Abnormal Psychology Clinical and Scientific Perspectives [6 ed.] 1517802822, 9781517802820 - EBIN.PUB (2022)

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Sixth Edition

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Charles A. L~ons

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harles A. Lyons is Professor of Psychology at Eastern Oregon University, where he teaches courses in abnormal psychology, behavior analysis, clinical interventions, evolution and behavior, human sexuality, and psychological assessment. He earned his PhD from Utah State University, with a specialization in the analysis of behavior. As a licensed clinical psychologist, he worked for several years with inpatient populations at a large state psychiatric facility, where he provided treatment, assessment, and forensic evaluations. As a researcher, he has published articles on animal behavior, basic learning processes, language, and addictive behaviors. His most recent research interests include social and compulsive gambling and largescale public lotteries.

arclay Martin is professor emeritus at the University of North Carolina at Chapel Hill. After receiving his PhD in psychology from Stanford University, he taught at the University of Wisconsin at Madison before joining the faculty at UNC. The author of numerous articles and books, he enjoys his retirement in Chapel Hill.

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Brief Contents Preface .. .. .. ... .. ............ . ....... ... . ...... . . .. . .. . ............ ... .. ..... . ............ . . .. .. . .. xii Supplements & Resources . ..................................................................... xiv

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Introduction and Methods of Research .. . .. . ... . .. . ..... ... .. . . . ............... . .... . .. . . 2 Historical Perspectives. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 22

ch~ter

Contemporary Frameworks. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 48

chJ/.ter

Classification, Diagnosis, and Assessment. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 86 Stress- and Trauma-Related Disorders .... ... . .. .. ....... . . . . . .. .. . . .......... . . . . ... . . . 112 Anxiety and Obsessive-Compulsive Disorders ... . . .. ... ..... .... . . ..................... 138 Somatic Symptom and Dissociative Disorders .. . ... . .... . .. .. . . . .................... . . . 164 Personality Disorders . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 190 Sexual and Gender Disorders . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 220 Schizophrenia and Psychotic Disorders . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 250 Mood Disorders and Suicide ...... . .. ..... ... . . . ....... .. .. . ... . .. . .. .... .... . . . .... . .. 288

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Substance-Related and Addictive Disorders . . ........... . . . .. . . . . . ........... . . .. ... . . . 324 Neurodevelopmental and Disruptive Disorders . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 360

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Eating, Sleep, and Elimination Disorders . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 394

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Legal, Ethical, and Professional Issues in Abnormal Psychology . . .. ... . . ........ .. ... . . . 446

Neurocognitive Disorders . ...... ... . . . .... .. . .. .. ..... . ...... . ... . . . . ... . .. . . .... .. . . . . 422

DSM-5 Classification ...... ... .... .. . ........... ... . ... .... ... ..... . .. .. ... . .. .......... .. .. ... . .. 468 Glossary . .. ... .. .... ... ... ..... .. . .. . .. . . ......... .. ... ....... . .. .... . ..... ... ................. . .. 478 Bibliography .. . ............ . .... ... . ... . .. ...... ..... . ... . .. ...... . .... .. .. .. ... .......... . .. . . . . 492 Name Index ... . ....... ... . .. . .... .. . .......... ... . . ... .... .. ........ .. . .... .. ......... . .. . . ... . . . 524 Subject Index . .. ... ... .... ... ... .... ... . ................. . ... . ..... . . ...... . .... .. ...... .. . .. . . .. 532

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Contents Preface xt1 Su pplements & Resources CHAPTER

2.3 Den1onology Today: Alive and \.Yell in the United States? .................... 29

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2.4 Hurnanitarian Reforn1s ...... •.. . ....... 31 2.4a The Early Asylums .......... . ..... • ....... 31

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Introduction and Methods of Research ............ . .......2 1.1 \>Vhat Is Abnonnal Beha,1or? ..... • . .. . ...3 Lia Cultural /Jiappropriateness. ......... • ....... 3 1.Jb Subjective Distre..,s .. . .............. •. . ..... .5 1.Jc Psychological Disability . . .......... ••• ......5

1.2 Abnortnality Is a Continnwn .... . •. ......6 1.3 \>Vhat Is t.tental Health'?.......... . .. ......6

2.4b Treating Mental Patients like Human Beings ............ •. .• ....... 31

2.5 The Organic Vie,v ........... . ........... 32 2.5a An Influential Classification System: Emil Kraepelin ............... . ........... 33 2.5b The Search for Physical Causes and Cures.. 34 2.5c An Example of Organic Causation: General Paresis. .............. . ........... 34

2.6 ll1e Psychological View ..... ............ 35 2.6a. Healing by Suggestion:

1.3a By What Name Shall We Call It? .. .. . . .. .... .1

Franz Anton Mesnier ......... , ........... 35

1.4 ll1e Prevalence of Abnonnality .... . ......9

2.6b The Scientific Study ofHysteria: Jean-Martin Charcot. ........ .. ........... 36 2.6c The Scientific Study of Learning and Behavior ..... . . . . . . .. ...... 38

1.5 The Scientific Study of Abnonual Beha,•ior .............. ............ . ...... 10 1.5a 1.5b 1.5c 1.5d l.5e

The C«se Study . ................ . .. ••. .... IO Epidemiological Research . ......... •• ..... 11 Sampling and Generalization .............. II Reliability and Validity ofMeasurement ... 12 Correlational Research .................... 13 J.!if Experimental Research . . ........... •• ..... .14

Chapter Review ........ . ................ . ..... 17 CHAPTER

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Historical Perspectives ...... ... ....... 22 2. I Models and Metaphors ................. 24 2.2 Den1on Possession Versus Katuralistic Explanations ............................ 25 2.2a 2.2b 2.2c 2.2d 2.2e

Early Denwnology .. ............... ••. .... Hippocrates . ....... . ............... .. .... Dtmce Mani«, in the lvliddle Ages.... ...... Demonology Triumphant: l•Vilchcraft. . ..... Voice.., efReason ..........................

Chapter Review ................ •.. •.. . ....... 43 CHAPTER

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Contemporary Frameworks ......... 48 3.1 Freud's Psychodynarnic Theory......... 49 3.Ja Basic Features ofFreud's Early 11,eory ..... 49 3.Jb AnxietyandtheJWechanisms efDefer,se.... 51 3.lc A Theory ofthe Mind: 11,e Higher-Order Abstractions . ........... 52 3.Jd A11 Illustration .. . ........ . .. . ............. 54 3.le Childhood Origins ofNeurotic Symptoms... 55 3.Jf Psychody namic Treatment. ................ 55 3.lg Variations in Psychodynan,ic Approaches. . 56

26 26 27 28

3.2 Behavioral Approaches ... . ............. 57

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3.2a. Operant Conditioning ... . .. . ............. 3.2b Operant Learning and Abnormal Behavior. 3.2c Behavioral Treatment... ... . .............. 3.2d Variations in BehavitJral Approaches . .....

58 62 63

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3.3 Biological Approaches ............. ..... 65 3.3a Heredity ........................ . ... . .... 65

5.3 'TI1e Nature ofStressors and 'TI1eir Severity .......................... 116

3.3b Research Methodsfor Studyi11g Hereditary !11jlue11ces . ............... . .... 68 3.3c 7he Human Brain .................... . .... 70

5.3a Stress and Cardiovascular Health ........ 118 5.3b Stress and l1111nune Functioning . ......... 119 5.3c Other Stress-Health Relationships ........ 122

3.3d Neurotransmi~sion ....................... 71 3.3e Biological Treatments ..................... 73

5.4 All ll lustration of tbe Range of Tran maaJJd Stressor-Related Disorders ....... 123

3.4 I Iu1nanistic-Experiential Approaches .. 77 3.5 Approaching an Integrated l\lodel ..... 78

5.5 Treatn1ent for Severe Stress Reactions ....................... 130

Chapter Review ......................... ..... 80

5.6 Other Stress-Related Disorders ........ 131 Chapter Review ............................. I 34

4 Classification, Diagnosis, and Assessment .. .. ............. ........ 86 CHAPTER

CHAPTER

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4.1 Classification ................... . ... . .... 87

Anxiety and Obsessive-Compulsive Disorders................................. 138

4.la Development ojt1 System q(C/assific,1/ion .. 88

6.1 fear and Anxiety ......... . ............. 139

4.2 Problems Associated ,vith Classification Syste1ns ............. . .... 94 4.2a The ReUt1bility of Categories ... ............ 94

6.2 Anxiety Disorders........... ........... 140

4.2b The Validity ofCategories ............ . .... 96

4.3 The Diagnostic Process ................. 97 4.3a 11,e Interview... .......................... 97 4.3b Observation ... ..... . ..................... 99 4.3c Psycho/ogiClJI Tests .................. . .... 99 4.3d Neuropsychological A~sessment .. . ... . ... 104

Chapter Review ........ . .................... 107

5 Stress- and Trauma-Related Disorders .......... 112 CHAPTER

5.1 Defining Stress ......................... 113 5.la 17,e Stress Respon.~e . ............. . ....... 113 5.2 'Il1e 1\ utonotnic Nervous System ... .... 114 5.2a Sympathetic Division .. .................. 114 5.2b Part1sympathetic Division . ............... 115 5.2c Regulation qfthe Autonomic Nervous System .............. 116

6.2a Characteristic Symptoms ................ 6.2b Panic Disorder .......................... 6.2c Agoraphobia ............................ 6.2d Specific Phobia .......................... 6.2e Social.Anxiety Disorder (Social Phobia) .. . 6.2f Generalized Anxiety Disorder. ............ 6.2g Separation AJLriet_y Disorder .. . .......... 6.2h Selective Matis,n . . . . . . . . . . . . . . . . . . . . . . . .

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142 14 4

146 149

150 151 152 6.2i Other AJLriety Disorders . ................. 152

6.3 Obsessive-Con1pulsive and Related Disorders ........... . .......... 153 6.3a Obsessive-Compulsive Disorder .......... 153 6.3b Body Dytmorphic Di.~order. .............. 156 6.3c Hoarding Disorder ............ . .......... 157 6.3d Trichotillomania (Hair-Pulling Disorder). 158 6.3e Excoriation {Skin-Picking} Disorder ...... 159 6.3f Other Obsessive-Compulsive Related Disorders. ....................... 159

Chapter Review ............................. 160

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CHAPTER

8.4 Cluster C Personality Disorders ....... 209

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Somatic Symptom and Dissociative Disorders.......... ...... 164 7.1 Can Physical and Psychological Sympton1s Be Falsified? ............... 165 7.Ja Malingering ....................... •• .... 165 7.lb Factitinus Disorder ............. . .. •• .... 166

7.2 Son1atic Syn1pton1 and Related Disorders ................ •. .... 167

8.4a Avoidant Personality Disorder ........... 209 8.4b Dependent Personality Disorder . ......... 210 8.4c Obsessive-Compulsive Personality Disorder ........ . ............ 211

8.5 Other Personalitv Disorders ........... 213 • 8.5a Personality Change Due to Another 1Wedica/ Condition .............. 213 8.5b Other Specified Personality Disorder ..... 213

8.6 Considerations for the Future ......... 213

7.2a Somatic Symptom Disorder ........ . ..... 168 7.2b Conversion Disorder (Functional Neuro/()gical Sympton, Disorder) ......... 171 7.2c 1/lne..,s Anxiety Disorder . ........... . ...... 174 7.2d P,ychologica/ Factors Affecting Other 1\1edical Conditions . ..................... 176 7.2e Other Somatic Symptom Disorders . . ..... 176

Chapter Review .... ............ . ............ 215

7.3 Dissociative Disorders ................. 177

9.2 Sexual Dysfunctions ...... . ............ 224

7.3a Dissociative Amnesia ................ .. . . 177 7.3b Dissociative Identity Disorder .. . ... . ..... 179 7.3c Depersonalizatim1/ Derealization Disorder ........................... . .... 183

9.2a Female Sexual Interest/Arousal Disorder .. 225 9.2b 114ale Hypoactive Sexual Desire Disorder . . 226 9.2c Erectile Disorder. ........................ 226 9.2d Female Orgasmic Disorder .. . ............ 230 9.2e Delayed Ejaculation .......... . .......... 230 9.2f Preniature (Early} Ejaculation ............ 230 9.2g Gen/ta-Pelvic Pain/Penetration Disorder .. 232 9.2h Other Sexual Dysfunctions .. ... . ......... 232 9.21 Future Considera~ions in the Treatn,ent q(Sexua/ DysjU11ctions . .... 233

7.4 A Concluding Conunent ......... . ..... 184

Chapter Review ........... ............ .. .... 185 CHAPTER

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Personality Disorders............. .... 190 8.1 1l1e Concept of Personality ...... . ..... 8.Ja Assessments ofPersonality ......... •..... 8.Jb Categories or Dimensions? ............... 8.lc Classifying Personality Disorders ... . ..... 8.ld Treating Per.sonality Disorders ...........

191 191 193 193 195

8.2 Cluster A Personality Disorders .... . . . 195 8.2a Paranoid Personality Disorder . .... . ..... 196 8.2b Schizoid Personality Disorder ... ... . ..... 197 .~.2c Schizotypal Personality Disorder ... . ..... 198

8.3 Cluster B Personality Disorders ....... 199 8.3a 8.3b 8.3c 8.3d

Antisocial Per.sonality Disorder ..... . .... 200 Borderline Persorwlity Disorder .. ........ 205 Histrionic Personality Disorder........... 207 Narcissistic Personality Disorder . .. . ..... 208

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Sexual and Gender Disorders ...... 220 9.1 Hu1nan Sexual Flll1ctioning ........... 222

9.3 ParaphHic Disorders ................... 2.34 9.3a. Exhibitionistic Disorder.. ... •• .... • ...... 235 9.3b Fetishistic Disorder . ........ •• . ••• • ...... 235 9.3c Frotteuristic Disorder ... .... •• .. •• ....... 236 9.3d Pedophilic Disorder .......... . . •. . ...... 236 9.3e Sexual Masochisn, Disorder . . . . . •. . ...... 237 9.3f Sexual Sadl,m Disorder ... .. . .... •• ...... 239 9.3g Tra1tsvestic Disorder . .......... . •. ....... 239 9.3h Voyeuristic Disllrder .... .... . ............ 239 9.3i Other Specified Paraphili.c Disorder . ...... 240 9.3j Causal Factors .............. . ............ 240 9.3k Treatn,ent ofParaphilic Disorder., . ....... 241

9.4 Gender Dysphoria............ . . . ....... 243 9.4a Cau.,al Factors . . ........... •• .... • ...... 244

Chapter Review ............. . .. .••. . .. ...... 246

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Schizophrenia and Psychotic Disorders ................................. 250 JO.I Psychosis ...... . . . ............. . ....... 251 10.lll Disturbtlnces in Lllnguageand Thought .. 251 JO.lb Disturbances in Sensation and Perception . . . . .... .......... . ...... 254 JO.Jc Disturbances in 1\;fotor Behavior ..... . ... 255 10.Jd Emotional Disturbance ......... . ... . ... 256 JO.le Social IVitlulrawal ...................... 256

11.2d Pren1e11strual Dysphoric Disorder ....... 297 J J. 2e Other Depressive Disorders . ............. 298

11.3 Causal Factors in Depressive Disorders ...... ........... 298 11.3a Biological Component., ................. 298 11.3b Psychosocial Components .... . .......... 301

l 1.4 Treat,nent of Depressive Disorders . .. 305 11.4a J1.4b J 1.4c 11.4d

10.2 Diagnosis of Psychotic Disorders .. ... 256 10.2a Schizophrenia .......................... 257

Biological Tret1tme11ts.... . ... . .......... 306 Psychological Trea.tments . ... . ....... . .. 308 Other Treatmentsfor Depression . ........ 310 Summary of1ret1tment for Unipolar Depression . ................... 310

11.5

Bipolar i\tood Disorders .............. 311

10.2b Schizvphreniform Disorder ............. 260 10.2c Schiz,Jajfective Disorder. ......... . ...... 261 10.2d BriefPsychotic Disorder ............ . ... 261 J0.2e Delusional Disorder ............ . ... . ... 261

11.Sa Bipolar I Disorder ...................... J J.Sb Bipc>lar 11 Disorder. .......... . .......... J J.Sc Cyclothyniic Disorder . .... . ............. J J.Sd Other Bipolar Disorders...... . ..........

10.2/ Additional Psychotic Disorders ...... . ... 262

10.3 CausaJ Factors in Psychotic Disorders .............. . ... 263 J0.3a Biolagiclll Factors .............. .... . ... 263 10.3h 1he Searchfor Neurobehavioral Markers . .......... . ... 269 JO.Jc Environmental Factors . ................. 270 J0.3d Psychosocial Factors ............... . ... 271 J0.•1e Causal Factors in Psychosis: A Summary . . .......................... 278

10.4 Treatlnen t of Psychotic Disorders .... 279 J0.4a Biolt,gical Therapy. ..................... 279 10.4b Psychosocial 7herapy . .............. . ... 281 Chapter Review ............... ....... ....... 283

CHAPTER

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Mood Disorders and Suicide ... .... 288

311 311

312 313

l 1.6 Causal Factors in Bipolar Disorders....... . ............. 313 11.7 Treat1nent of Bipolar Disorders ...... 313 11.7a Meclica.t itm .. .. .......... ............... 313

11.7b Psychosocial Treatments ................ 314 11.8 Suicide ...................... ....... ... 315

J1.8a Psychological Correlates . ............... 316 11.Sh Risk Factor$ . ................... ..... ... 317 11.Sc Suicide Prevention ...................... 318 Chapter Review ............. . ......... ..... . 319

12 Substance-Related and Addictive Disorders........ ........... 321 CHAPTER

12.1 Substa nce Use Disorders .. . ....... . .. 326 12.2 Substance-Induced Disorders ........ 328

Jl.l Diagnosis of Mood Disorders ..... .... 289 J1.1a A1ood Episodes .. .. ............. ........ 289

J.2.2a Substance Intoxication ................. 328 12.2b Substance Withdrawal. ...... . .......... 328

Jl.2 Depressive Disorders ............. . ... 295 11.2a Major Depressive Disorder .. ........ . ... 295

12.3 Developtnent of Substance Use Disorders ............................. 330

11.2b Persi.ttent Depressive Disorder (Dysthymia) ... . .. ... .................. 295 Jl.2c Disruptive Mood Dysregulutum Disorder. 296

12.3t1 Causal Factorsfor Substance Dependence.... .............. 330 12.3b Biologict1l Components ................. 334

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12.3c Psycfwsocial Componerits ......... • ..... 335 12.3d Swrunary ........................ • ..... 338

12.4 Developtnent of Su bstance-1 nduced Disorders . . ..... 339 12.4a Alcohol-Induced Disorders .............. 339 12.4b Stimula11t-lnduced Disorders ..... •..... 341 12.4c Caffeine-Induced Disorders ....... . ..... 342 12.4d CaJ1nabis-Jnduced Dlhilippc Pincl B. Ivan Pavlov C. Sigmund Freud D. Rene Ocsc.a rtes

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Emil Kracpclin's third category. paranoia. occurred less frequently t han his other two symptom patterns and consisted of _ _ _ _ _ symptom(s). A. one 8. two C. three D. four

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Bcnjrunin Rush advocated all of the following as effective treatments of abnormaJ behavior. except ______ A. spinning patients on boards 8. laying on of hands C. bloodletting 0. tranquilizing chairs

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8.

