICTABILITY Being exposed to uncontrollable and unpredictable stressful events (such as parental sepa- ration and divorce, family conflict, or sexual abuse) may play an important role in the development of social pho- bia (Mathew et al., 2001; Mineka & Zinbarg, 2006). In the case of Paul, the precipitating event seemed to be finding his fiancée in bed with his best friend. Perceptions of
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restructuring the therapist attempts to help clients with social phobia identify their underlying negative, automatic thoughts (“I’ve got nothing interesting to say” or “No one is interested in me”). After helping clients understand that such automatic thoughts (which usually occur just below the surface of awareness but can be accessed) often involve cognitive distortions, the therapist helps the clients change these inner thoughts and beliefs through logical reanalysis. The process of logical reanalysis might involve asking one- self questions to challenge the automatic thoughts: “Do I know for certain that I won’t have anything to say?” “Does being nervous have to lead to or equal looking stupid?”
In one highly effective version of such treatments, cli- ents may be assigned exercises in which they manipulate their focus of attention (internally versus externally) to demonstrate to themselves the adverse effects of internal self-focus. They may also receive videotaped feedback to help them modify their distorted self-images. Such tech- niques have been very successfully applied to the treatment of social phobia (Clark et al., 2006; Heimberg, 2002; Mörtberg et al., 2007). Many studies over the years have shown that exposure therapy and cognitive-behavioral ther- apy produce comparable results. However, one study sug- gests that this new, very effective variant on cognitive treatment may be more effective than exposure therapy (Clark et al., 2006). Moreover, at least one study has now shown that simply training individuals with social phobia to disengage from negative social cues during a 15-minute lab task that is repeated eight times over 4 to 6 weeks produced such remarkable reductions in social anxiety symptoms that nearly three out of four of the participants no longer met the criteria for social phobia (Schmidt et al., 2009).
An example of successful combined treatment can be seen in the case of Paul, the surgeon described earlier who had social phobia.
Paul’s Treatment
Since the onset of his social phobia 13 years earlier, Paul had taken an antidepressant at one point. The drug had helped stop his panic attacks, but he continued to fear them intensely and still avoided social situations. Thus, he had little relief from his social phobia. He had also been in supportive psychotherapy, which had helped his depression at the time but not his social phobia or his panic. When he went for treatment at a clinic that specialized in the treatment of anxiety disorders, he was not on any medication or in any other form of treatment. Treatment consisted of 14 weeks of cognitive-behavioral therapy. By the end of treatment, Paul was not panicking at all and was quite comfortable in most social situations that he had previ- ously avoided. He was seeing old friends whom he had avoided for years because of his anxiety, and he was beginning to date. Indeed, he even asked his female therapist for a date during the last treat- ment session! Although such a request was clearly inappropriate, it did indicate how much progress he had made.
stimuli and who are shy and avoidant are more likely to become fearful during childhood and, by adolescence, to show increased risk of developing social phobia (Hayward et al., 1998; Kagan, 1997). For example, one classic study was conducted on behavioral inhibition as a risk factor in a large group of children, most of whom were already known to be at risk for anxiety because their parents had an emotional disorder. Among these children, those who had been assessed as being high on behavioral inhibition between 2 and 6 years of age were nearly three times more likely to be diagnosed with social phobia (22 percent) even in middle childhood (average age of 10) than were chil- dren who were low on behavioral inhibition at 2 to 6 years (8 percent; Hirshfeld-Becker et al., 2007). Results from twin studies have shown that there is a modest genetic contribu- tion to social phobia; estimates are that about 30 percent of the variance in liability to social phobia is due to genetic factors (Hettema, Prescott, et al., 2005; Smoller et al., 2008). Nevertheless, these studies suggest that an even larger proportion of variance in who develops social phobia is due to nonshared environmental factors, which is consis- tent with a strong role for learning.
Treatments Treatment for social phobia is centered around both cog- nitive and behavior therapies and sometimes involves medication.
COGNITIVE AND BEHAVIORAL THERAPIES As with specific phobias, prolonged and graduated exposure to the feared situation (in this case, social situations), has proven to be a very effective treatment. As research has revealed the underlying distorted cognitions that characterize social phobia, cognitive restructuring techniques have been added to the behavioral techniques, generating a form of cognitive-behavioral therapy (Barlow et al., 2007). In cognitive
Infants and young children who are fearful and easily distressed by novel people or situations are sometimes high on the temperamental variable called behavioral inhibition. Such children show an increased risk of developing social phobia in adolescence.
Panic, Anxiety, Obsessions, and Their Disorders 187
Panic attacks often are “unexpected” or “uncued” in the sense that they do not appear to be provoked by identifiable aspects of the immediate situation. Indeed, they sometimes occur in situations in which they might be least expected, such as during relaxation or during sleep (known as nocturnal panic). In other cases, however, panic attacks are said to be situationally predisposed, occurring only sometimes while the person is in a par- ticular situation such as while driving a car or being in a crowd.
Because most symptoms of a panic attack are physi- cal, it is not surprising that as many as 85 percent of peo- ple having a panic attack may show up repeatedly at emergency departments or physicians’ offices for what they are convinced is a medical problem—usually cardiac, respiratory, or neurological (Korczak et al., 2007; White & Barlow, 2002).
Unfortunately, a correct diagnosis is often not made for years due to the normal results on numerous costly medical tests. Further complications arise because patients with cardiac problems are at a nearly twofold elevated risk for developing panic disorder (Korczak et al., 2007). Prompt diagnosis and treatment are also important because panic disorder causes approximately as much impairment in social and occupational functioning as that caused by major depressive disorder (Roy-Byrne et al., 2008) and because panic disorder can contribute to the development or worsening of a variety of medical problems (White & Barlow, 2002).
The case of Jackson is typical.
A Student’s Struggle with Panic
Jackson is a 21-year-old college student who came to his uni- versity’s mental health clinic complaining of unexplainable panic attacks. He reports experiencing these attacks for about a year, and is coming for treatment now because they have been increas- ing in frequency and have gotten to the point of interfering signifi- cantly with his ability to pay attention in class and to interact with his friends socially. Jackson describes his panic attacks as com- ing on completely out of the blue. They are typically characterized by feelings of derealization, extreme panic, and a strong desire to leave whatever situation he is in, and physical symptoms of racing heart, dizziness, sweating, chest pains, and shortness of breath. Jackson has these panic attacks at seemingly random times, but they occur most often in the shower, during his morning classes, and in the dining hall. Because of the distress experienced during these attacks and out of fear of having more attacks, Jackson has been showering less frequently, leaving class whenever he thinks a panic attack may be coming, and he no longer eats in the dining hall. He also has begun drinking alcohol earlier and earlier each evening because he has noticed that alcohol calms his anxiety and seems to decrease the amount of panic he experiences during the evening.
MEDICATIONS Unlike specific phobias, social phobia can sometimes be effectively treated with medications. The most effective and widely used medications are several categories of antidepressants (including the monoamine oxidase inhibitors and the selective serotonin reuptake inhibitors discussed extensively in Chapters 7 and 16; Ipser et al., 2008; Roy-Byrne & Cowley, 2007). In some studies, the effects of these antidepressant medications have been comparable to those seen with cognitive-behavioral treat- ments. However, in several studies, the newer version of cognitive-behavior therapy discussed earlier produced much more substantial improvement than did medication (Clark, Ehlers, et al., 2003). Moreover, the medications must be taken over a long period of time to help ensure that relapse does not occur (Stein & Stein, 2008). A distinct advantage of behavioral and cognitive-behavioral thera- pies over medications, then, is that they generally produce more long-lasting improvement with very low relapse rates; indeed, clients often continue to improve after treat- ment is over. Finally, several studies have also suggested that when d-cycloserine (discussed with treatment of specific phobias) is added to exposure therapy, the treat- ment gains occur more quickly and are more substantial (Guastella et al., 2008).
in review • What are the primary diagnostic criteria for social phobia and its
two subtypes?
• Identify three of the psychological causal factors for social phobia and two of the biological causal factors.
• Describe the major treatment approaches used for social phobia.
Panic Disorder 6.5 Describe the clinical features of panic disorder.
Panic disorder is defined and characterized by the occur- rence of panic attacks that often seem to come “out of the blue.” According to the DSM-5 criteria for panic disorder, the person must have experienced recurrent, unexpected attacks and must have been persistently concerned about having another attack or worried about the consequences of having an attack for at least a month (often referred to as anticipatory anxiety). For such an event to qualify as a full- blown panic attack, there must be abrupt onset of at least 4 of 13 symptoms. Most of these symptoms are physical, although three are cognitive (see the last three items in the DSM-5 box). Panic attacks are fairly brief but intense, with symptoms developing abruptly and usually reaching peak intensity within 10 minutes; the attacks often subside in 20 to 30 minutes and rarely last more than an hour. Periods of anxiety, by contrast, do not typically have such an abrupt onset and are more long lasting.
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outside their homes alone. In very severe cases, agorapho- bia is an utterly disabling disorder in which a person can- not go beyond the narrow confines of home—or even particular parts of the home.
The case of John D. is typical of someone with both panic disorder and agoraphobia.
John D.
John D. was a 45-year-old married European American man with three sons. Although well-educated and successful . . . John had been experiencing difficulties with panic attacks for 15 years . . . experi- encing two to five panic attacks per month. The previous week John had had a panic attack while driving with his family to a computer store. He recollected that before the panic attack he might have been “keyed up” over the kids making a lot of noise in the back seat; the attack began right after he had quickly turned around to tell the kids to “settle down.” Immediately after he turned back to look at the road, John felt dizzy. As soon as he noticed this, John experienced a rapid and intense surge of other sensations including sweating, accelerated heart rate, hot flushes, and trembling. Fearing that he was going to crash the car, John quickly pulled to the side of the road. . . .
John was having only a few panic attacks per month, but he was experiencing a high level of anxiety every day, focused on the possibility that he might have another panic attack at any time.
Agoraphobia Historically, agoraphobia was thought to involve a fear of the agora—the Greek word for “open gathering place.” In agoraphobia the most commonly feared and avoided situations include streets and crowded places such as shop- ping malls, movie theaters, and stores. Standing in line can be particularly difficult. Sometimes, agoraphobia develops as a complication of having panic attacks in one or more such situations. Concerned that they may have a panic attack or get sick, people with agoraphobia are anxious about being in places or situations from which escape would be difficult or embarrassing, or in which immediate help would be unavailable if something bad happened (see the DSM-5 box for diagnostic criteria). Typically people with agoraphobia are also frightened by their own bodily sensations, so they also avoid activities that will create arousal such as exercising, watching scary movies, drink- ing caffeine, and even engaging in sexual activity.
As agoraphobia first develops, people tend to avoid situations in which attacks have occurred, but usually the avoidance gradually spreads to other situations where attacks might occur. In moderately severe cases, people with agoraphobia may be anxious even when venturing
DSM-5 Criteria for. . . Panic Disorder
A. Recurrent unexpected panic attacks. A panic attack is an abrupt surge of intense fear or intense discomfort that reaches a peak within minutes, and during which time four (or more) of the following symptoms occur: Note: The abrupt surge can occur from a calm state or an anxious state.
1. Palpitations, pounding heart, or accelerated heart rate. 2. Sweating. 3. Trembling or shaking. 4. Sensations of shortness of breath or smothering. 5. Feelings of choking. 6. Chest pain or discomfort. 7. Nausea or abdominal distress. 8. Feeling dizzy, unsteady, light-headed, or faint. 9. Chills or heat sensations.
10. Paresthesias (numbness or tingling sensations). 11. Derealization (feelings of unreality) or depersonalization
(being detached from oneself). 12. Fear of losing control or “going crazy.” 13. Fear of dying.
Note: Culture-specific symptoms (e.g., tinnitus, neck sore- ness, headache, uncontrollable screaming or crying) may be seen. Such symptoms should not count as one of the four required symptoms.
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, hav- ing 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 unfamil- iar 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 dis- order (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).
Source: Reprinted with permission from the Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition (Copyright 2013). American Psychiatric Association.
Panic, Anxiety, Obsessions, and Their Disorders 189
Indeed, John had developed extensive apprehension or avoidance of driving, air travel, elevators, wide-open spaces, taking long walks alone, movie theaters, and being out of town.
[His] first panic attack had occurred 15 years ago. John had fallen asleep on the living room sofa at around 1:00 a.m. after return- ing from a night of drinking with some of his friends. Just after awak- ening at 4:30, John felt stomach pains and a pulsating sensation in the back of his neck. All of a sudden, John noticed that his heart was racing, too. . . . Although he did not know what he was suffering from, John was certain that he was dying.
John remembered having a second panic attack about a month later. From then on, the panic attacks began to occur more regularly. When the panic attacks became recurrent, John started to avoid situations in which the panic attacks had occurred as well as situa- tions in which he feared a panic attack was likely to occur. On three occasions during the first few years of his panic attacks, John went to the emergency department of his local hospital because he was sure that his symptoms were a sign of a heart attack.
Source: Adapted from Brown & Barlow, 2001, pp. 19–22.
Agoraphobia is a frequent complication of panic disor- der. As noted, the case of John D. is typical. However, many patients with agoraphobia do not experience panic. Recog- nizing this, in DSM-5 agoraphobia is now listed as a dis- tinct disorder. As agoraphobia develops, there is often a gradually spreading fearfulness in which more and more
aspects of the environment outside the home become threatening. The most recent estimate of the lifetime preva- lence of agoraphobia without panic is 1.4 percent (Kessler, Chiu, et al., 2006).
Prevalence, Age of Onset, and Gender Differences Approximately 4.7 percent of the adult population has had panic disorder with or without agoraphobia at some time in their lives, with panic disorder without agoraphobia being more common (Kessler, Chiu, et al., 2005). Panic disorder with or without agoraphobia typically begins in the 20s to the 40s, but sometimes begins in the late teen years (Kessler, Chiu, et al., 2006). Once panic disorder develops, it tends to have a chronic and disabling course, although the intensity of symptoms often waxes and wanes over time (White & Barlow, 2002). Indeed, one 12-year longitudinal study found that less than 50 percent of patients with panic disorder with agoraphobia had recovered in 12 years, and 58 percent of those who had recovered at some point had had a recurrence (new onset; Bruce et al., 2005). Panic disorder is about twice as prevalent in women as in men (Eaton et al., 1994; White & Barlow, 2002). Agoraphobia also occurs much more fre- quently in women than in men, and the percentage of women
DSM-5 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 dis- tress or impairment in social, occupational, or other important areas of functioning.
H. If another medical condition (e.g., inflammatory bowel dis- ease, 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 symp- toms 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). Note: Agoraphobia is diagnosed irrespective of the presence of panic disorder. If an individual’s presentation meets criteria for panic disorder and agoraphobia, both diagnoses should be assigned.
Source: Reprinted with permission from the Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition (Copyright 2013). American Psychiatric Association.
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research suggested that the link between panic and sui- cidal behavior is largely explained by the presence of comorbid disorders such as depression and substance abuse, leading researchers to conclude that panic itself doesn’t increase the risk of suicidal behavior (e.g., Vickers & McNally, 2004). However, two recent, very large epide- miological studies (one with 10,000 people from the United States and one with over 100,000 people from 21 countries) have found that panic disorder is indeed associated with increased risk for suicidal ideation and attempts independent of its relationship with comorbid disorders (Nock et al., 2009, 2010).
The Timing of a First Panic Attack Although panic attacks themselves appear to come “out of the blue,” the first one frequently occurs following feelings of distress or some highly stressful life circumstance such as loss of a loved one, loss of an important relationship, loss of a job, or criminal victimization (Barlow, 2002; Klauke et al., 2010). Although not all studies have found this, some have estimated that approximately 80 to 90 per- cent of people report that their first panic attack occurred after one or more negative life events.
increases as the extent of agoraphobic avoidance increases. Among people with severe agoraphobia, approximately 80 to 90 percent are female (Bekker, 1996; White & Barlow, 2002). Table 6.3 outlines gender differences in the prevalence of other anxiety disorders for comparison purposes.
People with severe agoraphobia are often fearful of venturing out of their homes into public places, in part because of their fear of having a panic attack in a place in which escape might prove physically difficult or psychologically embarrassing. They may even become housebound unless accompanied by a spouse or trusted companion.
Table 6.3 Association Between Gender and Lifetime Risk of Anxiety Disorders: Results from a Study of 15 Countries
Disorder Odds Ratio
Agoraphobia 2.0
Specific phobia 2.0
Panic disorder 1.9
Generalized anxiety disorder 1.7
Social phobia 1.3
NOTE: Odds ratios represent the increase in the odds of anxiety disorders associated with female (vs. male) gender. Source: WHO World Mental Health Survey Initiative (Seedat et al. [2009]. Cross-national associations between gender and mental disorders in the World Health Organization World Mental Health Surveys. Archives of General Psychiatry, 66, 785–95.).
The most common explanation of the pronounced gender difference in agoraphobia is a sociocultural one (McLean & Anderson, 2009). In our culture (and many oth- ers as well), it is more acceptable for women who experi- ence panic to avoid the situations they fear and to need a trusted companion to accompany them when they enter feared situations. Men who experience panic are more prone to “tough it out” because of societal expectations and their more assertive, instrumental approach to life (Bekker, 1996). Some evidence indicates that men with panic disorder may be more likely to self-medicate with nicotine or alcohol as a way of coping with and enduring panic attacks rather than developing agoraphobic avoid- ance (Starcevic et al., 2008).
Comorbidity with Other Disorders The vast majority of people with panic disorder (83 per- cent) have at least one comorbid disorder, most often gen- eralized anxiety disorder, social phobia, specific phobia, PTSD, depression, and substance-use disorders (especially smoking and alcohol dependence; Bernstein et al., 2006; Kessler, Chiu, et al., 2006; Zvolensky & Bernstein, 2005). Depression is especially common among those with panic disorder, with approximately 50 to 70 percent of people with panic disorder experiencing serious depression at some point in their lives (Kessler, Chiu, et al., 2006). Per- haps related to the fear of having a panic attack, they may also meet criteria for dependent or avoidant personality disorder (see Chapter 10).
Although people often think of suicide as being espe- cially associated with depression, a major study in the 1980s reported that panic disorder is a strong predictor of suicidal behavior (Weissman et al., 1989). Subsequent
Panic, Anxiety, Obsessions, and Their Disorders 191
anxiety disorders), but twin studies suggest that there is overlap in the genetic vulnerability factors for panic disor- der and both phobias and separation anxiety (Battaglia et al., 2009; Kendler, Walters, et al., 1995). This would be consistent with some preliminary evidence that people with a history of phobia are at heightened risk for develop- ing panic disorder (Biederman et al., 2006). However, another study suggests overlap in the genetic vulnerability for panic disorder, generalized anxiety disorder, and ago- raphobia (Hettema, Prescott, et al., 2005). Only further research can resolve these inconsistencies in findings (Norrholm & Ressler, 2009).
PANIC AND THE BRAIN One relatively early promi- nent theory about the neurobiology of panic attacks impli- cated the locus coeruleus in the brain stem (see Figure 6.1) and a particular neurotransmitter—norepinephrine—that is centrally involved in brain activity in this area (Goddard et al., 1996). However, today it is recognized that it is increased activity in the amygdala that plays a more cen- tral role in panic attacks than does activity in the locus coeruleus. The amygdala is a collection of nuclei in front of the hippocampus in the limbic system of the brain that is critically involved in the emotion of fear. Stimulation of the central nucleus of the amygdala is known to stimulate the locus coeruleus as well as the other autonomic, neuro- endocrine, and behavioral responses that occur during panic attacks (e.g., Gorman et al., 2000; LeDoux, 2000). Other recent research has also implicated the periaque- ductal gray area in the midbrain (Del-Ben & Graeff, 2009; Graeff & Del-Ben, 2008).
Nevertheless, not all people who have a panic attack following a stressful event go on to develop full-blown panic disorder. Current estimates are that nearly 23 percent of adults have experienced at least one panic attack in their lifetimes, but most do not go on to develop full-blown panic disorder (Kessler, Chiu, et al., 2006). Given that panic attacks are much more frequent than panic disorder, what causes full-blown panic disorder to develop in only a subset of these people? Several different prominent theories about the causes of panic disorder have addressed this question.
Biological Causal Factors The biological causal factors of panic disorder include genetics, brain activity, and biochemical abnormalities.
GENETIC FACTORS According to family and twin stud- ies, panic disorder has a moderate heritable component (Maron et al., 2010; Norrholm & Ressler, 2009). In a large twin study, López-Solà and colleagues (2014) estimated that 30 to 34 percent of the variance in liability to panic symptoms is due to genetic factors. As noted earlier, this genetic vulnerability is manifested at a psychological level at least in part by the important personality trait called neuroticism (which is in turn related to the temperamental construct of behavioral inhibition). Several studies have begun to identify which specific genetic polymorphisms are responsible for this moderate heritability (Strug et al., 2010), either alone or in interaction with certain types of stressful life events (Klauke et al., 2010).
Some studies have suggested that this heritability is at least partly specific for panic disorder (rather than for all
Limbic system
Locus coeruleus
Prefrontal cortex
Thalamus
Cingulate gyrus Fornix
Amygdala Hippocampus
Stria terminalis
Pituitary
Hypothalamus
Midbrain
Pons
Medulla oblongata
Brain stem
Figure 6.1 A Biological Theory of Panic, Anxiety, and Agoraphobia According to one theory, panic attacks may arise from abnormal activity in the amygdala, a collection of nuclei in front of the hippocampus in the limbic system. The anticipatory anxiety that people develop about having another panic attack is thought to arise from activity in the hippocampus of the limbic system, which is known to be involved in the learning of emotional responses. Agoraphobic avoidance, also a learned response, may also involve activity of the hippocampus and higher cortical centers (Gorman et al., 2000).
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example, some of these laboratory tests involve infusions of sodium lactate (a substance resembling the lactate our bodies produce during exercise; Gorman et al., 1989), inhaling air with altered amounts of carbon dioxide (Woods et al., 1987), or ingesting large amounts of caffeine (Uhde, 1990). In each case, such procedures produce panic attacks in panic disorder clients at a much higher rate than in normal subjects (Barlow, 2002). There is a broad range of these so-called panic provocation procedures, and some of them are associated with quite different and even mutually exclusive neurobiological processes. Thus, no single neuro- biological mechanism could possibly be implicated (Barlow, 2002; Roy-Byrne et al., 2006). However, as explained later in the section on causal factors, simpler bio- logical and psychological explanations can account for this pattern of results. These alternative explanations stem from the observation that what all these biological chal- lenge procedures have in common is that they put stress on certain neurobiological systems, which in turn produce intense physical symptoms of arousal (such as increased heart rate, respiration, and blood pressure).
At present, two primary neurotransmitter systems are most implicated in panic attacks: the noradrenergic and the serotonergic systems (Graeff & Del-Ben, 2008; Neumeister et al., 2004). Noradrenergic activity in certain brain areas can stimulate cardiovascular symptoms associ- ated with panic (Gorman et al., 2000). Increased serotoner- gic activity also decreases noradrenergic activity. This fits with results showing that the medications most widely used to treat panic disorder today—the selective serotonin reuptake inhibitors (SSRIs)—seem to increase serotonergic activity in the brain but also to decrease noradrenergic activity. By decreasing noradrenergic activity, these medi- cations decrease many of the cardiovascular symptoms associated with panic that are ordinarily stimulated by noradrenergic activity (Gorman et al., 2000).
The inhibitory neurotransmitter GABA has also been implicated in the anticipatory anxiety that many people with panic disorder have about experiencing another attack. GABA is known to inhibit anxiety and has been shown to be abnormally low in certain parts of the cortex in people with panic disorder (Goddard et al., 2001, 2004).
Psychological Causal Factors Panic disorder is caused by a number of psychological factors.
COGNITIVE THEORY OF PANIC The cognitive theory of panic disorder proposes that people with panic disorder are hypersensitive to their bodily sensations and are very prone to giving them the most dire interpretation possible (Beck et al., 1985; D. M. Clark, 1986, 1997). Clark referred to this as a tendency to catastrophize about the meaning of their bodily sensations. For example, a person who develops
Some research has suggested that the amygdala is the central area involved in what has been called a “fear net- work,” with connections not only to lower areas in the brain like the locus coeruleus but also to higher brain areas like the prefrontal cortex (Gorman et al., 2000). According to this view, panic attacks occur when the fear network is activated, either by cortical inputs or by inputs from lower brain areas. So according to this influential theory, panic disorder is likely to develop in people who have abnor- mally sensitive fear networks that get activated too readily to be adaptive. This theory about abnormally sensitive fear networks is also consistent with findings that individuals with panic disorder showed heightened startle responses to loud noise stimuli as well as slower habituation of such responding (Ludewig et al., 2005; see also Shin & Liberzon, 2009). Sakai and colleagues (2005), using functional neuro- imaging techniques, also found support for this neuroana- tomical hypothesis. Abnormally sensitive fear networks may have a partially heritable basis but may also develop as a result of repeated stressful life experiences, particu- larly early in life (Ladd et al., 2000).
But panic attacks are only one component of panic dis- order. People with panic disorder also become anxious about the possibility of another attack, and those with agora- phobia also engage in phobic avoidance behavior (Gorman et al., 2000). Different brain areas are probably involved in these different aspects of panic disorder. The panic attacks themselves arise from activity in the amygdala, either by cortical inputs (e.g., evaluating a stimulus as highly threat- ening) or by activity coming from more downstream areas like the locus coeruleus. For people who have one or more panic attacks and who go on to develop significant condi- tioned anxiety about having another one in particular contexts, the hippocampus (also a part of the limbic system, below the cortex, which is very involved in the learning of emotional responses; see Figure 6.1) is thought to generate this conditioned anxiety (Charney et al., 1998; Gray & McNaughton, 2000) and is probably also involved in the learned avoidance associated with agoraphobia (Gorman et al., 2000). Finally, the cognitive symptoms that occur dur- ing panic attacks (fears of dying or of losing control) and overreactions to the danger posed by possibly threatening bodily sensations are likely to be mediated by higher cortical centers (Etkin, 2010).
BIOCHEMICAL ABNORMALITIES Over 30 years ago, Klein (1981) and others (Sheehan, 1982, 1983) argued that panic attacks are alarm reactions caused by biochemical dysfunctions. This hypothesis initially appeared to be sup- ported by numerous studies during the past 40 years, showing that people with panic disorder are much more likely to experience panic attacks when they are exposed to various biological challenge procedures than are normal people or people with other psychiatric disorders. For
Panic, Anxiety, Obsessions, and Their Disorders 193
bodily sensations in a catastrophic manner (Teachman et al., 2007), and the greater the tendency to do so, the greater the severity of panic (Casey et al., 2005). The model also predicts that changing their cognitions about their bodily symptoms should reduce or prevent panic. Evidence that cognitive therapy for panic works is con- sistent with this prediction (D. M. Clark et al., 1994, 1999). In addition, a brief explanation of what to expect in a panic provocation study can prevent or reduce panic symptoms (D. M. Clark, 1997; Schmidt et al., 2006, for related results).
COMPREHENSIVE LEARNING THEORY OF PANIC DIS- ORDER A comprehensive learning theory of panic disor- der developed during the past few decades suggests that initial panic attacks become associated with initially neutral internal (interoceptive) and external (exterocep- tive) cues through an interoceptive conditioning (or exteroceptive conditioning) process, which leads anxiety to become conditioned to these CSs, and the more intense the panic attack, the more robust the conditioning that will occur. Other types of instrumental and avoidance learning are also involved but will not be explained here (see Bouton, 2005; Bouton et al., 2001; Mineka & Zinbarg, 2006).
This conditioning of anxiety to the internal or external cues associated with panic thus sets the stage for the devel- opment of two of the three components of panic disorder: anticipatory anxiety and, sometimes, agoraphobic fears. Specifically, when people experience their initial panic attacks (which are terrifying emotional events replete with strong internal bodily sensations), interoceptive and exteroceptive conditioning can occur to different kinds of cues, ranging from heart palpitations and dizziness to shopping malls. Because anxiety becomes conditioned to these CSs, anxious apprehension about having another attack, particularly in certain contexts, may develop, as may agoraphobic avoidance of contexts in which panic attacks might occur in a subset of individuals. Moreover, a recent study demonstrated that once an individual has developed panic disorder, that person shows greater gen- eralization of conditioned responding to other similar cues than do controls without panic disorder (Lissek et al., 2010). In individuals who have panic disorder, extinction of conditioned anxiety responses occurs more slowly than in normal controls (Michael et al., 2007). Because extinction involves inhibitory learning, which seems to be impaired in panic disorder, it is not surprising that individuals with panic disorder also show impaired discriminative condi- tioning because of their deficits in learning that a CS is a safety cue (Lissek et al., 2009).
However, another important effect is that panic attacks themselves (the third component of panic disorder) are also likely to be conditioned to certain internal cues. This leads to the occurrence of panic attacks that seemingly
panic disorder might notice that his heart is racing and con- clude that he is having a heart attack, or notice that he is dizzy, which may lead to fainting or to the thought that he may have a brain tumor. These very frightening thoughts may cause many more physical symptoms of anxiety, which further fuel the catastrophic thoughts, leading to a vicious circle culminating in a panic attack (see Figure 6.2). The per- son is not necessarily aware of making these catastrophic interpretations; rather, the thoughts are often just barely out of the realm of awareness (Rapee, 1996). These automatic thoughts, as Beck calls them, are in a sense the triggers of panic. Although it is not yet clear how the tendency to cata- strophize develops, the cognitive model proposes that only people with this tendency to catastrophize go on to develop panic disorder (D. M. Clark, 1997).
Several lines of evidence are consistent with the cog- nitive theory of panic disorder. For example, people with panic disorder are much more likely to interpret their
Trigger stimulus (internal or external)
Trigger stimulus (internal or external)
(e.g., exercise, excitement, anger, sexual arousal, co�ee, psychoactive drugs)
Perceived threat
Body sensations
Interpretation of sensations as catastrophic
Apprehension or worry (e.g., about having a panic attack or about
any distressing situation)
The Panic Circle
Figure 6.2 The Panic Circle Any kind of perceived threat may lead to apprehension or worry, which is accompanied by various bodily sensations. According to the cognitive model of panic, if a person then catastrophizes about the meaning of his or her bodily sensations, this will raise the level of perceived threat, thus creating more apprehension and worry as well as more physical symptoms, which fuel further catastrophic thoughts. This vicious circle can culminate in a panic attack. The initial physical sensations need not arise from the perceived threat (as shown at the top of the circle) but may come from other sources (exercise, anger, psychoactive drugs, etc., as shown at the bottom of the circle).
(Adapted from D. M. Clark, 1986, 1997.)
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“When I notice that my heart is beating rapidly, I worry that I might have a heart attack.” Anxiety sensitivity has been shown to predict the development of panic attacks (Li & Zinbarg, 2007; Schmidt et al., 1997), as well as the onset of other anxiety disorders (Schmidt et al., 2006).
In addition, several important studies have shown that simply having a sense of perceived control—for instance, over the amount of carbon-dioxide–altered air that is inhaled (a panic provocation procedure known frequently to bring on anxiety and panic)—reduces anxiety and even blocks panic (e.g., Sanderson et al., 1989; Zvolensky et al.,
Many people experiencing a panic attack mistake their symptoms (for example, chest pain and shortness of breath) for another medical problem—most often a heart attack.
come out of the blue when people unconsciously experi- ence certain internal bodily sensations (CSs). For example, one young man with panic disorder who was particularly frightened of signs that his heart was racing experienced a surprising and unexpected panic attack after hearing that his favorite presidential candidate had won. The panic attack thus occurred when he was happy and excited (which is what made it so surprising for him). However, from the standpoint of this theory, the attack was actually not surprising. Because the man was excited, his heart was racing, which probably served as an internal CS that trig- gered the panic (Mineka & Zinbarg, 2006). Notably, some people even have panic attacks while not consciously focused on their internal state at all—that is, while sleeping (see the Developments in Research box). This theory also underscores why not everyone who experiences an occasional panic attack goes on to develop panic disorder. Instead, people with certain genetic, temperamental or personality, or cognitive-behavioral vulnerabilities will show stronger conditioning of both anxiety and panic (Barlow, 2002; Bouton et al., 2001; Mineka & Zinbarg, 2006).
ANXIETY SENSITIVITY AND PERCEIVED CON- TROL Cognitive and learning explanations of panic and agoraphobia have looked at a number of different factors that can generally be explained within either the cognitive or learning perspective. For example, people who have high levels of anxiety sensitivity—a trait-like belief that certain bodily symptoms may have harmful conse- quences—are more prone to developing panic attacks and perhaps panic disorder (McNally, 2002; Pagura et al., 2009). People with anxiety sensitivity endorse statements such as
Developments in Research Nocturnal Panic Attacks
Although the majority of panic attacks experienced by people with panic disorder occur during waking hours, approximately 50 to 60 percent of people report that they have experienced a panic attack during sleep at least once (Barlow, 2002; O’Mahony & Ward, 2003). Nocturnal panic refers to waking from sleep in a state of panic. It seems to occur with some regularity in about 20 to 40 percent of people with panic disor- der and is frequently associated with insomnia and frequent awakenings during sleep (Craske et al., 2002; Overbeek et al., 2005; Papadimitriou & Linkowski, 2005). Although one might think that such panic attacks occur in response to nightmares, considerable research shows that this is not the case. Sleep has five stages that occur in a fairly invariant sequence multiple times throughout the night: one stage called REM sleep (rapid eye movement sleep) during which vivid dreaming occurs, and four stages of non-REM sleep (Stages 1–4) when vivid dreams do not occur. If nocturnal panic attacks occurred in response
to dreams, we would expect them to occur during REM sleep (when nightmares usually occur), but in fact they occur during Stage 2 and early Stage 3 sleep, usually a few hours after falling asleep.
It is important to note that nocturnal panic attacks are dif- ferent from “sleep terrors” or “night terrors,” which usually occur during Stage 4 sleep. Night terrors are usually experienced by children, who often scream and then fear that someone or something is chasing them around the room; however, they do not wake up (Barlow, 2002). Nocturnal panic attacks also differ from isolated sleep paralysis, which can sometimes occur dur- ing the transition from sleep to waking. Sleep paralysis involves awareness of one’s surroundings accompanied by a stark sense of terror (resembling that during a panic attack) and an inability to move, which seems to occur because the individuals are waking from REM (dream) sleep, when muscle activity below the neck is suppressed (Hinton et al., 2005).
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1998, 1999). In addition, if a person with panic disorder is accompanied by a “safe” person when undergoing a panic provocation procedure, that person is likely to show reduced distress, lowered physiological arousal, and reduced likelihood of panic relative to someone who came alone (without a “safe” person; Carter et al., 1995). More- over, anxiety sensitivity has a greater effect on panic symp- toms in people with low perceived control (Bentley et al., 2013). Finally, individuals with panic disorder may also be protected against the development of agoraphobic avoid- ance if they have relatively high levels of perceived control over their emotions and threatening situations (Suárez et al., 2009; White, Brown, et al., 2006).
SAFETY BEHAVIORS AND THE PERSISTENCE OF PANIC Why do people who have developed panic disor- der continue to have panic attacks in spite of the fact that their predictions of heart attacks, death, and insanity rarely, if ever, come true? Some people with panic disorder may, for example, have three or four panic attacks a week for 20 years; each time they may believe they are having a heart attack, and yet they never do. After experiencing hundreds or thousands of panic attacks without having a heart attack, one would think, from the cognitive perspec- tive, that this catastrophic thought would have been proved wrong so many times that it would finally go away. However, evidence suggests that such disconfirmation does not occur because people with panic disorder fre- quently engage in safety behaviors (such as breathing slowly or carrying a bottle with anxiolytic medication) before or during an attack. They then mistakenly tend to attribute the lack of catastrophe to their having engaged in this safety behavior rather than to the idea that panic attacks actually do not lead to heart attacks. Similarly, peo- ple who think they may faint will tend to lean against solid objects (D. A. Clark, 1997; Salkovskis et al., 1996). Research suggests that it is important during treatment to identify these safety behaviors so that the person can learn to give them up and finally see that the feared catastrophe still does not occur. Indeed, a good number of studies have found that asking people to drop their safety behaviors during cognitive-behavioral treatment can increase the effectiveness of the treatment (Rachman et al., 2008).
COGNITIVE BIASES AND THE MAINTENANCE OF PANIC Finally, many studies have shown that people with panic disorder are biased in the way they process threatening information. Such people not only interpret ambiguous bodily sensations as threatening (D. A. Clark, 1997; Teachman et al., 2006), but they also interpret other ambiguous situations as more threatening than do con- trols. People with panic disorder also seem to have their attention automatically drawn to threatening information in their environment such as words that represent things they fear, such as palpitations, numbness, or faint (see Lim &
Kim, 2005; Mathews & MacLeod, 2005; Mineka et al., 2003, for reviews). One study using fMRI techniques demon- strated that people with panic disorder showed greater activation to threat words than did normal people in brain areas involved in memory processing of threatening mate- rial (Maddock et al., 2003). Whether these information- processing biases are present before the disorder begins and help to cause it is as yet unclear, but these biases are certainly likely to help maintain the disorder once it has begun. For example, having one’s attention automatically drawn to threatening cues in the environment is likely to provoke more attacks.
In summary, research into both biological and psycho- social factors involved in panic disorder has provided important insights into this disorder since it was first identi- fied as a distinct disorder in 1980. It seems unlikely that research from either tradition alone will ever provide a com- plete account of this disorder, and more research is needed to synthesize these findings into a biopsychosocial theory.
Treatments Treatment for panic disorder includes behavioral and cognitive-behavioral approaches and different categories of medication.
BEHAVIORAL AND COGNITIVE-BEHAVIORAL TREAT- MENTS The original behavioral treatment for agoraphobia from the early 1970s involved prolonged exposure to feared situations, often with the help of a therapist or family mem- ber. Similar to what is done with specific and social phobias, the idea was to make people gradually face the situations they feared and learn that there was nothing to fear. Such exposure-based treatments were quite effective and helped about 60 to 75 percent of people with agoraphobia show clin- ically significant improvement (Barlow et al., 2007). These effects were generally well maintained at 2- to 4-year follow- up. But this left approximately 25 to 40 percent not improved to a clinically significant degree (Barlow et al., 2002).
One limitation of these original treatments was that they did not specifically target panic attacks. In the mid- 1980s, two new techniques were developed as clinical researchers increasingly recognized the importance of panic attacks to most people with agoraphobia. One technique involves the variant on exposure known as interoceptive exposure, meaning deliberate exposure to feared internal sen- sations. The idea was that fear of these internal sensations should be treated in the same way that fear of external ago- raphobic situations is treated—namely, through prolonged exposure to those internal sensations so that the fear may extinguish. For example, people are asked to engage in vari- ous exercises that bring on various internal sensations (e.g., spinning in a chair, hyperventilating, running in place) and to stick with those sensations until they subside, thereby allowing habituation of their fears of these sensations.
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MEDICATIONS Many people with panic disorder are prescribed anxiolytics (antianxiety medications) from the benzodiazepine category such as alprazolam (Xanax) or clonazepam (Klonopin). One major advantage of these drugs is that they act very quickly (30–60 minutes) and so can be useful in acute situations of intense panic or anxiety. How- ever, these anxiolytic medications can also have undesirable side effects such as drowsiness and sedation, which can lead to impaired cognitive and motor performance. Also, with prolonged use, most people using moderate to high doses develop physiological dependence on the drug, which results in withdrawal symptoms when the drug is discontin- ued (e.g., nervousness, sleep disturbance, dizziness, and fur- ther panic attacks). Withdrawal from these drugs can be very slow and difficult, and it leads to relapse in a high percentage of cases (Pollack & Simon, 2009; Roy-Byrne & Cowley, 2007). These are the reasons why benzodiazepines are no longer considered as a first-choice treatment (Katon, 2006).
The other category of medication that is useful in the treatment of panic disorder and agoraphobia is the antide- pressants (including primarily the tricyclics, the SSRIs, and most recently the serotonin-norepinephrine reuptake inhib- itors). These medications have both advantages and disad- vantages compared with anxiolytics. One major advantage is that they do not create physiological dependence in the way benzodiazepines can, and they also can alleviate any comorbid depressive symptoms or disorders (Pollack & Simon, 2009; Roy-Byrne & Cowley, 2007). However, it takes about 4 weeks before they have any beneficial effects, so they are not useful in an acute situation where a person is having a panic attack. Troublesome side effects (such as dry mouth, constipation, and blurred vision with the tricyclics, and interference with sexual arousal with the SSRIs) mean that large numbers of people refuse to take the medications or discontinue their use. Moreover, relapse rates when the drugs are discontinued are quite high (although not as high as with the benzodiazepines; Roy-Byrne & Cowley, 2007).
Today the SSRIs are more widely prescribed than the tricyclics because the SSRIs are generally better tolerated by most patients. Moreover, both are generally preferred by physicians to benzodiazepines because of the risks asso- ciated with the latter (Roy-Byrne & Cowley, 2007).
What about the combination of antianxiety medication and cognitive-behavioral therapy (CBT)? In the short term, such combined treatment sometimes produces a slightly superior result compared to either type of treatment alone (Barlow et al., 2007; Mitte, 2005). In addition, one study showed that those individuals who had received com- bined treatment showed fewer medication side effects and fewer dropouts than those who had used medication alone (S. M. Marcus et al., 2007). However, in the long term, after medication has been tapered (especially benzodiazepine medications), clients who have been on medication with or without cognitive or behavioral treatment seem to show a
Research Close-Up Clinically Significant
Not all statistically significant changes are of sufficient mag- nitude to be clinically significant. Clinical significance reflects how large the effects of a particular treatment or intervention are with respect to how much meaningful change they provide in a person’s level of functioning or well-being.
The second set of techniques that were developed is cognitive restructuring techniques, in recognition that cat- astrophic automatic thoughts may help maintain panic attacks. One kind of integrative cognitive-behavioral treat- ment for panic disorder—panic control treatment (PCT)— targets both agoraphobic avoidance and panic attacks. PCT has several aspects. First, clients are educated about the nature of anxiety and panic and how the capacity to expe- rience both is adaptive. A second part of the treatment involves teaching people with panic disorder to control their breathing. Third, clients are taught about the logical errors that people who have panic disorders are prone to making and learn to subject their own automatic thoughts to a logical reanalysis. Finally, they are exposed to feared situations and feared bodily sensations to build up a toler- ance to the discomfort. Generally, this integrative treat- ment produces better results than the original exposure-based techniques that focused exclusively on exposure to external situations (Arch & Craske, 2009; D. M. Clark, 1997). In many of the studies conducted using one of the variants on these treatments, 70 to 90 percent of people with panic disorder were panic free at the end of 8 to 14 weeks of treatment, and gains were well maintained at 1- to 2-year follow-ups (Arch & Craske, 2008; McCabe & Gifford, 2009). Overall, the magnitude of improvement is often greater with these cognitive and behavioral treatments than with medications (Arch & Craske, 2009; Barlow et al., 2002). Moreover, these treatments have been extended and shown to be very useful in treating people who also have noctur- nal panic (Arch & Craske, 2008).
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greater likelihood of relapse (Arch & Craske, 2008; Barlow et al., 2002; Marks et al., 1993). Perhaps this is because they have attributed their gains to the medication rather than to their personal efforts (Başoğlu et al., 1994; Mitte, 2005). The one medication that has shown promise for enhancing responsiveness of panic disorder to CBT is d-cycloserine— the same medication discussed earlier that can enhance the speed of treating specific and social phobias (Hofmann et al., 2015).
in review • You are experiencing a panic attack. What are your symptoms?
• Describe the major diagnostic features of both panic disorder and agoraphobia. Why do the two disorders often occur together?
• What biological causal factors have been implicated in panic disorder?
• Compare and contrast the learning or conditioning theory and cognitive models of panic disorder.
• Describe the major treatment approaches for panic disorder and their relative advantages and disadvantages.
Generalized Anxiety Disorder 6.6 Explain the clinical aspects of generalized anxiety
disorder.
Everyone experiences worry—a state of anxiety and uncertainty about something in the future. Indeed, this is an adaptive emotional state that helps us plan and prepare for possible threats. But for some people, worry about many different aspects of life (including minor events) becomes chronic, excessive, and unreasonable. In these cases, generalized anxiety disorder (GAD) may be diag- nosed. DSM-5 criteria specify that the worry must occur on more days than not for at least 6 months and that it must be experienced as difficult to control (see DSM-5 criteria box). The worry must be about a number of different events or activities, and its content cannot be exclusively related to the worry associated with another concurrent disorder, such as the possibility of having a panic attack. The subjec- tive experience of excessive worry must also be accompa- nied by at least three of six other symptoms, as listed in the DSM-5 box, such as muscle tension or being easily fatigued. There was discussion leading up to DSM-5 as to whether this is the optimal set of criteria for GAD (e.g., the 6-month duration requirement and the excessive worry require- ment; Lee et al., 2009; Ruscio et al., 2005) and whether this is the optimal name for the disorder (versus generalized worry disorder or pathological worry disorder; Andrews et al., 2010). However, ultimately a conservative approach was taken and no changes were made to this diagnosis.
Muscle tension, restlessness, and difficulty concentrating are all symptoms that people with generalized anxiety disorder may have. Such individuals also worry excessively and are hypervigilant for possible signs of threat in their environment.
People suffering from GAD live in a relatively con- stant, future-oriented mood state of anxious apprehen- sion, chronic tension, worry, and diffuse uneasiness that they cannot control. They also show marked vigilance for possible signs of threat in the environment and fre- quently engage in subtle avoidance activities such as procrastination, checking, or calling a loved one fre- quently to see if he or she is safe (Barlow, 2002). Such anxious apprehension also occurs in other anxiety disor- ders (for example, the person with agoraphobia shows anticipatory anxiety about future panic attacks and about dying, and the person with social phobia is anxious about possible negative social evaluation). But this apprehension is the essence of GAD, leading Barlow and others to refer to GAD as the “basic” anxiety disorder (Roemer et al., 2002; Wells & Butler, 1997).
The nearly constant worries of people with general- ized anxiety disorder leave them continually upset and discouraged. The most common areas of worry tend to be
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usual, and he had experienced some tingling sensations; this led him to worry that he might die. In another incident he had heard his name spoken over a loudspeaker in an airport and had worried that someone at home must be dying. He was also very worried about his future because his anxiety had kept him from completing his master’s thesis on time. Rodney also worried excessively about getting a bad grade even though he had never had one either in col- lege or in graduate school. In classes he worried excessively about what the professor and other students thought of him. Although he had a number of friends, he had never had a girlfriend because of his shyness about dating. He had no problem talking or socializing with women as long as it was not defined as a dating situation. He worried that he should date a woman only if he was quite sure, from the outset, that it could be a serious relationship. He also worried excessively that if a woman did not want to date him, it meant that he was boring.
In addition to his worries, which he perceived as uncontrollable, Rodney reported muscle tension and becoming easily fatigued. He also reported great difficulty concentrating and a considerable amount of restlessness and pacing. At times he had difficulty falling asleep if he was particularly anxious, but at other times he slept excessively, in part to escape from his worries. He frequently experi- enced dizziness and palpitations, and in the past he had had full- blown panic attacks.
Rodney’s mother was also quite anxious and had been treated for panic disorder. Rodney was obviously extremely bright and had managed to do very well in school in spite of his lifelong problems with anxiety. But as the pressures of finishing graduate school and starting his career loomed before him, and as he got older and had still never dated, the anxiety became so severe that he sought treatment.
family, work, finances, and personal illness (Roemer et al., 1997). Not only do those with GAD have difficulty making decisions, but after they have managed to make a decision they worry endlessly, even after going to bed, over possible errors and unforeseen circumstances that may prove the decision wrong and lead to disaster. They have no appre- ciation of the logic by which most of us conclude that it is pointless to torment ourselves about possible outcomes over which we have no control. As two researchers in this area put it, “The result is that they fail to escape the illusory world created in their thoughts and images and rarely experience the present moment that possesses the potential to bring them joy” (Behar & Borkovec, 2006, p. 184). It is not surprising then that those with GAD experience a simi- lar amount of role impairment and lessened quality of life to those with major depression (Hoffman et al., 2008).
The next case is fairly typical of generalized anxiety disorder.
A Graduate Student with GAD
Rodney was a 26-year-old, single graduate student in the social sciences at a prestigious university. He reported that he had had problems with anxiety nearly all his life, but they had become worse since he had left home and gone to an Ivy League college. During the past year his anxiety had seriously interfered with his function- ing, and he worried about several different spheres of his life such as his own and his parents’ health. During one incident a few months earlier, he had thought that his heart was beating more slowly than
DSM-5 Criteria for. . . Generalized Anxiety Disorder
A. Excessive anxiety and worry (apprehensive expectation), occur- ring 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 sig- nificant 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).
Source: Reprinted with permission from the Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition (Copyright 2013). American Psychiatric Association.
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panic disorder, social phobia, specific phobia, PTSD, and major depressive disorder (Kessler, Chiu, et al., 2005; Tyrer & Baldwin, 2006). In addition, many people with GAD (like Rodney) experience occasional panic attacks without quali- fying for a diagnosis of panic disorder (Barlow, 2002).
Psychological Causal Factors A number of psychological factors cause GAD.
THE PSYCHOANALYTIC VIEWPOINT According to this viewpoint, generalized or free-floating anxiety results from an unconscious conflict between ego and id impulses that is not adequately dealt with because the person’s defense mechanisms have either broken down or have never devel- oped. Freud believed that it was primarily sexual and aggressive impulses that had been either blocked from expression or punished upon expression that led to free- floating anxiety. Defense mechanisms may become over- whelmed when a person experiences frequent and extreme levels of anxiety, as might happen if id impulses are fre- quently blocked from expression (e.g., under periods of prolonged sexual deprivation). According to this view, the primary difference between specific phobias and free- floating anxiety is that in phobias, the defense mechanisms of repression and displacement of an external object or sit- uation actually work, whereas in free-floating anxiety these defense mechanisms do not work, leaving the person anx- ious nearly all the time. Unfortunately, this viewpoint is not testable and therefore has been largely abandoned among clinical researchers.
PERCEPTIONS OF UNCONTROLLABILITY AND UNPRE- DICTABILITY Uncontrollable and unpredictable aver- sive events are much more stressful than controllable and predictable aversive events, so it is perhaps not surprising that the former create more fear and anxiety, as we dis- cussed with specific and social phobias (Barlow, 2002; Craske & Waters, 2005; Mineka & Oehlberg, 2008). This has led researchers to hypothesize that people with GAD may have a history of experiencing many important events in their lives as unpredictable or uncontrollable. For example, having a boss or spouse who has unpredictable bad moods or outbursts of temper for seemingly trivial reasons might keep a person in a chronic state of anxiety.
Although the unpredictable and uncontrollable events involved in GAD are generally not as severe and traumatic as those involved in the origins of posttraumatic stress dis- order (PTSD), some evidence indicates that people with GAD may be more likely to have had a history of trauma in childhood than individuals with several other anxiety dis- orders (Borkovec et al., 2004; Kendler, Hettema, et al., 2003). Moreover, people with GAD have far less tolerance for uncertainty than nonanxious controls and even people with panic disorder (Dugas et al., 2004, 2005; Koerner & Dugas,
Prevalence, Age of Onset, and Gender Differences Approximately 3 percent of the population suffers from GAD in any 1-year period and 5.7 percent at some point in their lives (Kessler et al., 1994; Kessler, Berglund, Demler, et al., 2005; Kessler, Chiu, et al., 2005). It also tends to be chronic. One 12-year follow-up study of people diagnosed with GAD found that 42 percent had not remitted 13 years later and of those who had remitted, nearly half had had a recurrence (Bruce et al., 2005; see also Hoffman et al., 2008). After age 50 the disorder seems to disappear for many peo- ple (Rubio & Lopez-Ibor, 2007); however, it often tends to be replaced by a somatic symptom disorder and character- ized by physical symptoms and health concerns.
GAD is approximately twice as common in women as in men (see Table 6.3 for summaries of gender differences in the different anxiety disorders). Although GAD is quite common, most people with this disorder manage to func- tion (albeit with some role impairment) in spite of their high levels of worry and low perceived well-being (Stein, 2004). They are less likely to go to clinics for psychological treatment than are people with panic disorder or major depressive disorder. However, people with GAD do fre- quently show up in physicians’ offices with medical com- plaints (such as muscle tension or gastrointestinal and/or cardiac symptoms) and are known to be overusers of health care resources (similar to people with panic disor- der; Greenberg et al., 1999; Katon et al., 2002).
Age of onset is often difficult to determine because 60 to 80 percent of people with GAD remember having been anx- ious nearly all their lives, and many others report a slow and insidious onset (Roemer et al., 2002; Wells & Butler, 1997). However, research has also documented that GAD often develops in older adults, for whom it is the most common anxiety disorder (e.g., Mackenzie et al., 2011; Stein, 2004).
Comorbidity with Other Disorders Generalized anxiety disorder often co-occurs with other dis- orders, especially other anxiety and mood disorders such as
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• Coping and preparation (“Worrying about a predicted negative event helps me to prepare for its occurrence”; Borkovec, 1994, pp. 16–17; Borkovec et al., 2004).
Some evidence suggests that for a subset of people with GAD, these positive beliefs about worry play a key role in maintaining high levels of anxiety and worry, espe- cially in the early phases of the development of GAD (Dugas et al., 2007). In addition, exciting new discoveries about the functions that worry actually serves help reveal why the worry process is so self-sustaining. When peo- ple with GAD worry, their emotional and physiological responses to aversive imagery are actually suppressed. This suppression of aversive emotional physiological responding may serve to reinforce the process of worry (that is, to increase its probability; Borkovec et al., 2004; McLaughlin et al., 2007). Because worry suppresses physiological responding, it also insulates the person from fully experiencing or processing the topic that she or he is worrying about, and it is known that such full processing is necessary if extinction of that anxiety is to occur. Thus, the threatening meaning of the topic being worried about is maintained (Borkovec et al., 2004; Sibrava & Borkovec, 2006).
THE NEGATIVE CONSEQUENCES OF WORRY Although worry can be reinforcing, some of its effects are clearly negative (Mineka, 2004). For example, worry itself is certainly not an enjoyable activity and can actually lead to a greater sense of danger and anxiety (and lower posi- tive mood) because of all the possible catastrophic out- comes that the worrier envisions (McLaughlin et al., 2007). In addition, people who worry about something tend sub- sequently to have more negative intrusive thoughts than people who do not worry. For example, in one study in which people were showed a gruesome film, participants later told to worry in verbal form about the film experi- enced more intrusive images from the film relative to peo- ple told to imagine the events from the film (Wells & Papageorgiou, 1995). Perhaps not surprisingly then, people with GAD tend to experience more intense negative emo- tions when reacting to a sad film (McLaughlin et al., 2007).
Finally, there is now considerable evidence that attempts to control thoughts and worry may paradoxically lead to increased experience of intrusive thoughts and enhanced perception of being unable to control them (Abramowitz et al., 2001; Wells, 1999; Wells & Butler, 1997). Somewhat paradoxically, these intrusive thoughts can serve as further trigger topics for more worry, and a sense of uncontrollability over worry may develop in people caught in this cycle that occurs in GAD. As we have noted, perceptions of uncontrollability are also known to be asso- ciated with increased anxiety, so a vicious circle of anxiety, worry, and intrusive thoughts may develop (Mineka, 2004; Mineka & Zinbarg, 2006).
2008). This low tolerance for uncertainty in people with GAD suggests that they are especially disturbed by not being able to predict the future (as none of us can; Roemer et al., 2002). Moreover, the greater the intolerance of uncer- tainty, the more severe the GAD (Dugas et al., 2007). A simi- lar intolerance for uncertainty also seems to be elevated in people with obsessive-compulsive disorder (e.g., Behar et al., 2008), as discussed later in a section on that topic.
A SENSE OF MASTERY: THE POSSIBILITY OF IMMU- NIZING AGAINST ANXIETY A person’s history of con- trol over important aspects of his or her environment is another significant experiential variable strongly affecting reactions to anxiety-provoking situations. Although we cannot study this experimentally in humans, we can learn a lot from laboratory analogue studies in animals. For example, one longitudinal experiment with infant rhesus monkeys found that infant monkeys reared with a sense of mastery and control over their environments for 7 to 10 months later adapted more readily to frightening events and novel anxiety-provoking situations than did monkeys reared in environments that were identical except for the experiences with control (Mineka et al., 1986; see also Craske & Waters, 2005; Mineka & Zinbarg, 2006). In human children, experiences with control and mastery often also occur in the context of the parent–child relationship and so parents’ responsiveness to their children’s needs directly influences their children’s developing sense of mastery (Chorpita, 2001; Craske & Waters, 2005; Mineka & Zinbarg, 2006). Unfortunately, parents of anxious children often have an intrusive, overcontrolling parenting style, which may serve only to promote their children’s anxious behav- iors by making them think of the world as an unsafe place in which they require protection and have little control themselves (Craske & Waters, 2005).
THE REINFORCING PROPERTIES OF WORRY The worry process is now considered the central feature of GAD and has been the focus of much research in the past 20 years. One question that researchers have puzzled over is this: If worrying is so anxiety-provoking and distressing, why do people keep doing it? Borkovec and colleagues (Behar & Borkovec, 2006; Borkovec, 1994; Borkovec et al., 2004) investigated both what people with GAD think the benefits of worrying are and what actual functions worry serves. Several of the benefits that people with GAD most commonly think derive from worrying are:
• Superstitious avoidance of catastrophe (“Worrying makes it less likely that the feared event will occur”)
• Avoidance of deeper emotional topics (“Worrying about most of the things I worry about is a way to distract myself from worrying about even more emotional things, things that I don’t want to think about”)
Panic, Anxiety, Obsessions, and Their Disorders 201
Biological Causal Factors The biological factors involved in GAD can be attributed to genetics, neurotransmitter abnormalities, and neurobio- logical differences.
GENETIC FACTORS Evidence for genetic factors in GAD is mixed, but there does seem to be a modest heritability, although perhaps smaller than that for most other anxiety disorders except phobias (Hettema, Prescott, & Kendler, 2001). Part of the problem for research in this area has been the evolving nature of our understanding of GAD and what its diagnostic criteria should be. Several large twin studies have revealed that heritability estimates vary as a function of one’s definition of GAD, and indicate that 15 to 20 per- cent of the variance in liability to GAD is due to genetic fac- tors (Hettema, Neale, & Kendler, 2001; Kendler et al., 1992).
The evidence is increasingly strong that GAD and major depressive disorder have a common underlying genetic predisposition (Kendler, Gardner, et al., 2007). What determines whether individuals with a genetic risk for GAD and/or major depression develop one or the other disorder seems to depend entirely on the specific environ- mental experiences they have (nonshared environment). At least part of this common genetic predisposition for GAD and major depression is best conceptualized as the basic personality trait commonly known as neuroticism (Hettema et al., 2004; Kendler, Gardner, et al., 2007).
NEUROTRANSMITTER AND NEUROHORMONAL ABNORMALITIES
A Functional Deficiency in GABA In the 1950s, the benzodi- azepine category of medications was found to reduce anxi- ety. This discovery was followed in the 1970s by the finding that these drugs probably exert their effects by stimulating the action of GABA, a neurotransmitter now strongly impli- cated in generalized anxiety (Davis, 2002; LeDoux, 2002; Nutt et al., 2006). It appears that highly anxious people have a kind of functional deficiency in GABA, which ordi- narily plays an important role in the way our brain inhibits anxiety in stressful situations. The benzodiazepine drugs appear to reduce anxiety by increasing GABA activity in certain parts of the brain implicated in anxiety, such as the limbic system, and by suppressing the stress hormone corti- sol. Whether the functional deficiency in GABA in anxious people causes their anxiety or occurs as a consequence of it is not yet known, but it does appear that this functional deficiency promotes the maintenance of anxiety.
More recently, researchers have discovered that another neurotransmitter—serotonin—is also involved in modulat- ing generalized anxiety (Goodman, 2004; Nutt et al., 2006). At present, it seems that GABA, serotonin, and perhaps norepinephrine all play a role in anxiety, but the ways in which they interact remain largely unknown (LeDoux, 2002).
COGNITIVE BIASES FOR THREATENING INFORMA- TION Not only do people with GAD have frequent frightening thoughts, they also process threatening infor- mation in a biased way, perhaps because they have promi- nent danger schemas. Anxious people tend to preferentially allocate their attention toward threatening cues when both threat and nonthreat cues are present in the environment. Nonanxious people do not show a bias except under lim- ited circumstances, in which they actually may show the opposite bias (MacLeod & Mathews, 2012; Mathews & MacLeod, 2005). Further, this attentional vigilance for threat cues can occur at a very early stage of information processing, even before the information has entered the person’s conscious awareness. If a person is already anx- ious, having her or his attention automatically focused on threat cues in the environment would seem only to main- tain the anxiety or even make it worse. Moreover, recent evidence also strongly supports the idea that such atten- tional biases play a causal role in anxiety as well (MacLeod & Mathews, 2012; Mathews & MacLeod, 2002). For exam- ple, several studies have shown that training nonanxious individuals to show an attentional bias toward threat leads to their showing a greater increase in anxiety in stressful situations (MacLeod et al., 2002). Conversely, training anx- ious people to attend away from threat leads to a decrease in their anxiety symptoms (MacLeod & Mathews, 2012).
Anxious people are also more likely than nonanxious people to think that bad things are likely to happen in the future (MacLeod, 1999), and they have a much stronger tendency to interpret ambiguous information in a threat- ening way. For example, when clinically anxious subjects read a series of ambiguous sentences (e.g., “The doctor examined little Emma’s growth” or “They discussed the priest’s convictions”), they are more likely than nonanx- ious controls to remember the threatening interpretation of each sentence (Eysenck et al., 1991; see also MacLeod et al., 2004; Mathews & MacLeod, 2005; Ouimet et al., 2009). This tendency to interpret ambiguous information negatively has actually been shown to increase anxiety in several situations, including watching a stressful video (Wilson et al., 2006).
In summary, several psychosocial variables seem to promote the onset of generalized anxiety as well as its maintenance. Experience with unpredictable and/or uncontrollable life events may create a vulnerability to anxiety and promote current anxiety. People also believe that worry serves a number of important functions, and it may actually be reinforced because it dampens physiologi- cal arousal. But worry also has some negative consequences, including the fact that worry begets further worry and cre- ates a sense of perceived uncontrollability over the worry process, which further enhances anxiety. Finally, anxiety is associated with an automatic attentional and interpretive bias toward threatening information.
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The Corticotropin-Releasing Hormone System and Anxiety An anxiety-producing hormone called corticotropin- releasing hormone (CRH) has also been strongly implicated as playing an important role in generalized anxiety (and depression; Leonardo & Hen, 2006; Maier & Watkins, 2005). When activated by stress or perceived threat, CRH stimu- lates the release of ACTH (adrenocorticotropic hormone) from the pituitary gland, which in turn causes release of the stress hormone cortisol from the adrenal gland (Leonardo & Hen, 2006); cortisol helps the body deal with stress. CRH may play an important role in generalized anxiety through its effects on the bed nucleus of the stria terminalis (an exten- sion of the amygdala; see Figure 6.1), which is now believed to be an important brain area mediating generalized anxiety (Davis, 2006; Lang et al., 2000).
NEUROBIOLOGICAL DIFFERENCES BETWEEN ANXIETY AND PANIC As we noted at the beginning of this chapter, contemporary theorists are drawing several fundamental distinctions between fear, panic, and anxiety, including their neurobiological bases. Fear and panic involve activation of the fight-or-flight response, and the brain areas and neu- rotransmitters that seem most strongly implicated in these emotional responses are the amygdala (and locus coeruleus) and the neurotransmitters norepinephrine and serotonin. Generalized anxiety (or anxious apprehension) is a more dif- fuse emotional state than acute fear or phobia that involves arousal and a preparation for possible impending threat; and the brain area, neurotransmitters, and hormones that seem most strongly implicated are the limbic system (espe- cially the bed nucleus of the stria terminalis, an extension of the amygdala), GABA, and CRH (Davis, 2006; Lang et al., 2000). Although serotonin may play a role in both anxiety and panic, it probably does so in somewhat different ways. Recently, people with GAD have been found to have a smaller left hippocampal region similar to what is seen with major depression (Hettema et al., 2012); this may represent a common risk factor for the two disorders.
Treatments As noted earlier, most treatment for GAD involves medica- tion or cognitive-behavioral approaches.
MEDICATIONS Many clients with generalized anxiety disorder consult family physicians, seeking relief from their “nerves” or anxieties or their various functional (psy- chogenic) physical problems. Most often in such cases, medications from the benzodiazepine (anxiolytic) category such as Xanax or Klonopin are used—and misused—for tension relief, reduction of other somatic symptoms, and relaxation. Their effects on worry and other psychological symptoms are not as great. Moreover, they can create phys- iological and psychological dependence and withdrawal and are therefore difficult to taper. A newer medication called buspirone (from a different medication category) is also effective, and it is neither sedating nor does it lead to physiological dependence. It also has greater effects on psychic anxiety than do the benzodiazepines. However, it may take 2 to 4 weeks to show results (Roy-Byrne & Cowley, 2002, 2007). Several categories of antidepressant medications like those used in the treatment of panic disor- der are also useful in the treatment of GAD, and they also seem to have a greater effect on the psychological symp- toms of GAD than do the benzodiazepines (Goodman, 2004; Roy-Byrne & Cowley, 2002, 2007). However, they also take several weeks before their effects are apparent.
COGNITIVE-BEHAVIORAL TREATMENT CBT for gen- eralized anxiety disorder has become increasingly effective as clinical researchers have refined the techniques used. It usually involves a combination of behavioral techniques, such as training in applied muscle relaxation, and cogni- tive restructuring techniques aimed at reducing distorted cognitions and information-processing biases associated with GAD as well as reducing catastrophizing about minor events (Barlow et al., 2007; Borkovec, 2006). GAD initially appeared to be among the most difficult of the anxiety dis- orders to treat, and to some extent this is still true. How- ever, advances have been made, and a quantitative review of many controlled studies showed that CBT approaches resulted in large changes on most symptoms measured (Mitte, 2005). The magnitude of the changes seen with cognitive-behavioral treatment was at least as large as those seen with benzodiazepines, and it led to fewer drop- outs (i.e., it was better tolerated). Finally, CBT has also been found to be useful in helping people who have used benzo- diazepines for over a year to successfully taper their medi- cations (Gosselin et al., 2006).
CBT for Rodney’s GAD
The case of Rodney, the graduate student with GAD discussed ear- lier, serves as an example of the success of cognitive-behavioral therapy with this condition. Before receiving CBT, Rodney had seen someone at a student counseling center for several months, but he hadn’t found the “talk therapy” very useful. He had heard that CBT might be useful and had sought such treatment. He was in treat- ment for about 6 months, during which time he found training in
Panic, Anxiety, Obsessions, and Their Disorders 203
DSM-5). This new category includes not only OCD but also body dysmorphic disorder, hoarding disorder, excoriation (skin-picking) disorder, and trichotillomania (compulsive hair pulling).
Obsessive-Compulsive Disorder Obsessive-compulsive disorder is defined by the occur- rence of both obsessive thoughts and compulsive behav- iors performed in an attempt to neutralize such thoughts (see the DSM-5 box for diagnostic criteria). Obsessions are persistent and recurrent intrusive thoughts, images, or impulses that are experienced as disturbing, inappro- priate, and uncontrollable. People who have such obses- sions actively try to resist or suppress them or to neutralize them with some other thought or action. Compulsions involve overt repetitive behaviors that are performed as lengthy rituals (such as hand washing, checking, putting things in order over and over again). Compulsions may also involve more covert mental rituals (such as counting, praying, or saying certain words silently over and over again). A person with OCD usually feels driven to per- form this compulsive, ritualistic behavior in response to an obsession, and there are often very rigid rules regard- ing exactly how the compulsive behavior should be per- formed. The compulsive behaviors are performed with the goal of preventing or reducing distress or preventing some dreaded event or situation. OCD is often one of the most disabling mental disorders in that it leads to a lower quality of life and a great deal of functional impairment (Stein et al., 2009).
deep muscle relaxation helpful in reducing his overall level of ten- sion. Cognitive restructuring helped reduce his worry levels about all spheres of his life. He still had problems with procrastinating when he had deadlines, but this too was improving. He also began social- izing more frequently and had tentatively begun dating when treat- ment ended for financial reasons. He could now see that if a woman didn’t want to go out with him again, this did not mean that he was boring but simply that they might not be a good match.
in review • What are the key characteristics of GAD, and what is its typical
age of onset?
• Describe the various psychosocial causal factors that may be involved in GAD, and indicate what functions worry may serve for those with GAD.
• What are the major biological causal factors in GAD?
• Compare and contrast the biological and cognitive-behavioral treatments for GAD.
Obsessive-Compulsive and Related Disorders 6.7 Describe the clinical features of obsessive-
compulsive disorder and how it is treated.
Obsessive-compulsive and related disorders used to be classified in the DSM as anxiety disorders; however, as of DSM-5 they have been classified separately as their own type of disorder (see the box on Thinking Critically about
DSM-5 Thinking Critically about DSM-5 Why Is OCD No Longer Considered to Be an Anxiety Disorder?
In DSM-5, obsessive-compulsive disorder was removed from the
anxiety disorders category and placed into a new category called
“obsessive-compulsive and related disorders.” (As you already
know from Chapter 5, PTSD was also removed and put into a
new category called “trauma and stressor-related disorders.”)
One reason for moving OCD into the new category was that
anxiety is not generally used as an indicator of OCD severity.