Which of the following is true of general paresis? A. It is characterized by delusions of grandeur, dementia, and progressive paralysis and is caused by a sexually transmitted spirochete. B. It is a bizarre treatment for hysteria, from the early 1900s, in which individuals were exposed to blood infected with malaria. C. It is a symptom of dissociative identity disorder, caused by severe psychological anguish stemming from ritual abuse. D. It is an interesting side effect of hypnosis therapy, in which the hand or arm loses sensation and motor control while in the trance state.

9.

______ was a popular term in the late 1700s for procedures used to induce trances and other altered states of consciousness. A. Conditioni11g B. Mesmerism C. Autosuggestion D. Abasia

10. In hemia11estl1esia, the whole of one side of the body becon1es - - - - - · A. extremely cold B. overheated C. insensitive D. sensitive 11. Instead of being worried or depressed about their physical sy1nptoms, many hysterical patients appear calm and indeed quite cheerful in some cases, which is known a s - - - - - - · A. a characteristic of multiple personality disorder B. hemia11esthesia C. la belle indifference D. dualism 12. ______ is a learning process whereby a formerly neutral stimulus comes to elicit a respon se as a result of having been p aired with another stimulus that already causes that response. A. Generalization B. Opera11t conditioning C. Pavlovian conditioning D. General conditioning 13. Loud noises, such as his clock's a larm, cause Alvaro to startle into a state of high awareness. Just before the alarm goes off, the clock makes a light clicking noise, which initially Alvaro didn't even notice. Now that he has l1ad tl1e clock for some time, Alvaro has found that he startles into wakefulness when the clock makes the clicking noise, before the alarm even goes off. In this example, the unconditioned response is - - - - - - · A. the alarm B. the clicking noise C. being startled into a state of high awareness D. turning the alarm off

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14. _ _ _ _ _ occurs when Ute frequency and strength oftbc concLitioncd response tends to decrease. eventualJy to zero. after repeated presentations of

the conditioned stimulus without the unconditioned stimulus. A. GeneraJization

B. Discrimination C. Spontaneous recover)' 0. Extinction

15. Pavlovian conditioning focuses on t he stimuli that _ _ _ _ _ the response: operant conditioning emphasizes the stimuli that the response. A. follow / follow

8. precede / precede C. precede I follow 0. follow / precede

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CHAPTER OVERVIEW 3.1 Freud's Psychodynamic Theory ........ 49 Basic Features of Freud's Early Theory Anxiety and the Mechanisms of Defense A Theory of the Mind: The Higher-Order Abstractions An Illustration Childhood Origins of Neurotic Symptoms Psychodynamic Treatment Variations in Psychodynamic Approaches

3.2 Behavioral Approaches .................. 57 Operant Conditioning Operant Learning and Abnormal Behavior Behavioral Treatment Variations in Behavioral Approaches

3.3 Biological Approaches ................... 65 Heredity Research Methods for Studying Hereditary Influences The Human Brain Neurotransmission Biological Treatments

3.4 Humanistic--Experiential Approaches ........................... ..77 3.5 Approaching an Integrated Model ..... 78

CHAPTER OPENER QUESTIONS How does psychodynamic theory explain and treat psychological problems? What treatments have developed from the behavioral model? What is the biological perspective of abnormality? How does the humanistic approach differ from other perspectives? Can assessment of treatment outcomes contribute to a more unified framework?

Contemporary Framewor s C

hapter 2 traced the historical development of different models or paradigms of abnormal behavior. This chapter presents the current general models or frameworks of psychopathology. We begin with the framework developed from Sigmund Freud's perspective of the mind- the psychodynamic model-and its associated therapy, psychoanalysis. This framework becam e the first comprehensive theory for p sychology and psychiatry. The cardinal feature of the psychodynamic view is this: To comprehend abnormal behavior, one must understand the dynamic interplay of those intrapsychic events-motives, drives, emotions, fantasies, and conflicts-that underlie the surface manifestations of symptoms. Thus, psychological symptoms are seen as analogous to physical symptoms, such as fever, which can only be understood and effectively treated if the underlying disease process causing the symptom, such as an infection, is identified. Such a view clearly r epresents a variant of the illness metaphor. In this case, the underlying disease is not some physical lesion or infection but rather a pathological condition existing among the intrapsychic processes of tl1e mind- in short, a m ental disease.

3.1 Freud's Psychodynamic Theory A central idea in Freud's theory of psychological symptoms is that emotionally distressing past experiences may be put out of one's mind, or repressed, even as they continue to find expression in some manner, such as tl1rough bodily symptoms and altered states of consciousness. Freud came to view the mind as consisting of different "levels" of activity, with most of the action occurring outside of conscious awareness. Accordi11g to his depth hypothesis, the largest part of the mind is tl1e unconscious, ofwhich we are unaware and from which m aterial is normally unavailable. A much smaller part involves our conscious awareness and our psychological contact with the things around us. According to Freud's structural hypothesis, the mind can also be divided into three parts: tl1e id, which is concerned with basic instinctive drives of the unconscious; the ego, which serves to m ediate the expressions of the id in the real world; and the superego, containing our internalized values and corresponding to som etl1ing like a ''conscience." The relationship of these levels and structures of the mind can be illustrated by an iceberg metaphor: Only a sm all amount is easy to observe, while m ost exists subm erged and unseen (Figure 3-1).

3.1a Basic Features of Freud's Early Theory Unconscious Motivation In the course of working w ith m a ny patients, Freud elaborated on the basic them e of unacceptable impulses struggling for and finding expression in various disguises. He thus developed the concept of unconscious motivation, which he used to explain not only hyst erical and otl1er symptoms but also all manner of irrational huma n behavior. There is, in fact, nothing incomprehensible about any human behavior (according to Fr eud) once we understand the underlying unconscious motivation. All behavior is completely determined. A slip of the tongue, for example, is not a chance mistake but quite precisely reflects som e unconscious conflict.

Unconscious

In psychoanalytic tl1eory, that part of the rnind outside of conscious awareness, containing l1idden instincts, impulses, and 111e1nor1es

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50

Chaple< 3

Abnormal 1'$ychology

Figure 3·1 The Iceberg Metaphor of the Mind [emailprotected] Publ ishi ng

. , - - - - - --

Conscious - --t Mind Preconscious Mind

(111ternahzed ideals) Id (unconsoous psychic energy)

Austrian neur ologist Sigmund Freud. I he foun der of psych oanalysis (SiMm1md J.'n,ud Anau.oo by 04-rid Wd1b QV'ili lable m,dc,-• Cff'llih-e Comm,uw; AH.rihn:tion

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(Olltsade awareness but accessible)

Unconsdous Mind

Dreams. likewise. arc not nonsensical collections of images and feelings: they arc determined to the last detail by experiences of the recent and remote past. by w1.conscious motivations and connicts. and by defensive strategics designed to keep the dreamer unaware of the dream's-true"' meaning. According to Freud. most- perhaps all- dreams include clements of wish fulfillment.

The Sexual Basis of Psycholog1cal Sy1npto1ns As Freud helped patients explore further and further in to the hidden and disguised bases of their symptoms, it seemed that the trail inevitably led to a sexual conmct.. At first he thought that many. perhaps all. of his patients had actually cxperjenced in childhood sorne kind of sexual attack or seduction by an adult. which had caused the sexual conflict and its associated anxiety. Freud soon abandoned this theory and proposed instead that the patient as a young child had imagined that such events had taken place and, in retrospect. was unable to distinguish clearly between what had been wish and fear and what had. in fact. happened. ·m.e sexual basis ofsymptom~producing conflicts remained a cornerstone of Freud's theory and was the feature that provoked the strongest critical reactions. not only from the public at large. but from his professional colleagues as we.II. 1'o Freud's mind. the intensity and the irrationality of the attacks on him and his theory seemed to further prove the validity of his position. \t\lhy would people resist the idea so strongly ifit were not tapping their ow11 unconscious sexual conflicts?

Contempo,ary Frameworks

S1

111e Oedipal Conflict (t was not just any sexual conflict that seemed to be at the root of hysterical and othc.r symptoms. however. the sexual problem seemed to take a rather special form- the Oedipa..J conO ict. l n essence, the Oedipal conflict involves a sexual attraction to the othcr•scx parent, accompanied b)' feelings of competit ion and antagonism toward the same,.scx parcnL. as in the Greek rnyth of Oedipus. who, unaware of their true identity. slew his fatJ1er and married his mother. ·nlc Oedipal conflict (usually rcac.hing its peak around 4- 5 years of age) has no easy solution for the young child because the child cannot. in reality, affect a sexual liaison with the otber...sex parent nor vanqu ish the compeUtor- that is, the same•sex parent. 1he con nict is fu rthc.r fueled by fantasized elaborations. A boy, for example. may harbor death wishes against his father and begin. in turn. to imagine that his father wiU do bodily harm to him as a punishment for his (the boy"s) own impulses and fcclings.11le imagined harm at the hands of his father is likely to take the form of castration because it is sexual pleasure associated with his penis that is causing all the troublc.1lms. castration anxiety becomes a dri\li.ng force behind the Oedipal con Oict and its eventual resolution. lite young girl. discovering that she has no penis, assumes she has already been castrated. As a result. she experiences -penis envy.- which leads her to seek a man as a possessor of a penis. In her sexual desire for her father. her mother is her rNal. 1llc young child of either sex copes with this seemingly insoluble problem by pushing the whole thing- erotic interest in the othcr•scx parent. hostile wishes toward the samc•sex parent. and fears of retaliation- out of his or her mind. fn short. by repression. Normally. their sexual urges arc later redirected to others. and they may in the end marry someone like mom or dad. If children have had to deaJ with an especially intense QedjpaJ conflict, they are vulnerable in adolescence and yowlg adulthood. when the scxua] drive becomes increasingly intense. to rcarousals of the conflict and ineffective reprcssi\le defenses. 111e result. according to Freud. can be symptoms of psychological disorders.

3.1 b Anxiety and the Mechanisms of Defense In Freud's thinking. the motivation to avoid awareness and overt expression of unacceptable impulses came to center around the concept of anxiety.a powerful and unpleasant emotion thought by Freud to have its primitive beginnings in the infant's experience of being overwhelmed by uncontrollable stimulation. As the child grows older. anxiety begins to serve as a signal that warns of some impending danger. 111e danger may be internal. in the form of some disturbing instinctual impulse that threatens to break into awareness and possibly be expressed jn overt behavior. or external. such as a perceived threat of loss of love or physical injury from significant people in the. child's lifo.111c child then learns 1 \ arious strategies. known as d efense mech anisms. to prevent anxiety-arousing impulses from entering awareness or being overtly expressed in ,,1ays that might evoke retaliation (sec Figure 3 °2). Repression. the primary defense mechanism in Freud's early writ ing. is the unconscious but intentional forgetting of memories associated with anxiety-arousing impulses and conflicts. ln time. Freud expanded the concept of defense to incJude several other mechanisms in addition to the more basic one of repression. Reaction fo rmation represents an extension of the basic repressive strategy. In this defense. people take the additional step of believing and acting as though they were motivated to do just the opposite of the unacceptable impulse: A man behaves in a kindl)', considerate fashion when. in fact. he has an impulse lo be mean, sadistic. or cruel; a woman is excessively

Alber t Greiner as Oedipus in an 18% theatrical p roduction of OtdipusRe.i.. fOccbpu• by Alben Gremer Jr 11.,·llilllhlc under a Cre.11.h"' COllUtlOlUAltrihutioo L i e -

cc B\'·SA l.(I at hHp•:/1 COil! lll(!Cl$."''i ki med1a.o~' wik i/ tilc:Ot'dJpu•.JP\C}

Oedipal conflict In Freuclian theory, the erotic attachment to the other-sex parent. in\lolving feelings of competition and hostiLity toward the same-sex parent and fears ofretaJiation (castration anxiety in boys) from the samesex parent

Defense mecbanisrt1 In Freuclian theory, strategy whereby a person avoids anxiety• arousing experiences

Repression lJefunse mechanism in which the anxiety• arousing memory or impulse is prevented from becoming conscious

Reaction formation lJefunse mechanism in ,,,hich a person behaves in a way directly opposite from some underlying impulse

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Figure 3-2

The Purpose of Defense Mechanisms

Defense mechanisms serve to shield the ego from the harsh aspects of reality. Source: Adapted from Adjustment and Personal Growth, 2nd ed., by F. J. Bruno, 1983, New York, NY: Wiley. Copyright © 1983 by F. J. Bruno.

Defense Mechanisms

Isolation Defense mechanism in which a person separates emotional from intellectual co11te11t or otherwise separates experiences that would be anxiety arousing if permitted to occur together Displacement Defense mechanism in whicl1 tl1e person shifts a reaction from the original target person or situation to some otl1er person or situatio11 (e.g., anger displacement from boss to family) Projection Defense mechanism in which a person disowns son1e i1npulse and attributes it to another person Intrapsychic Unobservable mental eve11ts such as ideas,wishes,and unconscious conflicts Id In Freudian theory, that part of the mind from wl1ich instinctual impulses originate Ego In Freudian theory, that part of the mind that mediates between id impulses and external reality

Reality

Ego

neat, clean, and orderly, when underneath she wants to be messy and dirty; a person conducts a crusade against pornography to control (and, indirectly, to gratify) unconscious sexual interests. Reaction formations of this kind are likely to become long-standing character traits that color the whole personality. Isolation refers to isolating a memory or impulse in such a way that it no longer creates anxiety. The most common form this defense takes is the separation of an idea from its associated distressing emotions. The person may become able to tl1ink of this idea in a cold, emotionless way. An incest wish, for exa1nple, may be experienced as an abstract, intellectual idea, bereft of both the attracting and repelling emotions previously associated with it. In displacement, a disturbing emotion or conflict is transferred from its original source to some less threatening object or situation. A fear of castration might be displaced to a fear of dogs, for example. 111 projection, the person disow11s some impulse or attitude and projects it onto another person. "It's not I who am filled with a murderous rage against you; it's you who have it in for 1ne." "It's not I who have a homosexual attraction for you; it's you who are making homosexual passes at me." The defensive aim of such a mechanism is clear. This list of defense mechanism s is not complete. In fact, there is no one standard list. Different psychoanalytic authors put together various combinations of ways in which people defend against unacceptable impulses. What is agreed is that it is normal, even healthy, for people to make use of defenses-up to a point. However, excessive use of defenses interferes with healthier methods of coping and functioning in the face of life's demands.

3.lc

A Theory of the Mind: The Higher-Order Abstractions

Psychoanalytic theory is not so mucl1 concerned with overt behavior (what people do) as with what they think and feel. The basic inquiry of psychoanalysis is: What are the 1nental events-the i11trapsychic processes-that help us understand other mental events such as dreams and anxieties? As Freud's theory developed further, some aspects beca1ne quite abstract and complex.

The Structure of the Mind Superego In Freudian tl1eory, the i11ternalized representative of pare11tal or cultural values

As noted earlier, Freud proposed tl1at the mind could be conceptualized as consisting of tl1ree primary parts: the id, which is the source of basic insti11ctual drives seeking immediate gratification; the ego, which attempts to mediate between the urgings ofthe id and the demands of exter11al reality; and the superego, an internalized and partially irrational representation of parental or cultural values (see Table 3-1). 1l1e ego, according to Freud, governs such processes

Contempo,ary Framewo,ks Table 3-1 Structure

SJ

Mental Structure Accord ing to Freud Contents and Fu nctions

Consciousness

Id

Unconscious

Basic impulses (sex and aggression): seeks lmmediate gratification. regardles.-; of consequences: impervious to reason and logic: immediate. irrational. impulsive

£go

PredominanlJy conscious

Executive mediating between id 1mpulse·s and superego inhibitions: tests. reality: seeks safely und survivnl: rational. log1caJ. takes account of space and time

Supereg o

Both conscious and unconscious

(deals and morals: strh·es for perfection: observes. dictates. criticizes. and prohibits: imposes limitation.son satisfactions: becomes the conscience of the indh'ldual

as perception. learning, a nd thinki ng. whereby the person regulates the commerce between the id's imp ulses a nd reality: it also includes t hose mechanjsms of defense already described. 1hc s uperego was t hought to develop prima riJy in the course of resolution of t he Oedipal conflict. when children incorporate or internalize their irrational percept ion of t he same~sex parent. 'Otis internalization is another kind of defense mechan ism in which the ch i]d identifies with t he same~sex parent a nd thereby avoids his or her displeasure- a strat egy of~(fyou can't beat 'em. join 'em:· 111creafter. this internalized parental representa tion becomes a source of praise or condemnation: it becomes, in other words. one·s conscience.