Indeed, for people with certain forms of OCD such as symmetry-
related obsessions and compulsions, anxiety is not even a prom-
inent symptom. It was also noted that anxiety occurs in a wide
range of disorders, so the presence of some anxiety is not a valid
reason to regard OCD as an anxiety disorder. Indeed D. J. Stein et
al. (2010) wrote that “the highly stereotyped, driven, repetitive, and
nonfunctional quality of compulsive behaviors differentiate OCD
from normal acts and from the types of avoidance that occur in
other anxiety disorders” (p. 497).
Yet another reason is that the neurobiological underpinnings
of OCD appear to be rather different from those of other anxiety
disorders, focusing on frontal-striatal neural circuitry including the
orbitofrontal cortex, anterior cingulate cortex, and striatum (espe-
cially the caudate nucleus). Studies examining the “OCD-related
disorders” such as body dysmorphic disorder (obsessing about
perceived or imagined flaws in physical appearance) and trichotil-
lomania (chronic hair pulling) also suggest shared involvement of
frontal-striatal neural circuitry. Finally, other anxiety disorders
respond to a wider range of medication treatments than does
OCD, which seems to respond selectively to SSRIs.
How compelling do these reasons sound to you? What kinds
of research findings might further support the grouping of OCD
with related disorders such as hoarding or trichotillomania? On the
contrary, what research findings might incline you to think that it
was wrong to remove OCD from the anxiety disorders category?
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In addition, the person must recognize that the obses- sion is the product of his or her own mind rather than being imposed from without (as might occur in schizophrenia). However, there is a continuum of “insight” among persons with OCD about exactly how senseless and excessive their obsessions and compulsions are (Ruscio et al., 2010). In a minority of cases, this insight is absent most of the time. Most of us have experienced minor obsessive thoughts, such as whether we remembered to lock the door or turn the stove off. In addition, most of us occasionally engage in repetitive or stereotyped behavior, such as checking the stove or the lock on the door or stepping over cracks on a sidewalk. One recent study found that more than 25 percent of people in the United States report expe- riencing obsessions or compulsions at some time in their lives (Ruscio et al., 2010). With OCD, however, the thoughts are excessive and much more persistent and distressing, and the associated compulsive acts interfere with everyday activities. Diagnosis requires that obsessions and compul- sions take at least 1 hour per day, and in severe cases they may take most of the person’s waking hours. It is impor- tant to note that normal and abnormal obsessions and compulsive behaviors exist on a continuum, differing in the frequency and intensity of the obsessions and in the degrees to which the obsessions and compulsions are resisted and are troubling (Steketee & Barlow, 2002).
Many obsessive thoughts involve contamination fears, fears of harming oneself or others, and pathological doubt. Other fairly common themes are concerns about or need for symmetry (e.g., having magazines on a table arranged in a way that is “exactly right”), sexual obsessions, and obses- sions concerning religion or aggression. These themes are quite consistent cross-culturally and across the life span (Steketee & Barlow, 2002). Obsessive thoughts involving themes of violence or aggression might include a wife being obsessed with the idea that she might poison her husband or child, or a daughter constantly imagining pushing her mother down a flight of stairs. Even though such obsessive thoughts are very rarely acted on, they remain a source of often excruciating torment to a person plagued with them. The following case of Mark is fairly typical of severe OCD.
Obsessions about Confessing and Compulsive Checking
Mark was a 28-year-old single male who, at the time he entered treatment, suffered from severe obsessive thoughts and images about causing harm to others such as running over pedestri- ans while he was driving. He also had severe obsessions that he would commit a crime such as robbing a store of a large amount of money or poisoning family members or friends. These obsessions were accompanied by lengthy and excessive checking rituals. For example, one day when he drove, he began obsessing that he had caused an accident and hit a pedestrian at an intersection, and he felt compelled to spend several hours driving and walking around all parts of that intersection to find evidence of the accident.
At the time Mark went to an anxiety disorder clinic, he was no longer able to live by himself after having lived alone for several years since college. He was a very bright young man with considerable artistic talent. He had finished college at a prestigious school for the arts and had launched a successful career as a young artist when the obsessions began in his early 20s. At first, they were focused on the possibility that he would be implicated in some crime that he had not committed; later, they evolved to the point where he was afraid that he might actually commit a crime and confess to it. The checking rituals and avoidance of all places where such confessions might occur eventually led to his having to give up his career and his own apartment and move back in with his family.
At the time he presented for treatment, Mark’s obsessions about harming others and confessing to crimes (whether or not he had committed them) were so severe that he had virtually confined himself to his room at his parents’ house. Indeed, he could leave his room only if he had a tape recorder with him so that he would have a record of any crimes he confessed to out loud because he did not trust his own memory. The clinic was several hours’ drive from his home; his mother usually had to drive because of his obsessions about causing accidents with pedestrians or moving vehicles and because the associated checking rituals could punctuate any trip with several very long stops. He also could not speak at all on the phone for fear of confessing some crime that he had (or had not) committed, and he could not mail a letter for the same reason. He also could not go into a store alone or into public bathrooms, where he feared he might write a confession on the wall and be caught and punished.
As we have noted, people with OCD feel compelled to perform acts repeatedly that often seem pointless and absurd even to them and that they in some sense do not want to perform. There are five primary types of compul- sive rituals: cleaning (hand washing and showering), checking, repeating, ordering or arranging, and counting (Antony et al., 1998; Mathews, 2009), and many people exhibit multiple kinds of rituals. For a smaller number of people, the compulsions are to perform various everyday acts (such as eating or dressing) extremely slowly (primary obsessional slowness), and for others the compulsions are to have things exactly symmetrical or “evened up” (Mathews, 2009; Steketee & Barlow, 2002).
Panic, Anxiety, Obsessions, and Their Disorders 205
DSM-5 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, repeat- ing words silently) that the individual feels driven to per- form 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 dread- ed event or situation; however, these behaviors or men- tal 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 impor- tant 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 appear- ance, 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; stereoty- pies, as in stereotypic movement disorder; ritualized eating behavior, as in eating disorders; preoccupation with sub- stances 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 paraphilic disorders; impulses, as in disruptive, impulse-control, and conduct disorders; guilty ruminations, as in major depres- sive disorder; thought insertion or delusional preoccupa- tions, as in schizophrenia spectrum and other psychotic disorders; or repetitive patterns of behavior, as in autism spectrum disorder).
Source: Reprinted with permission from the Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition (Copyright 2013). American Psychiatric Association.
People who suffer from OCD often exhibit repetitive behaviors that are structured around rigid rules for performance. For example, this person turns the key in the lock a set number of times every time she leaves the house.
Washing or cleaning rituals vary from relatively mild ritual-like behavior such as spending 15 to 20 minutes washing one’s hands after going to the bathroom, to more extreme behavior such as washing one’s hands with disin- fectants for hours every day to the point where the hands bleed. Checking rituals also vary in severity from rela- tively mild (such as checking all the lights, appliances, and locks two or three times before leaving the house) to very extreme (such as going back to an intersection where one thinks one may have run over a pedestrian and spending hours checking for any sign of the imagined accident, much as Mark does in the case study). Both cleaning and checking rituals are often performed a specific number of times and thus also involve repetitive counting. The per- formance of the compulsive act or the ritualized series of acts usually brings a feeling of reduced tension and satis- faction, as well as a sense of control, although this anxiety relief is typically fleeting. This is why the same rituals need to be repeated over and over (Purdon, 2009; Steketee & Barlow, 2002).
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Howard Stern, a famous radio personality and author, as with other people who have suffered from OCD, found relief in a compulsive act or ritualized series of acts to bring about a feeling of reduced tension and a sense of control. In his book Miss America, Stern describes behaviors such as turning pages in magazines only with his pinky finger, walking through doors with the right side of his body leading, and flipping through television stations in a particular order before turning the set off.
Prevalence, Age of Onset, and Gender Differences Approximately 2 to 3 percent of people meet criteria for OCD at some point in their lifetime, and approximately 1 percent meet criteria in a given year (Ruscio et al., 2010). Over 90 percent of treatment-seeking people with OCD experience both obsessions and compulsions (Foa & Kozak, 1995; Franklin & Foa, 2007). When mental rituals and compulsions such as counting are included as compul- sive behaviors, this figure jumps to 98 percent.
Divorced (or separated) and unemployed people are somewhat overrepresented among people with OCD (Torres et al., 2006), which is not surprising given the great difficulties this disorder creates for interpersonal and occupational functioning. Some studies showed little or no gender difference in adults, which would make OCD quite different from most of the rest of the anxiety disor- ders. However, one British epidemiological study found a gender ratio of 1.4 to 1 (women to men; Torres et al., 2006). OCD typically begins in late adolescence or early adult- hood, but also can occur in children, where its symptoms are strikingly similar to those of adults (Poulton et al., 2009; Torres et al., 2006). Childhood or early adolescent onset is more common in boys than in girls and is often associated with greater severity (Lomax et al., 2009) and greater heritability (Grisham et al., 2008). In most cases the
disorder has a gradual onset, and once it becomes a seri- ous condition, it tends to be chronic, although the severity of symptoms sometimes waxes and wanes over time (Mataix-Cols et al., 2002).
Many of us show some compulsive behavior, but people with OCD feel compelled to perform repeatedly some action in response to an obsession, in order to reduce the anxiety or discomfort created by the obsession. Although the person may realize that the behavior is excessive or unreasonable, he or she does not feel able to control the urge. Obsessive-compulsive hand washers may spend hours a day washing and may even use abrasive cleansers to the point that their hands bleed.
Comorbidity with Other Disorders OCD frequently co-occurs with other anxiety disorders, most commonly social phobia, panic disorder, GAD, and PTSD (Kessler, Chiu, Demler, et al., 2005; Mathews, 2009). Moreover, approximately 25 to 50 percent of peo- ple with OCD experience major depression at some time in their lives and as many as 80 percent experience sig- nificant depressive symptoms (Steketee & Barlow, 2002; Torres et al., 2006), often at least partly in response to having OCD.
Psychological Causal Factors The following psychological factors may cause obsessive- compulsive disorder.
OCD AS LEARNED BEHAVIOR The dominant behav- ioral or learning view of obsessive-compulsive disorder is derived from Mowrer’s two-process theory of avoidance learning (1947). According to this theory, neutral stimuli become associated with frightening thoughts or experi- ences through classical conditioning and come to elicit anx- iety. For example, touching a doorknob or shaking hands might become associated with the “scary” idea of contami- nation. Once having made this association, the person may discover that the anxiety produced by shaking hands or touching a doorknob can be reduced by hand washing.
Panic, Anxiety, Obsessions, and Their Disorders 207
distress-induced grooming (such as washing) or tidying rituals seen in people with OCD, which are often provoked by obsessive thoughts that elicit anxiety.
COGNITIVE CAUSAL FACTORS
The Effects of Attempting to Suppress Obsessive Thoughts Quick, don’t think about a white bear! Gotcha. When most people attempt to suppress unwanted thoughts they sometimes experience a paradoxical increase in those thoughts later (Wegner, 1994). As already noted, people with normal and abnormal obsessions differ primarily in the degree to which they resist their own thoughts and find them unacceptable. Thus, one factor contributing to the frequency of obsessive thoughts, and the negative moods with which they are often associated, may be these attempts to suppress them (similar to what was discussed earlier about the effects of attempts to control worry in people with GAD). For example, when people with OCD are asked to record intrusive thoughts in a diary, both on days when they were told to try to suppress those thoughts and on days without instructions to suppress, they reported approximately twice as many intrusive thoughts on the days when they were attempting to suppress them (Salkovskis & Kirk, 1997). In addition, thought suppression leads to a more general increase in obsessive-compulsive symptoms beyond just the frequency of obsessions (Purdon, 2004). Finally, naturalistic diary studies of people with OCD reveal that they engage in frequent, strenuous, and time-consuming attempts to control the intrusive thoughts, although they are generally not effective in doing so (Purdon et al., 2007).
Washing his or her hands extensively reduces the anxiety, and so the washing response is reinforced, which makes it more likely to occur again in the future when other situa- tions evoke anxiety about contamination (Rachman & Shafran, 1998). Once learned, such avoidance responses are extremely resistant to extinction (Mineka & Zinbarg, 2006). Moreover, any stressors that raise anxiety levels can lead to a heightened frequency of avoidance responses in animals or compulsive rituals in humans (Cromer et al., 2007).
Several classic experiments conducted by Rachman and Hodgson (1980) supported this theory. They found that for most people with OCD, exposure to a situation that provoked their obsession (e.g., a doorknob or toilet seat for someone with obsessions about contamination) did indeed produce distress, which would continue for a moderate amount of time and then gradually dissipate. If the person was allowed to engage in the compulsive ritual immedi- ately after the provocation, however, her or his anxiety would generally decrease rapidly (although only tempo- rarily) and therefore reinforce the compulsive ritual.
This model predicts, then, that exposure to feared objects or situations should be useful in treating OCD if the exposure is followed by prevention of the ritual, enabling the person to see that the anxiety will subside naturally in time without the ritual (see also Rachman & Shafran, 1998). This is indeed the core of the most effective form of behav- ior therapy for OCD, as discussed later. Thus, the early behavioral model has been very useful in helping us understand what factors maintain obsessive-compulsive behavior, and it has also generated an effective form of treatment. However, it has not been so helpful in explain- ing why people with OCD develop obsessions in the first place and why some people never develop compulsive behaviors.
OCD AND PREPAREDNESS The preparedness concept described earlier that considers the evolutionarily adaptive nature of fear and anxiety for our early ancestors also can help us to understand the occurrence and persistence of OCD (De Silva, Rachman, & Seligman, 1977; Rapoport, 1989). The fact that many people with OCD have obses- sions and compulsions focused on dirt, contamination, and other potentially dangerous situations has led many researchers to conclude that these features of the disorder likely have deep evolutionary roots (Mineka & Zinbarg, 1996, 2006). In addition, some theorists have argued that the displacement activities that many species of animals engage in under situations of conflict or high arousal resemble the compulsive rituals seen in obsessive- compulsive disorder (Craske, 1999; Mineka & Zinbarg, 1996; Rapoport, 1989; Winslow & Insel, 1991). Displace- ment activities often involve grooming (such as a bird preening its feathers) or nesting under conditions of high conflict or frustration. They may therefore be related to the
Quick, don’t think about a white bear!
Appraisals of Responsibility for Intrusive Thoughts Salkovskis (e.g., 1989), Rachman (1997), and other cognitive theorists have distinguished between obsessive or intrusive thoughts
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per se and the negative automatic thoughts and cata- strophic appraisals that people have about experiencing such thoughts. For example, people with OCD often seem to have an inflated sense of responsibility. In turn, in some vulnerable people, this inflated sense of responsibility can be associated with beliefs that simply having a thought about doing something (e.g., a mother’s thought about harming her infant) is morally equivalent to actually hav- ing done it, or that thinking about the behavior increases the chances of actually doing so. This is known as thought– action fusion (Berle & Starcevic, 2005; Rachman et al., 2006). This inflated sense of responsibility for the harm they may cause can motivate compulsive behaviors to try to reduce the likelihood of anything harmful happening (Rachman et al., 2006). Thus, part of what differentiates normal people who have obsessions and can ordinarily dismiss them from people with OCD is this sense of responsibility that makes the thought so concerning to them.
Cognitive Biases and Distortions Cognitive factors have also been implicated in OCD. More specifically, people with OCD have an attentional bias toward disturbing material relevant to their obsessive concerns, much as occurs in the other anxiety disorders (McNally, 2000; Mineka et al., 2003). They also have difficulty blocking out negative, irrelevant input or distracting information, so they may attempt to suppress negative thoughts stimulated by this information (McNally, 2000). As we have noted, trying to suppress neg- ative thoughts may paradoxically increase their frequency. Moreover, those with OCD have low confidence in their memory ability (especially for situations they feel responsi- ble for), which may contribute to their repeating their ritu- alistic behaviors over and over again (Cougle et al., 2007; Dar et al., 2000). An additional factor contributing to their repetitive behavior is that people with OCD have deficits in their ability to inhibit both motor responses (Morein-Zamir et al., 2010) and irrelevant information (Bannon et al., 2008).
Biological Causal Factors In recent years there has been an increase in research on the possible biological basis for OCD, ranging from studies about its genetic basis to studies of abnormalities in brain function and neurotransmitter abnormalities. The evidence accumulating from all three kinds of studies suggests that biological causal factors may play a stronger causal role for OCD relative to the other disorders discussed in this chapter.
GENETIC FACTORS Evidence from twin studies reveals a moderately high concordance rate for OCD for monozy- gotic twins and a lower rate for dizygotic twins. One review of 14 published studies included 80 monozygotic pairs of twins, of whom 54 were concordant for the diagno- sis of OCD, and 29 pairs of dizygotic twins, of whom 9 were concordant. This is consistent with a moderate genetic
heritability, although it may be at least partially a nonspe- cific “neurotic” predisposition (Hanna, 2000; van Grootheest et al., 2007). Consistent with twin studies, most family studies have found 3 to 12 times higher rates of OCD in first-degree relatives of OCD clients than would be expected from current estimates of the prevalence of OCD (Grabe et al., 2006; Hettema, Prescott, & Kendler, 2001). Finally, evidence also shows that early-onset OCD has a higher genetic loading than later-onset OCD (Grisham et al., 2008; Mundo et al., 2006).
Further compelling evidence of a genetic contribution to some forms of OCD concerns a type of OCD that often starts in childhood and is characterized by chronic motor tics (Lochner & Stein, 2003). This form of tic-related OCD is linked to Tourette’s syndrome, a disorder characterized by severe chronic motor and vocal tics that is known to have a substantial genetic basis (see Chapter 15). For example, one study found that 23 percent of first-degree relatives of peo- ple with Tourette’s syndrome had diagnosable OCD even though Tourette’s syndrome itself is very rare (Pauls et al., 1986, 1991, 1995).
Finally, in recent years a number of molecular genetic studies have begun to examine the association of OCD with specific genetic polymorphisms (naturally occurring variations of genes; Grisham et al., 2008; Mundo et al., 2006; Stewart et al., 2007). Preliminary findings indicate that different genetic polymorphisms are implicated in OCD with Tourette’s syndrome and in OCD without Tourette’s syndrome, suggesting that these two forms of OCD are at least partially distinguishable at a genetic level (Stewart et al., 2007).
OCD AND THE BRAIN The search for brain abnormalities in OCD has been intense in the past 30 years as advances have been made in brain-imaging techniques. This research has revealed that abnormalities occur primarily in certain cortical and subcortical structures such as the basal ganglia. The basal ganglia are in turn linked at the amygdala to the limbic sys- tem, which controls emotional behaviors. Findings from a good number of studies using PET scans have shown that people with OCD have abnormally high levels of activity in two parts of the frontal cortex (the orbital frontal cortex and the cingulate cortex/gyrus), which are also linked to the lim- bic area. People with OCD also have abnormally high levels of activity in the subcortical caudate nucleus, which is part of the basal ganglia (see the three-dimensional depiction of the relevant brain parts in Figure 6.3). These primitive brain cir- cuits are involved in executing primitive patterns of behavior such as those involved in sex, aggression, and hygiene con- cerns. Indeed, activity in some of these areas is further increased when symptoms are provoked by relevant stimuli that activate obsessive thoughts (e.g., dirt; Evans, Lewis, & Iobst, 2004; Rauch & Savage, 2000). Studies have also shown partial normalization of at least some of these abnormalities
Panic, Anxiety, Obsessions, and Their Disorders 209
behavior) and from hygiene concerns (e.g., cleaning). Thus, the overactivation of the orbital frontal cortex, which stimu- lates the “stuff of obsessions,” combined with a dysfunc- tional interaction among the orbital frontal cortex, the corpus striatum or caudate nucleus, and the thalamus (which is downstream from the corpus striatum) may be the central component of the brain dysfunction in OCD. According to Baxter’s theory, the dysfunctions in this circuit in turn pre- vent people with OCD from showing the normal inhibition of sensations, thoughts, and behaviors that would occur if the circuit were functioning properly. In this case, impulses toward aggression, sex, hygiene, and danger that most peo- ple keep under control with relative ease “leak through” as obsessions and distract people with OCD from ordinary goal-directed behavior. Evidence suggests that at least part of the reason that this circuit does not function properly may be due to abnormalities in white matter in some of these brain areas; white matter is involved in connectivity among vari- ous brain structures (Szeszko et al., 2004; Yoo et al., 2007).
Considering these problems, Baxter and colleagues pro- posed that we can begin to understand how the prolonged and repeated bouts of obsessive-compulsive behavior in people with OCD may occur (Baxter et al., 1991, 1992, 2000). Several other slightly different theories have also been pro- posed as to the exact nature or source of the dysfunctions, but there seems to be general agreement about most of the brain areas involved (Friedlander & Desrocher, 2006; Harrison et al., 2009; Saxena & Rauch, 2000).
with successful treatment through either medication or behavior therapy (Baxter et al., 2000; Saxena et al., 2002, 2009).
The orbital frontal cortex seems to be where primitive urges regarding sex, aggression, hygiene, and danger come from (the “stuff of obsessions”; Baxter et al., 1991, p. 116). These urges are ordinarily filtered by the caudate nucleus as they travel through the cortico–basal–ganglionic– thalamic circuit, allowing only the strongest to pass on to the thalamus. The caudate nucleus or corpus striatum (part of the set of structures called the basal ganglia, which are involved in the execution of voluntary, goal-directed move- ments) is part of an important neural circuit linking the orbital frontal cortex to the thalamus. The basal ganglia also include two other structures—the globus pallidus and the substantia nigra—that are also involved in this cortico– basal–ganglionic–thalamic circuit. The thalamus is an important relay station that receives nearly all sensory input and passes it back to the cerebral cortex.
This cortico–basal–ganglionic–thalamic circuit is nor- mally involved in the preparation of complex sets of interre- lated behavioral responses used in specific situations such as those involved in territorial or social concerns. Several theo- ries have been proposed regarding what the sources of dys- function in this circuit are. For example, Baxter and colleagues (1991, 2000) cited evidence that when this circuit is not func- tioning properly, inappropriate behavioral responses may occur, including repeated sets of behaviors stemming from territorial and social concerns (e.g., checking and aggressive
Putamen and Globus pallidus
Caudate nucleus
Cerebral cortex
Cingulate gyrus/cortex
Frontal cortex
Cerebellum Thalamus Orbital frontal cortex
Corpus callosum
Basal ganglia
Figure 6.3 Neurophysiological Mechanisms for Obsessive-Compulsive Disorder This three-dimensional view illustrates parts of the brain implicated in OCD. The overlying cerebral cortex has been made transparent so that the underlying areas can be seen. The orbital frontal cortex, cingulate gyrus/cortex, and basal ganglia (especially the caudate nucleus) are the brain structures most often implicated in OCD. Increased meta- bolic activity has been found in each of these three areas in people with OCD.
210 Chapter 6
NEUROTRANSMITTER ABNORMALITIES Pharmaco- logical studies of causal factors in OCD intensified with the discovery in the 1970s that a tricyclic drug called clomip- ramine (Anafranil) is often effective in the treatment of OCD even though other tricyclic antidepressants are gen- erally not very effective (Dougherty et al., 2007). Research shows that this is because clomipramine has greater effects on the neurotransmitter serotonin, which is now strongly implicated in OCD (Pogarell et al., 2003; Stewart et al., 2009). Moreover, several other antidepressant drugs from the SSRI category that also have relatively selective effects on serotonin, such as fluoxetine (Prozac), have also been shown to be about equally effective in the treatment of OCD (Dougherty, Rauch, et al., 2002, 2007).
The exact nature of the dysfunction in serotonergic systems in OCD is unclear. Current evidence suggests that increased serotonin activity and increased sensitivity of some brain structures to serotonin are involved in OCD symptoms. Indeed, drugs that stimulate serotonergic sys- tems lead to a worsening of symptoms. In this view, long- term administration of clomipramine (or fluoxetine) causes a downregulation of certain serotonin receptors, further causing a functional decrease in the availability of sero- tonin (Dolberg, Iancu, et al., 1996; Dolberg, Sasson, et al., 1996). That is, although the immediate short-term effects of clomipramine or fluoxetine may be to increase serotonin levels (and exacerbate OCD symptoms too), the long-term effects are quite different. This is consistent with the find- ing that these drugs must be taken for at least 6 to 12 weeks before significant improvement in OCD symptoms occurs (Baxter et al., 2000; Dougherty, Rauch, et al., 2002, 2007). However, it is also becoming clear that dysfunction in sero- tonergic systems cannot by itself fully explain this complex disorder. Other neurotransmitter systems (such as the dopaminergic, GABA, and glutamate systems) also seem to be involved, although their role is not yet well under- stood (Dougherty et al., 2007; Stewart et al., 2009).
In summary, a substantial body of evidence now impli- cates biological causal factors in OCD. This evidence comes from genetic studies, from studies of abnormalities in brain function, and from studies of neurotransmitter abnormali- ties. Although the exact nature of these factors and how they are interrelated is not yet fully understood, major research efforts that are currently under way are sure to enhance our understanding of this disorder, which is often very serious and disabling.
Treatments Treatment for OCD includes behavioral and cognitive- behavioral approaches as well as medication.
BEHAVIORAL AND COGNITIVE-BEHAVIORAL TREAT- MENTS The most effective treatment for OCD is a behav- ioral treatment called exposure and response prevention
(Franklin & Foa, 2007; Stein et al., 2009). The exposure com- ponent involves having individuals with OCD repeatedly expose themselves (either in guided fantasy or directly) to stimuli that provoke their obsessions (e.g., for someone with contamination fears this may involve touching a toilet seat in a public bathroom). The response prevention com- ponent requires that they then refrain from engaging in the rituals that they ordinarily would perform to reduce their anxiety or distress. Preventing the rituals is essential so that they can see that if they allow enough time to pass, the anxiety created by the obsession will dissipate naturally down to at least 40 to 50 on a 100-point scale, even if this takes several hours. This is often as distressing as it sounds, and so the treatment typically starts out with manageable first steps in the person’s fear hierarchy (e.g., touching the bottom of their shoe) and only over time, gradually works up to more intense exposures (e.g., sitting on the floor of a dirty public restroom).
Exposure and response prevention treatment for OCD involves having the patient encounter the source of their obsessions, such as the germs imagined to lurk in a dirty bathroom, and preventing them from engaging in compulsive behaviors, such as repetitive cleaning. The treatment is often not fun for the patient, but can be very effective in decreasing OCD symptoms.
In intensive versions of this treatment, clients who, for example, are used to spending 2 to 3 hours a day shower- ing and hand washing may be asked to not shower at all for 3 days at a time (and when they finally do, to spend no more than 10 minutes in the shower). Later in treatment they are encouraged to shower for only 10 minutes a day,
Panic, Anxiety, Obsessions, and Their Disorders 211
(clomipramine) intolerable and gave it up within a few weeks. For the behavioral treatment, he was directed to get rid of the tape recorder and was given a series of exercises in which he exposed himself to feared situations where he might confess to a crime or cause harm to others, including making phone calls, mailing letters, and enter- ing stores and public bathrooms (all things he had been unable to do). Checking rituals (including the tape recorder) were prevented. Although the initial round of treatment was not especially helpful, in part because of difficulty in getting to treatment, he did eventually make a commitment to more intensive treatment by moving to a small apartment closer to the clinic. Thereafter, he did quite well.
MEDICATIONS Whereas the other anxiety disorders respond to a range of drugs, OCD seems to respond best to medications that affect the serotonin system. These medi- cations, such as clomipramine (Anafranil) and fluoxetine (Prozac) reduce the intensity of OCD symptoms, with approximately 40 to 60 percent of people showing at least a 25 to 35 percent reduction in symptoms (relative to 4 to 5 per- cent on placebo; Dougherty et al., 2007; Iancu et al., 2000). Some clients show greater improvement than this, but about 30 to 50 percent do not show any clinically signifi- cant improvement (Mancebo et al., 2006). In approximately one-third of people who fail to respond to these serotoner- gic medications, small doses of certain antipsychotic medi- cations may produce significantly greater improvement (Bloch et al., 2006).
A major disadvantage of medication treatment for OCD, as for other anxiety disorders, is that when the medication is discontinued relapse rates are generally very high (as high as 50 to 90 percent; Dougherty et al., 2007; Simpson & Liebowitz, 2006). Thus, many people who do not seek alternative forms of behavior therapy that have more long-lasting benefits may have to stay on these medi- cations indefinitely. Studies in adults have generally not found that combining medication with exposure and response prevention is much more effective than behavior therapy alone (Foa et al., 2005; Franklin & Foa, 2002, 2007), although one large study showed that a combination treat- ment was superior in the treatment of children and adoles- cents with OCD (March & Franklin, 2006; Pediatric OCD Treatment Study, 2004).
Finally, because OCD in its most severe form is such a crippling and disabling disorder, psychiatrists have begun to examine the usefulness of certain neurosurgical tech- niques for the treatment of severe, intractable OCD (which may afflict as many as 10 percent of people diagnosed with OCD; Mindus et al., 1994). Given the invasiveness of this intervention, before such surgery is even contemplated, the person must have had severe OCD for at least 5 years and must not have responded to any of the known treat- ments discussed so far (medication or behavior therapy). Several studies have shown that approximately 35 to 45 per- cent of these intractable cases respond quite well (at least a
with no more than five 30-second hand washings at meal- times, after bathroom use, and after touching clearly soiled objects. In addition to the exposures conducted during therapy sessions, “homework” is liberally assigned. For example, on one occasion well into treatment, a therapist drove a patient who was terrified of being contaminated by “dog dirt,” bathroom germs, garbage, and dead animals in the road to a place where she had observed a dead cat on the roadside. The therapist insisted that the patient approach the “smelly” corpse, touch it with the sole of her shoe, and then touch her shoe. A pebble lying close by and a stick with which she had touched the cat were presented to the patient with the instruction that she keep them in her pocket and touch them frequently throughout the day. (Franklin & Foa, 2008, pp. 192–205).
Although some people refuse such treatment or drop out early, most who stick with it show a 50 to 70 percent reduction in symptoms (Abramowitz et al., 2009; Steketee, 1993), as well as improvement in quality of life (Diefenbach et al., 2007). Approximately 50 percent are much improved or very much improved, and another 25 percent are moder- ately improved; about 76 percent maintain their gains at several-year follow-ups. These results are superior to those obtained with medication (Abramowitz et al., 2009; Franklin & Foa, 2008). There is also evidence that d-cycloserine (the drug known to facilitate extinction of fear) enhances the effectiveness of CBT; however, this enhancement is blocked if the person is also taking an antidepressant (Andersson et al., 2015). Finally, during the past 20 years a form of cognitive- behavioral therapy has also been developed by Salkovskis and colleagues (Salkovskis & Wahl, 2003). Some of the goals were to determine whether it might help a higher percent- age of people with OCD, or help increase the degree of symptom improvement, or decrease dropout rates. Current evidence suggests that this form of treatment can also be quite effective, but unfortunately it has not been shown to be superior to exposure and response prevention therapy in any of the predicted ways (Abramowitz et al., 2009; D. A. Clark, 2005). Moreover, some researchers have concluded that exposure and response prevention treatment might be enhanced by the addition of cognitive therapy (Abramowitz et al., 2009). Given that OCD rarely remits completely, leav- ing the client with some residual obsessional problems or rituals (Abramowitz et al., 2009; Franklin & Foa, 2007), there is clearly a need to improve further the efficacy of these treatments.
The successful use of this exposure and response pre- vention treatment in the case of Mark, the young artist with severe OCD, is described here briefly.
Mark’s Treatment
Mark was initially treated with medication and with exposure and response prevention. He found the side effects of the medication
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one-third reduction in symptoms) to neurosurgery designed to destroy brain tissue in one of the areas impli- cated in this condition (Dougherty, Baer, et al., 2002; Jenike, 2000; Rück et al., 2008). However, a significant number of these have adverse side effects. The results of these tech- niques are discussed in greater detail in Chapter 16.
Body Dysmorphic Disorder Body dysmorphic disorder (BDD) was classified as a somatoform disorder in DSM-IV-TR because it involves preoccupation with certain aspects of the body. However, because of its very strong similarities with OCD, it was moved out of the somatoform category and into the OCD and related disorders category in DSM-5. People with BDD are obsessed with some perceived or imagined flaw or flaws in their appearance to the point they firmly believe they are disfigured or ugly (see DSM-5 criteria). This preoccupation is so intense that it causes clinically significant distress and impairment in social or occupational functioning. Although it is not considered necessary for the diagnosis, most peo- ple with BDD have compulsive checking behaviors (such as checking their appearance in the mirror excessively or hiding or repairing a perceived flaw). Another very com- mon symptom is avoidance of usual activities because of fear that other people will see the imaginary defect and be repulsed. In severe cases, they may become so isolated that they lock themselves up in their houses and never go out, even to work, with the average employment rate estimated at only about 50 percent (Neziroglu et al., 2004). Not sur- prisingly, their average quality of life is quite poor (IsHak et al., 2012). Table 6.4 illustrates the range of activities with which BDD interferes.
People with body dysmorphic disorder are preoccupied with perceived defects in certain aspects of their body and frequently spend an inordinate amount of time obsessively checking their appearance in the mirror.
People with BDD may focus on almost any body part: Their skin has blemishes, their breasts are too small, their face is too thin (or too fat) or disfigured by visible blood vessels that others find repulsive, and so on. Some of the more common locations for perceived defects include skin (73 percent), hair (56 percent), nose (37 percent), eyes (20 percent), breasts/chest/nipples (21 percent), stomach (22 percent), and face size/shape (12 percent) (Phillips, 2005). Many sufferers have perceived defects in more than one body part. It is very important to remember that these are not the ordinary concerns that most of us have about our appearance; they are far more extreme, leading in many cases to complete preoccupation and significant emotional pain. Some researchers estimate that about half the people with BDD have concerns about their appear- ance that are of delusional intensity (Allen & Hollander, 2004). It is important to remember that others do not even see the defects that the person with BDD believes she or he has, or if they do, they see only a very minor defect within the normal range.
Another common feature of BDD is that people with this condition frequently seek reassurance from friends and family about their defects, but the reassurances almost never provide more than very temporary relief. They also fre- quently seek reassurance for themselves by checking their appearance in the mirror countless times in a day (although some avoid mirrors completely). They are usually driven by the hope that they will look different, and sometimes they
Table 6.4 BDD Interference in Functioning
Problem
Percentage of People with BDD Who Experienced the Problem
Interference with social functioning (e.g., with friends, family, or intimate relation- ships) due to BDD
99
Periods of avoidance of nearly all social interactions because of BDD
95
Ever felt depressed because of BDD 94
Interference with work or academic functioning because of BDD
90
Ever thought about suicide because of BDD*
63
Completely housebound for at least 1 week because of BDD
29
Psychiatrically hospitalized at least once because of BDD
26
Ever attempted suicide 25
Ever attempted suicide because of BDD 14
Average Number of Days Missed
Days of work missed because of BDD* 52 days
Days of school missed because of BDD* 49 days
*Since BDD began.
SOuRCE: Adapted from Katherine A. Phillips. The Broken Mirror: Understanding and Treating Dysmorphic Disorder. © 2005 Oxford University Press. Reprinted with permission.
Panic, Anxiety, Obsessions, and Their Disorders 213
may think their perceived defect does not look as bad as it has at other times. However, much more commonly they feel worse after mirror gazing (Veale & Riley, 2001). They frequently engage in excessive grooming behavior, often trying to camouflage their perceived defect through their hairstyle, clothing, or makeup (Sarwer et al., 2004).
The following case illustrates the primary features of this disorder.
Seeing Spots
Steve is a 24-year-old engineer who presented for treatment at the request of his wife. He was recently fired from his job after refusing to go into work for a 2-week period because of his extreme concerns about his appearance. He explains that he could no longer tolerate the enormous birth marks that cover his face, and so he has begun trying to pluck them off his face with nail clippers. This led to notice- able cuts and scabs on his face, which embarrassed him further and prevented him from going to work. Steve’s wife reports that although he does have a few very small and hardly noticeable freckles on this face, Steve has never had any significant birth marks or detectable skin discoloration.
Steve explained that ever since he can remember he has “not been thrilled” with the beauty marks on his face, but in the past year that have really bothered him to the point of thinking about them constantly and wishing they were gone. His wife said that Steve spends at least an hour in the mirror each morning and evening looking at the marks, asking her if she really loves him despite their presence, and researching ways to eliminate them via facial plastic surgery, bleaching, or some other cosmetic procedure. His job loss and facial lacerations were enough to push Steve’s wife to insist that he see a psychologist for treatment, and Steve has agreed to do so.
DSM-5 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 indi- vidual has performed repetitive behaviors (e.g., mirror checking, excessive grooming, skin picking, reassurance seeking) or mental acts (e.g., comparing his or her appear- ance 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.
Source: Reprinted with permission from the Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition (Copyright 2013). American Psychiatric Association.
PREVALENCE, AGE OF ONSET, AND GENDER DIFFER- ENCES Good estimates of the prevalence of BDD are dif- ficult to obtain because of the great secrecy that usually surrounds this disorder. Some leading researchers estimate that it is not a rare disorder, affecting perhaps 1 to 2 percent of the general population and up to 8 percent of people with depression (Buhlmann et al., 2010; Phillips, 2005; Rief et al., 2006). The prevalence seems to be approximately equal in men and women, although the primary body parts that are focused on tend to differ in men and women (Phillips, 2005; Phillips & Diaz, 1997). Men are more likely to obsess about their genitals, body build, and balding, whereas women tend to obsess more about their skin, stomach, breasts, buttocks, hips, and legs (Phillips, Menard, & Fay, 2006). The age of onset is usually in adolescence, when many people start to become preoccupied with their appearance. People with BDD very commonly also have a depressive diagnosis (with most estimates being over 50 percent; Allen & Hollander, 2004), and it can even lead to suicide attempts or death (Neziroglu et al., 2004; Phillips & Menard, 2006). Indeed, of nearly 200 patients with BDD, Phillips and Menard (2006) found that 80 percent reported a history of suicidal ideation, and 28 percent had a history of a suicide attempt. Rates of comorbid social phobia and obsessive-compulsive disorder are also quite substantial, although not as high as for depression (Allen & Hollander, 2004; Coles et al., 2006). Not surprisingly, BDD, like OCD, is often associated with a poor quality of life (IsHak et al., 2012).
Sufferers of BDD commonly make their way into the office of a dermatologist or plastic surgeon, one estimate being that over 75 percent seek nonpsychiatric treatment (Phillips et al., 2001). One study found that 8 percent of those seeking cosmetic medical treatments met criteria for BDD (Crerand et al., 2004), although other studies have estimated this to be as high as 20 percent (Phillips, 2005). An astute doctor will not do the requested procedures and may instead make a referral to a psychologist or psychia- trist. All too often, though, the patient does get what he or she requests—and unfortunately is almost never satisfied with the outcome. Even if they are satisfied with the out- come, such patients still tend to retain their diagnosis of BDD (Tignol et al., 2007).
RELATIONSHIP TO OCD AND EATING DISOR- DERS People with BDD, like those with OCD, have prominent obsessions, and they engage in a variety of ritu- alistic behaviors such as reassurance seeking, mirror check- ing, comparing themselves to others, and camouflage. Moreover, they are even more convinced that their obses- sive beliefs are accurate than are people with OCD (Eisen et al., 2003). In addition to these similarities in symptoms, there is overlap in the potential causes. For example, the same neurotransmitter (serotonin) and the same sets of brain structures are implicated in the two disorders (Rauch
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et al., 2003; Saxena & Feusner, 2006), and the same kinds of treatments that work for OCD are also the treatments of choice for BDD (Phillips, 2005).
Some researchers have noted similarities between BDD and eating disorders, especially anorexia nervosa. Perhaps the most striking similarities between these disor- ders are the excessive concern and preoccupation about physical appearance, dissatisfaction with one’s body, and a distorted image of certain features of one’s body (Allen & Hollander, 2004; Cororve & Gleaves, 2001). It is important to remember, however, that people with BDD look normal and yet are terribly obsessed and distressed about some aspect of their appearance. By contrast, people with anorexia are emaciated and generally satisfied with this aspect of their appearance (Phillips, 2005).
WHY NOW? BDD has existed for centuries and seems to be a universal disorder, occurring in all European countries, the Middle East, China, Japan, and Africa (Phillips, 2005). Why, then, did its examination in the literature begin only recently? One possible reason is that its prevalence may actually have increased in recent years as contemporary Western culture has become increasingly focused on “looks as everything,” with billions of dollars spent each year on enhancing appearance through makeup, clothes, plastic surgery, and other means (Fawcett, 2004). A second reason BDD has been understudied is that most people with this condition never seek psychological or psychiatric treat- ment. Rather, they suffer silently or go to dermatologists or plastic surgeons (Crerand et al., 2004; Phillips, 2001; Tignol et al., 2007). Reasons for this secrecy and shame include worries that others will think they are superficial, silly, or vain and that if they mention their perceived defect, others will notice it and focus more on it. Part of the reason why more people are now seeking treatment is that starting in the past 15 years the disorder has received a good deal of media attention. It has even been discussed on some daily talk shows, where it is sometimes called “imaginary defect disorder.” As increasing attention is focused on this disor- der, the secrecy and shame often surrounding it should decrease, and more people will seek treatment.
CAUSAL FACTORS: A BIOPSYCHOSOCIAL APPROACH TO BDD Our understanding of what causes BDD is still at a preliminary stage, but recent research seems to suggest that a biopsychosocial approach offers some reasonable hypotheses. First, one recent twin study found that over- concern with a perceived or slight defect in physical appearance is a moderately heritable trait (Monzani et al., 2012). Second, BDD seems to be occurring, at least today, in a sociocultural context that places great value on attractive- ness and beauty, and people who develop BDD often hold attractiveness as their primary value. This means that their self-schemas are heavily focused around such ideas as “If my appearance is defective, then I am worthless” (endorsed
by 60 percent in one study) (Buhlmann & Wilhelm, 2004, p. 924). One possibility why this occurs is that, in many cases, people with BDD were reinforced as children for their overall appearance more than for their behavior (Neziroglu et al., 2004). Another possibility is that they were teased or criticized for their appearance, which caused conditioning of disgust, shame, or anxiety to their own image of some part of their body. For example, one study of individuals with BDD found that 56 to 68 percent reported a history of emotional neglect or emotional abuse, and approximately 30 percent reported a history of physi- cal or sexual abuse or physical neglect (Didie et al., 2006).
In addition, substantial empirical evidence now demon- strates that people with BDD show biased attention and interpretation of information relating to attractiveness (Buhlmann & Wilhelm, 2004). They selectively attend to pos- itive or negative words such as ugly or beautiful more than to other emotional words not related to appearance, and they tend to interpret ambiguous facial expressions as contemp- tuous or angry more than do controls. When they are shown pictures of their own face that have been manipulated to be more or less symmetrical than in reality, they show a greater discrepancy than controls between judgments of their “actual” face and their “ideal” face. Asked to choose the pic- tures that best matched their faces, controls’ choices were more symmetrical than their real faces, while patients with BDD lacked this bias (Lambrou et al., 2011). Moreover, sev- eral fMRI studies have found that patients with BDD showed fundamental differences in visually processing other peo- ple’s faces relative to controls. Specifically, they showed a bias for extracting local, detailed features rather than the more global or holistic processing of faces seen in controls (Feusner et al., 2007). A second study showed that when patients with BDD are shown a picture of their own face, they demonstrate greater activation than do healthy controls in brain regions associated with inhibitory processes and the rigidity of behavior and thinking (the orbitofrontal cortex and the caudate) (Feusner et al., 2010). Similarly, compared to controls, patients with BDD demonstrate performance deficits on tasks that measure executive functioning (e.g., manipulating information, planning, and organization), which is thought to be guided by prefrontal brain regions (Dunai et al., 2010). Whether or not these factors play a causal role is not yet known, but certainly having such biases and deficits in processing information would, at a minimum, serve to perpetuate the disorder once it has developed.
TREATMENT OF BODY DYSMORPHIC DISORDER The treatments that are effective for BDD are closely related to those used in the effective treatment of OCD. Some evi- dence indicates that antidepressant medications from the SSRI category often produce moderate improvement in patients with BDD, but many are not helped or show only a modest improvement (Phillips, 2004, 2005; Phillips,
Panic, Anxiety, Obsessions, and Their Disorders 215
lack of responsiveness to the same medications that are often successful in reducing the severity of other forms of OCD and with recent findings that different genes seem to be implicated in OCD without hoarding versus OCD with hoarding (Pertusa et al., 2010; Samuels et al., 2007).
Part of the reason compulsive hoarding has become a focus of significant research attention stems from the real- ization that, on average, compulsive hoarders are signifi- cantly more disabled (both occupationally and socially) than people with OCD but without compulsive hoarding symptoms (Mataix-Cols et al., 2010; Pertusa et al., 2010). They are also at high risk for fire, falling, poor sanitation, and serious health problems (Saxena et al., 2011; Steketee & Frost, 2004). In addition, these individuals have a poorer prognosis for treatment than do people without hoarding symptoms. Notably, although the medications typically used to treat OCD are generally not effective in treating people with compulsive hoarding symptoms, some studies have suggested that one antidepressant can be somewhat effective (Saxena, 2007). Traditional behavioral therapy using exposure and response prevention is also less effec- tive than for traditional OCD (Saxena, 2007), although there are some promising, new intensive and prolonged behavioral treatments that include home visits, which seem to be more effective (2008).
Trichotillomania Trichotillomania (also known as compulsive hair pulling) has as its primary symptom the urge to pull out one’s hair from anywhere on the body (most often the scalp, eye- brows, or arms), resulting in noticeable hair loss. In earlier editions of the DSM, trichotillomania was categorized as an impulse-control disorder. However, reflecting its rela- tionship to OCD, in DSM-5 it is now placed in the obsessive- compulsive and related disorders category. The hair pulling is usually preceded by an increasing sense of ten- sion, followed by pleasure, gratification, or relief when the hair is pulled out. The symptoms must cause clinically sig- nificant distress or impairment in some important areas of functioning. It usually occurs when the person is alone (or with immediate family members) and the person often examines the hair root, twirls it off, and sometimes pulls the strand between their teeth and/or eats it. The onset can be in childhood or later, with onset post-puberty being associated with a more severe course (Odlaug & Grant, 2012). Research on trichotillomania is in very early stages and much remains to be learned about this condition.
in review • Summarize the major symptoms of obsessive-compulsive
disorder.
• How have conditioning and cognitive factors been implicated in OCD?
Pagano, & Menard, 2006). However, in some cases show- ing only limited improvement, it is possible that inade- quate doses of the medication were used, thus leading to an underestimation of their true potential effects. In gen- eral, it seems that higher doses of these medications are needed to effectively treat BDD relative to OCD (Hadley et al., 2006). In addition, a form of cognitive-behavioral treatment emphasizing exposure and response prevention has been shown to produce marked improvement in 50 to 80 percent of treated patients (Sarwer et al., 2004; Simon, 2002). These treatment approaches focus on getting the patient to identify and change distorted perceptions of his or her body during exposure to anxiety-provoking situa- tions (e.g., when wearing something that highlights rather than disguises the “defect”) and on prevention of checking responses (e.g., mirror checking, reassurance seeking, and repeated examination of the imaginary defect). The treat- ment gains are generally well maintained at follow-up (Looper & Kirmayer, 2002; Sarwer et al., 2004).
Hoarding Disorder Hoarding is a condition that had received very little research attention until the past 15 to 20 years. It has been brought into public awareness recently through several TV series such as A&E’s Hoarders or TLC’s Hoarding: Buried Alive. Traditionally, hoarding was thought of as one partic- ular symptom of OCD, but this categorization was increas- ingly questioned (Mataix-Cols et al., 2010) and hoarding was added as a new disorder in DSM-5. Compulsive hoarding (as a symptom) occurs in approximately 3 to 5 percent of the adult population, and in 10 to 40 percent of people diagnosed with OCD (Mataix-Cols et al., 2010; Steketee & Frost, 2004). People with hoarding disorder both acquire and fail to discard many possessions that seem useless or of very limited value, in part because of the emotional attachment they develop to their possessions. In addition, their living spaces are extremely cluttered and disorganized to the point of interfering with normal activi- ties that would otherwise occur in those spaces, such as cleaning, cooking, and walking through the house. In severe cases people have literally been buried alive in their own home by their hoarded possessions.
Recent neuroimaging research has found that people diagnosed with OCD who have compulsive hoarding symptoms also show patterns of activation in certain brain areas when their symptoms are provoked. These brain acti- vation patterns are different from those of people diag- nosed with OCD who do not have hoarding symptoms (Mataix-Cols et al., 2004, 2010; Pertusa et al., 2010). This has led some to suggest that people with compulsive hoarding may be neurologically distinct from people with OCD (Mataix-Cols et al., 2010; Saxena, 2008). This conclusion would also be consistent with some findings of a relative
216 Chapter 6
• What are the major biological causal factors for OCD?
• What are the primary symptoms of body dysmorphic disorder, and how are they related to obsessive-compulsive disorder?
• What are the primary symptoms of hoarding disorder and why is it often so debilitating?
• What are the primary symptoms of trichotillomania?
Cultural Perspectives 6.8 Summarize some examples of cultural differences
in sources of worry.
Cross-cultural research suggests that although anxiety is a universal emotion, and anxiety disorders probably exist in all human societies, there are some differences in preva- lence and in the form in which the different disorders are expressed in different cultures (Barlow, 2002; Good & Kleinman, 1985; Kirmayer et al., 1995). Within the United States, lifetime prevalence rates of several anxiety disor- ders vary in somewhat surprising ways across different racial and ethnic groups (Breslau et al., 2006). Specifically, lifetime risk for social phobia, generalized anxiety disor- der, and panic disorder is somewhat lower among ethnic minority groups than among the non-Hispanic whites.
These differences were slightly larger for people under age 45 and from lower socioeconomic classes. However, once a disorder has developed, the disorders are equally persis- tent across ethnic groups.
Latin Americans from the Caribbean (especially those from Puerto Rico), and other people from the Caribbean, do show higher rates of a variant of panic disorder called ataque de nervios (Guarnaccia et al., 2010; Hinton et al., 2008; Hinton, Lewis-Fernandez, & Pollack, 2009) than do other groups. Most of the symptoms of ataque de nervios are the same as in a panic attack, but they may also include burst- ing into tears, anger, and uncontrollable shouting. Other symptoms can include shakiness, verbal or physical aggres- sion, dissociative experiences, and seizure-like or fainting episodes. Such attacks are often associated with a stressful event relating to the family (e.g., news of a death), and the person may have amnesia for the episode. At least in Puerto Rico, this disorder is quite common in children and adoles- cents as well, affecting about 9 percent (Guarnaccia et al., 2005). Individuals who experience ataque de nervios also seem to be vulnerable to a wider range of other anxiety and mood disorders (Guarnaccia et al., 2010).
Looking at anxiety disorders from a cross-national perspective, one very large study of more than 60,000 peo- ple across 14 countries (8 developed and 6 less developed)
The World Around Us Taijin Kyofusho
Some evidence indicates that the form that certain anxiety dis- orders take has actually evolved to fit certain cultural patterns (Hinton, Park, et al., 2009). A good example is the Japanese disorder taijin kyofusho, which is related to the Western diagno- sis of social phobia. Like social phobia, it is a fear of interper- sonal relations or of social situations (Kim et al., 2008; Kirmayer, 1991). However, Westerners with social phobia are afraid of social situations where they may be the object of scrutiny or criticism. By contrast, most people with taijin kyofusho are con- cerned about doing something that will embarrass or offend others (Kim et al., 2008). For example, they may fear offending others by blushing, emitting an offensive odor, staring inappro- priately into the eyes of another person, or through their per- ceived physical defects or imagined deformities (which can reach delusional levels; Kim et al., 2008). This fear of bringing shame on others or offending them is what leads to social avoid- ance (Kleinknecht et al., 1997). Body dysmorphic disorder, described earlier, also commonly occurs in people with taijin kyofusho (Nagata et al., 2006).
Kirmayer (1991) and colleagues (1995) have argued that the pattern of symptoms that occurs in taijin kyofusho has clearly been shaped by cultural factors. Japanese children are raised to be highly dependent on their mothers and to have a fear of the outside world, especially strangers. As babies and young children,
they are praised for being obedient and docile. A great deal of emphasis is also placed on implicit communication—being able to guess another’s thoughts and feelings and being sensitive to them. People who make too much eye contact are likely to be considered aggressive and insensitive, and children are taught to look at the throat of people with whom they are conversing rather than into their eyes. The society is also very hierarchical and structured, and many subtleties in language and facial communication are used to communicate one’s response to social status.
At a more general level, cross-cultural researchers have noted that recognition of the cognitive component of most anx- iety disorders leads one to expect many cross-cultural varia- tions in the form that different anxiety disorders take. Anxiety disorders can be considered, at least in part, disorders of the interpretive process. Because cultures influence the categories and schemas that we use to interpret our symptoms of dis- tress, there are bound to be significant differences in the form that anxiety disorders take in different cultures (Barlow, 2002; Good & Kleinman, 1985; Kirmayer et al., 1995).
Should different manifestations of anxiety seen in different cultures be considered different disorders, or simply different manifestations of the same underlying condition?
Panic, Anxiety, Obsessions, and Their Disorders 217
Unresolved Issues The Choice of Treatments: Medications or Cognitive-Behavior Therapy?
Many people with anxiety or obsessive-compulsive disorders are unaware of the treatment options that are available to them. They also know little about the pros and cons of different types of treat- ment. Many mental health professionals are similarly uninformed or lack the training to conduct some of the more specialized treat- ments. For these reasons they may not recommend referral to what could be a more effective form of treatment. For example, in the United States specialized training in exposure and response preven- tion treatment for OCD is often not given to therapists in training. Many graduate programs in clinical psychology are also not very scientifically based (Baker et al., 2008).
Some people prefer treatment with medications because they believe it is easier to take pills than to engage in cognitive- behavior therapy (which might be more costly or involve home- work assignments). On the other hand, therapy (unlike medications) does not typically lead to unpleasant side effects other than briefly elicited fear or anxiety. Over the longer term,
therapy can also be more cost effective because people treated with medications routinely stay on them indefinitely, but therapy usually has very long-lasting effects that do not wear off with time. Medications sometimes also have limited effectiveness relative to the treatment effects that are seen with properly administered cognitive-behavior therapy.
Finding a well-trained cognitive-behavior therapist, however, is far from easy. And even trained therapists are frequently limited in the range of disorders they have been trained to treat. One solution is to provide therapists in training with proficiency in treat- ing a broader range of disorders. The Association for Psychologi- cal Science is trying to improve this situation by developing a new system for accrediting clinical training programs that teach their students well-validated forms of effective treatments. Although progress is being made, the pace of change is much slower than would be desirable.
by the World Health Organization (WHO World Mental Health Survey Consortium, 2004) showed that anxiety dis- orders were the most common category of disorder reported in all but one country (Ukraine). However, reported prevalence rates for all the anxiety disorders com- bined varied from 2.4 percent (Shanghai, China) to 18.2 percent (United States). Other countries with moderately high rates of reported anxiety disorders were Colombia, France, and Lebanon, and other countries with moderately low rates were China, Japan, Nigeria, and Spain. We now turn to several examples of cultural variants on anxiety disorders that illustrate the range of expressions of anxiety that are exhibited worldwide.
In the Yoruba culture of Nigeria, three primary clusters of symptoms are associated with generalized anxiety: worry, dreams, and bodily complaints. However, the sources of worry are very different than those in Western society; they focus on creating and maintaining a large family and on fertility. Dreams are a major source of anxi- ety because they are thought to indicate that one may be bewitched. The common somatic complaints are also unusual from a Western standpoint: “I have the feeling of something like water in my brain,” “Things like ants keep on creeping in various parts of my brain,” and “I am con- vinced some types of worms are in my head” (Ebigbo, 1982; Good & Kleinman, 1985). Nigerians with this syn- drome often have paranoid fears of malevolent attack by witchcraft (Kirmayer et al., 1995). In India also there are many more worries about being possessed by spirits and
about sexual inadequacy than are seen in generalized anxi- ety in Western cultures (Carstairs & Kapur, 1976; Good & Kleinman, 1985).
Another culture-related syndrome that occurs in places like China and other Southeast Asian countries is koro, which for men involves intense, acute fear that the penis is retracting into the body and that when this pro- cess is complete the sufferer will die. Koro occurs less fre- quently in women, for whom the fear is that their nipples are retracting and their breasts shrinking. Koro tends to occur in epidemics (sometimes referred to as a form of mass hysteria; Sinha, 2011)—especially in cultural minor- ity groups when their survival is threatened—and it is often attributed to either malicious spirits or contaminated food. A variant on this syndrome also occurs in West Afri- can nations, where afflicted individuals report shrinking of the penis or breasts (but not retraction), which they fear will lead to loss of sexual functioning and reproductive capacity (but not death). Frequently, another person who was present at the time is blamed and often severely beaten or otherwise punished (Dzokoto & Adams, 2005). They both occur in a cultural context where there are serious concerns about male sexual potency (Barlow, 2002; Kirmayer et al., 1995).
in review • What are some examples of cultural differences in sources of
worry?
Summary 6.1 Distinguish between fear and anxiety.
• The anxiety disorders have anxiety or panic or both at their core. They were initially considered a subset of the neuroses, but this term was largely abandoned after DSM-III.
• Fear or panic is a basic emotion that involves activa- tion of the fight-or-flight response of the autonomic nervous system; it occurs in response to imminent danger.
• Anxiety is a more diffuse blend of emotions that includes high levels of negative affect, worry about possible threat or danger, and the sense of being unable to predict threat or to control it if it occurs.
6.2 Describe the essential features of anxiety disorders.
• Anxiety disorders all are characterized by unrealistic, irrational fears or anxieties that cause significant dis- tress and/or impairments in functioning.
• Among the anxiety disorders recognized in DSM-5 are specific phobia, social phobia (social anxiety disorder), panic disorder, agoraphobia, and generalized anxiety disorder.
• People with these varied disorders differ from one another both in terms of the amount of fear or panic ver- sus anxiety symptoms that they experience and in the kinds of objects or situations that most concern them.
6.3 Explain the clinical features of specific phobias.
• With specific phobias, an individual has an intense and irrational fear of specific objects or situations that leads to a great deal of avoidance behavior; when confronted with a feared object, the person with a phobia often shows activation of the fight-or-flight response, which is also associated with panic.
6.4 Discuss the clinical features of social phobia.
• In social phobia, a person has disabling fears of one or more social situations, usually because of fears of neg- ative evaluation by others or of acting in an embarrass- ing or humiliating manner; in some cases a person with social phobia may actually experience panic attacks in social situations.
• People with social phobia also have prominent percep- tions of unpredictability and uncontrollability and are preoccupied with negative self-evaluative thoughts that tend to interfere with their ability to interact in a socially skillful fashion.
6.5 Describe the clinical features of panic disorder.
• In panic disorder, a person experiences recurrent, unex- pected panic attacks that often create a sense of stark terror and numerous other physical symptoms of the fight-or-flight response; panic attacks usually subside in a matter of minutes.
• Many people who experience panic attacks develop anxious apprehension about experiencing another attack; this apprehension is required for a diagnosis of panic disorder.
• Many people with panic disorder also develop agora- phobic avoidance of situations in which they fear that they might have an attack.
• Biological theories of panic disorder emphasize that the disorder may result from biochemical abnormali- ties in the brain as well as abnormal activity of the neu- rotransmitters norepinephrine and serotonin.
• Panic attacks may arise primarily from the brain area called the amygdala, although many other areas are also involved in panic disorder.
• The learning theory of panic disorder proposes that panic attacks cause the conditioning of anxiety primarily to external cues associated with the attacks and conditioning of panic itself primarily to interocep- tive cues associated with the early stages of the attacks.
• The cognitive theory of panic disorder holds that this condition may develop in people who are prone to making catastrophic misinterpretations of their bodily sensations, a tendency that may be related to preexist- ing high levels of anxiety sensitivity.
6.6 Explain the clinical aspects of generalized anxiety disorder.
• In generalized anxiety disorder, a person has chronic and excessively high levels of worry about a number of events or activities and responds to stress with high levels of psychic and muscle tension.
• Generalized anxiety disorder may occur in people who have had extensive experience with unpredict- able or uncontrollable life events.
• People with generalized anxiety seem to have danger schemas about their inability to cope with strange and dangerous situations that promote worries focused on possible future threats.
• The neurobiological factor most implicated in gen- eralized anxiety is a functional deficiency in the
218
Panic, Anxiety, Obsessions, and Their Disorders 219
neurotransmitter GABA, which is involved in inhibit- ing anxiety in stressful situations; the limbic system is the brain area most involved.
• Once a person has an anxiety disorder, mood-congruent information processing, such as attentional and inter- pretive biases, seems to help maintain it. This explains why, without treatment, anxiety disorders are often chronic conditions.
• Many people with anxiety disorders are treated by phy- sicians, often with medications designed to allay anxi- ety or with antidepressant medications that also have antianxiety effects when taken for at least 3 to 4 weeks. Such treatment focuses on suppressing the symptoms, and some anxiolytic medications have the potential to cause physiological dependence. Once the medications are discontinued, relapse rates tend to be high.
• Behavioral and cognitive therapies have a very good track record with regard to treatment of the anxiety disorders. A key ingredient of effective treatment is prolonged exposure to feared situations.
• Cognitive therapies focus on helping clients under- stand their underlying automatic thoughts, which often involve cognitive distortions such as unrealistic predictions of catastrophes that in reality are very unlikely to occur. Then they learn to change these inner thoughts and beliefs through a process of logical reanalysis known as cognitive restructuring.
6.7 Describe the clinical features of obsessive- compulsive disorder and how it is treated.
• In obsessive-compulsive disorder, a person experiences unwanted and intrusive distressing thoughts or images that are usually accompanied by compulsive behaviors performed to neutralize those thoughts or images. Checking and cleaning rituals are most common.
• Biological causal factors are also involved in obsessive- compulsive disorder, with evidence coming from genetic studies, studies of brain functioning, and psy- chopharmacological studies.
• Once this disorder begins, the anxiety-reducing quali- ties of the compulsive behaviors may help to maintain the disorder.
• Behavior therapies that involve exposure are effective in the treatment of OCD. Rituals must also must be prevented following exposure to the feared situations.
6.8 Summarize some examples of cultural differences in sources of worry.
• In Nigeria, sources of worry center on creating and maintaining a large family, being bewitched in one’s dreams, and having problems with one’s brain (such as experiencing insects or worms crawling in the brain).
• In China and other Southeast Asian countries that have cultural concerns about male sexual potency, a common source of worry is the penis retracting into the body.
agoraphobia, p. 188 amygdala, p. 191 anxiety, p. 174 anxiety disorders, p. 176 anxiety sensitivity, p. 194 blood-injection-injury
phobia, p. 178 body dysmorphic disorder
(BDD), p. 212 cognitive restructuring, p. 186 compulsions, p. 203
exposure and response prevention, p. 210
exposure therapy, p. 181 exteroceptive conditioning, p. 193 fear, p. 174 generalized anxiety disorder
(GAD), p. 197 hoarding disorder, p. 203 interoceptive conditioning, p. 193 neurotic disorders, p. 174 obsessions, p. 203
obsessive-compulsive disorder (OCD), p. 174
panic attack, p. 174 panic disorder, p. 187 panic provocation procedures, p. 192 phobia, p. 177 prepared learning, p. 180 social phobia, p. 183 specific phobia, p. 177 trichotillomania, p. 215
Key Terms
220
Learning Objectives
7.1 Describe the types of mood disorders, their primary symptoms, and their prevalence.
7.2 Distinguish between the different types of depressive disorders.
7.3 Describe the factors believed to cause unipolar mood disorders.
7.4 List and distinguish between different types of bipolar disorders.
7.5 Describe the causal factors influencing the development and maintenance of bipolar disorders.
7.6 Explain how cultural factors can influence the expression of mood disorders.
7.7 Describe and distinguish between different treatments for mood disorders.
7.8 Describe the prevalence and clinical picture of suicidal behaviors.
7.9 Explain the efforts currently used to prevent and treat suicidal behaviors.
Chapter 7
Mood Disorders and Suicide
Mood Disorders and Suicide 221
by intense and unrealistic feelings of excitement and euphoria. Some people with mood disorders experience only time periods or episodes characterized by depressed moods. However, other people experience manic episodes at certain time points and depressive episodes at other time points. Normal mood states can occur between both types of episodes. Manic and depressive mood states are often conceived to be at opposite ends of a mood contin- uum, with normal mood in the middle. Although this con- cept is accurate to a degree, sometimes an individual may have symptoms of mania and depression during the same time period. In these mixed-episode cases, the person experi- ences rapidly alternating moods such as sadness, eupho- ria, and irritability, all within the same episode of illness.
Types of Mood Disorders We will first discuss unipolar depressive disorders, in which a person experiences only depressive episodes, and then move onto bipolar and related disorders, in which a person experiences both depressive and manic episodes.
The most common form of mood disturbance involves a depressive episode, in which a person is markedly depressed or loses interest in formerly pleasurable activi- ties (or both) for at least 2 weeks, as well as other symp- toms such as changes in sleep or appetite, or feelings of worthlessness (see the DSM-5 box for diagnostic criteria).
The other primary kind of mood episode is a manic episode, in which a person shows a markedly elevated, euphoric, or expansive mood, often interrupted by occa- sional outbursts of intense irritability or even violence— particularly when others refuse to go along with the manic person’s wishes and schemes. These extreme moods must persist for at least a week for this diagnosis to be made. In addition, three or more additional symp- toms must occur in the same time period, ranging from behavioral symptoms (such as a notable increase in goal- directed activity), to mental symptoms where self-esteem becomes grossly inflated and mental activity may speed up (such as a “flight of ideas” or “racing thoughts”), to physical symptoms (such as a decreased need for sleep or psychomotor agitation). (See the Criteria for Manic Episode DSM-5 box.)
In milder forms, similar kinds of symptoms can lead to a diagnosis of hypomanic episode, in which a person experiences abnormally elevated, expansive, or irritable mood for at least 4 days. In addition, the person must have at least three other symptoms similar to those involved in mania but to a lesser degree (inflated self-esteem, decreased need for sleep, flights of ideas, pressured speech, etc.). Although the symptoms listed are the same for manic and hypomanic episodes, there is much less impairment in social and occupational functioning in hypomania, and hospitalization is not required.
A Successful “Total Failure” Sophie, a junior in college, was getting all A’s in her classes, working in her spare time as a research assistant in a psychology laboratory, and had a lot of great friends and a 2-year relationship with the guy of her dreams. Things soon changed, however, when her boyfriend unexpectedly told her that he was leaving her for someone else. Fol- lowing her initial shock and rage, she began to have uncontrollable crying spells and doubts about her other relationships and even about her abilities in the classroom and research lab. Decision mak- ing became an ordeal. Her spirits rapidly sank, and she began to spend more and more time in bed, refusing to talk with anyone. Her alcohol consumption increased to the point where she was seldom entirely sober. Within a period of weeks, her grades plummeted due to her inability, or refusal, to attend class or complete any assign- ments. She felt she was a “total failure,” even when her friends reminded her of her considerable achievements; indeed, her self- criticism gradually spread to all aspects of her life and her personal history. Finally, her parents intervened and forced her to accept an appointment with a clinical psychologist.
Was something “wrong” with Sophie, or was she merely expe- riencing normal human emotions because of her boyfriend having deserted her? The psychologist concluded that she was suffering from a serious mood disorder and initiated treatment. The diagnosis, based on the severity of the symptoms and the degree of impair- ment, was major depressive disorder. Secondarily, she had also developed a serious drinking problem—a condition that frequently co-occurs with major depressive disorder.
Most of us feel depressed from time to time. Failing an exam, arguing with a friend, not being accepted into one’s first choice of college or job, and breaking up with a roman- tic partner are all examples of events that can cause a depressed mood in many people. However, mood disor- ders involve much more severe alterations in mood for much longer periods of time. In such cases the disturbances of mood are intense and persistent enough to lead to seri- ous problems in relationships and work performance.
Mood disorders are diverse in nature, as is illustrated by the many types of depression recognized in the DSM-5 that we will discuss. Nevertheless, in all mood disorders (formerly called affective disorders), extremes of emotion or affect—soaring elation or deep depression—dominate the clinical picture. Other symptoms are also present, but abnormal mood is the defining feature.
Mood Disorders: An Overview 7.1 Describe the types of mood disorders, their
primary symptoms, and their prevalence.
The two key moods involved in mood disorders are depression, which usually involves feelings of extraordi- nary sadness and dejection, and mania, often characterized
222 Chapter 7
(following anxiety disorders), with a 12-month prevalence ranging from 1 to 10 percent across different countries (WHO World Mental Health Survey Consortium, 2004) (see Figure 7.1).
Moreover, rates for unipolar major depression are always much higher for women than for men (usually about 2:1), similar to the sex differences for most anxiety disorders (see Chapter 6) (Hasin et al., 2005; Nolen- Hoeksema, 2012; Nolen-Hoeksema & Hilt, 2009). These differences occur in most countries around the world. In the United States, this sex difference starts in adolescence and continues until about age 65, when it seems to disap- pear. Yet among schoolchildren, boys are equally likely or slightly more likely to be diagnosed with depression.