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The Libido One of Freud's most radical notions was that aJI motivation. o ther t han a few simple physiologicaJ d rives such as hunger and thirst. arises from the sexuaJ instinct. or t he libid o. Many fo rms of beh avior t ha t, on th e surface. seem to have nothing to do with sex. Freud considered sublimated expressions of the libidinal instinct. ~Illus. a scientist's c u riosity a bout t he workings of nature might be considered to re flect a sexu a l curiosity t ha t has been redirected to a more socially accepta ble and reward ing area of investigation. 111e motive is descxuo.lized. or changed so tha t it is no longer recogn ized as sexual. Sublimation is considered a psychologically healthy mech anism since it aJlows relatively fu ll expression of the underlying instinctu aJ e nergy. Later, Freud recognized the death inst inct (tha.natos) as a second major motivational system, accounting for aJI destructive b ehavior. whether people directed it against themselves or others. Not a lJ or Freud ·s colJcague-s. however. were willing to accept the existence of a n independent death jnstinct.

Stages of Psychosexual Deve/optnent AccorcHng to the psychoana.Jytic t heory of personality development. the individuaJ progresses th rough certain biologicall}•dctc.r mined stages of psychoscxual development in which t he basicsex-ua l instinct or libido see.ks gratificat ion via oral. anal, a nd genital zones of t he body (sec Table 3-2). 'the genital stage can be subdivided into t he phallic .~tage, corresponding to the Oedipal period from ages 4 to 6: the latency period. starting with the rep ression of all

Table 3-2 Stage

Freud's Stages of Psychosexual Development Time Span

focus of Sex ual GnUfic.a tion

Oral

Birth tJ-iough first 12-18 months

Ups and mouth

Anal

12-18 monlhs lo age 3

Anal are.a

Phallic

Age 3 lo ag-e 5-6

Genitals

Latency

Age 5 o r 6 to p uberty

No focus-sexual dn\-es unexpressed

Genital

P'rom pubert}•on

Sexual relabons with people outside lhe family

Libido

Psychoanalytic concept reforring to scxuaJ instincts

Sublin,ation lJefunse mechanism in which sexual instincts are rcchannelcd into substitute activities

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sexuality as a way of coping with Oedipal conflict and lasting u11til adolescence; and then the adult genital stage, in which the libido finds expression in a m ature heterosexual relationship. Fixations at and regressions to tl1ese various st ages of development influence later personality traits, including features of abnormal symptomatology. Fixation r efers to an undue investment of the sexual instincts at one of these stages of development-for example, oral fixation would tend to involve a conti11uing i11terest in oral activities such as the ingestion of liquids and sucking or chewing on objects. An anal fixation might involve excessive interest in messy, dirty activities (because of their symbolic relation to the process of defecation) or in "bathroom" l1umor. Fixations are thougl1t to occur because the p erson h as been either overindulged or unduly deprived of gratification at a particular stage. If persons are later frustrated or otherwise experience stress at a more "m ature" level of psychosexu al development, they are likely to regress to the stage at whicl1 they had previously become partially fixated. In the face of difficult life circumstances, for example, a person orally fixated might regress to oral sources of satisfaction and eat or drink excessively. The anal character is commonly thought to show stinginess (related to anal retentiveness), stubbornness (related According t o Freud's theory, a habit of anxious nailto opposition to bowel training), and compulsive orderliness and biting could be considered a form of oral fixation. (Shutterstock) pedantry (reaction formations against urges to be messy and sloppy).

3.ld

Fixation In Freudian theory, an unusual investment of libidinal energy at a certain psycl1osexual stage Regression In Freudian theory, a return to some earlier state of psycl1osexual development in the face of some current frustration Phobia Strong, irrational fear of so1ne specific object, ani1nal, or situatio11

An Illustration

An example of Freudian analysis in tl1e case of anxiety is "Little Hans." Hans was a 5-yearold boy who had developed a phobia (a fear) of going out in tl1e street b ecause a horse might bite him. Freud described his analysis of the cause of the phobia in his paper, "Analysis of a Phobia in a Five-Year-Old Boy" (Freud, 1909/ 1955). Most of Freud's information came not from Hans but from the boy's father, who sent detailed correspondence weekly to Freud about the situation and its background. Freud's report on t he case ran 140 pages; it will b e only briefly described h ere. Tracing the origin of the phobia required a complete history from Hans's father about the boy's developing sexual interest. At age 3, Hans began sh owing interest in his p enis (which he called his "widdler"). On one occasion, Hans was discovered tou ching his widdler by his mother, who responded by telling Hans that if h e did not stop playing with it, he might be sent to a doctor to "h ave it removed." Still, Han s's interest in his genital area continued. He admitted to playing with his widdler in bed at 11ight b efore going to sleep. He 11oticed that his sist er did not have a widdler, and t his was puzzling to him. At age 4, after a bath , Hans's 1nother was drying him and powdering him, carefully avoidin g touching l1is penis, when Hans said, "Why don't you put your finger h er e?" His mother r esponded that "it wouldn't be proper," to which Ha11s replied witl1 a laugl1, "But it would b e great fun!" Talking with his father, Hans sought to learn more about widdlers. He noted that animals h ad widdler s, and large animals had large ones. He assumed that his fath er had a large widdler too. In fact, Hans told his father about a horse h e had seen that h ad a large widdler. Horses were fan1iliar objects on tl1e Vienna streets at the ti1ne, and Hans saw tl1em frequently. Recently, Ha ns had been warned by his nursemaid to be careful around a large white horse because it might bite his finger. As the phobia deep en ed, Hans was afraid that a horse might come into his room and bite him. In addition to tracing the developments of the situation through the father's letter s, Freud interviewed Hans in his office. Asked what it was about horses that frightened him, Hans said h e was afraid of what horses wore around their eyes and the black thing around their mouths. He also recalled an accident involving a horse that had fallen to the ground, kicking; Ha11s was afraid the horse was dead.

Contemporary Frameworks

Freud's analysis ofHans's fear followed directly from his views on the Oedipal co11flict. Hans's fear of horses was symbolic of his unconscious fear of his father. His seductive episode after his batl1 revealed his sexual desire for his mother, whose remark about having his '"riddler removed only heightened his castration anxiety and fear of his father, whose widdler was larger. The things that horses wore around their eyes and mouth, which Hans found so frightening, symbolized his father's eyeglasses and moustache. Freud's conclusion was that the phobia had developed as Hans repressed these unacceptable feelings about his father a11d displaced them onto horses instead. Once the true nature ofhis fear was revealed to Hans, Freud reported that the child becam e less anxious and developed into a "cheerful, good-natured" boy.

3.le

Childhood Origins of Neurotic Symptoms

Neurotic (tl1at is, a nxiety-drive11) symptoms, according to Freud, r esult from the interplay b etween instinctual impulses striving for expression and defensive strategies. The key to understanding the strength of the forces involved lies in an appreciation of their early childhood origin, as the case of"Little Hans" illustrates. The conflict underlying hysteria, for example, is not between som e adult sexual urge and some adult view of ethics and morality. While this m ay indeed be a source of co11flict and stress, it does not result in the severe incapacitation of neurotic symptoms. Some t emptation, rejection, or other stress in the current life situation usually does precipitat e the disorder; however, its crucial feature is a rearousal of urges, fantasies, and fears Freud believed the key to under standing neuroses was to from early childhood, a time when loss of parental love or determine their early childhood origin. (Shutterstock) threats of punishment were experienced as catastrophic events. The defenses used to cope with these reawak ened emotions are likewise not adult modes of handling psychological problems but those used by the young child in a desp erate attempt to cope with what, from a child's view, are matters of emotional life or death.

3.lf

Psychodynamic Treatment

The psychoanalytic techniques that Freud introduced have been modified over the years but are still used in their general for1n by various psycl1odynamically oriented therapists. The goal of psychoanalysis essentially remains the sam e: to make the unconscious conscious, as a way to facilitate greater understanding and insight into the self. Through the relationship between therapist and patient, conflict s can be revealed, How does psychodynamic emotions can be experienced, and the patient can theory explain and treat b e changed, through n ew insights, in positive ways. psychological problems? Although Freud originally used hypnosis as a tool to connect with the patient's unconscious, h e soon found that inducing a trance state was not necessary. He instead developed his method of free association, in which the patient is instructed to express whatever com es to mind, no matter how seemi11gly irrelevant, trivial, or embarrassing. Rather than actively organizi11g thoughts, the patient is encouraged to adopt a passive attitude-reporting the ideas, feelings, and images that come into awareness as though they were scenes observed from a train window. Freud did not expect the patient to b e able to comply fully with this instruction; sooner or later the patient drew a blank, began to m ake well-planned sp eeches, got into disputes with the therapist, or in many other ways resisted the basic rule of free association. Resistance, as this is called, became a primary focus of attention for the therapist, who then attempted to h elp the patient through su ch resistances by interpretation. Since the way a

Free a sso ciation Basic procedure in psychoanalysis in which the patient is asked to say, without ce11sorsl1ip, whatever comes to mind Resis ta nce

In psychoanalysis, the phenome11on in which patients unconsciously resist gai11ing insight into unconscious motives and conflicts

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Abnormal Psychology

patient resists is likely to reflect styles of ego defenses used in other situations, insight about these resistances is considered an important tl1erapeutic benefit. Dreams were also viewed as ,-vindows to the u11conscious. Freud eagerly sought reports ofpatients' dreams for interpretation of symbols, since ego defenses disguised unacceptable impulses symbolically before allowing them to enter conscious11ess by way of the dream state. The content of dreams, therefore, seemed to provide much valuable information about the sources of conflicts and anxiety hidden deep within the patient's n1ind. Within the intimacy of the therapeutic relationship, the patient often begins to interact with tl1e therapist in ways similar to how the patient reacted to important persons from childhood or later life. Transference involves the projection of thoughts and feelings from these otl1er relatio11sl1ips to the therapist; in essence, the therapist becomes, in some ways, the mother, father, son, lover, or judgmental authority for whom the patient harbors strong feelings and impulses. Psychodynamic therapists do not try to avoid transference; on the contrary, they expect and welcome it as an opportunity to help a patient work through relationships with an absent significa nt figure. Transference and countertransference (that is, the therapist's reaction to the patient's projections) become important tools for insight therapy.

3.1g Variations in Psychodynamic Approaches

Swiss psychiatrist Carl Jung (Getty Images)

Transference

Irrational emotional reaction of a patient to the tl1erapist (usually in psychoanalysis) in which early attitudes toward parents are "transferred" to tl1e therapist

As with a11y movement-whether intellectual, political, or religious-in which individuals propound points of view radically different from the prevailing beliefs, a band of followers developed a round Freud, devoted to protecting the embryonic psychoanalytic movement fro1n the attacks of the establishment. Just as inevitably, there emerged splinter groups and individuals who disagreed ,-vith the developing orthodoxy of psychoanalytic theory. The universal role of sexual conflict in the causation of neurotic disorders was the point on which a number of early adherents began to disagree. Since this proposit ion was based on interpretations of memories, dream s, and so on provided by patients in the course of treatment, it could not be proved or disproved with any finality. Other analysts began to believe that the symptoms produced by their patients could be interpreted differently. Alfred Adler, for example, came to believe that it was not sexual conflict that lay bel1ind neurotic symptoms but conflicts revolving around needs to dominate or triumph over others. The free associations of his patients seemed always to lead to a central problem in which they were striving to be superior as a way of compe11sating for underlying feelings of inferiority. Carl G. Jung also doubted that all human motivation could be traced to sexual urges, and he questioned whetl1er all significa nt personality characteristics were essentially molded in the first 5 years of life. Jung went on to emphasize the unconscious as an energy source from which positive, creative acts arose as well as lusts a nd meanness. He also had a strong mystical bent, reflected for example in his theory of the collective or racial unconscious-the idea that all humanity shares certain racial memories. These common racial memories, according to Jung, are expressed sy1nbolically in the mythologies of all present a11d past cultures. Both Adler and Jung broke with Freud and developed their own movements, known respectively as individual p sychology and analyticalpsychology. Other individuals developed their own brands of neo-Freudian theories, most rejecting Freud's exclusively sexual interpretation ofhu1nan motivation and his overly restrictive vie,-v of biologically determined stages of psychosexual development. Neo-Freudians-such as Harry Stack Sullivan, Karen Horney, and Erich Fromm-put more emphasis on the social environment as a det ermina nt of personality developm ent. Sullivan, for example, became kno,-vn for his interpersonal theory ofpsychological disorders, supplementing the Freudian

Contemporary Frameworks

preoccupation with intrapsychic dynamics with an equal concern about who is doing what to wl1om in the external world of social interaction. Horney believed that most neurotic disorders could be traced back to a basic anxiety that has its origins in early childhood. She argued that all children develop aggressive or hostile impulses toward tl1eir parents because of the inevitable frustrations tl1at even the best-intentioned parents impose. This hostility can produce strong basic anxiety over the possibility that children may alie11ate their parents by some hostile or antagonistic expression and thus find tl1emselves deprived of love, their only source of acceptance and nurturance. Growing children, and even adults, engage in all manner of protective maneuvers to ensure that this does not happen. For example, they become overly dependent, submissive, placating, achieving, or competitive to guard against this loss. More recent extensions of psychoanalytic thought include object-relations theory, wl1ich analyzes psychological problems in terms of how features of a person's prese11t life symbolize the early social bonds formed by the developing child. These early relationships are internalized; in future relations, the person projects the internalized object-for example, the good mother, the demanding teacher, the loving child-onto the situation, effectively reliving the object relations of childl1ood in the present. The therapistPsycl1ologist Karen Horney b elieved t h at most neurotic patient relationship is seen as a symbolic expression of what disorders could be traced lJack to a basic anxiety tl1at has it s is pathological in the patient's life and, therefore, tl1e avenue origins in early childl1ood. (Shutterstock) to produce change. Althougl1 psychoanalysis is not as dominant in the treatment of abnormal behavior as it once was, it and its derivatives retain a significant following. The impact of its concepts has historically been stronger in psychiatry than in psychology, presumably because Freud trained as a physician. In fact, for most of the 20th century, advanced psychoanalytic training was available only to students admitted to medical schools-a situation that was not resolved until the 1980s, when the American Psychological Association won a lawsuit opening psychoanalytic institutes to psycl1ology students as well. Because its ter1ns do not easily lend themselves to precise definition, objective measurement, or scientific evaluation, psychoanalysis has not compiled a strong research base of support. Its influence, l1owever, can still be widely felt in psychology, and its rich and complex symbolism continues to fascinate philosophers, artists, and writers.

3.2 Behavioral Approaches The work of Ivan Pavlov in Russia began to attract the attention of U.S. psychologists in the early 20th century. At the time, the common approaches used by psychologists in research and therapy-introspection and psychoanalysis-were under attack by some researchers as being too u11reliable and subjective. One of these critics i11 particular, John Watson, claimed that psychology would never achieve scientific status by using these techniques. Watson, the leading psychologist in America at the time, knew of Pavlov's conditioning studies, and he saw the value in applying this consistently objective, measurable scientific methodology to the study of human bel1avior. Watson outlined such an approach, which he called behaviorism, and promoted it extensively as the only scientific path open to psychologists: Psychology as tl1e behaviorist views it is a purely objective experimental brancl1 of natural science. Its theoretical goal is the prediction and control of behavior. Introspection forms no essential part of its methods, nor is the scientific value of its data dependent upon the readiness with which they lend themselves to interpretation in terms of consciousness. (Watson, 1913, p. 158)

Behavioris m

An approach to understanding behavior that emphasizes tl1e relatio11 between observable behavior and specifiable environmental events (or stimuli)

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Abno rmal Psychology

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B. F. Skinner, founder of behavior analysis (B. F. Skinner at Harvard circa 1950 by Silly rabbit, available under a Creative Con1n1ons Attribution License CC BY 3.0 at https://commons.wikirnedia. org/ wiki/ File:B.F._ Skinner_at_ Ilarvard_circa_1950.jpg)

Watson's view was that tl1e principles of conditioning could explain all behavior, both normal and abnormal. The powerful laws of learning seemed to him a much more reasonable foundation for the developing science of psychology than the subjective a nd untestable concepts proposed by Freud. Watson set out to demonstrate this idea in experiments, including a famous example involving the development of a phobic response in a young boy, "Little Albert" (Watson & Rayner, 1920). Albert was reportedly a 11or1nal, ll-mo11th-old boy with no unusual characteristics or behaviors. In the experiment conducted by Watson and his graduate student Rosalie Rayner, the boy was shown an array of objects, most of them furry, such as a white rat, a rabbit, a dog, and cotton. Albert showed no signs of fear in their presence. To induce fear, the investigators used an unexpected loud noise produced by striking a steel bar with a ha1nmer closely bel1i11d the infant. In the first session, the bar was struck on two occasions when Albert reached out to touch a white rat. TI1e loud noise startled Albert a nd caused him to jump and whimper. A week later, five more paired presentations of rat and noise were given. On the eighth trial, the rat alo11e was presented, and Albert im1nediately bega11 to cry and to crawl away rapidly. In conditioning terms, the loud noise was the unconditioned stimulus, and the startle reaction was the unconditioned response. After being paired with tl1e loud noise, the rat became the conditioned stimulus, eliciting the conditioned response of fear. Five days later, Albert was tested for generalization of the fear response. He played as usual with wooden blocks, showing no sign s of fear. When the rabbit was put in front of him, he responded at once-leaning as far away from the animal as possible, whimpering, and finally bursting into t ears. Albert showed similar, though not as strong reactions, to the dog, cotto11, and other furry objects, sucl1 as a Santa Claus mask. Albert had acquired a phobia of white rats and related furry objects by a simple process of classical conditioning. Subsequent research using different methods also supported a conditioning model for the acquisition of phobias. For example, in a much later experiment, Campbell, Sanderson, and Laverty (1964) used drug-induced respiratory paralysis with volu11tary subject s. They found that with just one pairing of this l1orrific experience witl1 a tone, indications of fear, such as palms sweating and cha nge in heart rate, became conditioned to the tone and showed no signs of extinguishing over a 3-week p eriod and 100 presentations of the tone by itself. There is much indirect and anecdotal evidence to suggest that fear responses do, indeed, becom e associated with previously neutral stimuli on the basis of a few fear-arousing experiences. Some young children's reactions to the white-coated doctor from whom they have received shots on previous occasions are well known to m any parents. Individuals who develop intense fear about riding on trains, cars, or motorcycles after having experienced one accident are other examples. It seems likely, then, that some fears can be learned by classical conditioning. In fact, Wolpe and Rach man (1960) reanalyzed Freud's case of "Little Hans" and suggested that this celebrated example of a phobia could also be explained by a simple conditioning account. Clearly, Watson's approach to the study of anxiety was very different from that of Freud. Th e version of behaviorism promoted by Watson was incomplete because he relied solely on classical conditioning as an explanatory m echanism and because he downplayed biological contributions to behavior, largely in reactio11 to tl1eir overstated role proposed by instinct theorists of the time. Still, Watson's attempt to promot e a rigorous and objective approach to the study of behavior was groundbreaking a nd provided a n enticing and parsimonious alternative to psychodynamic theory.