The other type of major mood disorder, bipolar disorder (in which both manic and depressive episodes occur), is
The Prevalence of Mood Disorders Major mood disorders occur with alarming frequency—at least 15 to 20 times more frequently than schizophrenia, for example, and at almost the same rate as all the anxiety disorders taken together. Of the two types of serious mood disorders, major depressive disorder (MDD), in which only major depressive episodes occur (also known as unipolar major depression), is the most common, and its occurrence has apparently increased in recent decades (Kessler et al., 2003). The most recent epidemiological results from the National Comorbidity Survey Replication (NCS-R) found lifetime prevalence rates of unipolar major depression at nearly 17 percent (12-month prevalence rates were nearly 7 percent; Kessler, Chiu, et al., 2005). Worldwide, mood disorders are the second most prevalent type of disorder
DSM-5 Criteria for. . . Major Depressive Disorder
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 indi- cated 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 inappropri-
ate 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 indecisive- ness, 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 impair- ment in social, occupational, or other important areas of functioning.
C. The episode is not attributable to the physiological effects of a substance or another medical condition.
Note: Criteria A–C constitute a major depressive episode. Major depressive episodes are common in bipolar I disorder but are not required for the diagnosis of bipolar I disorder. Note: Responses to a significant loss (e.g., bereavement, finan- cial ruin, losses from a natural disaster, a serious medical illness or disability) may include the feelings of intense sadness, rumi- nation about the loss, insomnia, poor appetite, and weight loss noted in Criterion A, which may resemble a depressive episode. Although such symptoms may be understandable or consid- ered appropriate to the loss, the presence of a major depressive episode in addition to the normal response to a significant loss should also be carefully considered. This decision inevitably requires the exercise of clinical judgment based on the individu- al’s history and the cultural norms for the expression of distress in the context of loss.
D. The occurrence of the major depressive episode is not better explained by schizoaffective disorder, schizophrenia, schizo- phreniform disorder, delusional disorder, or other specified and unspecified schizophrenia spectrum and other psychotic disorders.
E. There has never been a manic episode or a hypomanic episode.
Note: This exclusion does not apply if all of the manic-like or hypo- manic-like episodes are substance-induced or are attributable to the physiological effects of another medical condition.
Source: Reprinted with permission from the Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition (Copyright 2013). American Psychiatric Association.
Mood Disorders and Suicide 223
among African Americans than among European white Americans and Hispanics, whose rates are comparable (Kessler, Chiu, et al., 2005; Williams et al., 2007). Native Americans, by contrast, have significantly elevated rates compared to white Americans (Hasin et al., 2005). There are no significant differences among such groups for bipolar disorder.
much less common. The NCS-R estimated that the lifetime risk of developing the classic form of this disorder is about 1 percent (see also Goodwin & Jamison, 2007), and there is no discernible difference in the prevalence rates between the sexes.
Nationally representative surveys of U.S. residents suggest that mood disorders occur less frequently
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 unim-
portant 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., pur- poseless 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 fool- ish business investments).
C. The mood disturbance is sufficiently severe to cause marked impairment in social or occupational functioning or to neces- sitate 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 treat- ment) or to another medical condition. Note: A full manic episode that emerges during antidepres- sant treatment (e.g., medication, electroconvulsive therapy) but persists at a fully syndromal level beyond the physiological effect of that treatment is sufficient evidence for a manic epi- sode and, therefore, a bipolar I diagnosis.
Note: Criteria A–D constitute a manic episode. At least one lifetime manic episode is required for the diagnosis of bipolar I disorder.
Source: Reprinted with permission from the Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition (Copyright 2013). American Psychiatric Association.
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12-Month Prevalence of Any DSM-IV Mood Disorder
Figure 7.1 Annual Prevalence of Mood Disorders Around the World This figure shows the annual (12-month) prevalence of mood disorders using data collected via household surveys in 17 different coun- tries as part of the WHO World Mental Health Survey Initiative
(Adapted from WHO World Mental Health Survey Consortium, 2004.)
224 Chapter 7
in review • What are the primary distinctions between depressive disorders
and bipolar disorders?
• How prevalent are the two types of mood disorders?
• How do the prevalence rates of depressive and bipolar disorders differ between the sexes?
• What are some of the basic demographic differences in the United States influencing rates of unipolar and bipolar disorders?
Unipolar Depressive Disorders 7.2 Distinguish between the different types of
depressive disorders.
Sadness, discouragement, pessimism, and hopelessness about matters improving are familiar feelings to most peo- ple. Feelings of depression are unpleasant when we are experiencing them, but they usually do not last long, dis- sipating on their own after a period of days or weeks or after they have reached a certain intensity level. Indeed, mild and brief depression may actually be “normal” and adaptive in the long run. By slowing us down, mild depres- sion sometimes saves us from wasting a lot of energy in the futile pursuit of unobtainable goals (Keller & Nesse, 2005; Nesse, 2000). Usually, normal depressions would be expected to occur in people undergoing painful but com- mon life events such as significant personal, interpersonal, or economic losses.
Major Depressive Disorder The diagnostic criteria for major depressive disorder (MDD; also known as “major depression”) require that a
Other epidemiologic research indicates that rates of unipolar depression are inversely related to socioeconomic status (SES); that is, higher rates occur in lower socioeco- nomic groups (Kessler, Chiu, et al., 2005; Monroe et al., 2009). This may be because low SES leads to adversity and life stress (Dohrenwend, 2000; Monroe & Hadjiyannakis, 2002). However, in spite of earlier indications that rates of bipolar disorder are elevated among those in higher socio- economic groups, current evidence from carefully con- trolled studies has not found bipolar disorder to be related to socioeconomic class (Goodwin & Jamison, 2007).
Another group that has elevated rates of mood disorders consists of individuals who have high levels of accomplish- ments in the arts. Indeed, a good deal of evidence has shown that both unipolar and bipolar disorder, but especially bipo- lar disorder, occur with alarming frequency in poets, writers, composers, and artists (Jamison, 1993; Murray & Johnson, 2010). Jamison has also documented for a number of such famous creative individuals how their periods of productiv- ity co-vary with the manic, or hypomanic, and depressive phases of their illnesses. One possible hypothesis to explain this relationship is that mania or hypomania actually facili- tates the creative process and/or that the intense negative emotional experiences of depression provide material for creative activity. A study of the eminent nineteenth-century American poet Emily Dickinson provides support for the lat- ter part of this hypothesis—that is, evidence supports the idea that Dickinson’s painful experiences with panic disor- der and depression provided ideas for her especially high- quality work during those times. However, a detailed analysis of her hypomanic periods suggests that her hypo- manic symptoms increased her motivation and output but not her creativity per se (Ramey & Weisberg, 2004).
Virginia Woolf (1882–1941) suffered from bipolar disorder. As a writer, she showed intense creative productivity during manic phases, and unproductive periods when depressed. She died by suicide by drowning herself.
A person with major depressive disorder may experience a loss of energy, too much or too little sleep, decreased appetite and weight loss, an increase or slowdown in mental and physical activity, difficulty concentrating, irrational guilt, and recurrent thoughts of death or suicide.
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and anxiety disorders (e.g., Kessler et al., 2007; Watson, 2005). The issues surrounding the co-occurrence of depres- sion and anxiety, which have received a great deal of atten- tion in recent years, are very complex.
DEPRESSION AS A RECURRENT DISORDER When a diagnosis of MDD is made, it is usually also specified whether this is a first, and therefore single (initial), episode or a recurrent episode (preceded by one or more previous episodes). Depressive episodes typically last about 6 to 9 months if untreated. In approximately 10 to 20 percent of people with MDD, the symptoms do not remit for over 2 years, in which case persistent depressive disorder is diagnosed (Boland & Keller, 2009; Gilmer et al., 2005). Chronic major depression has been associated with serious childhood family problems and an anxious personality in childhood (Angst et al., 2011).
Although most depressive episodes remit (which is not said to occur until symptoms have largely been gone for at least 2 months), depressive episodes often return at some future point. This return of symptoms is of one of two types: relapse and recurrence. Relapse refers to the return of symptoms within a fairly short period of time, a situation that probably reflects the fact that the underly- ing episode of depression has not yet run its course (Boland & Keller, 2002; Frank et al., 1991). For example, relapse may commonly occur when pharmacotherapy is terminated prematurely—after symptoms have remitted but before the underlying episode is really over (Hollon & Dimidjian, 2009).
Recurrence, which refers to the onset of a new episode of depression, occurs in approximately 40 to 50 percent of people who experience a depressive episode (Monroe & Harkness, 2011). The probability of recurrence increases with the number of prior episodes and also when the per- son has comorbid disorders. Unfortunately, people who experience multiple depressive episodes often are not symptom-free in between episodes, but instead have some depressive symptoms half to two-thirds of the time (Judd et al., 1998). Moreover, people with some residual symp- toms, or with significant psychosocial impairment, follow- ing an initial depressive episode are more likely to have recurrences than those whose symptoms remit completely (Judd et al., 1999; Solomon et al., 2004).
DEPRESSION THROUGHOUT THE LIFE CYCLE Although the onset of unipolar depressive disorders most often occurs during late adolescence up to middle adult- hood, such reactions may begin at any time from early childhood to old age. Depression was once thought not to occur in childhood, but more recent research has estimated that about 1 to 3 percent of school-age children meet the criteria for some form of unipolar depressive disorder, with a smaller percentage exhibiting dysthymic disorder (discussed later) than major depression (see Avenevoli
person must be in a major depressive episode and never have had a manic, hypomanic, or mixed episode.
The following account illustrates a moderately severe case of MDD.
Jennifer
Jennifer is a 35-year-old graphic designer who is married and has three young children at home. She has been running a successful, and growing, business out of her home office, which she has really enjoyed because working from home allows her the time and flexibil- ity to be with her children when they are not in school. Jennifer expe- rienced a major life stressor 6 months ago when her husband of 15 years, Michael, told her that he is leaving her for a younger woman he met at his job. Jennifer was totally blindsided by this news. After an initial period of trying to work things out, Michael moved out of the house. Jennifer continued on with her business and managing of her household for several weeks, but then things started to change. She felt increasingly sad and would have long periods of crying throughout the day several times per week. Whereas she used to enjoy work, time with her children, and going out with her girlfriends, none of that seemed fun anymore. Even “movie nights” at home with the kids, which was one of her favorite times of the week, just wasn’t enjoyable to her anymore. Her body felt heavier and heavier and she lacked the energy to keep up appointments, leading her business to decline—she began losing even her most loyal clients. Jennifer also had difficulties managing her household, on several occasions forgetting to pick up her chil- dren from school and not remembering to make dinner for the family. Her eating and sleeping both declined drastically, and she spent hours lying in bed feeling like she had let down her husband, her children, and her friends. In addition to her extreme sadness, Jennifer began to experience extreme anxiety and worry in multiple domains. How would her business succeed? If she lost her business, wouldn’t she lose her house? Would she lose her children as well? Who would take care of them? She wanted to address all of these things but felt paralyzed and unable to take action. This led her to feel even more like a failure. She believed she was completely worthless and began contemplating whether everyone wouldn’t be better off if she was dead, which increased to explicit and frequent thoughts of suicide.
Jennifer’s case illustrates that a person with MDD shows not only mood symptoms of sadness but also a vari- ety of symptoms that are more severe than those in milder forms of depression. Jennifer lacks energy and the ability to carry out her activities of daily life. Her physical symp- toms include loss of appetite and sleep disturbance. She also shows cognitive symptoms of worthlessness and thoughts of death and suicide.
Note also that few if any depressions—including milder ones—occur in the absence of significant anxiety (e.g., Merikangas et al., 2003; Mineka et al., 1998; Watson, 2005). Indeed, there is a high degree of overlap between measures of depressive and anxious symptoms in self- reports and in clinician ratings. At the diagnostic level, there are very high levels of comorbidity between depressive
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Psychotic symptoms, characterized by loss of contact with reality and delusions (false beliefs) or hallucinations (false sensory perceptions), may sometimes accompany other symptoms of major depression. In such cases the diagnosis is severe major depressive episode with psy- chotic features. Ordinarily, any delusions or hallucinations present are mood congruent—that is, they seem in some sense appropriate to serious depression because the con- tent is negative in tone, such as themes of personal inade- quacy, guilt, deserved punishment, death, or disease. For example, some people with severe depression hold the delusional idea that their internal organs have totally dete- riorated. Individuals who are psychotically depressed are likely to have longer episodes, more cognitive impairment, and a poorer long-term prognosis than those suffering from depression without psychotic features (Bora et al., 2010; Flores & Schatzberg, 2006), and any recurrent epi- sodes are also likely to be characterized by psychotic symp- toms (Fleming et al., 2004). Treatment generally involves an antipsychotic medication as well as an antidepressant (Keller et al., 2007).
A third important specifier is used when the individ- ual shows “atypical features.” Major depressive episode with atypical features includes a pattern of symptoms characterized by mood reactivity; that is, the person’s mood brightens in response to potential positive events. In addition, the person must show two or more of the four symptoms listed in Table 7.1. A disproportionate number of individuals who have atypical features are females, who have an earlier-than-average age of onset and who are more likely to show suicidal thoughts (Matza et al., 2003). Research has also shown that atypical depression is linked to a mild form of bipolar disorder that is associated with hypomanic rather than manic episodes (Akiskal & Bena-
et al., 2008; Garber et al., 2009). As in adults, recurrence rates are high in children.
The incidence of depression rises sharply during adolescence—a period of great turmoil for many people. Indeed, approximately 15 to 20 percent of adolescents expe- rience major depressive disorder at some point, and sub- clinical levels of depression affect a further 10 to 20 percent (Avenevoli et al., 2008; Lewinsohn & Essau, 2002). It is dur- ing this time period that sex differences in rates of depres- sion first emerge (Hankin et al., 2008; Nolen-Hoeksema, 2012). The Developments in Research box later in the chap- ter provides some insights into why this might be. The long-term effects of major depressive disorder in adoles- cence can last at least through young adulthood, when such individuals show small but significant psychosocial impair- ments in many domains, including their occupational lives, interpersonal relationships, and general quality of life (e.g., Lewinsohn et al., 2003; Rudolph, 2008). Moreover, major depression that occurs in adolescence is very likely to recur in adulthood (Avenevoli et al., 2008; Rudolph, 2008).
The occurrence of major depression continues into later life. Although the prevalence of major depression is significantly lower in people over age 65 than in younger adults (Kessler et al., 2010), MDD in older adults is still considered a major public health problem (Blazer & Hybels, 2009; Kessler, Berglund, Demler, et al., 2005). Unfortunately, depression in later life can be difficult to diagnose because many of the symptoms overlap with those of several medical illnesses and dementia (Alexo- poulos et al., 2002; Harvey et al., 2006). Yet it is very impor- tant to try and diagnose it reliably because depression in later life has many adverse consequences for a person’s health, including doubling the risk of death in people who have had a heart attack or stroke (e.g., Davidson et al., 2010; Schulz et al., 2002).
SPECIFIERS FOR MAJOR DEPRESSIVE EPISODES Some individuals who meet the basic criteria for diagnosis of a major depressive episode also have additional patterns of symptoms or features that are important to note when making a diagnosis because these patterns have implica- tions for understanding more about the course of the disor- der and its most effective treatment. These different patterns of symptoms or features are called specifiers in DSM-5 (see Table 7.1 for a summary of the major specifi- ers). One such specifier is major depressive episode with melancholic features. This designation is applied when, in addition to meeting the criteria for a major depressive epi- sode, a patient either has lost interest or pleasure in almost all activities or does not react to usually pleasurable stimuli or desired events. This subtype of depression is more her- itable than most other forms of depression and is more often associated with a history of childhood trauma (Harkness & Monroe, 2002; Kendler, 1997).
Table 7.1 Specifiers of Major Depressive Episodes
Specifier Characteristic Symptoms
With Melancholic Features
Three of the following: early morning awakening, depression worse in the morning, marked psychomotor agitation or retardation, loss of appetite or weight, excessive guilt, qualitatively different depressed mood
With Psychotic Features
Delusions or hallucinations (usually mood congruent); feelings of guilt and worthlessness common
With Atypical Features
Mood reactivity—brightens to positive events; two of the four following symptoms: weight gain or increase in appetite, hypersomnia, leaden paralysis (arms and legs feel as heavy as lead), being acutely sensitive to interpersonal rejection
With Catatonic Features
A range of psychomotor symptoms from motoric immobility to extensive psychomotor activity, as well as mutism and rigidity
With Seasonal Pattern
At least two or more episodes in past 2 years that have occurred at the same time (usually fall or winter), and full remission at the same time (usually spring). No other nonseasonal episodes in the same 2-year period
Mood Disorders and Suicide 227
few weeks (and for a maximum of 2 months). These inter- mittently normal moods are one of the most important characteristics distinguishing persistent depressive disor- der from MDD. Nevertheless, in spite of the intermittently normal moods, because of its chronic course people with persistent depressive disorder show poorer outcomes and as much impairment as those with MDD (Klein, 2008, 2010).
Although persistent depressive disorder is distinct from MDD, the two disorders sometimes co-occur in the same person, a condition given the designation double depression (Boland & Keller, 2009; Klein, 2010). People with double depression are moderately depressed on a chronic basis (meeting symptom criteria for persistent depressive disorder) but undergo increased problems from time to time, during which they also meet criteria for a major depressive episode. One clinical sample of nearly 100 individuals with early-onset dysthymia (onset before age 21) was followed for 10 years, during which time 84 percent experienced at least one major depressive episode (Klein et al., 2006; see also Keller et al., 1997). Although nearly all individuals with double depression appear to recover from their major depressive episodes (although usually just to their previous level of dysthymia), recur- rence is common (Boland & Keller, 2002; Klein, 2008, 2010; Klein et al., 2006). In DSM-5, double depression is classi- fied as a form of persistent depressive disorder.
Persistent depressive disorder is quite common, with a lifetime prevalence estimated at between 2.5 and 6 percent (Kessler, Berglund, Demler, et al., 2005). The average dura- tion of persistent depressive disorder is 4 to 5 years, but it can last for 20 years or more (Klein et al., 2006). Chronic stress has been shown to increase the severity of symptoms over a 7.5-year follow-up period (Dougherty et al., 2004). Persistent depressive disorder often begins during adoles- cence, and over 50 percent of those who present for treat- ment have an onset before age 21. One 10-year prospective study of 97 individuals with early-onset dysthymia found that 74 percent recovered within 10 years but that, among those who recovered, 71 percent relapsed, with most relapses occurring within approximately 3 years of follow- up (Klein et al., 2006; see also Klein, 2010).
The following case is typical of this disorder.
A Persistently Depressed Student
Rosa, a 20-year-old college student, came into the university clinic for an evaluation at the encouragement of her roommate. She reports that “ever since high school” she has “felt sad, like, all of the time . . . it doesn’t seem normal and I don’t know why.” Rosa notes that there was no major stressor that she can remember that trig- gered her feelings of sadness, “just the normal high school stuff.” But her feelings of sadness have persisted for nearly 4 years now. When asked about what her sadness is like, she tells the psychologist that she just feels like she is not as good as everyone else—not as smart as the other students, not as attractive as the other girls, and can’t
zzi, 2005). This is also an important specifier because there are indications that individuals with atypical features may preferentially respond to a different class of antidepres- sants—the monoamine oxidase inhibitors—than do most other individuals with depression.
A fourth specifier is used when the individual shows marked psychomotor disturbances. Major depressive epi- sode with catatonic features includes a range of psycho- motor symptoms, from motoric immobility (catalepsy—a stuporous state) to extensive psychomotor activity, as well as mutism and rigidity. Catatonia is known more as a sub- type of schizophrenia, but it is actually more frequently associated with certain forms of depression and mania than with schizophrenia (Fink & Taylor, 2006).
A fifth specifier is used when individuals who experi- ence recurrent depressive episodes show a seasonal pattern, recurrent major depressive episode with a seasonal pattern, also commonly known as seasonal affective disorder. To meet DSM-5 criteria for this specifier, the per- son must have had at least two episodes of depression in the past 2 years occurring at the same time of the year (most commonly fall or winter), and full remission must also have occurred at the same time of the year (most com- monly spring). In addition, the person cannot have had other, nonseasonal depressive episodes in the same 2-year period, and most of the person’s lifetime depressive epi- sodes must have been of the seasonal variety. Prevalence rates suggest that winter seasonal affective disorder is more common in people living at higher latitudes (north- ern climates) and in younger people.
Persistent Depressive Disorder Persistent depressive disorder (formerly called dysthymic disorder or dysthymia) is a disorder characterized by persis- tently depressed mood most of the day, for more days than not, for at least 2 years (1 year for children and adoles- cents). In addition, individuals must have at least two of six additional symptoms when depressed (see the DSM-5 box for diagnostic criteria). Periods of normal mood may occur briefly, but they usually last for only a few days to a
228 Chapter 7
with how to appropriately diagnose (or not) a person’s response to them.
LOSS AND THE GRIEVING PROCESS We usually think of grief as the psychological process one goes through fol- lowing the death of a loved one—a process that appears to be more difficult for men than for women (Bonanno & Kaltman, 1999). Grief often has certain characteristics. Bowlby’s (1980) classic observations revealed that there are usually four phases of normal response to the loss of a spouse or close family member: (1) numbing and disbelief, (2) yearning and searching for the dead person, (3) disorga- nization and despair that sets in when the person accepts the loss as permanent, and (4) some reorganization as the person gradually begins to rebuild his or her life.
For decades this was generally considered as a normal pattern, and in 2007 a careful study of over 200 individuals who had lost a loved one due to natural causes docu- mented that this is indeed the typical sequence (Maciejew- ski et al., 2007). The normal nature of exhibiting a certain number of grief symptoms led DSM-IV-TR to suggest that a major depressive disorder usually should not be diag- nosed for the first 2 months following the loss, even if all the symptom criteria are met. However, in a controversial move, this 2-month bereavement exclusion was dropped in DSM-5 (see the Thinking Critically about DSM-5 box). Another controversial change is described in the Develop- ments in Thinking box.
seem to have fun and enjoy college like everyone else seems to be doing. Rosa was very active and popular early in high school: She was a member of the track team, in honors classes and an A stu- dent, and had a wonderful and supportive network of friends. How- ever, during her junior and senior years, she lost interest in track and school, and just didn’t feel close to her friends anymore and so over time stopped hanging out with them. No one seemed to care or try to change things, which really affected Rosa’s self-esteem and to this day causes her to think that no one “really” cares about her. In addition to her feelings of sadness, Rosa has been having trouble sleeping several nights per week, tossing and turning throughout the night. She also weighs about 20 pounds less than she did in high school, not because of diet or exercise but because she “doesn’t really enjoy food much anymore.” All of this has led to problems with Rosa’s ability to care about school or to be motivated to apply her- self in class, and so this once A student is now barely passing her classes. Rosa’s roommate has been asking her to come in to talk with someone about all of this for months, and Rosa’s declining attendance at school and decreasing contact with her family and friends led her roommate to walk her to the clinic for an evaluation today—to make sure she came in for help.
Other Forms of Depression Depressions are nearly always precipitated by stressful life events. Some of the most stressful events possible are those involving the loss of life, as well as the creation of new life. Indeed, these dramatic events often can push a person into a depressive episode, and psychologists have struggled
DSM-5 Criteria for. . . Persistent Depressive Disorder
A. Depressed mood for most of the day, for more days than not, as indicated by either subjective 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 or adolescents) of the disturbance, the individual 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 schizo- affective disorder, schizophrenia, 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 or impairment in social, occupational, or other important areas of functioning.
Note: Because the criteria for a major depressive episode include four symptoms that are absent from the symptom list for persistent depressive disorder (dysthymia), a very limited number of individu- als will have depressive symptoms that have persisted longer than 2 years but will not meet criteria for persistent depressive disorder. If full criteria for a major depressive episode have been met at some point during the current episode of illness, they should be given a diagnosis of major depressive disorder. Otherwise, a diagnosis of other specified depressive disorder or unspecified depressive dis- order is warranted.
Source: Reprinted with permission from the Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition (Copyright 2013). American Psychiatric Association.
Mood Disorders and Suicide 229
DSM-5 Thinking Critically about DSM-5 Was It Wise to Drop the Bereavement Exclusion for Major Depression?
One feature of DSM-IV-TR was that it contained a bereavement
exclusion criterion for major depression. This stipulated that peo-
ple who had recently been bereaved, but who otherwise meet
diagnostic criteria for a major depressive episode, could be
excluded from being diagnosed with clinical depression for up to
2 months post-loss. This criterion was designed to distinguish
true disorder from normal sadness, thus reducing diagnostic
false-positives, unnecessary treatment, potential stigmatization,
and inflated prevalence rates (Wakefield et al., 2007).
However, no exclusion was made for other types of loss. This
raised the issue of whether it was justifiable to consider depression
in response to the loss of a loved one as normal, and depression
in response to other losses as a form of mental disorder. In an
examination of this Wakefield and colleagues (2007) found that
bereavement-triggered depression and depression triggered by
other forms of loss were very similar on eight of nine symptoms of
depression (the exception being that bereaved individuals, not sur-
prisingly, thought about death more). There was therefore no evi-
dence to support granting bereavement special status.
In DSM-5, many people expected that the specific bereave-
ment exclusion would be dropped and replaced by an expanded
exclusion that included other types of loss (loss of a job, divorce)
as well as death of a loved one. However, in a controversial deci-
sion, the bereavement exclusion has not only not been expanded,
but it has been removed completely from DSM-5.
What are the issues here? Dropping the bereavement exclu-
sion may now create the risk that a normal grief reaction becomes
misdiagnosed as a major depressive episode leading to unnec-
essary treatment, stigmatization, or other negative conse-
quences. On the other hand, the assumption that any depressive
response to the loss of a love one is “normal” could lead to
delays in receiving needed treatment. One finding in support of
keeping the bereavement criterion as it was in DSM-IV-TR is that
people who experience symptoms of major depression following
death of a loved one are not at elevated risk for a recurrence of
later major depression the way people who have major depres-
sive episodes under other conditions are. So they may indeed be
a special group. What do you think? Is grief normal? How is grief
different from depression? Does the removal of the bereavement
criterion in DSM-5 now pathologize grief? Going forward, what
do you think some of the consequences of this change in DSM-5
might be?
It is important to note that not all loss is followed by depression. Recent studies of those experiencing the loss of a spouse, life partner, or parent reveal that about 50 percent exhibit genuine resilience in the face of loss, with minimal, very short-lived symptoms of depression or bereavement. Also, in contrast to what was previously thought, these resil- ient individuals are not emotionally maladjusted or unat- tached to their spouses (e.g., Bonanno et al., 2004, 2005).
POSTPARTUM “BLUES” Although you might think the birth of a child is always a happy event, postpartum depression sometimes occurs in new mothers (and occa- sionally fathers) and it is known to have adverse effects on child outcomes (e.g., Ramchandani et al., 2005). In the past it was believed that postpartum major depression in moth- ers was relatively common, but more recent evidence sug- gests that only “postpartum blues” are very common. The
Developments in Thinking A New DSM-5 Diagnosis: Premenstrual Dysphoric Disorder
After years of study, surrounded by some controversy, a new disorder called premenstrual dysphoric disorder has been added to the depressive disorders category in DSM-5. This dis- order is diagnosed if a woman has had a certain set of symp- toms in the majority of her menstrual cycles for the past year. In particular, she must have at least one of the following four symptoms in the final week before the onset of menses; these symptoms must start to improve within a few days after the onset of menses, and become minimal or absent in the week post-menses. The four symptoms of which one must occur include (1) marked affective lability such as mood swings; (2) marked irritability or anger or increased interpersonal
conflicts; (3) marked depressed mood, or feelings of hopeless- ness or self-deprecating thoughts; or (4) marked anxiety, ten- sion, or feelings of being “keyed up” or “on edge.” Seven other symptoms are listed and a total of five symptoms must be experienced. These other symptoms include (1) decreased interest in usual activities; (2) subjective sense of difficulties in concentration; (3) lethargy, easy fatigability, or lack of energy; (4) marked changes in appetite or overeating; (5) hypersomnia or insomnia; (6) a sense of being overwhelmed or out of control; and (7) physical symptoms such as breast tenderness or swell- ing, a sense of bloating, weight gain, etc. This is one form of depression where hormones clearly play an important role.
230 Chapter 7
in review • What are the major features that differentiate dysthymic disorder
and major depressive disorder?
• Distinguish between recurrence and relapse.
• What are three common specifiers of major depressive disorder?
Causal Factors in Unipolar Mood Disorders 7.3 Describe the factors believed to cause unipolar
mood disorders.
In considering the development of unipolar mood disor- ders, researchers have focused on the possible roles of bio- logical, psychological, and sociocultural factors. Although each set of factors has usually been studied separately, ulti- mately the goal should be to understand how these differ- ent kinds of causal factors are interrelated in order to develop a biopsychosocial model.
Biological Causal Factors It has long been known that a variety of diseases and drugs can affect mood, leading sometimes to depression and sometimes to elation or even mania. Indeed, this idea goes back to Hippocrates (c. 400 B.C.), who hypoth- esized that depression was caused by an excess of “black bile” in the system. As we will discuss, in the past half century investigators attempting to establish a biological basis for unipolar disorders have considered a wide range of factors.
GENETIC INFLUENCES Family studies have shown that the prevalence of mood disorders is approximately two to three times higher among blood relatives of persons with clinically diagnosed unipolar depression than it is in the population at large (e.g., Levinson, 2006, 2009; Wallace et al., 2002). Twin studies, which can provide much more conclusive evidence of genetic influences on a disorder, also suggest a moderate genetic contribution to MDD. Monozygotic co-twins of a twin with MDD are about twice as likely to develop the disorder as are dizygotic co-twins, with about 31 to 42 percent of the variance in liability due to genetic influences (Sullivan, Neale, & Kendler, 2000). The estimate is substantially higher (70 to 80 percent) for more severe, early-onset, or recurrent depressions (see also Levinson, 2009; McGuffin et al., 2007). Notably, how- ever, even more variance in the liability to most forms of MDD is due to nonshared environmental influences (i.e., experiences that family members do not share) than to genetic factors.
Taken together, the results from family and twin stud- ies make a strong case for a moderate genetic contribution
symptoms of postpartum blues typically include changeable mood, crying easily, sadness, and irritability, often liberally intermixed with happy feelings (Miller, 2002; Reck et al., 2009). Such symptoms occur in as many as 50 to 70 percent of women within 10 days of the birth of their child and usually subside on their own (Miller, 2002; Nolen-Hoeksema & Hilt, 2009). Hypomanic symptoms are also frequently observed, intermixed with the more depression-like symptoms (Sharma et al., 2009).
Actress Brook Shields describes her experience with postpartum depression in her popular book Down Came the Rain. In it, she writes, “I wasn’t simply emotional or weepy, like I had been told I might be. This was something quite different. This was sadness of a shockingly different magnitude. It felt as if it would never go away.”
It appears that major depression in women occurs no more frequently in the postpartum period than would be expected in women of the same age and socioeconomic sta- tus who have not just given birth (Hobfoll et al., 1995; O’Hara & Swain, 1996). Thus, the once firmly held notion that women are at especially high risk for major depression in the postpartum period has not been upheld. There is, however, a greater likelihood of developing major depres- sion after the postpartum blues—especially if they are severe (Henshaw et al., 2004; Reck et al., 2009).
Hormonal readjustments (Miller, 2002; O’Hara et al., 1991) and alterations in serotonergic and noradrenergic functioning (Doornbos et al., 2008) may play a role in post- partum blues and depression, although the evidence on this issue is mixed. It is obvious that a psychological com- ponent is present as well. Postpartum blues or depression may be especially likely to occur if the new mother has lack of social support or has difficulty in adjusting to her new identity and responsibilities, or if the woman has a per- sonal or family history of depression that leads to height- ened sensitivity to the stress of childbirth (Collins et al., 2004; Miller, 2002; O’Hara & Gorman, 2004).
Mood Disorders and Suicide 231
McGuffin, 2010; see also Karg et al., 2011). Such results sug- gest that the search for candidate genes that are likely to be involved in the etiology of major depression is likely to be much more fruitful if researchers also test for genotype– environment interactions, beyond examining the effects of a genotype itself (see Moffitt et al., 2005).
NEUROCHEMICAL FACTORS Ever since the 1960s, the view that depression may arise from disruptions in the delicate balance of neurotransmitter substances that regu- late and mediate the activity of the brain’s nerve cells has received a great deal of attention. A large body of evidence suggested that various biological therapies (discussed later in this chapter) that are often used to treat severe mood disorders—such as electroconvulsive therapy and antide- pressant medications—affect the concentrations or activity of neurotransmitters at the synapse. Such early findings encouraged the development of neurochemical theories of the etiology of major depression.
Early attention in the 1960s and 1970s focused primar- ily on two neurotransmitters of the monoamine class—nor- epinephrine and serotonin—because researchers observed that antidepressant medications seemed to have the effect of increasing these neurotransmitters’ availability at syn- aptic junctions (Thase & Denko, 2008). This observation led to the once influential monoamine theory of depression—that depression was at least sometimes due to an absolute or
to the causal patterns of MDD, although not as large a genetic contribution as for bipolar disor- der (Farmer et al., 2005; Goodwin & Jamison, 2007). Unfortunately, the evidence for a genetic contribution to persistent depressive disorder is slim because there has been very little research on the topic (Klein, 2008).
Attempts to identify specific genes that may be responsible for these genetic influences have not yet been successful, although there are some promising leads (Levinson, 2006, 2009; Wallace et al., 2002). As discussed in Chapter 3, one candi- date for a specific gene that might be implicated is the serotonin-transporter gene—a gene involved in the transmission and reuptake of serotonin, one of the key neurotransmitters involved in depression. Two different kinds of versions or alleles are involved: the short allele (s) and the long allele (l). People either have two short alleles (s/s), two long alleles (l/l), or one of each (s/l). Previous work with animals had suggested that having ss alleles might predispose a person to depression relative to a person having l/l alleles, but human work on this issue provided mixed results. In 2003, Caspi and colleagues published a landmark study in which they tested for the pos- sibility of a genotype–environment interaction involving these two alleles of the serotonin-transporter gene. They studied 847 people in New Zealand who had been followed from birth to 26 years of age, at which time the researchers assessed diagnoses of major depressive episodes in the past year and the occurrence of stressful life events in the previous 5 years. Their results were very striking: As illustrated in Figure 7.2, individuals who pos- sessed the genotype with the s/s alleles were twice as likely to develop a major depressive episode following four or more stressful life events in the past 5 years as those who possessed the genotype with the l/l alleles and had experi- enced four or more stressful events (those with the s/l alleles were intermediate). Moreover, they found that those who had the ss alleles and had experienced severe mal- treatment as children were also twice as likely to develop a major depressive episode as those with the l/l alleles who had had severe maltreatment and also as compared to those with the ss alleles who had not been maltreated as children. These findings strongly support a diathesis–stress model; many other (but not all) studies being conducted have found similar results (e.g., Kendler et al., 2005; Uher & McGuffin, 2010). However, in 2009 a quantitative review by Risch and colleagues (2009) challenged these results; this led to a major controversy in the field. Fortunately by 2011 other quantitative reviews had demonstrated that the gene–environment result is robust if the studies use sensi- tive interview-based measures of life stress (Uher &
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Figure 7.2 Number of Stressful Life Events Versus Probability of Major Depressive Episode Results demonstrate the association between the number of stressful life events (between ages 21 and 26 years) and probability of a major depressive episode at age 26 as a function of the 5-HTT genotype. Life events predicted a diagno- sis of major depression among carriers of the s allele (s/s or s/l), but not among carriers of two l alleles (l/l).