3.2a Operant Conditioning The behavioral model was expanded and significantly strengthened by anotl1er U.S. psychologist , B. F. Skinner (1904-1990). In his book, The Behavior

Contemporary Frameworks

59

of Organisms (1938), Skinner recognized two basic and distinct learning processes: classical conditioning, which concerned reflexive or elicited behaviors, and operant conditioning, which involved "voluntary" or emitted bel1aviors. The latter derived from Thorndike's "law of effect," which was restated to eliminate subjective experience, so that satiefi,ers and annoyers became reinforcers and punishers-that is, they were defined by their effect on behavior. Skinner created a laboratory environment (still called a Skinner box) to initially focus his approach, which he termed "the experimental analysis of behavior," on simple activities sucl1 as lever pressing by rats and key pecking by pigeons under controlled environmental situations. The animal subjects were placed inside the apparatus, which automatically recorded the target responses and provided access to food or water contingent on responses occurring at certain ti1nes, such as wl1en a light was illuminated. By systematically manipulati11g different components of the experimental procedure, he was able to describe lawful relationships between behavior and its consequences and to produce and control patterns of responding. Although Skinner began his work on the simple, observable responses of animals, he made it clear tl1at he intended to expand his analysis of behavior to complex l1uman activities, including language, and to internal or private events such as feeling and thinking. He considered the barrier of the skin to be unimportant in terms of the law of effect and viewed thoughts and beliefs not as causes of behavior but rather as behaviors themselves, evoked by the environmental co11text and shaped (that is, influenced and directed) by their consequences. The essence of operant conditioning is that the organism learns to make a response that operates on the environment so as to produce some consequence favorable to the organism. Skinner and others have used the term reinforcement to refer to a co11seque11ce that strengtl1ens or increases the likelil1ood that a response will be repeated. Some consequences are almost universally reinforcing: water when thirsty, food when hungry, sleep when tired, and sexual activity after deprivation. These biologically important consequences are called primary reinforcers, and hun1ans share similar sensitivities to these types of consequences. Other reinforcers, however, such as money, praise, and social status, are called secondary or conditioned reinforcers, which are established by their association with other reinforcers. Different types ofconsequences weaken or suppress the behaviors that produce them, and these are called punishers. Punishers can also be primary or secondary. A primary punisher (or aversive stimulus) is electric shock, for example, while a secondary punisher might be criticism or disapproval. There is no sure way of knowing whether a given consequence will, in fact, be reinforcing or punishing for a given individual, but this does not matter for the behavioral approach. Reinforcement simply involves a consequence that increases behavior, and punishment involves a consequence that decreases b ehavior. Because they have had different learning histories, people differ in the sorts ofsecondary reinforcers and punishers that affect them. The value of a reinforcer also changes due to satiation and deprivation conditions, its delay in time, and the momentary context of other available reinforcers. In addition, internal events can serve as reinforcers and punishers. For example, feelings of envy, a fond recollection, a sense of accomplishment, or relief from pain could weaken or strengthen the activities that produced them. We ca.n further organize the effect of consequences by considering wl1ether the behavioral contingency involves the presentation of something or the removal of something. When behavior i11creases because of the presentatio11 of a positive result (such as winning a jackpot after placing a bet), it is positive reinforcement (we become 1nore likely to gamble again in the future). When behavior increases because of the removal of som ething unpleasant, the result is called negative reinforcement. For example, if taking aspirin relieves a headache, we become more likely to use aspirin again in tl1e future. On the other l1and, after receiving a painful burn from a hot stove, we are much less likely to touch it again; the presentation of pain is a punisher for that response. A final type of punishment involves the loss of sometl1ing positive. For instance, a traffic fine for speeding entails the removal of money; once having paid the fine, we are less likely to commit the same offense in a similar setting in tl1e future. These relationships are illustrated in Table 3-3.

Reinforcement Consequence that strengthens the future probability of a response that produces it Primary reinforcer Event, usually biological i1111ature, that almost always provides reinforcement, such as eating when hungry (Primary reinforcers do not acquire their rei11forcing properties througl1 learning.) Conditioned reinforcer Consequence that has gained ITS reinforcing value by being paired with other reinforcers Punisher Type of consequence that weakens or suppresses the beha,riors that produce it Contingency The specified dependency between a behavior and its antecedents a11d conseq t1ences

Positive reinforcement The contingent presentatio11 of a pleasant result, which strengthens stibsequent responding Negative reinforcement The conti11gent removal of an unpleasant sti1nult1s, wl1ich strengthens stibsequent responding

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Another important concept in the oper a nt learning model is the discriminative stimulus. What the organism learns is not just to make a r esponse but also to make it only under cer tain circumst ances. For example, people learn to tell humorous off-color jokes, but not in church, where such activity often earns disapproval. Similarly, touching a hot stove is punished unless we are using a protective oven mitt so that a bur11 would 11ot occur. The settings or situations signaling that r esponses are likely t o produce reinforcing outcomes are called discrim inative stimuli, and they serve t o guide our actions. Although we quickly learn to discriminate (that is, to distinguish) the particular setting in which a response will produce reinforce1nent from the setting in which it will not, we can a lso gener alize our operant resp on ses to simila r situations that we've never encountered before. So, based on only a few experiences, we may learn how to operate any type Careft1l bala11cing of your ba11k account is 11egatively of automobile or not to trust any stranger. As generalization reinforced because overdraft fees are avoided. (Shutterstock) proceed s, our responses may become topographica lly varied while remaining functionally similar; they 1nay for1n generalized resp onse classes (such as "making excuses" or "telling jokes"), which include many different specific activities that achieve similar reinforcing functions.

Three Levels of Selection

Dis criminative stimulus

A stimulus that serves as a signal that a certain response will lead to a rei11forcer

Thorndike had originally assumed that the typ e of learning he studied in the puzzle box was the result of selection by the environment- that is, behavioral variability was present , and environmental consequences selected the effective actions and eliminat ed ineffective ones. In a classic paper, Skinner (1981) furt her developed this idea. Specifically, he proposed that operant conditioning and 11atural selection were actually the sam e process, operating over different time spans and on different asp ect s of the organism. He called that process selection by consequences. In natural selection (or Level 1 selection), many variations exist b et ween organism s within a species. Some are larger, heavier, faster, or n1ore sensit ive to light; some have different m arkings or colors. If any variation provided an advantage, however slight, to an organism in terms of succeeding at r eproduction, that advantage could be passed on to offspring. Over time, the adva ntageous t rait would becom e more common in the population, and event ually tl1e sp ecies would become different from their ancestors. Said another way, tl1e consequence in natural selection is reproduction, and the effect is that organism s are slowly modified in ways that m ake r eproduction more likely. The unit of this level of selection is the gene; given enough time (perhaps hundreds or thousands of generations), the result is evolution, or a change in species. In the case of opera nt conditioning (Level 2 selection), variations also exist within tl1e behavioral rep ertoire of an individual organism. If any behavioral variation provides a n advantage in acquiring reinforcem ent or avoiding punishment in a par ticular situation, that behavior will become 1nore likely the next time a si1nilar circumst ance occurs, a11d other competing actions will become less likely. In t ime, the overall pattern of behavior is altered

Table 3-3

Basic Contingencies of Operant Conditioning Consequence Involves Presentation of Stimulus

Consequence Involves Removal of Stimulus

Stimulus is pleasant.

Positive reinforcement

Punishment

Stimulus is aversive.

Punishment

Negative rei11forcement

Contemporary Frameworks

by the result. The consequence of operant conditioning is reinforcement, and the reinforcing environment modifies an organism's actions to make certain behavior more likely. The unit of this level of selection is individual behavior, and on this time scale (1noments), the result is a change in the repertoire of activities the organism displays. A third level of selection is cultural selection. Variations exist within the practices of a culture or social group-such as in language, religion, business, politics, scientific research, or the practice of medicine. If a cultural practice provides an advantage to the group in ter1ns of maintaining its survival or stability in tl1e face of challenges, that variation tends to be maintained. Cultures that provide effective educational practices, for example, are more likely to continue than those that do not. The consequences of selection at this level include the strengthening of tl1e cultural practice. On this ti1ne scale (decades or centuries), the result of selection is the emergence and evolution of cultures. According to Skinner, the 1nechanism for these three levels of selection is the sa1ne: selection by consequences. On the shortest time span, individual behavior is modified. On a longer ti1ne span, cultures are modified; and given enough time, species are modified-all by the consequences that variations have produced. Since humans have been on this planet for many thousands of years, Skinner proposed that any co1nplete explanation of l1uman behavior and of human problems always involved an appeal to all three levels. As one example, consider the problem of overconsumption of calories and the resultant obesity that we see in the United States at this time. At the species level (Level 1), humans have inherited genetic attributes that make us susceptible to sweet and high-fat foods and that provide ways to store excess calories in the body in the form of fat. Presumably, this is adaptive because our ancestors had to endure ti1nes of limited food availability or fa1nine. At the individual level (Level 2), we have learned particular food preferences and how to accumulate tasty foods for quick consumption or easy preparation; to modify their flavors with condiments and dressings; and perhaps to follow the meal with delicious, high-calorie desserts such as ice cream. We have also learned to eat while doing other thi11gs and to snack-both to satisfy hunger and as a way to pass tl1e time or perhaps to enhance an activity such as viewing a movie. At the cultural level (Level 3), we are exposed to constant promotions for fast food and sugary treats and find opportunities to consume large portions ofhigh-calorie, high-fat foods on every highway and in every shopping mall in every town in the country. Fast foods are easy to consume because the culture keeps them inexpensive, conve11ient, and readily available; so it is much easier to order a burger and fries than it is to cook a healthy meal. The result of selection on these three levels is a dramatic increase in the percentage of the U.S. population that is obese. Similar analyses could be made for alcoholism, pornography, and aggression. To Skinner, then, the origin of behavior is the same as the origin of species: variation and selection. However, we are not yet able to intervene effectively in the selective process at the genetic level. In the case of obesity, we cannot change the genome of obese persons. Intervention at the cultural level is possible, but much time and effort is required to alter our fast-food culture, and economically powerful institutions, such as the food industry, would likely At the cultural level, we are exposed to constant pro1notions resist the effort. Only at the individual level can we quickly for fast food, sugary treats, and alcohol. The result is a and effectively intervene by shaping different eating habits dramatic increase i11 the percentage of people wl10 are obese and food choices. Thus, operant conditioning provides the or who drink frequently. (Shutters tock) most effective way to change behavior.

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3.2b Operant Learning and Abnormal Behavior RcversaJ design An experimental design in which

new reinforccme.11t contingencies arc instated for a period of lime. foUowed by reinstatc.mcnt of the old reinforcement contingencies. and

finally the installment ofthc origmnl. new con ti ngcncies (Sometimes a fourth reversal is included to show that the new contingencies arc causing any observed changes in beha\.";or.)

Although Skinner himself did not work in the area of abnormal behavior. many other investigators have used the operant model as a way of understanding the development of abnormal reactions and as a basis for devising treatment proccdurcs.111eir basic assumption is that abnormal behavior is shaped because it produces reinforcing consequences in some way: thus. it should be subject to unlearning ifU1c setting conditions and consequences arc appropriately changed. From this point of view, children may develop strong and recurrent temper tantrums because such behavior is reinforced by parental attention or by giving in to the child's demands. A depressed person who expresses feelings of worthlessness and preoccupation with physical complaint.~ may be reinforced because his family comforts him at these times. An alcoholic may escape from strcssors in life. ach ieve a temporary sense of enjoyment. and avoid unpleasant withdrawal symptoms by continuing to drink. lhc most impressive demonstrations of the power of external consequences to influence our behavior arc experimental studies in which the investigator changes U1e consequences in such a way that old behavior is eliminated and new behavior is instituted. (n a rcvcrsaJ design, the e..xperimentcr subsequently reinstates t he original consequences and observes whether the fom1er behavior returns.1l1en the new consequences arc put into effect a second time to see whether the new behavior again rep]accs the old behavior. It is hard to argue witl1 data of this kind; different cxtcrnaJ consequences clearly have led to different behavior. A reversal design js illustrated in the following clinical reporL

1~1111's S11iness Is Mo,lifie,t bi Cl1a11gi11g Co11se,11.1e11ces Ann was a 4-ycar-old girl who had become more and more isolated from the other children in her preschoo1. showing an increasing preference for interaction with the adult teachers. As time went by. she spent an even greater proportion of her time simply standing and looking. Mild. tic-like behaviors. such as picking her lower lip. puUing a strand of hair. or fingering her check. also devc1oped. Careful observation or Ann's behavior indicated that she was using many techniques for gaining and prolonging the attention ofadults and that most adult attention was contingent upon (was a consequence of) behaviors that were incompatible with playing with peers. An intervention program was instituted in which Ann received adult attention as a consequence of play with another chikl lbis attention. of course, had to be given in such a way that it did not draw her away from her interaction wiU1 the other children. No adult attention was given for isolate behavior or in response to bids for interaction with adults. Almost jmmcdiatcly after these new consequences were introduced. Ann:~ play-with other children increased drrunaticaJly and her interactions with adults decreased (see Figure 3·3). After 5 days of the new consequences. the procedure was reversed. The teachers responded as they had originally, giving attention when Ann was showing isolate behavior or intcractingwith adults. Ann's peer intc-raction quick ly dropped to its previous level. After 5 more days. the new consequences were once more provided. again with immediate effects on Ann's behavior. During the last days of the second reversal period. the teachers gave increasingly intermittent (nonsystem• a tic) attention for interaction with other children. Many laboratory studies have shown that such interm ittent or partial reinforcement increases the resistance to extinction of newl)r learned responses. No systematic attempt was made to maintain the program after the 25U1 day. On days 31. 38.40. and 51. checks of Ann's behavior indi• cat.ed that her new rate of interaction with peers was holding up moderately well. Perhaps enjoyable play with other children had come to serve increasingly as reinforcement in its own right for social interaction with peers.

Con.tempOf'ary Frameworks

Figure 3 -3

Effects of Social Reinforcement on Shyness

Percentage of time Ann spent in social interaction with adu lts and with peers during approximately 2 hours of each morning session Sow-ce: Dat a from ~Effects of Social Reh1forceme.n1.on lso-late Beh;wlor of aNur..sery School Child.~ by K. E. Allen. B. Jfar t,J. S. Buell. F. R. Harrlg,, a ,ld M. M. Wolf. 196-l. C/11/d D6ve/opme11t. 35. p. SIS. Originally published In Child De1't!lopmen1. Copyright~ 1964 by 1J,eSoelety fo r Researeh in Child Oevelo1>ment.

100

With Adults

80

60 40

~

20

V~\?'-

;;;:

i 100

• • •

~

~

~

With Children

80

• •

60

40

20

1 2 3

4 5 6 7 8 9 10 11 12 13 14 1S 16 17 18 19 20 21 22 23 24 25 Interaction with Interaction with Children Baseline Reversal Children Reinforced Reinforced

31384051

Post Checks

Oays

3.2c Behavioral Treatment A variety of treatment interventions have been developed within the behavioral model. ''fypic.ally. when building new behaviors. a contingency management technique like that

illustrated in Ann's case is attempted. The baseline level of the t."trgct behavior is assessed, and then a contingency is implemented such that engaging in the target behavior produces a reinforcing consequence. At first. thescareartificial arrangements: however. once the behavior is established, an attempt is made to fade into more natural cons!!quences that will maintain the improvement after the contingency management program, ends. In Ann's case. adult attention initially was the reinforcer. but later the natural consequences of peer play came to maintain the sociaJ interactions. Sometimes. these sorts of contingency arrangements can be What treatments have made between couples in marriage counseling; at developed from the behavioral other times. behavioral contacting m.ight be used to model? outline the contingencies in a sc.Jf•control program. Because peers can hold strong influence over a client's behavior. modeUng is an important intervention. If a model pcrform.s the appropriate behavior. it is more likely to be i1nitated by other members of the peer group. 1]1is is especially true if the mode] receives positive consequences for his or her actions. A variety of posith•e behaviors. such as social interactions.

Modeling Teaching a behavior by performing the behavior and having the learner imitate it

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Abnormal Psychology

problem solving. persistence at academic tasks. and important safety behaviors. have bcc.n taught by employing peer models who demonstrate succcssful approaches to problems. lhcrc are times when punishment prograrns are applied- for example. when seriously disturbed children engage in self-destructive acts such as head banging. Unpleasant consequences. such as a squirt of lemon juice into the mouth or a mist of water onto the face. have been used quite effectively as punishcrs in stopping self-destructive activities among autistic and intellcctuall)r deficient children (Dorscy. lwata. Ong. & McSwecn. 1980). Because ofimportant ethic.al considerations. punishment is usuaJly a last-resort intervention. applied only when the behavior is seriously harmful and needs to be stopped quickly. More often. extinction tec.hniques arc used to decrease an unwanted behavior. In either case. the treatment would also include rcinforcernent components to build an alternative (and more appropriate) behavior. Other behavioral treatments have been derived from classic.al condition ing. Strong emotional reactions like fear and anxiety arc similar to reflexive responses in that they can come to b0tentia1 that represents either a striving for"'good·· constructjvc personality growth or a strhring for-evil .. or destructive.ends. \¥hat exactl)' arc the metaphors used to explain abnormal behavior in the humanistic framework? One such metaphor deriving from existential philosophy and mentioned previously is that symptoms of mental disorder occur when individuals make too many inauthentic choices and fail to confro nt the existential anxiety associate.cl with taking responsibility for their own lives. Another. perhaps more common. metaphor is that symptoms occur when persons cut themselves off from their own expcricncings. 'fh is metaphor is quite similar to the psychodynamic metaphor and perhaps differs primarily in avoiding theorizing about s uch constructs as id. superego. ego. fixations. and so on. It is useful to be reminded that our subjective experiences are rich, varied. and- in many respects- likely to be unique for each of us; thus. any t heoretical formulation will probably not capture all t he nuances ofthc-se cxpc.ricncings. '£here is aJso an ethicaJ quality of humaneness that pc.rvadcs this approach. Adherents of other approaches can be. and frequently arc~ just as humane: but the humanistic writers have most insistently reminded us that a bnormally behaving people arc persons. not cases to be considered only as interesting examples of p sychopathology. On t he other hand. the humanistic approach has not generated much research that has illuminated the nature of abnormal beha\-,.ior.111is is not surprising in light of the negative views of its adherents toward cntc.gori z.i ng. quantifying. and experimenting with human bchavjor. Although humanistic writers sometimes imply that we arc on the verge of sornc new methodology for studying subjective experience. how can they or anyone everdirectlystudysomebodyclse's subjective experience- short of some kind of extrasensory. telepathic communication?