(Adapted from Caspi et al., 2003. Influence of life stress on depression: Moderation by a polymorphism in the 5-HTT gene. Science, 301, 386–89. Reprinted with permission from Science, 18 July 2003, Vol. 301. Copyright © 2003 AAAS.)
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mood disorder (Southwick et al., 2005; Thase, 2009a). The majority of attention has been focused on the hypothalamic- pituitary-adrenal (HPA) axis, and in particular on the hor- mone cortisol, which is excreted by the outermost portion of the adrenal glands and is regulated through a complex feedback loop. The human stress response is associated with elevated activity of the HPA axis, which is partly con- trolled by norepinephrine and serotonin. The perception of stress or threat can lead to norepinephrine activity in the hypothalamus, causing the release of corticotrophin-releas- ing hormone (CRH) from the hypothalamus, which in turn triggers the release of adrenocorticotropic hormone (ACTH) from the pituitary. The ACTH then typically trav- els through the blood to the adrenal cortex of the adrenal glands, where cortisol is released. Elevated cortisol activity is highly adaptive in the short term because it promotes survival in response to life-threatening or overwhelming life circumstances. However, sustained elevations are harmful to the organism, including promoting hyperten- sion, heart disease, and obesity (which are all elevated in depression) (Stetler & Miller, 2011; Thase, 2009a). Blood plasma levels of cortisol are known to be elevated in some 20 to 40 percent of outpatients with depression and in about 60 to 80 percent of hospitalized patients with severe depression (Thase et al., 2002). Sustained elevations in cor- tisol—a “hallmark of mammalian stress responses”—can result from increased CRH activation (for example, during sustained stress or threat), increased secretion of ACTH, or the failure of feedback mechanisms.
One line of evidence that implicates the failure of feed- back mechanisms in some patients with depression comes from robust findings that in about 45 percent of patients with serious depression, dexamethasone, a potent suppres- sor of plasma cortisol in normal individuals, either fails entirely to suppress cortisol or fails to sustain its suppres- sion (Carroll, 2009; Thase et al., 2002). This means that the HPA axis is not operating properly in these “dexametha- sone nonsuppressors.” It was initially thought that dexa- methasone nonsuppressor patients constituted a distinct subgroup of people with severe or melancholic depression (Holsboer, 1992). However, subsequent research has shown that several other groups of psychiatric patients, such as those with panic disorder, also exhibit high rates of non- suppression, suggesting that nonsuppression may merely be a nonspecific indicator of generalized mental distress.
Research also has revealed that patients having depres- sion with elevated cortisol also tend to show memory impairments and problems with abstract thinking and complex problem solving (Belanoff et al., 2001). Some of these cognitive problems may be related to other findings showing that prolonged elevations in cortisol result in cell death in the hippocampus—a part of the limbic system heavily involved in memory functioning (e.g., Southwick et al., 2005; Thase, 2009a). Other research has shown that
relative depletion of one or both of these neurotransmitters at important receptor sites in the brain (Schildkraut, 1965). This depletion could come about through impaired synthe- sis of these neurotransmitters in the presynaptic neuron, through increased degradation of the neurotransmitters once they were released into the synapse, or through altered functioning of postsynaptic receptors (Thase, 2009a). Collectively, these neurotransmitters are now known to be involved in the regulation of behavioral activ- ity, stress, emotional expression, and vegetative functions (involving appetite, sleep, and arousal)—all of which are disturbed in mood disorders (Garlow & Nemeroff, 2003; Southwick et al., 2005; Thase, 2009a).
However, by the 1980s it was clear that no such straightforward mechanisms could possibly be responsible for causing depression (Krishnan & Nestler, 2010). For example, some studies have found exactly the opposite of what is predicted by the monoamine hypothesis—that is, net increases in norepinephrine activity in patients with depression—especially in those with severe or melancholic depression (Thase & Denko, 2008). Moreover, only a minor- ity of patients with depression have lowered serotonin activity, and these tend to be patients with high levels of suicidal ideation and behavior. Finally, even though the immediate, short-term effects of antidepressant drugs are to increase the availability of norepinephrine and sero- tonin, the long-term clinical effects of these drugs do not emerge until 2 to 4 weeks later, when neurotransmitter lev- els may have normalized.
Other more recent research suggests that dopamine dysfunction (especially reduced dopaminergic activity) plays a significant role in at least some forms of depression, including depression with atypical features and bipolar depression (Krishnan & Nestler, 2010; Thase, 2009a). Because dopamine is so prominently involved in the expe- rience of pleasure and reward, such findings are in keeping with the prominence of anhedonia, the inability to experi- ence pleasure, which is such an important symptom of depression.
Unfortunately, the early monoamine theory has not been replaced by a compelling alternative. Altered neu- rotransmitter activity in several systems is clearly associ- ated with major depression, but research for the past 20 to 25 years has focused on complex interactions of neu- rotransmitters (Treadway & Pizzagalli, 2014). A number of integrative theories have been proposed that include a role for neurotransmitters, not alone but rather as they interact with other disturbed hormonal and neurophysiological patterns and biological rhythms (Garlow & Nemeroff, 2003; Thase, 2009a).
ABNORMALITIES OF HORMONAL REGULATORY AND IMMUNE SYSTEMS Research interest has focused on possible hormonal causes or correlates of some forms of
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activity on the left side of the prefrontal cortex in depres- sion is thought to be related to symptoms of reduced posi- tive affect and approach behaviors to rewarding stimuli, and increased right-side activity is thought to underlie increased anxiety symptoms and increased negative affect associated with increased vigilance for threatening infor- mation (Pizzagalli et al., 2002).
Abnormalities also have been detected in several other brain areas in patients with depression, as illustrated in Figure 7.3 (Davidson et al., 2009; Koolschijn et al., 2009). For example, several regions of the prefrontal cortex, including the orbital prefrontal cortex, which is involved in responsivity to reward (Haber & Knutson, 2010), show decreased volume in individuals with recurrent depression relative to normal controls (Koolschijn et al., 2009; Phillips et al., 2003). Lower levels of activity in the dorsolateral pre- frontal cortex, which are associated with decreased cogni- tive control, have also been observed in individuals with depression compared to controls (Disner et al., 2011; see also Chang et al., 2011), and seem to normalize following treatment with antidepressant medication (Fales et al., 2009). Another area involved is the hippocampus, which is critical to learning and memory and regulation of adreno- corticotropic hormone. As noted earlier, prolonged depres- sion can lead to decreased hippocampal volume, which could be due to cell atrophy or cell death (e.g., Koolschijn et al., 2009; Sapolsky, 2000). In addition, evidence of decreased hippocampal volume in never-depressed indi- viduals who are at high (versus low) risk for depression suggests that reductions in hippocampal volume may pre- cede the onset of depression (Chen et al., 2010).
A third such area is the anterior cingulate cortex, which shows both decreased volume and abnormally low levels of activation in patients with depression (Koolschijn et al., 2009). This area is involved in selective attention, which is important in prioritizing the most important information available, and therefore in self-regulation and adaptability— all important processes that are disrupted in depression.
Finally, the amygdala, which is involved in the percep- tion of threat and in directing attention, tends to show increased activation in individuals with depression (and anxiety disorders), which may be related to their biased attention to negative emotional information (Davidson et al., 2009; Disner et al., 2011; Phillips et al., 2003).
SLEEP AND OTHER BIOLOGICAL RHYTHMS Although findings of sleep disturbances in patients with depression have existed as long as depression has been studied, only recently have some of these findings been linked to more general disturbances in biological rhythms.
Sleep Sleep is characterized by five stages that occur in a relatively invariant sequence throughout the night (Stages 1–4 of non-REM sleep and REM sleep make up a sleep
stress in infancy and early childhood can promote long- term changes that increase the reactivity of the HPA axis, which may in turn help explain why children reared in environments with early adversity are at higher risk for developing depression later in life when they are exposed to acute stressors (e.g., Southwick et al., 2005).
The other endocrine axis that has relevance to depres- sion is the hypothalamic-pituitary-thyroid axis (Garlow & Nemeroff, 2003; Thase, 2009a; Thase et al., 2002). People with low thyroid levels (hypothyroidism) often become depressed, and approximately 20 to 30 percent of patients with depression who have normal thyroid levels nevertheless show dysregulation of this axis. Moreover, some patients who do not respond to traditional antidepressant treat- ments show improvement when administered thyrotropin- releasing hormone, which leads to increased thyroid hormone levels (Garlow & Nemeroff, 2003; Thase, 2009b).
Finally, in recent years many studies have shown that depression is also accompanied by dysregulation of the immune system (Dantzer et al., 2009). Specifically, depres- sion is associated with activation of the inflammatory response system as evidenced by increased production of proinflammatory cytokines such as interleukin and inter- feron (Dowlati et al., 2010). Both of these can contribute directly to the development of depressive symptoms.
NEUROPHYSIOLOGICAL AND NEUROANATOMICAL INFLUENCES Exciting neurophysiological research in recent years has followed up on earlier neurological find- ings that damage (for example, from a stroke) to the left, but not the right, anterior prefrontal cortex often leads to depression (Davidson et al., 2009; Robinson & Downhill, 1995). This led to the idea that depression in people with- out brain damage may nonetheless be linked to lowered levels of brain activity in this same region. A number of studies have supported this idea. Studies measuring the electroencephalographic (EEG) activity of both cerebral hemispheres in people who are depressed reveals an asym- metry or imbalance in the EEG activity of the two sides of the prefrontal regions of the brain. People with depression show lower activity in the left hemisphere in these regions and higher activity in the right hemisphere (Davidson et al., 2009; Stewart et al., 2010, 2011). Similar findings have been reported using positron emission tomography (PET) neuroimaging techniques (Davidson et al., 2009; Phillips et al., 2003). Notably, patients in remission show the same pattern (Henriques & Davidson, 1990; Stewart et al., 2010, 2011), as do children at risk for depression (Bruder et al., 2007). These latter findings hold promise as a way of iden- tifying persons at risk both for an initial episode and for recurrent episodes. Indeed, a recent study found that left frontal asymmetry in never-depressed individuals pre- dicted onset of major and minor depressive episodes over a 3-year period (Nusslock et al., 2011). The relatively lower
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than-normal amount of deep sleep. Both the reduced latency to enter REM sleep and the decreased amount of deep sleep often precede the onset of depression and per- sist following recovery, which suggests that they may be vulnerability markers for certain forms of major depres- sion (Hasler et al., 2004; Thase et al., 2002).
Circadian Rhythms Humans have many circadian (24-hour, or daily) cycles that the body uses to respond appropri- ately to the changing environment (e.g., sleep–wake cycle, locomotor activity cycle). These circadian rhythms are con- trolled by two related central “oscillators,” which act as internal biological clocks. Research has found some abnor- malities in all of these rhythms in patients with depression including drastic changes in mood, sleep, appetite, and social interactions. Although psychologists are still work- ing to figure out exactly how circadian rhythm abnormali- ties might contribute to the symptoms of depression, it is clear that circadian rhythms, the human stress response, and disorders such as depression are closely related (Landgraf et al., 2014).
Sunlight and Seasons Another, rather different kind of rhythm abnormality or disturbance is seen in people with
cycle). REM sleep (rapid eye movement sleep) is character- ized by rapid eye movements and dreaming as well as other bodily changes; the first REM period does not usu- ally begin until near the end of the first sleep cycle, about 75 to 80 minutes into sleep. This normal sleep–wake cycle is thought to be regulated by the suprachiasmatic nucleus of the hypothalamus (Steiger, 2007; Thase, 2009a). People who are depressed often show one or more of a variety of sleep problems, ranging from difficulty falling asleep, to periodic awakening during the night (poor sleep mainte- nance), to early morning awakening. Such changes occur in about 80 percent of hospitalized patients with depres- sion and in about 50 percent of outpatients with depres- sion, and are particularly pronounced in patients with melancholic features.
Moreover, research using EEG recordings has found that many patients with depression enter the first period of REM sleep after only 60 minutes or less of sleep (15 to 20 minutes sooner than nondepressed patients), show greater amounts of REM sleep during the early cycles, and have more intense and frequent rapid eye movements (Tsuno et al., 2005). Most deep sleep occurs during Stages 3 and 4, and people with depression also appear to get a lower-
Orbital prefrontal cortex
Ventromedial prefrontal cortex
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Figure 7.3 The key brain regions involved in affect and mood disorders are the (A) orbital prefrontal cortex and ventromedial prefrontal cortex, (B) dorsolateral prefrontal cortex, (C) hippocampus and amygdala, and (D) anterior cingulate cortex
(Adapted from R. J. Davidson, Diego Pizzagalli, and Jack Nitschke. (2002). The representation and regulation of emotion in depression. In I. H. Gotlib and C. L. Hammen (Eds.), Handbook of Depression (pp. 219–244). New York: Guilford.)
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who are already at high risk (for example, by being at high genetic risk), hormonal fluctuations may trigger depres- sive episodes, possibly by causing changes in the normal processes that regulate neurotransmitter systems (Deecher et al., 2008; Naninck et al., 2011). Some studies have sug- gested that women have a greater genetic vulnerability to depression than men, but many other studies have not supported this idea (e.g., Nolen-Hoeksema & Hilt, 2009; Wallace et al., 2002).
Psychological Causal Factors The evidence for important psychological causal factors in most unipolar mood disorders is at least as strong as the evidence for biological factors. However, it is likely that the effects of some psychological factors such as stressful life events are mediated by a cascade of underlying biological changes that they initiate. One way in which stressors may act is through their effects on biochemical and hormonal balances and on biological rhythms (Hammen, 2005; Monroe, 2008).
STRESSFUL LIFE EVENTS AS CAUSAL FACTORS Envi- ronmental stressors are known to be involved in the onset of a variety of disorders, ranging from some of the anxiety disorders to schizophrenia, but nowhere has their role been more carefully studied than in the case of unipolar major depression. Many studies have shown that severely stress- ful life events often serve as precipitating factors for unipo- lar depression (e.g., Hammen, 2005; Monroe et al., 2009). This is especially true for young female adults for whom stressful life events are more likely to show a stronger stress–depression relationship than is the case for men (Harkness et al., 2010).
Most of the episodic stressful life events involved in precipitating depression concern loss of a loved one, seri- ous threats to important close relationships or to one’s occupation, or severe economic or serious health problems (Monroe et al., 2009). The stress of being the caregiver to a spouse with a debilitating disease such as Alzheimer’s is also known to be associated with the onset of both major depression and generalized anxiety disorder in the care- giver (e.g., Russo et al., 1995).
An important distinction has been made between stressful life events that are independent of the person’s behavior and personality (independent life events, such as losing a job because one’s company is shutting down or having one’s house hit by a hurricane) and events that may have been at least partly generated by the depressed person’s behavior or personality (dependent life events). For example, people with depression sometimes gener- ate stressful life events through their poor interpersonal problem solving (such as being unable to resolve con- flicts with a spouse), which is often associated with depression. The poor problem solving in turn leads to
seasonal affective disorder, in which most of those affected seem to be responsive to the total quantity of available light in the environment (Oren & Rosenthal, 1992). A majority (but not all) of people with seasonal affective dis- order become depressed in the fall/winter and normalize in the spring/summer (Goodwin & Jamison, 2007). Research in animals also has documented that many sea- sonal variations in basic functions such as sleep, activity, and appetite are related to the amount of light in a day (which, except near the equator, is much greater in summer than in winter). A good deal of research on patients with seasonal affective disorder supports the therapeutic use of controlled exposure to light, even artificial light, which may work by reestablishing normal biological rhythms (Fava & Rosenbaum, 1995; Goodwin & Jamison, 2007). Although antidepressant medications can also be useful, the use of light therapy is more cost efficient in the long term (Cheung et al., 2012).
People who live in higher latitudes (northern climates for those in the Northern Hemisphere) are more likely to exhibit seasonal affective disorder, in which depression occurs primarily in the fall and winter months and tends to remit in the spring or summer months.
BIOLOGICAL EXPLANATIONS FOR SEX DIFFERENCES Before we leave the topic of possible biological causal fac- tors for depression, we should note that it has been sug- gested that hormonal factors such as normal fluctuations in ovarian hormones account for sex differences in depres- sion (Deecher et al., 2008). However, studies examining this hypothesis have yielded inconsistent results and over- all are not very supportive (Nolen-Hoeksema & Hilt, 2009). It seems that for the majority of women, hormonal changes occurring at various points (e.g., at the onset of puberty, before menstruation, in the postpartum period, and at menopause) do not play a significant role in causing depression. However, it remains possible that there is a causal association that has not yet been discovered because of real methodological difficulties in conducting conclu- sive research on this topic (Naninck et al., 2011; Sanborn & Hayward, 2003). Moreover, for a small minority of women
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Mildly Stressful Events and Chronic Stress Whether mildly stressful events are also associated with the onset of depression is less clear, with conflicting findings in the literature. Studies applying more sophisticated strategies for assessing life stress have generally not found minor stressful events to be associated with the onset of clini- cally significant depression (Dohrenwend et al., 1995; Stueve et al., 1998). An interesting hypothesis has been raised that minor events may play more of a role in the onset of recurrent episodes than in the initial episode (Stroud et al., 2011).
A number of studies have demonstrated that chronic stress is associated with increased risk for the onset, main- tenance, and recurrence of major depression (Hammen, 2005; Monroe et al., 2007). Chronic stress (or chronic strain or difficulties) has been defined in different ways, but usu- ally refers to one or more forms of stress ongoing for at least several months (e.g., poverty, marital discord, medi- cal problems, having a child with a disability).
Vulnerability and Responses to Stressors It is important to keep in mind that there are important individual differ- ences in how people respond to the experiences of episodic or chronic life stress. For example, women (and perhaps men) at genetic risk for depression not only experience more stressful life events but also are more sensitive to them (Kendler et al., 1999a). More specifically, those at high genetic risk for depression appear to be much more likely to respond to stressful life events with depression (an example of a gene–environment interaction) than those at low genetic risk (Caspi et al., 2003).
higher levels of interpersonal stress, which in turn leads to further symptoms of depression. Another example of a dependent life event is failing to keep up with routine tasks such as paying bills, which may lead to a variety of troubles. Evidence to date suggests that dependent life events play an even stronger role in the onset of major depression than do independent life events (Hammen, 2005; Kendler et al., 1999a).
Research on stress and the onset of depression is com- plicated by the fact that people with depression have a dis- tinctly negative view of themselves and the world around them (Beck, 1967; Clark, Beck, & Alford, 1999). Thus, their own perceptions of stress may result—at least to some extent—from the cognitive symptoms of their disorder rather than cause their disorder (Dohrenwend, 2006; Monroe, 2008; Monroe & Hadjiyannakis, 2002). That is, their pessimistic outlook may lead them to evaluate events as stressful that other nondepressed people would not. Therefore, researchers have developed more sophisticated interview-based measures of life stress that do not rely on the depressed person’s self-report of how stressful an event is and that take into account the biographical context of a person’s life. Trained independent raters evaluate what the impact of a particular event would be expected to be for an average person who has experienced this event in these particular life circumstances; the person’s subjective evalu- ations of stress are not recorded or taken into account in the rating of impact (Monroe, 2008). For example, the stress value of divorce for a woman who has already begun to establish a new relationship would probably not be rated as highly as the divorce of a woman whose husband left her for a younger woman. There is widespread agreement that conclusions derived from studies using these more sophisticated interview-based techniques are more reliable and valid in predicting depressive episodes (e.g., Monroe, 2008; Uher & McGuffin, 2010).
Several recent reviews of studies that employed these sophisticated measurements of life stress suggest that severely stressful episodic life events play a causal role (most often within a month or so after the event) in about 20 to 50 percent of cases (Hammen, 2005; Monroe & Hark- ness, 2005). Moreover, people with depression who have experienced a stressful life event tend to show more severe depressive symptoms than those who have not experi- enced a stressful life event (Monroe & Hadjiyannakis, 2002). This relationship between severely stressful life events and depression is much stronger in people who are having their first onset than in those undergoing recurrent episodes (Kendler, Thornton, & Gardner, 2000). It has been estimated that about 70 percent of people with a first onset of depression have had a recent major stressful life event, whereas only about 40 percent of people with a recurrent episode have had a recent major life event (Monroe & Harkness, 2005).
If a woman living in poverty is already genetically at risk for depression, the stresses associated with living in poverty may be especially likely to precipitate a major depression in her.
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short-term and a long-term vulnerability to depression. Such factors operate, at least in part, by increasing an indi- vidual’s sensitivity to stressful life events in adulthood, with similar findings having been observed in animals (Slavich et al., 2011). The long-term effects of such early environmental adversities may be mediated by both bio- logical variables (such as alterations in the regulation of the hypothalamic-pituitary stress response system) and psy- chological variables (such as lower self-esteem, insecure attachment relationships, difficulty relating to peers, and pessimistic attributions; Goodman & Brand, 2009; Hark- ness & Lumley, 2008). However, it is also important to real- ize that certain individuals who have undergone early adversity remain resilient, and if the exposure to early adversity is moderate rather than severe, a form of stress inoculation may occur that makes the individual less sus- ceptible to the effects of later stress (Parker et al., 2004). These stress-inoculation effects seem to be mediated by strengthening socioemotional and neuroendocrine resis- tance to subsequent stressors.
Summary As we have discussed, several different types of biological and psychological diatheses for unipolar depression have been studied, and some of these have been formulated as diathesis–stress theories, as we review in the following sections. Nevertheless it is important to keep in mind that these theories of vulnerability are not mutually exclusive, and some may simply be describing the same diathesis in different terms or at different levels of analysis. For example, there is a moderately strong genetic basis for neuroticism, and neuroticism is strongly corre- lated with pessimism (Clark, Watson, & Mineka, 1994), so these proposed diatheses are clearly somewhat interre- lated. Moreover, dysfunctional early parenting, emotional abuse, and parental loss have been strongly implicated in the formation of some of the other cognitive diatheses (Alloy et al., 2004; Bowlby, 1980; Goodman & Brand, 2009). Thus, these two proposed diatheses may simply differ in whether they operate distally (poor early parenting) or proximally (negative thinking patterns) in contributing to vulnerability for depression.
We now turn to five major psychological theories of depression that have received much attention over the years.
PSYCHODYNAMIC THEORIES In his classic paper “Mourning and Melancholia” (1917), Freud noted the important similarity between the symptoms of clinical depression and the symptoms seen in people mourning the loss of a loved one. Freud and his colleague Karl Abraham (1927) both hypothesized that when a loved one dies the mourner regresses to the oral stage of development (when the infant cannot distinguish self from others) and introjects or incorporates the lost person, feeling all the same feelings toward the self as toward the lost person. These feelings were thought to include anger and hostility
DIFFERENT TYPES OF VULNERABILITIES FOR UNIPO- LAR DEPRESSION In addition to genetic variables, there are a host of other psychological and social variables that may make some people more vulnerable, and other people less vulnerable, to developing depression after experienc- ing one or more stressful life events.
Personality and Cognitive Diatheses Researchers have concluded that neuroticism is the primary personality variable that serves as a vulnerability factor for depression (and anxiety disorders; Klein et al., 2009; Zinbarg et al., 2011). Recall that neuroticism, or negative affectivity, refers to a stable and heritable personality trait that involves a temperamental sensitivity to negative stimuli. Thus, peo- ple who have high levels of this trait are prone to experi- encing a broad range of negative moods, including not only sadness but also anxiety, guilt, and hostility. More- over, several studies have also shown that neuroticism predicts the occurrence of more stressful life events, which frequently lead to depression (Kendler, Gardner, & Prescott, 2003; Uliaszek et al., 2012). In addition to serving as a vulnerability factor, neuroticism is associated with a worse prognosis for complete recovery from depression. Finally, some researchers attribute sex differences in depression to sex differences in neuroticism (Kendler et al., 2002; Sutin et al., 2010).
There is more limited evidence that high levels of introversion (or low positive affectivity) may also serve as vulnerability factors for depression, either alone or when combined with neuroticism (Watson et al., 2005). Positive affectivity involves a disposition to feel joyful, energetic, bold, proud, enthusiastic, and confident; people low on this disposition tend to feel unenthusiastic, unenergetic, dull, flat, and bored. It is therefore not surprising that this might make them more prone to developing clinical depression, although the evidence for this is very mixed.
The cognitive diatheses that have been studied for depression generally focus on particular negative patterns of thinking that make people who are prone to depression more likely to become depressed when faced with one or more stressful life events. For example, people who attri- bute negative events to internal, stable, and global causes may be more prone to becoming depressed than are peo- ple who attribute the same events to external, unstable, and specific causes (Abramson et al., 2002). A pessimistic or depressive attribution for receiving a low grade in an exam might be “I’m stupid,” whereas a more optimistic attribution for the same event might be “The teacher delib- erately wrote a difficult test to make us all realize we need to study harder.”
Early Adversity as a Diathesis A range of adversities in the early environment (such as family turmoil, parental psy- chopathology, physical or sexual abuse, and other forms of intrusive, harsh, and coercive parenting) can create both a
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energy, cause the person with depression to experience lower rates of reinforcement, which in turn may help main- tain the depression. Interestingly, exciting new research has demonstrated that a novel form of behavioral treat- ment inspired by these behavioral theories—behavioral activation treatment—seems to be an effective treatment for depression (Dimidjian et al., 2011; Martell, 2009).
BECK’S COGNITIVE THEORY Since 1967 one of the most influential theories of depression has been that of Aaron Beck (b. 1921), a psychiatrist who became disen- chanted with psychodynamic theories of depression early in his career and developed his own cognitive theory of depression (Beck, 1967, 2005). Whereas the most prominent symptoms of depression have generally been considered to be the affective or mood symptoms, Beck hypothesized that the cognitive symptoms of depression often precede and cause the affective or mood symptoms rather than vice versa (see Figure 7.4). For example, if you think that you are a failure or that you are ugly, it would not be surprising for those thoughts to lead to a depressed mood.
because Freud believed that we unconsciously hold nega- tive feelings toward those we love, in part because of their power over us. This is what led to the psychodynamic idea that depression is anger turned inward. Freud hypothe- sized that depression could also occur in response to imag- ined or symbolic losses. For example, a student who fails in school or who fails at a romantic relationship may experi- ence this symbolically as a loss of his or her parents’ love.
Later psychodynamic theorists proposed a number of variants on Freud and Abraham’s early psychodynamic theories (Levy & Wasserman, 2009). Perhaps the most important contribution of the psychodynamic approaches to depression has been their noting the importance of loss (both real and symbolic or imagined) to the onset of depres- sion and noting the striking similarities between the symp- toms of mourning and the symptoms of depression (Bowlby, 1980).
Children who have lost a parent through death or permanent separation may become vulnerable to depression if they receive poor subsequent care from another parent or guardian and if their environment and routine are disrupted.
BEHAVIORAL THEORIES In the 1970s and 1980s, sev- eral theorists in the behavioral tradition developed behav- ioral theories of depression, proposing that people become depressed either when their responses no longer produce positive reinforcement or when their rate of negative expe- riences increases (Ferster, 1974; Lewinsohn & Gotlib, 1995). Such theories are consistent with research showing that people with depression do indeed receive fewer positive verbal and social reinforcements from their families and friends than do people who are not depressed and also experience more negative events. Moreover, they have lower activity levels, and their moods seem to vary with both their positive and their negative experiences rates (Lewinsohn & Gotlib, 1995; Martell, 2009). Nevertheless, although such findings are consistent with behavioral the- ories, they do not show that depression is caused by these factors. Instead, it may be that some of the primary symp- toms of depression, such as pessimism and low levels of
Formation of dysfunctional beliefs
Early experience
Critical incident(s)
Symptoms of depression
Beliefs activated
Negative automatic thoughts
Behavioral
A�ective
Motivational Cognitive
Somatic
Depression
Figure 7.4 Beck’s Cognitive Model of Depression According to Beck’s cognitive model of depression, certain kinds of early experiences can lead to the formation of dysfunctional assumptions that leave a person vulnerable to depression later in life if certain critical incidents (stressors) activate those assumptions. Once activated, these dysfunctional assumptions trigger automatic thoughts that in turn produce depressive symptoms, which further fuel the depressive automatic thoughts.
(Adapted from Fennell, 1989.)
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didn’t have a moment of pleasure or fun today” not because this is true but because he or she selectively remembers only the negative things that happened.
• Arbitrary inference, which involves jumping to a con- clusion based on minimal or no evidence. A depressed person might say, after an initial homework assign- ment from a cognitive therapist did not work, “This therapy will never work for me.” (Examples from Fennell, 1989, p. 193)
It is easy to see how each of these cognitive distortions tends to maintain the negative cognitive triad. That is, if the content of your thoughts regarding your views of yourself, your world, and your future is already negative and you tend to minimize the good things that happen to you or draw negative conclusions based on minimal evidence, those negative thoughts are not likely to disappear. In addi- tion, just as the underlying dysfunctional beliefs (such as “If everybody doesn’t love me, then my life is worthless”) elicit the negative cognitive triad when activated, so too does the negative thinking produced by the negative triad serve to reinforce those underlying beliefs. Thus, each of these com- ponents of cognitive theory serves to reinforce the others, as shown in Figure 7.4. Moreover, these negative thoughts can produce some of the other symptoms of depression such as sadness, dejection, and lack of motivation.
Evaluating Beck’s Theory as a Descriptive Theory An enormous amount of research has been conducted to test various aspects of Beck’s theory, and it has generated a
Beck’s theory, a diathesis–stress theory in which negative cognitions are central, has become somewhat more elaborate over the years while still retaining its primary tenets (Beck, 1967, 2005; Clark & Beck, 2010). First, there are the underlying dysfunctional beliefs, known as depressogenic schemas, which are rigid, extreme, and counterpro- ductive. An example of a dysfunctional belief (that a person is usually not con- sciously aware of) is “If everyone doesn’t love me, then my life is worthless.” Accord- ing to cognitive theory, such a belief would predispose the person holding it to develop depression if he or she perceived social rejection. Alternatively, a person with the dysfunctional belief “If I’m not perfectly successful, then I’m a nobody” would be vulnerable to developing negative thoughts and depressed mood if she or he felt like a failure. These depression-producing beliefs or schemas are thought to develop during childhood and adolescence as a function of negative experiences with parents and sig- nificant others, and they are thought to serve as the underlying diathesis, or vulnerability, to developing depression (Beck, 1967; Ingram et al., 2006; Morley & Moran, 2011). Although they may lie dormant for years in the absence of significant stressors, when dysfunctional beliefs are activated by current stressors or depressed mood, they tend to fuel the current thinking pattern, cre- ating a pattern of negative automatic thoughts—thoughts that often occur just below the surface of awareness and involve unpleasant, pessimistic predictions. These pessi- mistic predictions tend to center on the three themes of what Beck calls the negative cognitive triad, which include negative thoughts about (1) self (“I’m worth- less”); (2) world (“No one loves me”); and (3) future (“It’s hopeless because things will always be this way”) (Clark, Beck, & Alford, 1999; see Figure 7.5 ).
Beck also postulated that the negative cognitive triad tends to be maintained by a variety of negative cognitive biases or errors (see also Scher et al., 2005). Each of these involves biased processing of negative self-relevant infor- mation. Examples include:
• Dichotomous or all-or-none reasoning, which involves a tendency to think in extremes. For example, someone might discount a less-than-perfect performance by saying, “If I can’t get it 100 percent right, there’s no point in doing it at all.”
• Selective abstraction, which involves a tendency to focus on one negative detail of a situation while ignoring other elements of the situation. Someone might say, “I
“I’m ugly/ worthless/ a failure.”
“No one loves me.”
“It’s all hopeless because things will always be this way.”
The Self
The World
The Future
Figure 7.5 Negative Cognitive Triad Beck’s cognitive model of depression describes a pattern of negative automatic thoughts. These pessimistic predictions center on three themes: the self, the world, and the future.
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prospective study design. People who are not depressed are tested for their cognitive vulnerability (usually, dys- functional beliefs) at Time 1 and then are followed for 1 or more months or years, after which measurements of life stress are administered. Only some studies have found that dysfunctional beliefs or attitudes at Time 1, in interaction with stressful life events, predict depression at Time 2. Lewinsohn and colleagues (2001) assessed about 1,500 adolescents for their dysfunctional beliefs or attitudes and then followed them for 1 year, at which point stressful life events during that year were assessed. Results indicated that those who had started with high levels of dysfunc- tional beliefs and who experienced high stress were more likely to develop major depression than those with low stress or than those with low dysfunctional beliefs and high stress. Another study with a large community sample of 700 women (average age was 41) also found that dys- functional beliefs at the outset of a 3-year follow-up period predicted new onsets and recurrences of major depressive episodes over the next 3 years (Otto et al., 2007). However, this study did not find evidence of a diathesis–stress inter- action, and dysfunctional beliefs did not have additional predictive value beyond that afforded by knowing a prior history of the person’s depressive episodes. Because of inconsistencies in results across studies, more research is still needed to fully assess the causal aspects of Beck’s cog- nitive theory of depression.
THE HELPLESSNESS AND HOPELESSNESS THEORIES OF DEPRESSION Whereas Beck’s theory grew out of his clinical observations and research on the pervasive pat- terns of negative thinking seen in patients with depression, the learned helplessness theory of depression originated out of observations in an animal research laboratory. Mar- tin Seligman (1974, 1975) first proposed that the laboratory phenomenon known as learned helplessness might pro- vide a useful animal model of depression. In the late 1960s, Seligman and his colleagues (Maier et al., 1969; Overmier & Seligman, 1967) noted that laboratory dogs who were first exposed to uncontrollable shocks later acted in a pas- sive and helpless manner when they were in a situation where they could control the shocks. In contrast, animals first exposed to equal amounts of controllable shocks had no trouble learning to control the shocks.
Seligman and his colleagues (Maier et al., 1969; Over- mier & Seligman, 1967) developed the learned helplessness hypothesis to explain these effects. It states that when ani- mals or humans find that they have no control over aver- sive events (such as shock), they may learn that they are helpless, which makes them unmotivated to try to respond in the future. Instead they exhibit passivity and even depressive symptoms. They are also slow to learn that any response they do make is effective, which may parallel the negative cognitive set in human depression. Seligman’s
very effective form of treatment for depression known as cognitive therapy. In addition, it has been well supported as a descriptive theory that explains many prominent char- acteristics of depression (Clark, Beck, & Alford, 1999). Patients with depression of all the subtypes are consider- ably more negative in their thinking, especially about themselves or issues highly relevant to the self, than are persons who are not depressed, and they are also more negative than they usually are when they are not depressed. Moreover, persons with depression think more negatively about themselves and the world around them, especially their own personal world, than do persons who are not depressed, and are quite negative about the future, espe- cially their own future (the negative cognitive triad). By contrast, people who are not depressed show a tendency to process emotional information in an overly optimistic, self- enhancing manner, which may serve as a protective factor against depression (Mezulis et al., 2004).