3.5 Approaching an Integrated Model 1l1erc arc. of course. many other psychological perspectives t hat have not been covered here. aJthough most could be viewed, to some extent. within these four basic frameworks. It is also true that t he models presented here arc not as distinct as they seen\, Psychodynamic and biological frameworks have long coexisted within the practice of psychiatry, while t he behavioral. cognitive. and biological models combined within the ncurosciences. Some merging between humanistic concerns Can assessment of treatment and behavioral methodologies is evident in the outcomes contribute to a more emergence of ~positive psychologyH approaches. unified framework? which emphasize empir ic.ally based interventions to increase personal happiness (Seligman. Steen. Park. & Peterson. 2005). Practicing psychotherapists commonly draw from humanistic. behavioral. and cognitive models while interacting with clients. At the same time. our understanding of psychopathology remains very incomplete, and many questions remain unanswered. An eclectic approach. many wou.ld agree. is U1e best one for the current state of affairs. Research is progressing rapidly, noneth eless, on many fro nts, and it seems very likely that a more unified or integrated model will be Ute result. 'lbe activity ofscience opens many new doors and also closes old ones. Psychotropic medications arc subjected to controlled demons trations of their effectiveness and risks. and the cstabl ished formulary contains

Contempo,ary Framewo,ks

Table 3·5

Well-Established and Probably Efficacious Psychotherapies for Selected Disorders

Disord e r Anxiety

Probably E ffica cious Treatme nts Cogniuve-behavioraJ therapy f()r panic d1sorder Cogniuve-behavioral therapy fhr generalized am:iety disorder Exposure treatment for agoraphobia Exposure.and response prevention for obsessive-compulsh:e disorder

Depressfon

Behavior therapy for depression CogniUve therap)' for depressfon lnterpersonaJ therapy for depression

Applied relaxation for panic disorder Applied relaxation for generalfaed anxiel)' disorder Cognitwe-beha\·ioraJ therapy for soc ial phobia Cogniti.,.e therapy for obsessive-compulsive disonler Exposure treatment for post-traumatic slres.s disorder £ye movement desem;1tization and reprogramming for post• traumatic stress disorder Syslemabc des.ensitiz.ation forsociaJ anxiety

Bnefdynamic therapy for depression Cogniti.,.e therapy for geriatric depression Self-control Lherapy for depression

Healtll problems

Behavior therapy for headache CogmtJve-behavioraJ therapy fqr bulimia CogmtJve-behavioraJ therapy for rheumatic pain CogmtJve-behavioraJ therapy with relapse prevention for smoking cessation

Behavior therapy for chi1dhood obesity Cognill','e•behavioraJ therapy for b1nge•eatmg disorder Cognill','e•behavioraJ therapy for chronic pain EMG (eleersonal identity. so the person is uncertain about important personal information (including name. residence. or profession). An individual with dissociative fugue may wander for periods of time ranging from brief journeys (of il few hours or days) to several months over thousands of miles. Most often. the person in the fugue state docs not form a new identity: when that docs occur. it appears to include more outgoing and uninhibited traits than the original one (American Psychiatric Association. 2000). Sometimes. however, new identities can be quite e.~tcnsive. including assumption of a different name. a new residence. and involvement in new. complex social acti\'itics and functions. Amnesia associated with dissociatjve fugue can remain after the fugue state remits. Severe strcssors or overwhelming life events arc typical ly related to onset: offset is often hastened by removal from the stressful situation (Arneric.an Psychiatric Association. 20l3).

Somatic Symptom and Dissociative Disorders

179

Causal Factors There is no clear evidence of genetic or biological influences in the development of the disorder. Most case reports and reviews have suggested that severe stressors or traumas trigger dissociative amnesia. Coons and Milstein (1992) found multiple stressful precipitants among tl1e cases they reviewed. Among precipitating stressors for fugue, the most common appear to be marital discord, financial and occupational problems, and war-related events (Maldonado et al., 2002). The psychoanalytic perspective presumes that the memory loss is the result of unconscious repression (rather than suppression) of the memory due to its tl1reatening or unacceptable content, thus" dissociating" the memory from the person. The behavioral perspective assumes (similarly) that the amnesia is in some way negatively reinforced as an avoidance or escape response.

Treatment for Dissociative Amnesia

Dissociative amnesia is a memory disorder characterized by extreme memory loss that is caused by extensive psychological stress rather than physical causes. (Sbutterstock)

For years, the typical approaches to treating dissociative amnesia i11volved hypnosis or the drug sodium amytal, (also called amobarbital, a barbiturate derivative), together with free association, to uncover unconscious memories and bring them to the surface. Supportive therapy takes place i11 a safe environment, working to facilitate recall and provide reintegration of the dissociated memories. No careful studies of the effectiveness of these treatments for dissociative am11esia exist, however (Maldonado et al., 2002). Because people with dissociative disorders are quite suggestible, tl1ere is a risk that the memories recovered during therapy may be produced through iatrogenesis. In other words, a false or altered memory could be created, inadvertently, during the therapy process as the client and therapist interact. There have been several experimental demonstrations of induced false memories i11 both children and adults, showi11g that it is possible to get people to remember events that never happened (Loftus, 1997). Simply having people read a set of short articles that describe witnessing the "possession" of someone else caused subjects to rate this implausible event as more plausible and rendered them less certain that they had not experienced tl1e eve11t i11 childhood (Mazzoni, Loftus, & Kirsch, 2001). Results such as these suggest that iatrogenic false memories for clinically significant phenomena could be created rather easily. Indeed, there have now been legal cases involving clients who have accused their therapists of implanting false memories for the purpose of financial gain. One lawsuit involves a 41-year-old woman who claimed her tl1erapist used hyp11osis to implant false memories of rape, involvement in satanic cult rituals, and multiple personalities after she sought treatment originally for an eating disorder. Other women at the same treatment center have made similar allegations (Caron, 2011). At the same time, there is strong criticism about the validity of the concept of repressed memory, which some consider illusionary (Bonanno, 2006). The heated debate, which in part is an argument about the foundations of psychoanalytic theory, continues to be very active, with defenders of the notion insisting that repression is a valid concept and others claiming that the empirical evidence shows that trauma, in general, enhances memory (Rofe, 2008).

7.3b

Dissociative Identity Disorder

Dissociative identity disorder (DID), formerly called multiple personality disorder, is perhaps the most unusual of the dissociative disorders. Perhaps because its symptoms are so strange (see Table 7-7), it has also received the most attention in the literature and remains the most controversial. The diagnosis requires the presence of two or more distinct personalities

Iatrogenesis The inadverte11t and avoidable indt1ction of a condition or d isorder by a therapist during the treatment process

180

Chaple< 7 Abnormal Psychology

Table 7·7

Summary of DSM-5 Diagnostic Criteria for Dissociative Identity Disorder

Person's 1dentily is disrupted by at least two di.slinct personalil)' states. often described as an experience of possession. Disruption involves notable discontinuity in sense of selfand agency. along with related d1anges in behavior, memory. cognition. affefit or pleasure. 3. lmpulsi~·ity or failure lo plan ahead. 4. Irritability and aggressi\'eness. as indicated by repeated physical fights or assau lts. 5. Reckless disregard for the safety of selr or olhers. 6. Consistent iITesponsibility. as indicated by repeated failure to s ustain consistent work behavior or honor finan ciaJ obligations. 7. Lack of remorse. as indicated by being indifferent to or rnlionali.zing having hurt. mistreated. or stole n from another. 8. The individual i.-; at feast age IS years. C. There is evidence of a conduct disorder with onset before age l3 years. D. The occurrence of antisoc:ial behavior is not exclusive1y d uring the course ofschizophrenia o r a bipolar disorder. Sou rce: Reprinted with perml!.s:ion from the Diagnostic o,1d Stat/sJ.leol Mmwalo/MenUJI Di.,;ordt.r-!J. 5th ed. (Copyright 2013}. American PS)'Chlat.rk Association.

Personality Disorders

201

antisocial personality disorder were 5 times rnorc likely to be receiving physical disability benefits than were the patients without the disorder (Byrne. Cherniack. & Petry, 2013). Although it is tempting to equate a rep~ted pattern of criminal activity with antisocial personality disorder. it is not accurate to say that all career criminals can be so diagnosed In fact. a subclinicaJ label. or ~v.codc.'" that better applies to many such persons is ~adult antisocial behavior.Ha DSJ\.1-Slistingmeant to apply to situations in which the focus of clinical attention is antisocial behavior that is not due to a mental disorder. Distinguishing adult antisocial behavior from antisocial personality disorder requires sufficient information to diagnose a personaHtydisorder. in addition to evidence of a conduct disorder before age 15. Antisocial personality disorder is estimated to occur in 3% of males and l% of fcmalcs in the general population- although fomale,1, may be undcrdiagnosed because of male aggression bias in the conduct disorder diagnosis. However. it is much more prevalent (over 70%) in certain settings. such as substance abuse treatment groups among the legal ly incarcerated (Amcrican Psychiatric Association. 2013).111c behavior pattcl'ns characteristic of antisocial personality disorder have been the focus of. perhaps. more attention from psychologists than other personality disorders: thus. a review of tJlat history is ,-.•orthwhile.

Background of tile Diagnosis ln 1835.Jamcs Cowles Prichard described a kind of"moraJ insanity- in which intellect seemed unimpaired but moral principles were "pe,r vcrtcd or depraved." the ..power of self-government" wa.1o lost or diminished. and the pc.rson was incapable orconducting himselfwith decency and propriety in the business oflifc." Later writers (e.g.. House. 1923) us.eel the term constil-utional p.rychopathic inferiority to refor to this pattern of behavior. strongly implying a biological and possibly hereditary etiology. Until the 1960s. the term psychopathic personality (or just 1>sycb opatb) was the most common label. ~me DSM described the pattern as ~antisocial personality disorder- in its diagnostic series. although the term psychopath is still wide]y used. Writers have compiled lists of varying lengths to describe the essential features of the psychopathic or antisocial personality. 11le following six charactel'istics represent a synthesis of earlier descriptions by various authors. especially Cleckley (1976). and McCord and McCord (1964). 1.

lack ofconscience orfeelings ofremorse \Vhcn most of us have violated some moral standard. especiaUy if we have hurt another person physically or cmotionaJI)'· we arc likely to feel some regret. remorse. or "twinge of conscience." 'Che psychopath docs not. One psychopath describes how he murdered three people: lhc two little kids started crying. wanting water. I gave them some and she !their mother] drove a while- and I turned around and started shooting in the back sc.atand then turned back and shot her. She fell over against me and onto the floor" (Smrkal & 1horne. 1951. p. 31 1). After giving the children a cl.rink of water. he shot them and later related the story without compassion or remorse. In psychoanalytic terminology. the psychopath has little or no superego and no gu-Llt feelings about wrongdoing.

2.

lmpulsivit-y: inability to delaygratification Psychopaths tend to act upon the impulse of the moment. l11cy seem unable or unwilling to delay gratification for rnore long-term rcwards.11lcreforc. they arc likely to commit impulsive. poorly planned criminal acts: Oit from one mate to another (with or without marriage): quit or be fired from job after job because they cannot stand the restrictions or demands of ordinary work: and. in general. lead erratic and unstable lives. \1/ltcn frustrated in seeking immediate gratification. they arc likely to respond with aggression or violence against their perceived frustrators.

3.

Inability to profit.from mistakes Most people caught in some criminal or antisocial act and given some appropriate punishment e ither dcvcJop their criminal expertise

Psychopath Antisocial personal..ity involving characteristics such as lack of empathy or concern for others. frequent rule violations. impulsivity. and superficial charm

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Abnormal Psychology

so that they are less likely to get caught the next time or give up criminal activities. Not so with psychopaths. Although they may be caught in many crimes and receive varying kinds of punish1nent, they do 11ot seem to lear11 from these experiences and frequently repeat the same antisocial behavior in tl1e future.

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4.

Lack ofemotional ties to other people Emotionally, psychopaths are loners; they seem incapable of binding ties or loyalties to other people. Although they may form fleeting attachments, these lack emotional depth and tenderness and, not uncommonly, end abruptly in aggressive explosions. They can behave as callously toward their own wives, children, or parents as toward anyone else. Other people are treated as objects to be manipulated for tl1e psycl1opath's own pleasure.

5.

Stimulus seeking Most psychopaths become bored quickly with the l1umdrum of everyday life. They search constantly for new thrills and experiences-daring robberies, impersonations, confidence games, new varieties of drugs, and deviant sexual behavior.

6.

Ability to make a good impression on others There is no reason to believe that psychopaths, on the average, are any more or less intelligent than the rest of us. Many of them have learned as part of their manipulative strategies to appear intelligent, likable, charming, and witty. Frequently, they talk their way out of tight spots; "con" people into dubious investments; or convince judges, juries, probation officers, or therapists of their good intentions for the future.

Studies at that time suggested that the psychopath's inability to profit from mistakes derived from a lack of anxiety about future punishment and an impaired ability to learn responses motivated by avoidance of pain or other forms of punishment. Punishment is effective in deterring most people from repeating undesired behavior because the person learns to respond with anxiety in anticipation of being caught. In a study by Hare (1965a), the subjects watched consecutive numbers 1-12 appear on a display. They were told that each time the number 8 appeared, they would receive an electric shock equal in intensity to one earlier determi11ed to be tl1e strongest tl1ey could tolerate. Both normals a11d nonpsychopathic criminals showed anticipatory rises in palmar sweat gland activity (galvanic skin response, or GSR), but psychopathic criminals did not. Given a relative lack of anticipatory anxiety, one would expect psychopaths to learn conditioned electrodermal GSR responses less well than no11psychopaths; this was shown to be the case (Hare, 1965b). GSR responses were conditioned to auditory stimuli, preceded by electric shock as the unconditioned stimulus (see Figure 8-1). Other work similarly showed that psychopaths demonstrate poorer learning in shock-avoidance experiments (Lykken, 1957; Schmauk, 1970). A general conclusion might be that psychopaths, defined according to Cleckley's (1976) criteria, show less anxiety than nonpsychopaths in stressful situations, perhaps contributing to psychopaths' willingness to indulge in risky behavior and their difficulty in learning to inhibit antisocial behavior. Quay (1977) theorized that a prin1ary cl1aracteristic of psychopatl1s that might explain much of their behavior is an inordinate need for increases or changes in stimulation. Others (e.g., Hare, 1993) have suggested that psychopaths are physiologically underaroused and thus seek stimulation to bring themselves up to an optimal state of pleasurable arousal. Either of these proposals might explain the deficient anxiety conditioning seen in psychopaths. However, Fowles (1993) suggested that a deficient behavioral inhibition system together with a normal or overactive behavioral activation system distinguishes psychopaths. Factor analytic studies remain active as well. Cooke and Michie (2001) suggested the three main factors in psychopathy are arrogant and deceitful interpersonal style, deficient affective experience, and impulsive and irresponsible behavioral style.

Personal ity Disorders

Figure 8-1 Conditioning of the Galvanic Skin Response (GSR) in Psychopathic and Nonpsychopathic Criminals

203

Nonpsychopaths

12 V> a:: 10

Source: Data fro1n Adapted from "Acquisitions and Generalization of a conditioned-Fear Response in Psychopathic and Nonpsychopathic Criminals," by R. D. Hare,1965, 1hejournal of Psy chology: Interdisciplinary and Applied, 59, pp. 367- 370

....u 0

.... e in new activities. -Fear of ru}ection. disapproval. or criticism creates an avoidance ofoccupationaJ acti\•ilies that mvolve sign.ificant interpersonal con.tact. -Has a preoccupation with being rejected or crilid:r.-ed 10 social situations. -Belie\1es they are inferior. socially inept. or personaUy unappeaJing to o thers. Source: American P.sychlattic Assoclalkln. 2013.

Causal Factors No infonnation on familial patterns is provided in DSJl1-5. ald1ough Oahl (1993) indicated that it is: more common among close relatives of those with the disorder. The significant overlap of symptoms and high comorbidity bctv.-een avoidant personality disorder and social phobia may suggest a common biological underpinning (Koenigsberg ct al.. 2002}. Others, however. argue that avoidant personaJity disorder should be considered within the schizophrenic spectrum (Gooding. Tallent. & Matts. 2007). Possible psychological causes include parentaJ or peer rejection in childhood. although little empirical evidence exists for any specific causal factors.

Treatment of Avoidant Personality Disorder

Avoidnnt personaUty disorder inrnlves social inhihitmn. hypersensillvit)' to cnticism, and feehngs ofinadequacy. These individuals may resist new re.lation.shtps or friendslups when feeling uncertajn lhat they will be acc:epted or li.ked. fiSiod:I

Pharmacologica l approaches to treatment of avoidant personality disorder essentially assume that the condition has a common basis with that of social phobia. Caso reports suggest certain antidepressant medications (MAO-ts and SSR ls) may be helpful. but controlled studies are needed (Koenigsberg et al.. 2002). One randomized controlled trial showed that behavioral treatments that involved graduated exposure and social skills training were more effective than a wait-list control: less r'igorous comparative studies and case studies have also supported cognitive therapy and supportive expressive dynamic therapy (Crits•Christoph & Barber. 2002).

8.4b Dependent Personality Disorder 'Che central characteristic ofdependent personality d isorder (Table 8~10) is an excessive need to be taken care ofby others.1hat persistent need is associated with fears ofseparation and dinging and submissive behavior designed to evoke carcgiving. Individuals with dependent personality disorder are uncomfortable bcing a lone because they fear being unable to care for tJ1cmselves; thus. they will urgently seek a replacement relationship if a close relationship ends. 1'ypically, they allow others to make import.ant decisions about most life areas. including employment. use of free time, and choice of friends. 1l1ey may volunteer to do unpleasant tasks or participate in unwanted activities in hopes of securing the care and support they need. 1J1cir pattern of dependency tends to keep them dcpcndc.nt because they do not gain the skills needed for self-support.

Personality Disorders

Table 8·10

Summary of DSM-5 Diagnostic Criteria for Dependent Personality Disorder

E.xcess1ve need lo be taken care of that Jeads to fears ofseparabon. as well as submi.s.sl\'e and c:Jingmgbehavior. This pervasn,e pattern has occurred since early aduJthood and is expressed by at least 6n~of the following: -Need,;: others to be responsjbJe for most major areas oflheir life. -Exaggerated fears of being unable 1.o care for themselves causes helplessness or discomfort when alone. -When a close relationship ends. immediately seeks another relationship for support and care. -Requires an excessive amount of reassurance and advic:e from others in Mder to make e\'eryday dec1smns. -Has difficultydomg things on their own or m1tiatingprojects due to a laok of approval or suppor L -Expressingdisagrttment with 0U1ers is challenging due to fears about loss of support or approval Realistic fears of retribulion are not included in thi.s cr-iteria. -Makes excessive efforts to obtain support and nurtu.rance £rom others. e\'en volunteering to do things that are unpleasanL -Unrealistic preoccupatmn with fearofbe.i.ng lefi to take care of themselves.. Source: American PsychialJ'ic AssoclatJon. 2013.

People with dependent personality disorder sccthcmsclvc-s as inept and totally dependent on the advice and assistan ce of others. 10 maintain the dependent bond. they may accept verbal. physical, or sexual abuse. '£he condition tends to co--occur \'lith borderline personality disorder and with mood and anxiety disorders. Jt is diagnosed more often among females than males. and its prevalence appears to be less than !%of the population (American Psychiatric Association. 2013).

Causal Factors 'Ote DSJ\1~.5 provides no information about any farniUal influences in dependent personality disorder. Some have speculated about possible histories of abuse. overprotective pa.renting. or delayed Hweaning from nurturance" in childhood (_Meyer & Deitsch. 1996). However. no empirical evidence appears to support any particular genetic. biological. or psychological causal factors at present.

Treatn1ent of Dependent Personality Disorder No evidence is available from control.led reports concerning the rcJativc effectiveness of medication or psychotherapy for dependent pcrsonaJity disorder. Symptomatic treatments for depression or anxiety and directed skills training for assertiveness. independent living. and problem solving may be attempted.

8.4c Obsessive-Compulsive Personality Disorder Obsessive-compulsive personality disorder (Table 8-11) involves a preoccupation with control, orderliness. and perfectionism. People with this condition are overinvolved with rules. schedules. and details and arc insensitive to the resulting annoyance of others to the extent that inflex:ibility of procedure is more important than cfficiency. Thc)r tend to be stubborn and inflexible about checking details. so that deadlines tend to he missed despite excessive devotion to work. lhc same preoccupation with and dedication to tasks interfe res with friendships or leisure activit ies. 1l1cir emphasis is on perfect performance and r igid devotion to principles. and they typically do not trusl the abilities of others toward these ends. Consequently, they rarely delegate tasks or collaborate with coworkers.

211

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Abnormal Psychology

Table 8·11

Summary of DSM-5 Diagnostic Criteria for Obsessive-Compulsive Personality Disorder

P-reocc upation with perfectionism. orderliness. and mentaJ/interpers.onal control. at the oosl of efficiency. flex1h1Jity. and openness. This pervasiw pattern has occurred since early adult.hood and is expressed by at least four of the fc,llowin_g: -Difficulty completing tasks due l() a need for perfec:tionism {e.g .. their overt)' stnct sl:andards cause the inability to finish a project) -Inflexible. scrupulous. or excessively c onscientious about ethics. \lalues. or mat te n. of moraJily. whicb cannot be accounted for by any cuJtural or religious affiliation -Miserly i.n matters of spend mg monc.,y on themsel..-es or others: feels lhe need to hoard money in case offul-ure catastrc;,phes -Reluctant tu work with others or delegate t.ask..,o; unJess others agree to do tbingi. precisely their way

-The major pmnt of activities becomes lost due- to a preoc:cupalion with order. ruJes. detaits.. hsts. schedules. and organization -Forgoes letsure activities and friendships due 1.o an excessive dei.'Otion to work and produc tivity that lS not an ob\1 ious economic necessity -Unable to gel rid of worthless or wom-oul things. e\1et1 items with no sentimental ,.·alue -DispJays stubborn. rigid behavior Sou rce: American Psychlalr1c Astociatlon. 2013.

Unlike obsessive.. compulsive disorder (described in Chapter 6). those with obsessive• compulsive personality disorder are not particularly distressed by their condition. In fact. they can appear to be emotionally insensitive and unexpressivc. Others may sec them as overly conscientious and moralistic. In addition. those with obsessive-compulsive personality disorder do not display true obsessions or compulsions. According to the DSiW~S. the condition may be among the rnost common personality disorder in the general popu lation. \'\'lth incidenc.e estimates ranging from 2% to nearly 8%. Its maJe-to•remale ratio is 2: I (American Psychiatric Association. 2013).

Causal Factors No evidence of familiaJ influences is provided in DSJ\1.s. People with anxiety d isorders may have a h igher risk for obsessive-compu l,;ive personality disorder. Many of the features of obsessive-compulsive personality disorder appear to overlap with Cluster A rather than Cluster C conditions. and there may be an association \\Tith eating disorders and depressive disorders (American Psychiatric.Association. 2013). Earlier Freudian perspectives in,•okcd fixation at the anal stage ofpsychosexua.J development Canal retentive.. personalities arc preoccupied with order and neatness. as compared to -anal expuL,;:ive" personalities. which are disorgan ized and messy). possibly related to overcontrolling parents. Later perspectives tend to emphasize overuse of defenses. 'W ithout empiric.a.I data. littJc is known abcmt these or other possible environmental or familial contributions to this condition.

Treatment of Obsessive-Compulsive Personality Disorder Blbliotbcrapy 'Che use of selected written materiaJs t..hat may have parucular life significance as an ndjunct in psychotherapy

'lhcre arc no controlled outcome studies on either p harmacological or psychologica l interventions for obsessive-compu lsive personality disorder. lbcrapy may be attempted for relaxation training or to reduce the nearly compuJsivc preoccupation with detail tJ1at is so characteristic of the behavior pattern. Meyer and Ocitsc.h {1996) recommend relaxation, modeling of hu rnor. bibliother apy techniques (use of written materials that may have life significance), and cognitive challengi ng. alth ough no empirical data support these interventions for obsessive-compulsive personality d isorder.

Personal ity Disorders

213

8.5 Other Personality Disorders 8.Sa Personality Change Due to Another Medical Condition One new personality disorder classification appears in the DSM-5: personality change due to another m edical condition. Sometimes, p ersistent p ersonality changes can be associated with chronic medical problems or events such as stroke, head trauma, epilepsy, autoimmune disorders, or other central nervous system dysfunctions. Those afflicted may show emotional inst ability, aggression, paranoia, apatl1y, or poor impulse control, among a host of other possible dysfunctions. When these changes can be directly linked to the underlying medical co11dition, this diagnosis would be appropriate.

8.Sb Other Specified Personality Disorder Quite often, individuals present symptoms that meet the general definition of a p ersonality disorder (see Table 8-1) but do not satisfy the specific criteria for any of the Cluster A, B, or C diagnoses. Usually, tl1ese appear to be co11ditions in which the symptoms of different personality disorders are mixed together. In those situations, a diagnosis of "other specified personality disord er" is given. Even w hen structured clinical interviews are employed in diagnosis, this classification is among the top three personality disorders in terms of prevalence; when interviews are not structured, this is the most common personality disorder diagnosis {Verheul & Widiger, 2004).

8.6 Considerations for the Future The overlap and intermingling of personality disorders with other DSM conditions weakens the argument about their independent status, and several writers have called their future status into question. Because categorical diagnoses of m any of these disorders involve matching client symptoms to "3 of the following 7" or "5 of the following 9" criteria, there can be a very large range of variability in the expression of any single p ersonality disorder. Thus, two persons with the same diagnosis may behave in different ways (a ch allenge to convergent validity), while others with differe11t diagnoses may act similarly (a challenge to divergent validity). Factor -analytic studies of the 10 p ersonality disorders did not support their categorical organization i11 theDSM-/V(Sheets & Craighead, 2007), and one evaluation of convergent and divergent validity and correspondence to the Big Five personality factors in the DSM-IVclassificatio11 system i11dicated that only borderline personality disorder met all criteria for a u seful and valid classification tl1at identifies functional impairment {Ryder et al., 2007). Others suggested that substantial revisions were needed in paranoid personality disorder b ecause of poor validity (Bernstein & Useda, 2007). The broad and persistent criticism of the personality disorders led the DSM-5 t ask force to consider major changes i11 their classification. In preparation for DSM-5, proposals to rethink the personality disorders by sl1ifting to diagnosis based on five-factor 1nodels of personality appeared (Widiger, Costa, & McCrae, 2002). Among the other options mentioned for the DSM-5 taskforce to consider were whether to abandon the classifications altogether or to redefi11e personality disorders as either early onset or chronic variants of existing DSM conditions {Widiger, 2007). It appeared certain that the DSM-5 would move toward a more dimensional,

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Chapter 8

Abnormal Psychology

and less categorical, model for diagnosis of personality disorders (Regier, Narrow, Kuhl, & Kupfer, 2009); early drafts of the DSM-5 proposed sweeping changes including reducing the nu1nber of disorders to six and adding a di1ne11sional assessment component based on a fivefactor model of p ersonality (curiously, not identical to the well-researched Big Five model). However, tl1e proposed changes were so extensive that many balked at what appeared to be confusing and time-consuming assessments, and in the final draft, the sweeping changes were voted down. Consequently, the DSM-5 retains the DSM-IVpersonality disorder categories with almost no changes, although the alternative personality trait model was placed in Section III for further study. Given the continued dissatisfaction with tl1eir current status, the personality disorders will most likely be revamped with the next revision of the DSM.

215

TO SUM UP ... •

Personality disorders are enduring and stable st yles of thinking, p erceiving, and behaving across many settings and situations that are evident at least since early adulthood and that cause distress for the person or for others.

Personality disorders may affect 9% of the population. Within clinical sa1nples, nearly half of p ersons receiving any DSM diagnosis also meet the criteria for some t yp e of personality disorder diagnosis.

Personality disorder symptoms generally clust er into three groups: those that are odd or eccentric; those that are dramatic, emotional, or erratic; and those that are anxious or fearful.

Very little is known about tl1e causes of personality disorders, which are presumed to originate in adolescence. Family studies tend to support either weak or only moderat e ge11etic influences.

There is significant overlap among the different p ersonality disorders and between personality disorders and several other mental disorders. The degree of comorbidity raises questions about the validity of the personality disorder categories. Diagnostic reliability also continues to be a problem for these conditions.

Mathematical studies of p ersonality assessments tend to support a dimen sional model of personality disorders rather than the current categorical model of personality disorders used by DSM-5.

Treatment of personality disorders is difficult. People diagnosed with these conditions often do not seek treatment and may be uncooperative patients. Several p sychological and pharmacological interventions have been attempted, but there is only limited evidence of their effectiveness.

KEY TERMS Agreeableness Bibliotherapy BigFive

Neuroticism

193

Open11ess to experience

212

Personality

192

Conscientiousness Extroversion

193

Ideas of reference

Phrenologist

191 192

Psychometrician

192

Factor analysis

192

192 198

Psychopath Psychoticism

201 192

192

192

216

QUESTIONS FOR STUDY •

Discuss l1ow a dimensional method of p ersonality disorder diagnosis migl1t work and whether it would be an improvement over a categorical one.

Imagine you are hosting a large party. You have invited people with each of the personality disorders. Which ones w ill accept your invitation, and which will refuse your i11vitation? Why?

Try to describe a person who would meet the diagnostic criteria for two personality disorders simultaneously.

POP QUIZ 1.

Dr. Brown believes that p ersonality is a collection of psychological characteristics, such as kindness or dependability, w hich can be identified a nd measured. She would be best described as a - - - - - · A. trait theorist B. humanist C. phrenologist D. psychoanalyst

2.

The DSM-5 lists _ _ _ _ _ different primary p ersonality disorders. A. 3 B. 6

C. 10 D. 12

3.

_ _ _ _ _ personality disorders tend to present symptoms that observers consider odd or eccentric. A. Cluster D B. Cluster C C. Cluster B D. Cluster A

4.

Personality disorders are difficult to treat because of all of the following reasons except thei r - - - - - · A. stability B. chronicity C. medical basis D. involvement in several life areas

217

5.

Which of the following personality disordered individuals would have recurrent suspicions, without justification, regarding the fidelity of a spouse or sexual partner? A. obsessive-compulsive personality disorder B. histrionic p ersonality disorder C. schizoid personality disorder D. paranoid personality disorder

6.

People with _ _ _ _ _ are largely indifferent to criticism. A. dependent personality disorder B. obsessive-compulsive personality disorder C. borderline personality disorder D. schizoid personality disorder

7.

_ _ _ _ _ individuals initially diagnosed with schizotypal personality disorder go on to develop schizophrenia. A. Only a small percentage of B. Nearly a third of C. Half of D. Most

8.

The Cluster B personality disorders include individuals who may be described as

-----· A. odd or eccentric B. emotional or dra1natic C. avoidant or fearful D. psycl1otic 9.

Individuals with antisocial personality disorder frequently are able to talk their way out of difficult situations and may "con" others into believing their good intentions for the future, demonstrating their-----· A. the inability to profit from mistakes B. the need for admiration C. impulsivity D. the ability to make a good impressio11 on others

10. Of those diagnosed with borderline personality disorder, _ _ _ _ _ are

female. A. 75%

B. 50% C. 25%

D.

5%

11. Frank believes he is more important than he really is. He has a grandiose se11se

of self-importance and is preoccupied with fantasies about his own success and brilliance. Frank would best be described as having - - - - -· A. narcissistic personality disorder B. histrionic p ersonality disorder C. dependent personality disorder D. obsessive-compulsive personality disorder

218

12. In the general population, _ _ _ _ _ display at least one of the personality

disorders. A. 1% B. 4%

C. 6% D. 9% 13. The most common personality disorder diagnosis is most likely-----·

A. B. C. D.

paranoid personality disorder dependent personality disorder other specified personality disorder schizoid personality disorder

14. The use of written materials that may l1ave life significance is called •

A. bibliotherapy

B. biotherapy C. autobibliotherapy D. biblicotherapy 15. Dialectical behavior therapy (DBT) is effective in treating which of the

following? A. antisocial personality disorder B. borderline personality disorder C. obsessive-compulsive personality disorder D. dependent personality disorder

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pierced. s hocked. or subject to other forms of physical or verbal a buse or humiliation; they must have persisted for6 monUlS and must cause distress or inlcrpersonal problems to qualify for the d iagnosis. In some cases. individuals act on these urges or fantasies during solitary sexual behavior. while others seek masochistic acts w ith partners. The course tends to be chronic, and the activities may remain relatively mild or may increase in intensity and dangerousness. Specifiers include in a controlled environment and in fuU remission. (t can also be sp ecified for one type of masochistic act- asphyxiophilia. which involves oxygen-depriving activities such as choking. hanging. or suffocating; seve ral accidental deaths occur from these practices each year in the United States (American Psychiatric Association. 2000). Prevalence estimates of about 2% of males and 1% of fem.ales have been reported in Australia. but t he U.S. incidence of t he disorder is unknown (American Psychiatric Association. 2013~ It is possible that the intcre.~t in masochisrn and sadism is increasing. as indicated by wjdcly available sadomasoch istic pornography and bcst-..s clling novels such as FiftyShades ofGrey. Some information exists that masochists arc more common among higher socioeconomic levels. and many arc highly educated and successful at work (Levitt. Mosc.r, & Jamison. 1994).

Sexual a nd Gender Disorders

2J9

9.3f Sexual Sadism Disorder 'Ole term sadism comes from the name of the Marquis de Sade ( 1740- 1814}, who wrote stories

a bout achieving sexual gratification by inflicting pain on his partners. Sexual sadism djsorder involves intense sexuaJ arousal and fantasies. persisting for 6 months, about causing physical or psychologicaJ s uffering to others. 1'0 receive the diagnosis. the person e ither has committed the act on a nonconsent:ing person or is distressed and impaired by the urges. Sad istic fantasies in volve themes of dorninancc and control over another person and typically include bondage. whipping. spanking, burning. torturing. raping. or otherwise inflicti ng suffering. lhe cou rse tends to be chronic. and the activities may remain relatively mild or may increase in intensity and dangerousness: when severe. especially involving those with antisocial lll~,rsonaJitydisorder, victims may be seriously injured or lolled (American Psychiatric rt-U.stress Iridium reaches for a glowing candle. preparing to Association. 2000). 1l1e condjtion can be specified as in a dribble hot wax.on her fellow performer. Miko. al tha S&:.Mcontrolled en\•ironment or in full remission. 'O,eprcvalencc 1.hemed rustaumnl La Nom.-elleJu~Une in New York. In addition to the perform..anoe. ClL'ilorners can purchase $20 services from is unknown, but less than 10% of civilly committed sex U1e -speci.n I fare~ me nu. such as s:panki ng from a vinyl•dad waiter offenders carry the diagnosis (American Psychiatric or waitress. (AJ• Photo! Emde \\VIUl~I Association. 2013).