Beck’s theory originally proposed that stressors are necessary to activate depressogenic schemas or dysfunc- tional beliefs that lie dormant between episodes, but more recent research has shown that stressors are not necessary to activate the latent depressive schemas between epi- sodes. Indeed, simply inducing a depressed mood (e.g., through listening to sad music or recalling sad memories) in an individual who was previously depressed (that is, at risk) is generally sufficient to activate latent depressogenic schemas (e.g., Ingram et al., 2006; LeMoult et al., 2009; Scher et al., 2005).
In addition to evidence for dysfunctional beliefs and negative automatic thoughts, there is also considerable evi- dence for certain cognitive biases for negative self-relevant information in depression. For example, people with depression show better or biased recall of negative infor- mation and negative autobiographical memories, whereas people who are not depressed tend to show biased recall of positive emotional information and positive autobiographi- cal memories (Gotlib & Joormann, 2010; Hertel & Brozovich, 2010; Mathews & MacLeod, 2005; Mineka et al., 2003). In addition, people with depression are more likely than peo- ple who are not depressed to draw negative conclusions that go beyond the information presented in a scenario and to underestimate the positive feedback they have received (Clark, Beck, & Alford, 1999). It is easy to see how, if one is already depressed, remembering primarily the bad things that have happened is likely to maintain or exacerbate the depression. Teasdale (1988, 1996) aptly called this the “vicious cycle of depression.”
Evaluating the Causal Aspects of Beck’s Theory Although research supports most of the descriptive aspects of Beck’s theory, research directed toward confirming the causal hypotheses of Beck’s theory has yielded more mixed results. The causal hypotheses are usually tested with a
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interaction with negative life events (Abramson et al., 1989; Alloy et al., 2008). Some results have supported this theory and some have not.
The helplessness theory has been used to explain sex differences in depression. This theory proposes that by vir- tue of their roles in society, women are more prone to expe- riencing a sense of lack of control over negative life events. These feelings of helplessness might stem from poverty, discrimination in the workplace, high rates of sexual and physical abuse against women (either currently or in child- hood), role overload (e.g., being a working wife and mother), and less perceived control over traits that men value when choosing a long-term mate, such as beauty, thinness, and youth (Heim et al., 2000; Nolen-Hoeksema & Hilt, 2009). There is at least some evidence that each of these conditions is associated with higher-than-expected rates of depression, although whether the effects involve a sense of helplessness has not yet been established (Nolen- Hoeksema et al., 1999). Combining the neuroticism theory with the helplessness theory, it is important to note that there is evidence that people who are high on neuroticism are more sensitive to the effects of adversity relative to those low on neuroticism (a genotype–environment inter- action; Kendler et al., 2004; Lahey, 2009). So given that women have higher levels of neuroticism and experience more uncontrollable stress, the increased prevalence of depression in women becomes less surprising.
The Hopelessness Theory of Depression A further revi- sion of this theory, known as the hopelessness theory, was later presented (Abramson et al., 1989; see Alloy et al., 2008). Abramson and colleagues (1989) propose that hav- ing a pessimistic attributional style in conjunction with one or more negative life events was not sufficient to produce depression unless one first experienced a state of hopeless- ness. A hopelessness expectancy was defined by the per- ception that one had no control over what was going to happen and by the absolute certainty that an important bad outcome was going to occur or that a highly desired good outcome was not going to occur. They also proposed that the internal/external dimension of attributions was not important to depression. Specifically, they proposed that depression-prone individuals not only tend to make global and stable attributions for negative events but also tend to make negative inferences about other likely nega- tive consequences of the event (e.g., that this means more bad things will also happen) and negative inferences about the implications of the event for the self-concept (e.g., that one is unworthy or deficient; Abramson et al., 2002).
Research during the past 25 years has been testing this theory. A major longitudinal prospective study of several hundred college students who were hypothesized to be at high risk for unipolar depression (because they had both a pessimistic attributional style and high levels
observations that the animals looked depressed captured his attention and ultimately led to his proposing a learned helplessness model of depression (Seligman, 1974, 1975). Subsequent research demonstrated that helpless animals also show other depressive symptoms such as lower levels of aggression, loss of appetite and weight, and changes in monoamine neurotransmitter levels. After demonstrating that learned helplessness also occurs in humans (Hiroto & Seligman, 1975), he went on to propose that learned help- lessness may underlie some types of human depression. That is, people undergoing stressful life events over which they have little or no control may develop a syndrome like the helplessness syndrome seen in animals.
The Reformulated Helplessness Theory Some of the research with humans on helplessness soon led to a major reformulation of the helplessness theory, addressing some of the complexities of what humans do when faced with uncontrollable events (Abramson et al., 1978). In particular, Abramson and colleagues proposed that when people (probably unlike animals) are exposed to uncontrollable negative events, they ask themselves why, and the kinds of attributions that people make are, in turn, central to whether they become depressed. These investigators pro- posed three critical dimensions on which attributions are made: (1) internal/external, (2) global/specific, and (3) stable/unstable. They proposed that a depressogenic or pessimistic attribution for a negative event is an internal, stable, and global one. For example, if your boyfriend treats you badly and you conclude that “It’s because I’m ugly and boring,” you are much more likely to become depressed than if you conclude that “It’s because he’s in a bad mood today and he is taking it out on me.”
Abramson and colleagues (1978) proposed that people who have a relatively stable and consistent pessimistic attributional style have a vulnerability or diathesis for depression when faced with uncontrollable negative life events. This kind of cognitive style seems to develop, at least in part, through social learning (Alloy, Abramson, Smith, et al., 2006). For example, children may learn this cognitive style by observing and modeling inferences made by their parents. Alternatively or additionally, the parents may communicate their own inferences about neg- ative events happening to their children, or engage in gen- erally negative parenting practices such as high levels of negative psychological control (criticism, intrusiveness, and guilt) as well as a lack of warmth and caring.
This reformulated helplessness theory led to a great deal of research. Many studies demonstrated that depressed people do indeed have this kind of pessimistic attributional style, but of course this does not mean that pessimistic attri- butional style plays a causal role. Using prospective designs, many studies have examined the ability of a pessimistic attributional style to predict the onset of depression in
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repetitive and relatively passive mental activity. Other peo- ple, by contrast, have a more action-oriented or problem- solving response to such feelings and, for example, distract themselves with another activity or actually try to do some- thing that will solve the problems that are leading to the sadness and distress. Research has consistently shown that there are stable individual differences in the tendency to ruminate and that people who ruminate a great deal tend to have more lengthy periods of depressive symptoms. They are also more likely to develop full-blown episodes of major depressive disorder (Nolen-Hoeksema, 2000; Nolen- Hoeksema & Hilt, 2009).
Interestingly, it seems that women are more likely than men to ruminate when they become depressed (Nolen- Hoeksema & Aldao, 2011; Nolen-Hoeksema & Corte, 2004). Moreover, self-focused rumination leads to increased recall of more negative autobiographical memories, thereby feed- ing a vicious circle of depression (Hertel & Brozovich, 2010; Lyubomirsky et al., 1998; Nolen-Hoeksema et al., 2008). Importantly, when gender differences in rumination are statistically controlled, gender differences in depression are no longer significant (Nolen-Hoeksema & Hilt, 2009).
Men, by contrast, are more likely to engage in a dis- tracting activity (or consume alcohol) when they get in a depressed mood, and distraction seems to reduce depres- sion (Nolen-Hoeksema, 2012; Nolen-Hoeksema & Corte, 2004). Distraction might include going to a movie, playing a sport, or avoiding thinking about why they are depressed. The origin of these sex differences in response to depres- sion is unclear, but if further research supports this hypoth- esis it would certainly suggest that effective prevention efforts might include teaching girls to seek distraction rather than to ruminate as a response to depression.
of dysfunctional beliefs) has yielded evidence supportive of some of the major tenets of the hopelessness theory (Abramson et al., 2002; Alloy, Abramson, Whitehouse, et al., 2006; Alloy et al., 2008). For example, in a 2.5-year fol- low-up period, students in the high-risk group who had never previously been depressed at the outset of the study were about four times more likely (16.2 versus 3.6 percent) to develop a first episode of major depression (or comorbid depression and anxiety) than those in the low- risk group. For those who had already had a previous epi- sode of depression prior to entry into the study, the high-risk group was about three times more likely to experience a recurrent episode of major depression in the 2.5-year follow-up period.
Additional support for the hopelessness theory has been accumulating as well. Several smaller studies have shown evidence for the interaction of cognitive vulnerabil- ity with life stress in predicting depressive symptoms and onset of depression (Hankin et al., 2004), although others have not (Alloy et al., 2008). Furthermore, research has begun to integrate hopelessness theory with a motivational theory of depression that posits that depression is associ- ated with decreased approach behavior (Nusslock et al., 2011). Specifically, some researchers have hypothesized that cognitively vulnerable individuals are at risk for decreased approach-related behavior as a result of increased hopelessness under stress, thereby contributing to depression. There is at least initial empirical support for this notion. For example, in one investigation of under- graduate students, cognitive vulnerability interacted with life stress to predict a decrease in goal-directed behavior, which was then associated with higher levels of depressive symptoms (Haeffel et al., 2008). The relationship between cognitive vulnerability and stress with goal- directed behavior was mediated by increased feelings of hopelessness. Additional tests of the hopelessness theory and its predictions are needed, but future research on the hope- lessness theory is likely to continue to pro- vide important insights into psychosocial causes of depression.
The Ruminative Response Styles Theory of Depression Nolen-Hoeksema’s ruminative response style cognitive theory of depression (1991, 2000, 2012) focuses on different kinds of responses that people have when they experi- ence feelings and symptoms of sadness and distress, and how their differing response styles affect the course of their depression. Specifically, when some people have such feel- ings, they tend to focus intently on how they feel and why they feel that way—a process called rumination, which involves a pattern of
Women are more likely than men to ruminate when they are depressed. Men, in contrast, tend to engage in distracting activities when they get into a depressed mood.
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have researchers begun to make significant advances in understanding the real scope of the problem. The overlap between measures of depression and anxiety occurs at all levels of analysis: patient self-report, clinician ratings, diagnosis, and family and genetic factors (Clark & Watson, 1991; Mineka et al., 1998; Watson, 2005). Just over half of the patients who receive a diagnosis of a mood disorder also receive a diagnosis of an anxiety disorder at some point in their lives, and vice versa (Hettema, 2008; Watson, 2005). Finally, there is considerable evidence from genetic and family studies of the close relationship between anxi- ety and unipolar depressive disorders (Garber & Weersing, 2010). The shared genetically based factor among these dis- orders seems to be at least in part the personality trait of neuroticism—a major risk factor for all of these disorders (Hettema, 2008; Watson et al., 2006).
Although depressed and anxious individuals cannot be differentiated on the basis of their high level of negative affect, they do differ in their reports of positive affect, which includes affective states such as excitement, delight, inter- est, and pride. Depressed persons tend to be characterized
The ruminative response styles theory of depression has been integrated with the two previously discussed cognitive theories of depression. For example, research reviewed recently by Alloy, Abramson, and colleagues (2008) shows that for people with high levels of dysfunc- tional attitudes and/or pessimistic attributional styles, their tendencies to ruminate moderated the effects of the negative cognitive styles on increasing vulnerability to depression. Specifically, those who had negative cognitive styles who also tended to ruminate a lot were most likely to develop depressive episodes. The researchers suggest that people with negative cognitive styles have a lot of negative content to their thoughts but that only if they dwell on this and brood about it (high ruminators) are they especially likely to develop clinical depression (see also Robinson & Alloy, 2003).
Comorbidity of Anxiety and Mood Disorders The issue of whether depression and anxiety can be differentiated in a reliable and valid way has received a good deal of atten- tion over the years. Only in the past two decades, however,
Developments in Research Why Do Sex Differences in Unipolar Depression Emerge During Adolescence?
It is interesting to consider why the sex difference in depression starts in adolescence (Essau et al., 2010; Hankin & Abramson, 2001; Hankin et al., 2008). It begins between ages 12 and 13 and reaches its most dramatic peak between ages 14 and 16, although it is actually more tied to pubertal status than to age per se (Becker et al., 2007; Conley & Rudolph, 2009; Sanborn & Hay- ward, 2003). This is a time of rapid physiological, environmental, and psychological changes known to create turmoil for many adolescents, but why are adolescent females more likely to become depressed? Hankin, Abramson, and colleagues (Hankin & Abramson, 2001; Hankin et al., 2008) have proposed an intrigu- ing cognitive vulnerability-stress model of the development of gender differences during adolescence. Building on ideas from the reformulated helplessness and hopelessness models of depression for adults, they summarize research indicating that children and adolescents, like adults, are prone to experiencing increases in depressive symptoms if they have a pessimistic attri- butional style and experience stressful life events (e.g., Hankin, 2006; Hankin & Abramson, 2001). Moreover, during early adoles- cence, gender differences in attributional style, in rumination, and in stressful life events emerge such that girls tend to have a more pessimistic attributional style, to show more rumination, and to experience more negative life events (especially interpersonal events; Rudolph, 2008). Thus, one can see how, with all three of these risk factors showing gender differences in adolescence, a synergistic effect might lead to the dramatic rise in depression in adolescent girls. Moreover, Hankin and Abramson (2001; see also Hankin et al., 2008) review evidence that the experience of
negative life events may contribute to greater cognitive vulnerabil- ity, which in turn further increases susceptibility to depressive symptoms. Furthermore, depressive symptoms in adolescent girls, as in adults, are likely to result in more dependent life stress being generated, which in turn may exacerbate depression (Liu & Alloy, 2010; Rudolph, 2008). Finally, girls not only experience more negative life events than boys but also encode them in greater detail and show better memory for emotional events (though not for nonemotional events).
Hankin and Abramson (2001) also emphasized the role of negative cognitions about attractiveness and body image in the emergence of sex differences in depression during adolescence. There is evidence that the development of secondary sexual characteristics is harder psychologically for girls than for boys. Body dissatisfaction goes up for females at this time, and down for males; moreover, body dissatisfaction is more closely related to self-esteem for girls than for boys. Much of girls’ dissatisfaction with their bodies comes from their realization of the discrepancy between our society’s ideal of a thin, prepubescent body shape for females and the fact that they are gaining fat as they mature sexually. Hankin and Abramson (2001) summarized evidence that girls are more likely than boys to make pessimistic attributions and other negative inferences about negative events that may occur (such as negative remarks) related to the domain of physi- cal attractiveness. Given that physical attractiveness may be more motivationally significant for girls than for boys, it becomes plausible that this may be one important factor that makes depression especially likely in adolescent girls.
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depressed if they experienced a severely stressful event. Many studies have since supported the idea that people who are lonely, socially isolated, or lacking social sup- port are more vulnerable to becoming depressed and that individuals with depression have smaller and less supportive social networks, which tends to precede the onset of depression (Cacioppo et al., 2006; Gotlib & Hammen, 1992; Ibarra-Rovillard & Kuiper, 2011). In addition, some people with depression have social-skills deficits. For example, they seem to speak more slowly and monotonously and to maintain less eye contact; they are also less skilled than people without depression at solving interpersonal problems (Ingram et al., 1999; Joiner & Timmons, 2009).
The Effects of Depression on Others Not only do people with depression have interpersonal problems, but, unfor- tunately, their own behavior also seems to make these problems worse. For example, the behavior of someone who is depressed often places others in the position of providing sympathy, support, and care. However, posi- tive reinforcement does not necessarily follow. Depres- sive behavior can elicit negative feelings (sometimes including hostility) and rejection in other people, includ- ing strangers, roommates, and spouses (Coyne, 1976; Ingram et al., 1999; Joiner & Timmons, 2009). Although these negative feelings may initially make the person who is not depressed feel guilty, which leads to sympa- thy and support in the short term, ultimately a down- wardly spiraling relationship usually results, making the person with depression feel worse (e.g., Joiner, 2002; Joiner & Metalsky, 1995). Social rejection may be espe- cially likely if the person with depression engages in excessive reassurance seeking (Joiner & Timmons, 2009; Prinstein et al., 2005).
Marriage and Family Life Interpersonal aspects of depres- sion also have been carefully studied in the context of mar- ital and family relationships. A significant proportion of couples experiencing marital distress have at least one partner with clinical depression, and there is a high corre- lation between marital dissatisfaction and depression for both women and men (Beach & Jones, 2002; Rehman et al., 2008; Whisman, 2007). In addition, marital distress spells a poor prognosis for a spouse with depression whose symp- toms have remitted. That is, a person whose depression clears up is likely to relapse if he or she has an unsatisfying marriage, especially one characterized by high levels of critical and hostile comments from the spouse (Butzlaff & Hooley, 1998; Hooley, 2007).
Why should criticism be linked to relapse? One pos- sibility is that criticism perturbs some of the neural cir- cuitry that underlies depression. Moreover, even after full recovery, criticism may still be a powerful trigger for those who are vulnerable to depression. In a novel study,
by low levels of positive affect, but anxious individuals usually are not (with the exception of people with social phobia; Naragon-Gainey et al., 2009; Watson et al., 2006). People with anxiety (especially those who experience panic), but not people with depression, also tend to be characterized by high levels of another mood dimension known as anxious hyperarousal, symptoms of which include racing heart, trembling, dizziness, and shortness of breath. This tripartite model of anxiety and depression thus explains what features anxiety and depression share (high negative affect) and what features they differ on (low positive affect for depression and anxious hyper- arousal for panic; Mineka et al., 1998). Each of the other anxiety disorders has its own separate and relatively unique component as well (Barlow, 2002; Prenoveau et al., 2010; Watson, 2005).
INTERPERSONAL EFFECTS OF MOOD DISORDERS Although there is no interpersonal theory of depression that is as clearly articulated as the cognitive theories, a con- siderable amount of research has been done on interper- sonal factors in depression. Interpersonal problems and social-skills deficits may well play a causal role in at least some cases of depression. In addition, depression creates many interpersonal difficulties—with strangers and friends as well as with family members (Hammen, 1995, 2005; Joiner & Timmons, 2009).
Lack of Social Support and Social-Skills Deficits Brown and Harris (1978), in their classic study of community women in a poor area of inner London, reported that women without a close, confiding relationship were more likely than those with at least one close confidant to become
Why are people without social support networks more prone to depression when faced with major stressors?
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control children who become depressed who do not have a parent with depression (see Hammen, 2009).
Some of these effects probably occur because these children inherit a variety of traits such as temperament (including shyness, behavioral inhibition, and neuroti- cism), low levels of positive emotions, and poor ability to regulate emotions that are all known risk factors for depression (Durbin et al., 2005; Hammen, 2009). In addi- tion, many studies have documented the damaging effects of negative interactional patterns between moth- ers with depression and their children. For example, mothers with depression show more friction and have fewer playful, mutually rewarding interactions with their children (Goodman & Gotlib, 1999). They are also less sensitively attuned to their infants and less affirm- ing of their infants’ experiences (Goodman & Brand, 2009). Furthermore, their young children are given mul- tiple opportunities for observational learning of nega- tive cognitions, depressive behavior, and depressed affect. Thus, although genetically determined vulnera- bility is clearly involved, psychosocial influences clearly also play an important role (Hammen, 2009; Natsuaki et al., 2010), and evidence is accumulating that inadequate parenting is what mediates the association between parental depression and their children’s depression (Goodman, 2007).
in review • Summarize the major biological causal factors for unipolar
depression, including genetic, biochemical, neuroendocrinologi- cal, and neurophysiological factors.
• What is the role of stressful life events in unipolar depression, and what kinds of diatheses have been proposed to interact with them?
• Describe the following theories of depression: Beck’s cognitive theory, the helplessness and hopelessness theories, ruminative response styles theory, and interpersonal theories.
Hooley and colleagues (2009) exposed healthy (never- depressed) controls and women with a past history of depression to critical remarks from their own mothers. While they were lying in a brain scanner, each participant heard her own mother making personally relevant critical remarks. Even though all the young women in the recovered- depressed group were completely well and had no symp- toms of depression, their brains still responded differently from the healthy controls when challenged by criticism. As you can see in Figure 7.6, there are differences in several brain areas that, as you have already learned, have been implicated in depression. When they heard criticism from their mothers, the recovered-depressed participants showed less brain activation in the dorsolateral prefrontal cortex and anterior cingulate cortex than the never- depressed controls did. In contrast, during criticism, brain activity in the amygdala was much higher in the recovered-depressed participants than it was in the con- trols. What was especially interesting was that all of this occurred without the recovered-depressed subjects being aware that they were responding differently to the criti- cisms. Taken together, these findings suggest that criticism might be associated with relapse in depression because it is capable of activating some of the neural circuits that are thought to be involved in the disorder. They also suggest that people who are vulnerable to depression may be especially sensitive to criticism even after they have made a full recovery.
The effects of depression in one family member can extend to children of all ages as well. Parental depression puts children at high risk for many problems, but espe- cially for depression (Goodman, 2007; Hammen, 2009; Hammen et al., 2011). Although these effects occur with both fathers and mothers with depression, the effects of maternal depression are somewhat larger (Hammen, 2009). Children of parents with depression who become depressed themselves tend to become depressed earlier and to show a more severe and persistent course than
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Figure 7.6 Brain Activation in Response to Maternal Criticism When healthy (never-depressed) participants hear criticism from their own mothers they show significantly greater activation in the dorso- lateral prefrontal cortex and anterior cingulate cortex than do people who have a history of depression but who are currently fully recovered. Amygdala activation during criticism is significantly greater in formerly depressed participants than it is in controls (Hooley et al., 2009).
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The following case illustrates cyclothymia.
A Cyclothymic Chef
Kevin is a 35-year-old chef who is seeking treatment at the sugges- tion of both his employer and girlfriend. His presenting problem is that “for the past 10 or so years I have been having extreme ups and downs . . . pretty serious mood swings.” Kevin says that he knows that some of his employees refer to him as “Dr. Jekyll and Mr. Hyde” behind his back, and his employer and girlfriend have said that they never know “which Kevin” they are going to see. He describes his mood swings as periods of ups and downs. The “ups” last 3 to 5 days during which he is happy, full of energy and creativity, often expanding his menu, creating new dishes, and experiencing “a deep love of life and everything in it.” The “downs” last a little bit longer, maybe 5 to 7 days, and during those periods he feels down, lacks energy, has to really push himself to get into work and prepare his menu, and is often agitated—yelling at his cooks, occasionally so loud that customers can hear him. This pattern of ups and downs has started to have a negative impact on his work, and is putting a significant strain on his relationship.
Bipolar Disorders (I and II) Recurrent cycles of mania and melancholia were recog- nized as early as the sixth century; however, it wasn’t until 1899 that Kraepelin introduced the term manic-depressive insanity and clarified the clinical picture. Kraepelin described the disorder as a series of attacks of elation and depression, with periods of relative normality in between. Today we call this illness bipolar disorder, although the term manic-depression is still commonly used as well.
Bipolar I disorder is distinguished from MDD by the presence of mania (see Table 7.2 for a summary). A mixed episode is characterized by symptoms of both full-blown manic and major depressive episodes for at least 1 week, either intermixed or alternating rapidly every few days. Mixed episodes were once thought to be relatively rare, but a recent review of 18 studies found that approximately 28 percent of bipolar patients experience mixed states at least some of the time. Moreover, many patients in a manic epi- sode have some symptoms of depressed mood, anxiety,
Bipolar and Related Disorders 7.4 List and distinguish between different types of
bipolar disorders.
As discussed earlier, bipolar disorders are distinguished from unipolar disorders by the presence of manic or hypo- manic episodes, which are nearly always preceded or fol- lowed by periods of depression. A person who experiences a manic episode has a markedly elevated, euphoric, and expansive mood, often interrupted by occasional outbursts of intense irritability or even violence—particularly when others refuse to go along with the manic person’s wishes and schemes. Hypomanic episodes can also occur; these involve milder versions of the same symptoms. Although the symptoms listed are the same for manic and hypo- manic episodes, there is much less impairment in hypoma- nia, and hospitalization is not required.
Cyclothymic Disorder Some people experience cyclical mood changes that are more severe than normal, but less severe than the mood swings seen in bipolar disorder. Cyclothymic disorder refers to the repeated experience of hypomanic symptoms for a period of at least 2 years. This is a less serious version of full-blown bipolar disorder because it lacks the extreme mood and behavior changes, psychotic features, and marked impairment seen in bipolar disorder.
Symptoms of the hypomanic phase of cyclothymia are essentially the opposite of the symptoms of persistent depressive disorder. In this phase of the disorder, the per- son may become especially creative and productive because of increased physical and mental energy. There may be significant periods between episodes in which the person with cyclothymia functions in a relatively adaptive manner. For a diagnosis of cyclothymia, there must be at least a 2-year span during which there are numerous peri- ods with hypomanic and depressed symptoms (1 year for adolescents and children), and the symptoms must cause clinically significant distress or impairment in functioning (although not as severe as in bipolar disorder). Individuals with cyclothymia are at greatly increased risk of later developing full-blown bipolar I or II disorder (Goodwin & Jamison, 2007).
In the depressed phase of cyclothymic disorder, a per- son’s symptoms are very similar to what is seen in persis- tent depressive disorder but without the duration criterion. The individual’s mood is dejected, and he or she experi- ences a distinct loss of interest or pleasure in customary activities and pastimes. In addition, the person may show other symptoms such as low energy, feelings of inadequacy, social withdrawal, and a pessimistic, brooding attitude.
Table 7.2 Distinguishing Between Bipolar I and Bipolar II Disorder
Bipolar I:
• Person has full-blown mania.
• Person experiences episodes of mania and periods of depression. Even if the periods of depression do not reach the threshold for a major depressive episode, the diagnosis of bipolar I disorder is still given.
Bipolar II:
• Person experiences periods of hypomania, but his or her symptoms are below the threshold for full-blown mania.
• Person experiences periods of depressed mood that meet the criteria for major depression.
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ods of pretty severe depression during which he becomes extremely sad, stops playing or making music, sleeps most of the day, and barely leaves the house. However, she has never seen him so sped up and out of control and he has become a completely different person these past few weeks.
DSM-5 also identifies a distinct form of bipolar disor- der called bipolar II disorder, in which the person does not experience full-blown manic (or mixed) episodes but has experienced clear-cut hypomanic episodes as well as major depressive episodes. Bipolar II disorder is equally or somewhat more common than bipolar I disorder, and, when combined, estimates are that about 2 to 3 percent of the U.S. population will suffer from one or the other disor- der (Kessler et al., 2007). Bipolar II disorder evolves into bipolar I disorder in only about 5 to 15 percent of cases, suggesting that they are distinct forms of the disorder (Coryell et al., 1995; Goodwin & Jamison, 2007). Recently, a subthreshold form of bipolar II disorder also has been rec- ognized and as many as 40 percent of individuals diag- nosed with MDD have a similar number of hypomanic symptoms, although not with a sufficient number or dura- tion to qualify for a hypomanic episode (Zimmerman et al., 2009). Findings like these are leading psychologists to rec- ognize that MDD is a far more heterogeneous category than previously recognized.
Bipolar disorder occurs equally in males and females (although depressive episodes are more common in women than men) and usually starts in adolescence and young adulthood, with an average age of onset of 18 to 22 years (Goodwin & Jamison, 2007; Merikangas et al., 2007). Bipolar II disorder has an average age of onset approxi- mately 5 years later than bipolar I disorder (Baldessarini et al., 2010). Both bipolar I and II are typically recurrent disorders, with people experiencing single episodes extremely rarely (Kessler et al., 2007). In about two-thirds of cases, the manic episodes either immediately precede or immediately follow a depressive episode; in other cases, the manic and depressive episodes are separated by intervals of relatively normal functioning. Figure 7.7 illustrates the different patterns of manic, hypomanic, and depressive symptoms and episodes that can be seen in bipolar-spectrum disorders. Most patients with bipolar disorder experience periods of remission during which they are relatively symptom-free, although this may occur on only about 50 percent of days (Kupka et al., 2007). Moreover, as many as 20 to 30 percent continue to experi- ence significant impairment (occupational and/or inter- personal) and mood lability most of the time, and as many as 60 percent have chronic occupational or interper- sonal problems between episodes. As with unipolar major depression, the recurrences can be seasonal in nature, in which case bipolar disorder with a seasonal pattern is diagnosed.
guilt, and suicidal thoughts, even if these are not severe enough to qualify as a mixed episode. People whose first episode of mania is a mixed episode have a worse long- term outcome than those originally presenting with a depressive or a manic episode (Baldessarini et al., 2010; Dodd et al., 2010).
If a person shows only manic symptoms, it is never- theless assumed that a bipolar disorder exists and that a depressive episode will eventually occur. Although some researchers have noted the probable existence of a unipolar type of manic disorder (i.e., “pure mania”; Kessler et al., 1997; Solomon et al., 2003), critics of this diagnosis argue that such patients usually have bipolar relatives and may well have had mild depressions that went unrecognized (Goodwin & Jamison, 2007; Winokur & Tsuang, 1996).
The following case illustrates both phases of bipolar I disorder.
Sped Up and Out of Control
Tim is a 25-year-old student and aspiring poet, rapper, and musi- cian. He was just admitted to a psychiatric hospital in an apparent manic episode. Although he has had a fairly stable life in which he lives with his girlfriend, Tessa, takes classes at the local community college, and works at a coffee shop in town, his behavior has become increasingly erratic. More specifically, his girlfriend reports that Tim has appeared to be “really sped up” the past month, talking faster than usual, expressing some pretty grandiose ideas (e.g., “I’m going to start and finish a PhD in poetry this year,” “I set up a meeting with Kanye West to discuss signing with him,” and “I am Tupac rein- carnated!”). Tessa reports that things have gotten much worse dur- ing the past 2 weeks, during which Tim sleeps just 1 to 2 hours per night and spends the rest of his time in the evenings making music, smoking marijuana, and buying expensive items online (he has maxed out their credit cards buying multiple guitars, turntables, a new refrigerator, and a five-star trip to Paris). She also reports that Tim disappeared for the past 4 days (skipping school and work as well), only to return home this morning saying that he “has been liv- ing with another woman he just met.” Tessa says that this is all very out of character for Tim. Since she has known him he has had peri-
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People with bipolar disorder suffer from more epi- sodes during their lifetimes than do persons with unipo- lar disorder (although these episodes tend to be somewhat shorter, averaging 3–4 months; Angst & Sellaro, 2000; Solomon et al., 2010). As many as 5 to 10 percent of per- sons with bipolar disorder experience at least four epi- sodes (either manic or depressive) every year, a pattern known as rapid cycling. In fact, those who go through periods of rapid cycling usually experience many more than four episodes a year. People who develop rapid cycling are slightly more likely to be women, to have a history of more episodes (especially more manic or hypo- manic episodes), to have an earlier average age of onset, and to make more suicide attempts (Coryell et al., 2003; Kupka et al., 2005; Nierenberg et al., 2010). Rapid cycling is sometimes precipitated by taking certain kinds of anti- depressants (Goodwin & Jamison, 2007; Kilzieh & Akis- kal, 1999). Fortunately, for about 50 percent of cases, rapid cycling is a temporary phenomenon and gradually disap- pears within about 2 years (Coryell et al., 1995, 2003).
Overall, the probabilities of “full recovery” from bipo- lar disorder are discouraging even with the widespread use of mood-stabilizing medications such as lithium, with one review estimating that patients with bipolar disorder spend about 20 percent of their lives in episodes (Angst & Sellaro, 2000). One 20-year prospective study in which over 200 patients were followed for an average of 17 years found that 24 percent had relapsed within 6 months of recovery; 77 percent had had at least one new episode within 4 years of recovery; and 82 percent had relapsed within 7 years (Coryell et al., 1995). Another prospective
FEATURES OF BIPOLAR DISORDER The duration of manic and hypomanic episodes tends to be shorter than the duration of depressive episodes, with typically about three times as many days spent depressed as manic or hypomanic (Goodwin & Jamison, 2007). There has been controversy over whether the symptoms of the depressive episodes of bipolar disorder are clinically distinguishable from those seen in unipolar major depressive episodes (Cuellar et al., 2005; Perris, 1992). Although there is a high degree of overlap in symptoms, there are some significant differences. The most widely replicated differences are that, relative to people with a unipolar depressive episode, people with a bipolar depressive episode tend to show more mood lability, more psychotic features, more psycho- motor retardation, and more substance abuse (Goodwin & Jamison, 2007). By contrast, individuals with unipolar depression, on average, show more anxiety, agitation, insomnia, physical complaints, and weight loss (Johnson et al., 2009). In spite of the high degree of similarity in symp- toms, research clearly indicates that major depressive epi- sodes in people with bipolar disorder are more severe than those seen in unipolar disorder, and, not surprisingly, they also cause more role impairment (Kessler et al., 2007).
Misdiagnoses are unfortunate because there are some- what different treatments of choice for unipolar and bipo- lar depression. Moreover, there is evidence that some antidepressant drugs used to treat what is thought to be unipolar depression may actually precipitate manic epi- sodes in patients who actually have as-yet-undetected bipolar disorder, thus worsening the course of the illness (Ghaemi et al., 2003; Whybrow, 1997).
M
D
m
d
Normal mood variation
Cyclothymic personality
Cyclothymic disorder
Bipolar II "Unipolar mania"
Bipolar I
The Manic-Depressive Spectrum
Figure 7.7 The Manic-Depressive Spectrum There is a spectrum of bipolarity in moods. All of us have our ups and downs, which are indicated here as normal mood variation. People with a cyclothymic personality have more marked and regular mood swings, and people with cyclothymic disorder go through periods when they meet the criteria for dysthymia (except for the 2-year duration) and other periods when they meet the criteria for hypomania. People with bipolar II disorder have periods of major depression and periods of hypomania. Unipolar mania is an extremely rare condition. Finally, people with bipolar I disorder have periods of major depression and periods of mania.
(Adapted from Frederick K. Goodwin and Kay R. Jamison. (2009). Manic Depressive Illness. Copyright © 1990. Oxford University Press, Inc.)
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unipolar disorder or any of the other major adult psychiat- ric disorders, including schizophrenia (Torrey et al., 1994).
Efforts to locate the chromosomal site(s) of the impli- cated gene or genes in this genetic transmission of bipolar disorder suggest that it is polygenic (Willcutt & McQueen, 2010). Although a great deal of research has been directed at identifying candidate genes through linkage analysis and association studies, no consistent support yet exists for any specific mode of genetic transmission of bipolar disor- der (Potash & DePaulo, 2000; Tsuang et al., 2004).
Another wrinkle in the story identified by recent stud- ies is that different disorders seem to share their genetic etiology. For instance, some of the genetic polymorphisms that are seen in those with bipolar disorder are also seen in those with schizophrenia (perhaps pointing toward why people with both disorders experience psychotic features) and with depression (perhaps explaining why people with these two disorders both experience depressive symp- toms) (Cross-Disorder Group of the Psychiatric Genomics Consortium, 2014).
NEUROCHEMICAL FACTORS The early monoamine hypothesis for unipolar disorder was extended to bipolar disorder, the hypothesis being that if depression is caused by deficiencies of norepinephrine or serotonin, then per- haps mania is caused by excesses of these neurotransmit- ters. There is good evidence for increased norepinephrine activity during manic episodes and less consistent evi- dence for lowered norepinephrine activity during depres- sive episodes (Goodwin & Jamison, 2007; Manji & Lenox, 2000). However, serotonin activity appears to be low in both depressive and manic phases.
As noted earlier, norepinephrine, serotonin, and dopamine are all involved in regulating our mood states (Howland & Thase, 1999; Southwick et al., 2005). Evidence for the role of dopamine stems in part from research show- ing that increased dopaminergic activity in several brain areas may be related to manic symptoms of hyperactivity, grandiosity, and euphoria (Cousins et al., 2009; Goodwin & Jamison, 2007). High doses of drugs such as cocaine and amphetamines, which are known to stimulate dopamine, also produce manic-like behavior (Cousins et al., 2009). Drugs like lithium reduce dopaminergic activity and are antimanic. In depression there appear to be decreases in both norepinephrine and dopamine functioning (Goodwin & Jamison, 2007; Manji & Lenox, 2000). Thus disturbances in the balance of these neurotransmitters seem to be one of the keys to understanding this debilitating illness.
ABNORMALITIES OF HORMONAL REGULATORY SYS- TEMS Some neurohormonal research on bipolar disorder has focused on the HPA axis. Cortisol levels are elevated in bipolar depression (as they are in unipolar depression), but they are usually not elevated during manic episodes (Goodwin & Jamison, 2007). Similarly, people with bipolar
study of 146 bipolar patients found that they experienced some symptoms (mostly subsyndromal) on an average of 47 percent of the weeks during the 13-year follow-up period. During the follow-up period, depressive symptoms were three times more common than manic or hypomanic symptoms (Judd et al., 2002; see also Judd et al., 2003).
in review • Describe the symptoms and clinical features of cyclothymia and
bipolar disorder.
• Describe the typical course of bipolar I and bipolar II disorders.
Causal Factors in Bipolar Disorders 7.5 Describe the causal factors influencing the
development and maintenance of bipolar disorders.
A host of causal factors for bipolar disorder have been pos- ited during the past century. However, biological causal factors are clearly dominant, and the role of psychological causal factors has received significantly less attention. The majority of research has concentrated on bipolar I disorder, which is what we focus on here.
Biological Causal Factors A number of biological factors are thought to play a causal role in the onset of bipolar disorder. These factors include genetic, neurochemical, hormonal, neurophysiological, neuroanatomical, and biological rhythm influences.
GENETIC INFLUENCES There is a greater genetic contri- bution to bipolar I disorder than to unipolar disorder. Approximately 8 to 10 percent of the first-degree relatives of a person with bipolar I illness can be expected to have bipolar disorder, compared to 1 percent in the general pop- ulation (Plomin et al., 2013; Willcutt & McQueen, 2010). The first-degree relatives of a person with bipolar disorder also are at elevated risk for unipolar major depression, although the reverse is not true (Akiskal & Benazzi, 2005; Goodwin & Jamison, 2007).
Although family studies cannot by themselves estab- lish a genetic basis for the disorder, results from twin stud- ies dating back to the 1950s also point to a genetic basis because the concordance rates for these disorders are much higher for identical than for fraternal twins. The average concordance rate is about 60 percent for monozygotic twins and only about 12 percent for dizygotic twins (Kelsoe, 1997). This and other studies suggest that genes account for about 80 to 90 percent of the variance in the liability to develop bipolar I disorder (Goodwin & Jamison, 2007; McGuffin et al., 2003). This is higher than heritability estimates for
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Other neurophysiological findings from patients with bipolar disorder have shown both similarities to and differ- ences from patients with unipolar disorder and normal controls. For example, several recent reviews suggest that there are deficits in activity in the prefrontal cortex in bipo- lar disorder. These seem related to neuropsychological deficits that people with bipolar disorder show in problem solving, planning, working memory, shifting of attention, and sustained attention on cognitive tasks (Chen et al., 2011; Haldane & Frangou, 2004; Malhi, Ivanovski, et al., 2004). This is similar to what is seen in unipolar depres- sion, as are deficits in the anterior cingulate cortex (Langan & McDonald, 2009). However, structural imaging studies suggest that certain subcortical structures, including the basal ganglia and amygdala, are enlarged in bipolar disor- der but reduced in size in unipolar depression. The decreases in hippocampal volume that are often observed in unipolar depression are generally not found in bipolar depression (Konarski et al., 2008). Some studies using func- tional magnetic resonance imaging (fMRI) also find increased activation in bipolar patients in subcortical brain regions involved in emotional processing, such as the thal- amus and amygdala, relative to unipolar patients and normal controls subjects (Chen et al., 2011; Malhi, Lagopoulos, et al., 2004). Overall, it is hard to draw firm conclusions in this area yet because there are so many inconsistencies in results across studies. However, there is initial meta-analytic sup- port for dysregulation in frontal-limbic activation in indi- viduals with bipolar disorder compared to controls (Chen et al., 2011). Hopefully more definitive findings will follow when much-needed technological innovations unfold (Goodwin & Jamison, 2007).
SLEEP AND OTHER BIOLOGICAL RHYTHMS There is considerable evidence regarding disturbances in biological rhythms such as circadian rhythms in bipolar disorder, even after symptoms have mostly remitted (Harvey, 2008; Murray & Harvey, 2010). During manic episodes, patients with bipolar disorder tend to sleep very little (seemingly by choice, not because of insomnia), and this is the most common symptom to occur prior to the onset of a manic episode. During depressive episodes, they tend toward hypersomnia (too much sleep). Even between episodes people with bipolar disorder show substantial sleep diffi- culties, including high rates of insomnia (Harvey, 2008; Millar et al., 2004). Bipolar disorder also sometimes shows a seasonal pattern in the same way unipolar disorder does, suggesting disturbances of seasonal biological rhythms, although these may be the result of circadian abnormalities in which the onset of the sleep–wake cycle is set ahead of the onset of other circadian rhythms. Given the cyclic nature of bipolar disorder itself, this focus on disturbances in biological rhythms holds promise for future integrative theories of the biological underpinnings of bipolar disorder.
disorder who are in a depressed episode show evidence of abnormalities on the dexamethasone suppression test (DST) at about the same rate as do people experiencing a unipolar depression, and these abnormalities persist even when the patients have been fully remitted and asymptomatic for at least 4 weeks (Langan & McDonald, 2009; Watson et al., 2004). During a manic episode, however, their rate of DST abnormalities generally has been found to be much lower (Goodwin & Jamison, 2007; Manji & Lenox, 2000, although see Langan & McDonald, 2009). Research also has focused on abnormalities of the hypothalamic-pituitary-thyroid axis because abnormalities of thyroid function are fre- quently accompanied by changes in mood. Many bipolar patients have subtle but significant abnormalities in the functioning of this axis, and administration of thyroid hormone often makes antidepressant drugs work better (Altshuler et al., 2001; Goodwin & Jamison, 2007). How- ever, thyroid hormone can also precipitate manic epi- sodes in patients with bipolar disorder (Goodwin & Jamison, 2007).
NEUROPHYSIOLOGICAL AND NEUROANATOMICAL INFLUENCES With PET scans, it is possible to visualize variations in brain glucose metabolic rates in depressed and manic states, although there is far less evidence regard- ing manic states because of the great difficulties studying patients who are actively manic. Several summaries of the evidence from studies using PET and other neuroimaging techniques show that, whereas blood flow to the left pre- frontal cortex is reduced during depression, during mania it is increased in certain other parts of the prefrontal cortex (Bermpohl et al., 2010; Goodwin & Jamison, 2007). Thus, there are shifting patterns of brain activity during mania and during depressed and normal moods (see Figure 7.8).
Figure 7.8 Mood Disorders and the Brain Brain imaging studies have revealed that people with mood disorders show abnormalities in several different brain regions, including the prefrontal cortex, basal ganglia, thalamus, anterior cingulate cortex, amygdala, and hippocampus.
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recurrences (Cohen et al., 2004; see also Alloy et al., 2010). There is also some evidence that personality and cognitive variables may interact with stressful life events in deter- mining the likelihood of relapse. For example, the person- ality variable neuroticism has been associated with symptoms of depression and mania (Quilty et al., 2009), and two studies have found that neuroticism predicts increases in depressive symptoms in people with bipolar disorder just as it does in unipolar disorder.
Moreover, personality variables and cognitive styles that are related to goal striving, drive, and incentive moti- vation have been associated with bipolar disorder (Alloy et al., 2009). For example, two personality variables associ- ated with high levels of achievement striving and increased sensitivity to rewards in the environment predicted increases in manic symptoms—especially during periods of active goal striving or goal attainment (such as studying for an important exam and then doing very well in it; Lozano & Johnson, 2001; Meyer et al., 2001). Another study found that students with a pessimistic attributional style who had also experienced negative life events showed an increase in depressive symptoms whether they had bipolar or unipolar disorder. Interestingly, however, the students with bipolar disorder who had a pessimistic attributional style and experienced negative life events also showed increases in manic symptoms at other points in time (Alloy et al., 2010; Reilly-Harrington et al., 1999).
in review • Summarize the major biological causal factors for bipolar disorder,
including genetic, biochemical, and other biological factors.
• What role do psychological factors, including stressful life events, seem to play in bipolar disorder?
Sociocultural Factors Affecting Unipolar and Bipolar Disorders 7.6 Explain how cultural factors can influence the
expression of mood disorders.
Research on the association of sociocultural factors with both unipolar and bipolar mood disorders is discussed together because much of the research conducted in this area has not made clear-cut diagnostic distinctions between the two types of disorders. Although the prevalence of mood disorders seems to vary considerably among differ- ent countries, it has been difficult to provide conclusive evidence for this because of various methodological prob- lems, including widely differing diagnostic practices in dif- ferent cultures, and because the symptoms of depression
This is particularly true because patients with bipolar dis- order seem especially sensitive to, and easily disturbed by, any changes in their daily cycles that require a resetting of their biological clocks (Goodwin & Jamison, 2007; Murray & Harvey, 2010).
Psychological Causal Factors Although biological factors play a prominent role in the onset of bipolar disorder, psychosocial factors have also been found to be involved in the etiology of the disorder. In particular, stressful life events, poor social support, and certain personality traits and cognitive styles have been identified as important psychological causal factors.
STRESSFUL LIFE EVENTS Stressful life events appear to be as important in precipitating bipolar depressive episodes as they are in triggering unipolar depressive episodes. Both stressful life events during childhood (e.g., physical and sexual abuse) and recent life stressors during adulthood (e.g., problems with friends and part- ners, financial hardship) increase the likelihood of ever developing bipolar disorder as well as having recur- rences (Gilman et al., 2015).
How might stressful life events operate to increase the chance of relapse? The diathesis–stress model would sug- gest that stressful life events influence the onset of epi- sodes by activating the underlying vulnerability. One hypothesized mechanism is through the destabilizing effects that stressful life events may have on critical bio- logical rhythms. Although evidence in support of this idea is still preliminary, it appears to be a promising hypothe- sis, especially for manic episodes (Bender & Alloy, 2011; Grandin et al., 2006).
OTHER PSYCHOLOGICAL FACTORS IN BIPOLAR DIS- ORDER Other social environmental variables may also affect the course of bipolar disorder. For example, one study found that people with bipolar disorder who reported low social support showed more depressive recurrences over a 1-year follow-up, independent of the effects of stressful life events, which also predicted more
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from Hong Kong and the United States found levels of depressive symptoms and hopelessness to be higher in the adolescents from Hong Kong (Stewart et al., 2004).
Cross-Cultural Differences in Prevalence Prevalence rates for mood disorders vary a great deal across countries, as revealed by large-scale epidemiologi- cal studies. For example, the WHO World Mental Health Survey, which assesses the prevalence and characteristics of psychological disorders across more than 20 countries, reveals that the 12-month prevalence of mood disorders varies from 0.8 percent in Nigeria to 9.6 percent in the United States, as shown earlier in the chapter in Figure 7.1 (WHO World Mental Health Survey Consortium, 2004). The reasons for such wide variation are undoubtedly very complex, and much work remains to be done before we fully understand them. The ideas that are being explored include differences in willingness to report the presence of a mental disorder due to stigma, as well as different levels of important psychosocial risk variables in different cul- tures and different levels of stress. For example, there appear to be cross-cultural differences in hypothesized risk variables such as pessimistic attributional style, although how these differences might translate into different rates of depression is unclear because we do not yet know whether the same risk variables are operative in different cultures. However, research is beginning to explore whether psy- chosocial risk factors for mood disorders operate across cultures, and there is some initial evidence that factors like rumination, hopelessness, and pessimistic attributional style (Abela et al., 2011) are associated with risk for depres- sion in other countries, such as China (Hong et al., 2010).
in review • What kinds of cross-cultural differences are there in depressive
symptoms, and what kinds of cross-cultural factors influence the prevalence of unipolar depression?
Treatments and Outcomes 7.7 Describe and distinguish between different
treatments for mood disorders.
Many patients with mood disorders (especially unipolar disorders) never seek treatment. Even without formal treatment, the great majority of individuals with mania and depression will recover (often only temporarily) within less than a year. However, given the enormous amount of personal suffering and lost productivity that these individuals endure, and given the wide variety of treatments that are available today, more and more people
appear to vary considerably across cultures (Chentsova- Dutton & Tsai, 2009; Kleinman, 2004).
Cross-Cultural Differences in Depressive Symptoms Depression occurs in all cultures that have been studied. However, the form that it takes differs widely, as does its prevalence (Chentsova-Dutton & Tsai, 2009; Marsella, 1980). For example, in Western cultures the “psychologi- cal” symptoms of depression (e.g., guilt, worthlessness, suicidal ideation) are prominent, whereas they are not prominently reported in non-Western cultures such as China and Japan, where rates of depression are relatively low. Instead people in non-Western cultures tend to exhibit the more “physical” symptoms (e.g., sleep distur- bance, loss of appetite, weight loss, and loss of sexual interest (Kleinman, 2004; Ryder et al., 2008; Tsai & Chentsova-Dutton, 2002).
Several possible reasons for these symptom differ- ences stem from Asian beliefs in the unity of the mind and body, a lack of expressiveness about emotions more gener- ally, and the stigma attached to mental illness in these cul- tures (Chentsova-Dutton & Tsai, 2009). Another reason why guilt and negative thoughts about the self may be common in Western but not in Asian cultures is that West- ern cultures view the individual as independent and autonomous, so when failures occur, internal attributions are made. By contrast, in many Asian cultures individuals are viewed as inherently interdependent with others. Nev- ertheless, as countries like China have incorporated some Western values over the course of becoming increasingly industrialized and urbanized, rates of depression have risen a good deal relative to several decades ago (Dennis, 2004; Zhou et al., 2000). Indeed, one study of adolescents
In some cultures the concept of depression as we know it simply does not exist. For example, Australian aborigines who are “depressed” show none of the guilt and self-abnegation commonly seen in more developed countries. They also do not show suicidal tendencies but instead are more likely to vent their hostilities onto others rather than onto themselves.
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not respond to an initial trial of medication will show a clinically significant response when switched to a different antidepressant or to a combination of medications (Hollon, Thase, & Markowitz, 2002).
Unfortunately, TCAs have unpleasant side effects for some people (e.g., dry mouth, constipation, sexual dys- function, and weight gain). Although these side effects often diminish over time, they are so unpleasant to many patients that they stop taking their medications before the side effects go away. In addition, because these drugs are highly toxic when taken in large doses, there is some risk in prescribing them for suicidal patients, who might use them for an overdose.
The side effects and toxicity of TCAs have led physi- cians to increasingly prescribe selective serotonin reup- take inhibitors (SSRIs) (Olfson & Marcus, 2009). SSRIs are generally no more effective than the tricyclics; indeed some findings suggest that TCAs are more effective than SSRIs for severe depression. However, the SSRIs tend to have many fewer side effects and are better tolerated by patients, as well as being less toxic in large doses. The primary nega- tive side effects of the SSRIs are problems with orgasm and lowered interest in sexual activity, although insomnia, increased physical agitation, and gastrointestinal distress also occur in some patients (Thase, 2009b).
who experience these disorders are seeking treatment. There was a rapid increase in the treatment of depression from 1987 to 1997, and there has been a more modest increase since 1998 (Marcus & Olfson, 2010). Interestingly, between 1998 and 2007, there was a decline in the reported use of psychotherapy, although the use of antidepressant medication remained relatively stable. These changes are happening in an era in which there is greatly increased public awareness of the availability of effective treatments and during a time in which significantly less stigma is associated with experiencing a mood disorder. Neverthe- less, only about 40 percent of people with mood disorders receive minimally adequate treatment, with the other 60 percent receiving no treatment or inadequate care (Wang, Lane, et al., 2005). Fortunately, the probability of receiving treatment is somewhat higher for people with severe uni- polar depression and with bipolar disorder than for those with less severe depression (Kessler et al., 2007).
Pharmacotherapy Antidepressant, mood-stabilizing, and antipsychotic drugs are all used in the treatment of unipolar and bipolar dis- orders (see Chapter 16 for further information about these medications). The first category of antidepressant medications—developed in the 1950s—is the monoamine oxidase inhibitors (MAOIs) because they inhibit the action of monoamine oxidase, the enzyme responsible for the breakdown of norepinephrine and serotonin once released. The MAOIs can be as effective in treating depres- sion as other categories of medications, but they have potentially dangerous (even potentially fatal) side effects if certain foods rich in the amino acid tyramine are consumed (e.g., red wine, beer, aged cheese, salami). Thus, they are not used very often today unless other classes of medica- tion have failed. Depression with atypical features is the one subtype of depression that seems to respond preferen- tially to the MAOIs.
For most patients who are moderately to seriously depressed, including those with persistent depressive dis- order, the drug treatment of choice from the 1960s to the early 1990s was tricyclic antidepressants (TCAs; called this because of their chemical structure) such as imipra- mine. TCAs increase neurotransmission of the mono- amines, primarily norepinephrine and to a lesser extent serotonin (Thase & Denko, 2008). The efficacy of TCAs in significantly reducing depressive symptoms has been demonstrated in hundreds of studies where the response of patients with depression who were given these drugs has been compared with the response of patients given a placebo. However, only about 50 percent show what is considered clinically significant improvement, and many of these patients still have significant residual depressive symptoms. Fortunately, about 50 percent of those who do
SSRIs are used not only to treat severe depression but also to treat people with mild depressive symptoms (Gitlin, 2002). Importantly, recent research has shown that antidepressant medication is superior to placebo only for patients with very severe depressive symptoms, with negligible treatment effects observed for those with less severe symptoms (Fournier et al., 2010; see Figure 7.9).
In the past decade, several new atypical antidepres- sants (neither tricyclics nor SSRIs) have also become increasingly popular, each with its own advantages (Mar- cus & Olfson, 2010). For example, bupropion (Wellbutrin) does not have as many side effects (especially sexual side effects) as the SSRIs and, because of its activating effects, is particularly good for depression involving significant weight gain, loss of energy, and oversleeping. In addition,
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25 percent of patients continuing to receive medication dur- ing the maintenance phase of treatment show recurrence of MDD (Solomon et al., 2005). Patients showing residual symptoms are most likely to relapse, indicating the impor- tance of trying to treat the patient to full remission of symp- toms (Keller, 2004; Thase & Denko, 2008).
LITHIUM AND OTHER MOOD-STABILIZING DRUGS Lithium therapy has now become widely used as a mood stabilizer in the treatment of both depressive and manic episodes of bipolar disorder. The term mood stabilizer is often used to describe lithium and related drugs because they have both antimanic and antidepressant effects—that is, they exert mood-stabilizing effects in either direction. Lithium has been more widely studied as a treatment of manic episodes than of depressive episodes, and estimates are that about three-quarters of those in a manic episode show at least partial improvement. In the treatment of bipolar depression, lithium may be no more effective than traditional antidepressants (study results are inconsistent), but about three-quarters show at least partial improve- ment (Keck & McElroy, 2007). However, treatment with antidepressants is associated with significant risk of pre- cipitating manic episodes or rapid cycling, although the risk of this happening is reduced if the person also takes lithium (Keck & McElroy, 2007; Thase & Denko, 2008).
Lithium is often effective in preventing cycling between manic and depressive episodes (although not
venlafaxine (Effexor) seems superior to the SSRIs in the treatment of severe or chronic depression, although the profile of side effects is similar to that for the SSRIs. Several other atypical antidepressants have also been shown to be effective (see Chapter 16).
THE COURSE OF TREATMENT WITH ANTIDEPRESSANT DRUGS Antidepressant drugs usually require at least 3 to 5 weeks to take effect. Generally, if there are no signs of improvement after about 6 weeks, physicians try a new medication because about 50 percent of those who do not respond to the first drug prescribed do respond to a second one. Also, discontinuing the drugs when symptoms have remitted may result in relapse. Recall that the natural course of an untreated depressive episode is typically 6 to 9 months. Thus, when depressed patients take drugs for 3 to 4 months and then stop because they are feeling better, they are likely to relapse because the underlying depressive episode is actually still present, and only its symptomatic expression has been suppressed (Gitlin, 2002; Hollon, Thase, & Markowitz, 2002; Hollon et al., 2006). Because depression is often a recurrent disorder, physicians have increasingly recommended that patients continue for very long periods of time on the drugs (ideally at the same dose) in order to prevent recurrence (Nutt, 2010). Thus, these medi- cations can often be effective in prevention, as well as treat- ment, for patients subject to recurrent episodes (Hollon et al., 2006; Thase & Denko, 2008). Nevertheless, approximately
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Figure 7.9 Effectiveness of Antidepressants Based on Severity of Depression This figure shows the amount of change in depressive symptoms, as measured by the Hamilton Rating Scale for Depression (HRSD), from treatment intake to the end of treatment for those receiving antidepres- sant medication (ADM; dark circles) relative to placebo (light circles). The size of the circle represents the number of data points that contributed to that mean. The two lines represent the estimated change in depressive symptoms. Note that the circles (and lines) are overlapping for those with low and moderate depressive symptoms at intake (the left half of the figure), and a difference between ADM and placebo only emerges for those with high depressive symptoms at intake (the right half of the figure). The take- home message: Antidepressants appear to be most effective for severe depression, but are no more effective than placebo for mild or moderate depression.
(Adapted from Fournier, J.C., DeRubeis, R. J., Hollon, S. D., Dimidjian, S., Amsterdam, J.D., Shelton, R. C., & Fawcett, J. (2010). Antidepressant drug effects and depression severity: A patient-level meta-analysis. JAMA, 303, 47–53.)
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among the elderly) and who may present an immediate and serious suicidal risk, including those with psychotic or melancholic features (Goodwin & Jamison, 2007). It is also used in patients who cannot take antidepressant medi- cations or who are otherwise resistant to medications (Heijnen et al., 2010; Mathew et al., 2005). When selection criteria for this form of treatment are carefully observed, a complete remission of symptoms occurs for many patients after about 6 to 12 treatments (with treatments adminis- tered about every other day). This means that a majority of patients with severe depression can be vastly better in 3 to 5 weeks (George et al., 2013). The treatments, which induce seizures, are delivered under general anesthesia and with muscle relaxants. The most common immediate side effect is confusion, although there is some evidence for lasting adverse effects on cognition, such as amnesia and slowed response time (Sackeim et al., 2007). Maintenance dosages of an antidepressant and a mood-stabilizing drug such as lithium are then ordinarily used to maintain the treatment gains achieved until the depression has run its course (Mathew et al., 2005; Sackeim et al., 2009). ECT is also very useful in the treatment of manic episodes; reviews of the evidence suggest that it is associated with remission or marked improvement in 80 percent of patients with mania (Gitlin, 1996; Goodwin & Jamison, 2007). Maintenance on mood-stabilizing drugs following ECT is usually required to prevent relapse.
TRANSCRANIAL MAGNETIC STIMULATION Although transcranial magnetic stimulation (TMS) has been available as an alternative biological treatment for some time now, only in the past decade has it begun to receive significant attention. TMS is a noninvasive technique allowing focal stimulation of the brain in patients who are awake. Brief but intense pulsating magnetic fields that induce electrical activ- ity in certain parts of the cortex are delivered (Goodwin & Jamison, 2007; Janicak et al., 2005). The procedure is pain- less, and thousands of stimulations are delivered in each treatment session. Treatment usually occurs 5 days a week for 2 to 6 weeks. Many studies have shown it to be quite effective—indeed in some studies quite comparable to uni- lateral ECT and antidepressant medications (George & Post, 2011; Janicak et al., 2005; Schulze-Rauschenbach et al., 2005). In particular, research suggests that TMS is a promising approach for the treatment of unipolar depression in patients who are moderately resistant to other treatments (George & Post, 2011). Moreover, TMS has advantages over ECT in that cognitive performance and memory are not affected adversely and sometimes even improve, as opposed to ECT, where memory-recall deficits are common (George et al., 2013). Finally, TMS appears to be safe for use with children and adolescents, with only low rates of mild and transient side effects such as headaches (12 percent) and scalp dis- comfort (3 percent) (Krishnan et al., 2015).
necessarily for patients with rapid cycling), and patients with bipolar disorder frequently are maintained on lithium therapy over long time periods, even when not manic or depressed, simply to prevent new episodes. Unfortunately, several large studies recently have found that only about one-third of patients maintained on lithium remained free of an episode over a 5-year follow-up period. Nevertheless, patients on lithium maintenance do have fewer episodes than patients who discontinue their medication (Keck & McElroy, 2007).
Lithium therapy can have some unpleasant side effects such as lethargy, cognitive slowing, weight gain, decreased motor coordination, and gastrointestinal difficulties. Long- term use of lithium is occasionally associated with kidney malfunction and sometimes permanent kidney damage, although end-stage renal disease seems to be a very rare consequence of long-term lithium treatment (Goodwin & Jamison, 2007; Tredget et al., 2010). Not surprisingly, these side effects, combined with the fact that many patients with bipolar disorder seem to miss the highs and the abun- dance of energy associated with their hypomanic and manic episodes, sometimes create problems with compli- ance in taking the drug.
In the past several decades, evidence has emerged for the usefulness of another category of drugs known as the anticonvulsants (e.g., carbamazepine, divalproex, and val- proate) in the treatment of bipolar disorder. These drugs are often effective in patients who do not respond well to lithium or who develop unacceptable side effects from it, and they may also be given in combination with lithium. However, a number of studies have indicated that risk for attempted and completed suicide was nearly two to three times higher for patients on anticonvulsant medications than for those on lithium (Goodwin et al., 2003; Thase & Denko, 2008), suggesting one major advantage of giving lithium to patients who can tolerate its side effects. Both people with bipolar or unipolar depression who show signs of psychosis (hallucinations and delusions) may also receive treatments with antipsychotic medications (see Chap- ters 13 and 16) in conjunction with their antidepressant or mood-stabilizing drugs (Gitlin, 2009; Keck & McElroy, 2002; Rothschild et al., 2004).
Alternative Biological Treatments In addition to the use of pharmacotherapy, there are sev- eral other biologically oriented approaches to the treat- ment of mood disorders. These approaches have been the subject of empirical study in recent years, and they appear to be promising treatment options.
ELECTROCONVULSIVE THERAPY Because antide- pressants often take 3 to 4 weeks to produce significant improvement, electroconvulsive therapy (ECT) is often used with patients who are severely depressed (especially
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problems rather than on the more remote causal issues that psychodynamic psychotherapy often addresses. For exam- ple, cognitive therapy consists of highly structured, sys- tematic attempts to teach people with unipolar depression to evaluate systematically their dysfunctional beliefs and negative automatic thoughts. They are also taught to iden- tify and correct their biases or distortions in information processing and to uncover and challenge their underlying depressogenic assumptions and beliefs. Cognitive therapy relies heavily on an empirical approach in that patients are taught to treat their beliefs as hypotheses that can be tested through the use of behavioral experiments.
One example of challenging a negative automatic thought through a behavioral experiment can be seen in the following interchange between a cognitive therapist and a patient with depression.
Therapy Session: “My Husband Doesn’t Love Me Anymore”
patient: My husband doesn’t love me anymore. therapist: That must be a very distressing thought. What makes you
think that he doesn’t love you? patient: Well, when he comes home in the evening, he never wants
to talk to me. He just wants to sit and watch TV. Then he goes straight off to bed.
therapist: OK. Now, is there any evidence, anything he does, that goes against the idea that he doesn’t love you?
patient: I can’t think of any. Well, no, wait a minute. Actually it was my birthday a couple of weeks ago, and he gave me a watch which is really lovely. I’d seen them advertised and mentioned I liked it, and he took notice and went and got me one.
therapist: Right. Now how does that fit with the idea that he doesn’t love you?
patient: Well, I suppose it doesn’t really, does it? But then why is he like that in the evening?
therapist: I suppose him not loving you any more is one possible reason. Are there any other possible reasons?
patient: Well, he has been working very hard lately. I mean, he’s late home most nights, and he had to go in to the office at the weekend. So I suppose it could be that.
therapist: It could, couldn’t it? How could you find out if that’s it? patient: Well, I could say I’ve noticed how tired he looks and ask
him how he’s feeling and how the work’s going. I haven’t done that. I’ve just been getting annoyed because he doesn’t pay any attention to me.
therapist: That sounds like an excellent idea. How would you like to make that a homework task for this week?
(From Fennell, M. J. V. (1989). Depression. In K. Hawton, P. M. Salkovskis, J. Kirk, & D. M. Clark (Eds.), Cognitive behaviour therapy for psychiatric problems: A practical guide. Oxford University Press.)
The usefulness of cognitive therapy has been amply documented in dozens of studies, including several stud- ies on hospital patients with unipolar depression and on patients diagnosed with depression with melancholic
DEEP BRAIN STIMULATION In recent years, deep brain stimulation has been explored as a treatment approach for individuals with refractory depression who have not responded to other treatment approaches, such as medica- tion, psychotherapy, and ECT. Deep brain stimulation involves implanting an electrode in the brain and then stimulating that area with electric current (Mayberg et al., 2005). Although more research on deep brain stimulation is needed, initial results suggest that it may have potential for treatment of unrelenting depression (see Chapter 16 for more details).
BRIGHT LIGHT THERAPY In the past decade an alterna- tive nonpharmacological biological method has received increasing attention: bright light therapy (see Pail et al., 2011, for a review). This was originally used in the treatment of seasonal affective disorder, but it has now been shown to be effective in nonseasonal depressions as well (Golden et al., 2005; Lieverse et al., 2011).
Psychotherapy Several forms of specialized psychotherapy, developed since the 1970s, have proved effective in the treatment of unipolar depression, and the magnitude of improvement of the best of these is approximately equivalent to that observed with medications. Considerable evidence also suggests that these same specialized forms of psychother- apy for depression, alone or in combination with drugs, significantly decrease the likelihood of relapse within a 2-year follow-up period (Hollon & Dimidjian, 2009; Hollon et al., 2005). Other specialized treatments have been devel- oped to address the problems of people (and their families) with bipolar disorder.
COGNITIVE-BEHAVIORAL THERAPY One of the two best-known psychotherapies for unipolar depression with documented effectiveness is cognitive-behavioral therapy (CBT) (also known as cognitive therapy), originally devel- oped by Beck and colleagues (Beck et al., 1979; Clark, Beck, & Alford, 1999). It is a relatively brief form of treatment (usually 10 to 20 sessions) that focuses on here-and-now
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from depression suggests that mindfulness-based cogni- tive therapy is an effective treatment for reducing risk of relapse in those with a history of three or more prior depressive episodes who have been treated with antide- pressant medication (Piet & Hougaard, 2011).
Although the vast majority of research on CBT has focused on unipolar depression, recently there have been indications that a modified form of CBT may be quite use- ful, in combination with medication, in the treatment of bipolar disorder as well (Lam et al., 2003, 2005; Miklowitz, 2009). There is also preliminary evidence that mindfulness- based cognitive therapy may be useful in treating bipolar patients between episodes (Williams et al., 2008).
BEHAVIORAL ACTIVATION TREATMENT A relatively new and promising treatment for unipolar depression is called behavioral activation treatment. This treatment approach focuses intensively on getting patients to become more active and engaged with their environment and with their interpersonal relationships. These techniques include scheduling daily activities and rating pleasure and mastery while engaging in them, exploring alternative behaviors to reach goals, and role-playing to address specific deficits. Traditional cognitive therapy attends to these same issues but to a lesser extent. Behavioral activation treatment, by contrast, does not focus on implementing cognitive changes directly but rather on changing behavior. The
features (Craighead et al., 2007; Hollon, Haman, & Brown, 2002; Hollon et al., 2006). When compared with pharmaco- therapy, it is at least as effective when delivered by well- trained cognitive therapists. It also seems to have a special advantage in preventing relapse, similar to that obtained by staying on medication (Hollon, 2011; Hollon & Ponniah, 2010). Moreover, evidence is beginning to accumulate that it can prevent recurrence several years following the epi- sode when the treatment occurred (Craighead et al., 2007; Hollon & Dimidjian, 2009). Perhaps not surprisingly, some recent interesting brain-imaging studies have shown that the biological changes in certain brain areas that occur fol- lowing effective treatment with cognitive therapy versus medications are somewhat different, suggesting that the mechanisms through which they work are also different (Clark & Beck, 2010; Hollon & Dimidjian, 2009). One pos- sibility is that medications may target the limbic system, whereas cognitive therapy may have greater effects on cor- tical functions.
Recent evidence suggests that CBT and medications are equally effective in the treatment of severe depression (DeRubeis et al., 1999; Hollon et al., 2006). For example, one important two-site study of moderate to severe depres- sion found that 58 percent responded to either cognitive therapy or medication (DeRubeis et al., 2005). However, by the end of the 2-year follow-up, when all cognitive therapy and medications had been discontinued for 1 year, only 25 percent of patients treated with cognitive ther- apy had had a relapse versus 50 percent in the medication group (Hollon & Dimidjian, 2009; Hollon et al., 2005). This is illustrated in Figure 7.10.
Another variant on cognitive therapy, called mindfulness-based cognitive therapy, has been developed in recent years to be used with people with highly recurrent depression (Segal et al., 2002, 2012; Teasdale, 2004). The logic of this treat- ment is based on findings that people with recur- rent depression are likely to have negative thinking patterns activated when they are simply in a depressed mood. Perhaps rather than trying to alter the content of their negative thinking as in traditional cognitive therapy, it might be more useful to change the way in which these people relate to their thoughts, feelings, and bodily sen- sations. This group treatment involves training in mindfulness meditati