9.3g Transvestic Disorder 1he essential feature of transvestic disorder is recurrent. intense, sexually arousing fantasies, urges. or behaviors that involve cross•dressing. 1lle pattern must persist for at least 6 months and must be associated with distress or social impairment. 111c transvestic act may range from occasionally wearing a single object ofwomen's clothing to complete cross-dressing with makeup. female mannerisms. and habits. Most indi·viduals with transvcstic disorder experience the sexual arousa l by imagining t hey are females. often visualiz ing female genitalia. In the DSJ\1.JV diagnosis. the disorder. by definition. occurred only in Most cases oftrnn.-."\·eslk disorder in\·olve males who crossheterosexual ,nales . 11w DSJllf.5 no longer carries that dress as (em ales. tShutt.t!nillldcl requirement. It is distinguished from the cross-dressing that may be involved i n gender dysphoria, which is not done for purposes of sexual arousal. lt is a rare disorder in males and extremely rare in females. t hough actual incidence is not known. lt can be specified with fetishism or with autogyneph ilia (arousal at thinking of self as a female) and if in a controlled environment or in fuU remission (American Psychiatric Association. 2013). AsphyxlopbUia

9.3h Voyeuristic Disorder Individuals with voyeuristic disorder experience intense sexual arousal connected to observing an unsuspecting person who is naked. disrobing, or engaged in sexua l activities. 1"he d iagnosis requires that the person has either acted on these urges or that the urges caus.c the person distress or impa.irm.cnt: signs of voyeurism must persist for at least 6 months. 'fyp icaUy. the voyeur does not seek sexual contact with the observed pc-rs.on. a lthough he may harbor a fantasy of such activity. It is the violation of privacy that seems to be most arousing to the voyeur, who may masturbate- during the viewing or at a later time while recalli ng the

Intentional depri\'ntion of oxygen to increase intensity of ~exual arousal or orgasm

Sadism t>rcfc.rence for obtaining sexual grati!ication by inflictingpain on one·s partner

240

Chapter 9

Abnormal Psychology

event. Voyeurism usually begins by age 15, tends to have a chronic course, and m ay be the person's exclusive sexual outlet when severe (Am erican Psychiatric Association, 2000). The diagnosis can be specified if in a co11trolled environment or in full re1nission. Prevalence could b e as high as 12% in males and one third that for females (American Psychiatric Association, 2013).

9.3i

Other Specified Paraphilic Disorder

There a re many additional forms of paraphilic conditions-all having in common the intense sexual arousal associated with urges, fantasies, and act s involving unusual sources of attraction. If these are recurrent and persist for at least 6 months and if they cause distress or social problems, they may be coded as other specifiedparaphilic disorder. Some examples tl1at have been reported include zoophilia (animals), necrophilia (corpses), coprophilia (feces), and klismaphilia (enemas).

9.3j

Causal Factors

The fantasies and behaviors involved in the p a raphilias often first app ear during childhood and become elaborated in adolescence a nd adulthood (American Psychiatric Association, 2013). For example, both m asochistic and sadistic fantasies are likely to have been present in childhood. Psychoanalytic perspectives suggest that paraphilias result from regression or fixatio11 at earlier stages of psychosexual development-that is, the individual reverts to sexual habits that aroused them earlier in life. Other p sychoanalysts consider them expressions of hostility to obtain revenge for a childhood in which parents punitively inhibited budding sexuality (Masters et al., 1992). Biological speculations have included excessive exposure to m ale hormones, focal brai11 damage, and chro1nosom al abnormalities; however, evidence is lacking to support any of these possibilities. Most of the data on the d evelopment of the various paraphilic disorders derive from retrospective reports of the individuals involved. TI1ese reports suggest that learned anxiety or inhibition with respect to more conventional heterosexual behavior n1igl1t be mixed with positive experiences associated with particular pedophilic sexu al expression in childhood. In one conditioning model, McGuire, Carlisle, and Young (1964) stressed the importa nce of som e early experience with the deviant sexual behavior, followed by a p eriod during which tl1e person masturbates while fa11tasizing about the deviant object or behavior. The repeated masturbation is thought to condition sexual arousal to the particular fantasized stimulus. The authors suggest ed that without the subsequent pa iring of masturbation with the fantasized object, the deviant behavior would probably not develop. McGuire and his associates reported several examples in which such conditioning could have occurred. Two exhibitionists r eported similar experiences in which they had b een urinating in a semipublic place when a woman passing by surprised them. They felt no sexual arousal at the time; rather, they were embarrassed and left hurriedly. It was only later that the sexual significance of the encounter occurred to them, and each had then m asturbated frequently to the m emory of the incident. Eventually, the thought of self-exposure becam e so sexually arousing that each had acted upon the idea. In another case, a 17-year-old male had seen, through a window, a girl dressed only in her underwear. He was sexually aroused a nd later masturbated repeatedly to this memory. In tin1e, the m emory of the actual girl became vagu e, but adver tisem ents and shop window displays continually reminded him of underwear; his masturbating fantasies gradually fixated on female underwear. Three years later, he had no sexual interest at all in girls but was sexually aroused by fem ale under wear, which he bought or stole. In accordance with a conditioning model, sexual arousal has been established to formerly neutral stimuli through classical conditioning procedures. Rachman (1966), for exa1nple, paired a photographic slide of black boots with a slide of an attractive nude woman. Subjects

Sexual and Gender Disorders

241

s ubsequently sl1owed penile arousal when the pictures of boots were presented alone. Those results were later replicated, tl1ough certain methodological problems in tl1ese studies prevent clear co11clusions. For example, the control procedures were inadequate; specifically, arousal to boots was not assessed before pairing them with the nude picture. More recent controlled research has demonstrated, however, that male sexual arousal can be classically conditioned (Gaither, Rosenkranz, & Plaud, 1998). Social learning models proposed that lack of parental care, physical punishment, and aggressive behavior within the family increase the chances of pedophilic development. People raised in such homes may demonstrate the low self-esteem, limited capacity for affection and intimacy, and impaired ability to postpone gratification that is reported among sexual offender samples (Maletzky, 2002). In a different take on self-esteem, LaTorre (1980) reported that college students who had been rejected for dates responded more positively to pictures of women's legs and panties and less positively to pictures ofwomen than did other men who had not been rejected, suggesting rejection as a factor in fetish development. At this point, conditio11ing and learning models remai11 plausible accounts for paraphilia development, though further controlled studies are necessary.

9.3k

Treatment of Paraphilic Disorders

People with paraphilic disorders do not often seek treatment unless mandated by legal authorities; they may claim that therapy is not needed. Lack of motivation for change represents a serious impediment to therapy; in fact, those in treatment may make deliberate attempts to fool the therapist into believing that the problem has improved when, in fact, it hasn't (Masters et al., 1992). Publisl1ed reports on the treat ment of most paraphilias are based on case studies, providing little guidance for identifying effective therapies. Some medication approaches appear to be partly directed by the apparent similarity of the paraphilic behavior to obsessive-compulsive disorder, which may be responsive to SSRis. As such, antidepressants for1n one general thrust of pharmacotherapy for paraphilias. Other pharmacological approacl1es attempt to inhibit sexual arousal by giving estrogen-like or progestin-like hormones to males. These drugs reduce the production and action of androgens, and they have been associated with reduced sexual activity, including masturbation, in small group trials (Cooper, Sandhu, Losztyn, & Cernovsky, 1992). The limited data available are perhaps stronger in support of antiandrogens, although controlled comparative research is needed (Gijs & Gooren, 1996). Behavioral treatments for paraphilias tend to include masturbatory retraining or aversion techniques. Masturbatory retraining may involve instructing the p erson to m asturbate while engaged in the paraphilic fantasy and to continue masturbating for a much longer time (e.g., 1-2 hours) than is pleasurable, even after ejaculating. Most males experience continued stimulation such as this as very uncomfortable; the goal is to make the paraphilic fantasy aversive. This technique can be combined with m asturbation to nondeviant stimuli, in which case masturbation stops after ejaculatio11. There have been positive case reports based on this type of orgasmic reconditioning, wl1ich has been termed masturbatory satiation or masturbatory extinction (Gaither et al., 1998). Aversion approaches attempt to reduce sexual arousal to deviant stimuli by pairing them with aversive events sucl1 as electric sl1ock or noxious odors. Data appear more convincing for olfactory aversive therapy, which has been found useful in several studies. In one successful treatment example (Earls & Castonguay, 1989), an adolescent p edophile was presented sexual stimuli relating to children and to adults while undergoing plethysmographic assessment. An aversive odor (ammonia) was presented contingent on penile arousal to the child stimuli but not after arousal to adult stimuli. Post-treatment assessments and follow-up indicated increased arousal to adult images and dramatic decreases in arousal to children. A different type of aversive therapy involves covert sensitization, in which imager y of the paraphilic act is paired with an anxiety-i11ducing or nausea-inducing verbal description.

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242

Chapter 9

Abnormal Psychology

Typically, tl1e perso11 imagines engaging in the paraphilia and then imagines a very unpleasant outcome. Imagery of appropriate behavior is paired witl1 descriptions of positive outcomes. An early example comes from Hayes, Brownell, and Barlow (1978). The client was an adult male with a history of attempted rape, exhibitionism, and sadistic fantasies. The exhibitionist scenes involved imagery of exposing himself, in which he was identified by his victim and tl1en located by police, who arrest him at home in front of his crying wife. The imagined scene was constructed to 1naximize the aversive conseque11ces he most feared. Similar scenes were prepared for sadistic imagery. The results are shown in Figure 9-2. The degree of arousal was assessed in two ways: the physiological assessment of penile erection and the self-report using a card sort technique with cards that described various sexual situations. The covert sensitization procedure appeared effective during therapy and across an 8-week follow-up in reducing arousal to paraphilic stimuli, while arousal to normal heterosexual stimuli did not cha11ge. A diverse set of cognitive-behavioral procedures involving cognitive restructuring, relapse prevention, and empathy training (identification

Figure 9-2

Treatment of Paraphilias with Covert Sensitization

These data were obtained in response to exhibitionistic, sadistic, and normal heterosexual stimuli during baseline, treatment, and follow-up phase. Card sort data are daily averages iI1 the baseline and treatment phases, and weekly averages in the follo,-v-up phase. Data source: "The Use of Self-Adminstered Covert Sensitization in the Treatment of Exhibitionism and Sadism," by S. C. Hayes, K. D. Brownell, and D. H. Barlow, 1978, Behavior Therapy, 9, pp. 283- 289.

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Sexual and Gender Disorders

with the victim) has also been employed in individual case studies with some positive results. These approaches may focus on identifying and correcting cognitive distortions, assumptions, and justifications for paraphilic acts. Combining these techniques with behavioral or conditioning approaches can result in better outcomes (Maletzky, 2002). The promising results from case studies involvi11g either psychotherapy or pharmaceutical treatments have not been supplemented by well-controlled or double-blind trials, and compariso11 group data are lacki11g. Recidivism continues to be a serious problem in the treatment of sex offenders, and most interventions are not seen as alternatives to incarceration for those groups. Relapse appears to be high when medications are discontinued, and combination therapies do not allow partition of the effective components. There is obviously a need for more careful research to r efine tl1e treatment of paraphilias.

9.4 Gender Dysphoria In gender dysphoria, both (a) strong and persistent cross-gender identification and (b) persistent discomfort with one's assigned sex or witl1 the gender role associated with it occur. As a result, the person experiences clinically significant distress or impairment in functioning. The disorder is diagnosed som ewhat differe11tly for children than for adults; the criteria for gender dysphoria in children are shown in DSM-5: Diagnostic Criteria for Gender Dysphoria in Children. Children with gender dysphoria may express the wish to grow the genitals of the other sex; they prefer the stereotypic play, mannerisms, and attire of the other gender. Boys may enjoy fe1ninine toys and playi11g l1ouse, often role-playing female figures such as mothers or sisters. They prefer girls as playmates to other boys. They may also adopt feminine mannerism s, such as sitting down to urinate. Girls m ay refuse to attend school or social events in which feminine attire is required, may cut their hair short, and may take on a boy's name. TI1ey sl1ow little interest in dolls What is gender dysphoria? Is it or typical girls' toys and prefer boys as playmates, different from homosexuality? enjoying rough-and-tumble play and contact sports.

Diagnostic Criteria for Gender Dysphoria in Children 302.6 (F64.2) Gender Dysphoriain Children

A. A marked incongruence between one's experience/expressed gender a11d assig11ed gender, of at least 6 months duration, as manifested by at least 6 of tl1e following (one of which must be Criterion Al): 1. A strong desire to be of the otl1er gender or an insistence that one is tl1e other gender (or some alternative gender different from one's assigned gender). 2. In boys (assigned ge11der), a strong preference for cross-dressing or simulating female attire; or in girls (assigned gender), a strong preference for wearing only typical masculine clotl1ing and a strong resistance to ,vearing feminine clothing. 3. A strong preference for cross-gender roles in make-believe play or fantasy play. 4. A strong preference for tl1e toys, games, or activities stereotypically used or engaged in by the other gender. 5. A strong preference for playmates of the otl1er ge11der. 6. In boys (assigned ge11der), a strong rejection of typically masculine toys, games, and activities and a strong avoidance of rough-and-tumble play; or in girls (assigned gender), a strong rejection of typically feminine toys, games, and activities. 7. A strong dislike of 011e's sexual anatomy. 8. A strong desire for the primary and secondary sex cl1aracteristics that match 011e's experienced gender. B. The co11ditio11 is associated with clinically significant distress or impairment in social, school, or otl1er important areas of functioning. Specify if: With a disorder of sex development (e.g., a congenital adrenogenital disorder such as 255.2 [E25.0] co11genital adrenal hyperplasia or 259.50 [E34.50] androgen insensitivity syndrome). Coding note: code the disorder of sex development as well as gender dysphoria. Source: Reprinted with permission fro1n the Diagnostic and Statistical Manual ofMental Disorders, 5th ed. (Copyright 2013). American Psychiatric Association.

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Abnormal Psychology

Transsexualism Condition in which sexual identity is contrary to biological gender Congenital adrenal hyperplasia Condition i11 which fetal exposure to androgens results in masculinization of the genitals of a genetic female Androgen insensitivity syndrome Condition in which a genetically male fetus is insensitive to tl1e effects of androgen and develops genitalia resembling a female

In adolescents and adults with gender dysphoria, there is frequent expression of the desire to live as or to become the other sex, including interest in sex-change surgery or hormonal treatments. Gender dysphoria in adolescents a nd adults can be sp ecified if post-tra nsition (that is, living as the other gender and preparing for or completing gender reassignment). Often, effective cross-dressing allows some people with this disorder to pass convincingly as a m ember of the other sex. Gender dysphoria appears to be quite rare, althougl1 little dat a exist; i11 clinical settings, n1ales with the disorder out number females by a factor of least 2 or 3 in the United States, although in some countries (e.g.,Japan and Poland), females with the condition m ay outnumber m ales (American Psychiatric Association, 2013). In the DSM-I V, the corresponding diagnosis of gender identity disorder (also called transsexualism) ,-vas not give11 if there was a concurrent i11tersex condition, although this is no longer the case for gender dysphoria in the DSM-5. Some biological conditions affect the development of sex charact eristics in the fetus; as a r esult, some people m ay have genitals tl1at appear to have both male and fem ale characteristics. In one of these intersex conditions, congenital adrenal hyperplasia (CAH, also t ermed adrenogenital syndrome), a genetic female (XX) fetus is exposed to high levels of androgens during fetal development. This m ay cause elongation of the clitoris to resemble a penis and fusion of the labia t o resemble a scrot al sac; thus, the ext ernal genitals appear m asculine. In another intersex condition, androgen insensitivity syndrome, a genetic male (XY) fetus shows general insensitivity during fetal development to androgens and is born with undeveloped sexual structures that, b y default, resemble the ext ernal fem ale genitalia. In cases of these and other pseudohermaphroditic conditions, individuals troubled by persist ent cross-gender identity may be diagnosed with ge11der dysphoria with the specifier "with a disorder of sex developme11t." Accurat e diagnosis of gender dysphoria may be difficult. Reliability data from field trials indicated that the DSM-III diagnostic criteria showed very poor reliability (from - .001 to - .002 in tl1e two phases). In the DSM-5, it must be distinguished from simple nonconformity t o stereotypic sex roles, and the cross-gender identification must not be based m er ely on the cultural a dvant ages of being the other sex. The cross-d ressing involved must b e distinguished from tra nsvestic disor der (in which ca se, cross-dressing produces sexual arousal), and t h e conviction of belonging to the ot her sex cannot be delusional, as may occur in schizophrenia . In addition, sexual attraction to others ofthe same biological gender, which those exp eriencing gender dysphoria m ay consider normal heterosexual at traction for someone who ident ifies with the other sex, must be distinguished from homosexuality, in which t here is not gender discomfort. The course of gender dysphoria is variable. Two traj ectories are highlighted in the DSM-5: early-onset gender dysphoria starts in childhood, while late-onset d syphoria begins at or after puber ty. Cross-gender behaviors t end to decline for most children w ith the disorder, perhap s due to social and parental shaping. It tends to be more persistent in girls. Most boys (two t hirds or more) who do not p ersist in gender dysphoria identify as gay or homosexual; girls who do not persist i11 the disorder identify as lesbian at lower rates. Adults m ay show fluctuating course, with late-onset fem ales more likely to engage in transvestic activities for a rousal. People with gender dysphoria often feel so cially isolated and may experience concurrent an xiet y disorders or depression (American Psychiatric Association, 2013).

9.4a Causal Factors Although chromosomal sex is determined at the time of conception, gender identity develops in early childhood and is u sually established by age 3, suggesting that caus al factors for gender identity disorder are located in prenat al or early postnatal development. No research has established sp ecific biological factors in the Can people change from development of gender identity disorder. However, male to female or from animal research has demonstrated that masculine female to male? b eh avior ca n b e incr eased in female animals by

Sexual and Gender Disorders

providing high levels of male hormones in the prenatal environment, while male animals behave more like females when not given sufficient amounts of male hormones prenatally. Goy (1970), for exa1nple, injected pregnant rhesus mo11keys with the male hormone testosterone. Masculinized female infants were born with genitals that included both male and female characteristics. When these females grew up, they showed 1nore rough-and-tumble play and ,-vere more masculine than normal females in other social behaviors. Similar effects have been noted i11 human female children. During the 1950s, a number of pregnant women were treated with synthetic progestin (a hormone that prepares the uterus for pregnancy) in order to reduce miscarriages. An unexpected side effect of this drug was that it caused an excess of male hormones and, thereby, affected the develop1nent of female fetuses. Compared with matched control girls, these girls had more traditionally Chromosomal sex is deternti11ed at conception, and gender "masculine" interests, gave higher priority to a career over identity is usually established by age 3. However, research marriage, were less interested in participating in baby care in animals has established that pre11atal exposure to of a you11ger sibling or a neighbor's cl1ild, and preferred to unusual levels of male or female hormones can affect gender develop1nent. (iStock) play with boys' toys such as cars, guns, and trucks rather than dolls (Erhardt, 1973). The prenatal exposure of male fetuses to female hormones (estrogen and progesterone) has also been reported to produce "fe1ni11ization" in boys (Yalom, Green, & Fisk, 1973). However, there is no direct evide11ce that hormonal exposure causes gender identity disorder in humans, and there are no clear hormonal distinctions between those with gender identity disorder and people with normal gender identity. Coolidge, Thede, and Young (2002) reported tl1at analysis of twin research supports a strong heritable component in gender ide11tity disorder. However, Segal (2006) reported nonconcordance of female-to-male transsexualism in two pairs of identical twi11s, suggesting prenatal hormonal influences as possible causal factors. The DSM-5 describes the evidence of familial transmission as weak, with stronger support for prenatal hormonal influences (American Psychiatric Association, 2013). Psychoanalytic models tend to emphasize issues in parental relationships in which children overidentify with the other-sex parent. No clear evidence exists to strongly support any particular causal tl1eory.

Treatment of Gender Dysphoria Sex reassignment surgery appears to be among the only effective treatments for chronic gender dysphoria in adults. It is recommended that the person preparing for sex reassignment first complete a year oflife-experience as the other sex and 6 months on continuous hormone treatments in order to be a candidate for surgery. Male-to-female operations typically involve plastic surgery for creating a vagina and labia from penile and scrotal skin and modifying the remnant penis into a sensitive clitoris. The female-to-male operation is less well established but can involve creating a phallus with skin from the forearm (Sohn & Bosinski, 2007). Sexual sensitivity can be maintained by using the clitoris as a base for the neophallus. Reviews of outcome literature revealed that most transsexuals are satisfied with the outcome of sex reassignment surgery (LeVay & Valente, 2006).

245

246

TO SUM UP ... •

The normal sexual r esponse cycle consist s of four phases: the excitem ent phase, the plateau phase, the orgasmic phase, and the resolution phase.

Masters and Johnson helped dispel previously held fallacies about direct stimulation of the clitoris, clitoral versus vaginal orgasms, simultaneous orgasms, and the relationship between the size of the p enis and sexual enjoyment.

Sexual dysfunctions are disorders in which there is a disturbance in the sexual r esponse cycle or in which pain occurs during sexual activity. Sexual dysfunctions are relatively common among the population.

Anxiety about sexuality plays an important role in the development of these dysfunctions. Masters and Johnson especially emphasized p erformance anxiety and a spectator role.

There are a variety of effective psychotherapies for the sexual dysfunctions. Medications are increasingly used to provide symptom r elief as well. Som e sex therapists are concerned about the growing m edicalization of treatment for sexual dysfunctions.

Paraphilias are disorders in which the disturba11ce concerns the focus or target of sexual desire. They are much more common among males than females. Some paraphilic disorders involve activities that are illegal.

Behavioral approaches to treating paraphilic disorders appear promising, especially those involving covert sen sitization and orgasmic reconditioning.

Gender dysphoria involving persistent cross-gender identification and discomfort with or rejection of 011e's biological sex is ver y rare. Unlike sexual dysfunctio11s and paraphilic disorders, which may display high diagnostic reliability, the gender identity disorders historically show very low diagnostic reliability.

The causes of and treatme11ts for gender identity disorder remai11 unclear. Most adults who undergo sex reassignment surger y are satisfied with the outcome.

247

KEY TERMS Androgen insensitivity syndrome 244

Pletl1ysmographic assessment

Sadism

Congenital adrenal hyperplasia Kegel exercise Masochism Paraphilia

244

232

239

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Squeeze technique

237 234

Performance anxiety

222

Refractory period

239

Asphyxiophilia

237

231

Transsexualism

244

Vasocongestion

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223

QUESTIONS FOR STUDY •

Discuss Masters andJohnson's pioneering studies of human sexuality. How was tl1erapy for sexual disorders influe11ced by their work?

Suggest a possible explanation for the large gender difference in the diagnosis of paraphilias.

Describe the differences between transvestic fetishism and gender dysphoria.

POP QUIZ 1.

The human sexual response cycle was defined by _ _ _ __ A. B. C. D.

Benjamin Rush Alfred Kinsey William Masters and Virginia Johnson Sigmund Freud

2.

The proper order of the sexual response cycle consists of which of the following? A. plateau phase, orgasmic phase, resolution phase, excitement phase B. excite1nent phase, plateau phase, orgasmic phase, resolution phase C. excitement phase, orgasmic phase, plateau phase, resolution phase D. plateau phase, orgasmic phase, excitement phase, resolution phase

3.

Which phase do men exp erience, but not women? A. plateau phase B. orgasmic phase C. resolution phase D. refractory period

248

4.

Sally, now age 33, has experienced sexual dysfunctions since sh e was 13 years old. The DSM-5 specifier choice for Sally's situation is - - - - - · A. early remission vs. full remissio11 B. lifelong type vs. acquired type C. generalized type vs. situational type D. due to psychological or to combined factors

5.

To meet criteria for a sexual dysfunction disorder, the minimum duration of dysfunction must be ______., A. There is no minimum duration of dysfunction required. B. 1 month C. 3 mo11ths D. 6months

6.

The hormone ______ may increase sexual desire in m en a nd women who experience sexual desire disorders. A. progesterone B. estrogen C. adrenaline D. testosterone

7.

About ______ of U.S. women report some difficulties with low sexual desire. A. one tenth

B. one third C. one half D. two thirds 8.

According to psychoanalytic theory, men and women with deficient sexual a rousal show inhibited sexual excitement becau se, unconsciously, they perceive sexu al activity a s - - - - - -· A. dangerous B. odd C. confusing D. dirty

9.

An effective treatm ent for deficient arousal in m ales is - - - - - - · A. sildenafil B. aphrodisiacs C. alcohol D. ginkgo biloba extract

10. Seth is fascinated by women's shoes and stockings. He has recurrent, intense sexually arousing fantasies, urges, or behaviors tl1at r evolve around high heels, panty hose, and patent leather. He has 20 pairs of shoes and has stolen shoes from women's dressing rooms and from female coworkers. He often masturbates while merely smelling them or when a partner wears tl1em. He would b e diagnosed w i t h - - - - - · A. fetishistic disorder B. exhibitionistic disorder C. frotteuristic disorder D. voyeuristic disorder

249

11. John has recently incorporated the masochistic act of _ _ _ _ _ into his sexual life. 'This involves oxygen-depriving activities such as choking, hanging or suffocating.

A. areophila B. coprophilia C. asphyxiophilia D. klismaphilia 12. Jane gets sexual gratification by inflicting pain on her partner through whippings and beatings with various hard leather objects and by inserting blunt objects into various orifices. She would be diagnosed with - - - - - ·

A. transvestic disorder B. sexual masochism disorder C. frotteuristic disorder D. sexual sadism disorder 13. A pharmaceutical treatment for males witl1 paraphilic disorders is to give hormones in an attempt to reduce sexual arousal. 'These drugs reduce the production and action of _ _ _ _ _ _ A. oxytocin B. progestins C. estrogens D. a11drogens 14. When a genetic male fetus does not physically respond to the effects of testosterone and develops genitalia resembling a female, this is known as

-----· A. androgen insensitivity syndrome B. adrenogenital syndrome C. congenital adrenal hyperplasia D. Klinefelter's syndrome 15. It is recommended that the person preparing for sex reassignment first complete _ _ _ _ _ of life-experience as the other sex and _ _ _ _ _ on

continuous hormone treat1nents in order to be a candidate for surgery. A. 3 months / 6 months B. 6 months / 6 montl1s C. 12 months / 6 montl1s D. 12 montl1s / 9 months

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CHAPTER OVERVIEW 10.1 Psychosis .................. ................251 Disturbances In Language and Thought Drst.urbances in Sens.a tion and Percepbon Drst.urbances in Motor Behavior

E.mobonal Otsturbance Socsal Wnhdrawal

10.2 Diagnosis of Psychotic Disorders .. ...256 Schizophrenia Sd11zophreniform Oisorde-r Schi.zoaffectlvc Disorder 13nef Psychouc Disorder Oclus.onal Orso,der Additional Psychouc Otsorders

10.3 Causal Factors in Psychotic Disorders ......... ... . ....263 Bmlogical Factors The Search for Neurobehav,oral Markers Envtronme:ntal Factors Psychosocial F'.actors Causal Factors rn Psychos~ A Summary

10.4 Treatment of Psychotic Disorders ... .. .. .. .. .. .. ..279 8mlogical Therapy PS)'chosoc,al Thcrap)'

CHAPTER OPENER QUESTIONS What are the signs of psychosis? Can schizophrenia be reliably diagnosed? How do various psychotic disorders differ? How strong are genetic influences in the development of schizophrenia? What nongenetic factors seem to contribute to psychosis?

What is the dopamine hypothesis? Can psychotic disorders be treated?

Schizophrenia and Psychotic Disorders T

he disorders considered in tllis chapter represent severe forms ofpsychopathology that are usually labeled psychoses. As d istinguished from the Freudian. anxiety-driven n eurosis that can result when id impulses threaten to overwhelm the ego. psychos-is concerns a more serious pathology that involves a loss of contact with reality. The J)S.M-5 category or schizophrenia spectrum and other psychotic disorders includes sc,·cral distinct diagnoses: the most well known is schizophrenia. which has been the focus of clinical and research attention for well over a hundred years. Lay terms for these conditions often include madness or insanity(the latter actuaJ ly has a specific le.gal meaning that will be d iscussed in a later chapter). These condjtions distinctly differ in scope and impairment fro m the disorders considered thus far. To better understand these psychotic disorders. a general ove.rvicwofpsychotic symptoms follows.

10.1 Psychosis 1l1c. presence of psychosis is inferred in the same way as all other mental disorders: from what people say during an interview and how they act when observed. Some symptoms- such as delusions. hallucinations. and grossly impaired speech or movement- arc considered direct evi dence of psychosis. almost as if bizarre attributes have been added to a person ·s psychological repertoire. Other symptoms provide indirect evidence of psychosis: impairment in self-care. restricted range of emotion. poverty of speech content. and inability to initiate goal• directed behavior. In a sense. these indirect symptoms Disturbances in thinking and language are among the key symptonL-. o f psychosj.s, hStndl make it seem as if something has been lost or removed from a person's psychological state. Tue d irect (or positive) symptoms and in direct {or negative) symptoms What are the signs of can be described as disturbances oflanguage and psychosis? thought. disturbances ofsensation and perception. disturbances of motor behavior. emotional disturbances. and social withdrawal. Neurosis

10.la Disturbances in Language and Thought Loosening of Associations One aspect of psychosis is a tendency toward loose. disjointed expression in speech. Bleu lcr (1950) referred to this problem as the "derailment of associations," by which he meant that the person becomes distracted by irrelevant associations. cannot suppress them. and. as a consequence. wanders further and further off the subject. Some writers (e.g.. Mech). 1962) used phrases like ..cognitive sJippage"' to describe how t heschizophrenic's train of thought seems to slip away from its intended goal. Others refer to t hese a.c;pects of impaired communication as '"tangentiality.- because the speaker seems to fo llow tangents in the original utterance that lead loosely to other semantic pathways.

Freudian term for the anxiety~drivcn condition that results when id impulses threaten lo 01,,•cnvhelm the ego

Psychosis Severe psychological disturbance involving personality disorganization and los.s of contact 'Atith reality

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Chapter 10 Abnormal Psychology

Intruding associations may sometimes be highly personal and result in speech that is c.g occntric or autistic and. in extreme instances. almost totalJy unintclligib1c.111c following e.xample, from 70 years ago. remains as illustrative as C\'cr: l11te.rviewer: \Vhy arc you in the Hospital?

Patient: I'm a cut dona tor. donated by double sacrifice. I get two days for everyone. lhat's known as double-sacrifice: in other words, standard cut donator. You know. we considered it. He couldn"t have an.ytJ1ing for the cut, or for these patients. /Jtte.rviewer: \Yell. what do you do here? l'atie11t: l do what is known as the double criminal treatment. Something that he badly wanted. he gets that. and seven days' crim inal protection. '£hat's all he gets. and the rest l do for my friend. l11ter11iewer. \,Vho is the other person t hat gets all this?

Patient~ That's the way the asylum cut is donated. l11terviewer: But who is the other person? Patient: He·s a criminal. He gets so much. He gets twenty years criminal treatment.

,-.Tou ld make fort-yyears: and he gets seven days criminal protection and that makes fourteen days. 11,at's all he gets. l11ter11iewer. And what are you?

J'atie,,t: \\!hat is known as cutdonator Christ. None of them couldn't be able to ha,re anything: so it has to be true works or prove true to have anything, too. He gets two days; and that twenty years makes forty years. (Came.ron. 1947. pp. 466- 467) Note that the patient's sentence structure or syntax is not impaired: tJ1ere is no evidence of educational or intellectual difficulties that might make communication ineffecti\te. Instead. although the form oflanguageappcars normal, the content is unusual. and the meaning seems lost.111e part.s maybe lo0&dyconncctcd- for instance. tJ1e -double sacrifice seems associated with the doublingof20years to 40 years and the doubling of? days to 14 days. However. in the utterance. the contribution of this connection to the information is obscure. 'IO many clin icians. such impaired communication has been considered evidence of a formal Lhought disorder. lhe DSl't1•5 distinguishes between loose associations or derailmenL which involve shifts bct\\leen clauses of topics or referential frames. and incoherence, which concerns shifts within c.lauses (American Psychiatric Association. 2000). The unusual results of loose language associations have sometimes been described as -word salad-- that is. psychotic speech can almost seem as if a collect.ion of words were thrown together and tossed. like a salad. before presentation. Of course. for the psychotic speaker, words may be associated in ways of which the listener is unaware. One example is called c.laogiug, which involves the use of a word not because ofi ts meaning but because of its sound (such as in rhyming or punning). In other cases. a psychotic speaker employs tJ1e use of ncologisnut or ~new words" that the speaker invents. Consider this letter from Larry P.. as written to the author jn request for release from the hospital: H

Clanging 'the use. of a word because of its sound rather than its meaning

Neologism New word that a speaker invents Alogla

Impovcrished speech that conveys little information

1he Physcological Sanity of my mind is conducted with Reason of sanity justice sedetating attempt to cooperated a sanity ofjustice deaJ of ordain lane. attempt of shock treatment oftolcratingaUcrgic reactions of dust acid attacks. 111is is my offering ofjustice answerable logk which says I'm sanity but I can't conduct. so please e.xcusc this era ofjoint settlement ofjoint delusion. I'm still please to hear of this place but I would like some kind of discussion about this reason of jurc demand. Other characteristics of psychotic language use include a Jogia. or impoverished speech. Replies to questions may be very brief and convey little information: speech may be repetitive, stereotyped. and nonspontaneous. Sometimes. psychotic language appears to be

Schizophrenia and Psychotic Disorders

overgeneralized and hypcrmetaphorical. An intere~~ting observation comes from Luria (1982), who proposed that in response to the question -v~"hat is a dog?'" those ofJow intelligence would give a concrete. one-dimensional answer. such as -a dog barks- or -a dog has four legs'°: a normal person might give a categorical response. such as-a dog is a mammal .. or -a dog is a peC; and a schizophrenic person might give an overgeneralized response. such as ..a dog is mass. attracted by gravity to the earth's core." Hyper-metaphorical speech is a form of overgencralization;'1t,/,.{,t instead of reporting. ~My arm fell asleep... a psychotic person might report. '"My arm died" (taking the s leep metaphor too far). Conversely. other psychotic speech shows r:: ..... ~ echolalia, in which the person repeats wha tcver someone else says. • •

-

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Bizarre delusions involve false beliefs that could not possibly be true, given what is known about the world. For example. a woman who insists she is pregnant. despite a series of negative tests. may be delusional. though the delusion L~ not a bizarre one. It is possible that a mistake was made: false negatives arc not unknown. However. a man who insists that he is pregnant is endorsing a belief that could not conceivably be true. Similarly, the delusion of being followed by Ute Cl.A is not c.ornpletcly implausible: however, a man who believes that his head is switched onto other bodies at night while he sleeps is engaging in a bizarre delusion.

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.Delusionaljealousy involves t he incorrect conviction that a person's spouse or sexual partner has been or is being unfaithful. Unlike -normal- suspicion about infidelity, delusional jealousy is unreasonably held. even in the face of proof or evidence to t he contrary.

Erotomanic delusions arc patently false beliefs that another person. often someone famous or of higher status or authority. is in love with the individual.

Gra.ndiose delusions involve grossly jn Hated sc)f..irnportancc, fame. power. wealth, or knowledge. lbcy may involve special relationships with powerfuJ or holy entities or identification with a great person from history, such as a politicaJ. military. or religious leader.

iWood•congruent delu.si.ons concern content t hat is enti rely consistent with c..xpressed mood. r:or e.~ample. the belief that one is responsible for a deadly tornado or that one's body is rotting would be congruent with depressed mood (as would other tJ1cn1es of death. guilt, or failure).

Mood-incongruent delusions involve content that is not consistent with the prevailing mood. Beliefs of unlimited wealth and power wou ld be jncongrucnt with depressed mood.

Echolalia Repetition of words or phrases spoken by another person Delusion False belief that is linnly held. conuary to evidence and the consensus of other people

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Delusions ofbeing controlled involve the belief that som e external force or agent is manipulating one's movements, thoughts, speech, or emotions. People may believe that a murderous impulse, a sexual fantasy, or an urge to com1nit suicide is imposed from the outside. The controlling agents may be gods, demons, parents, political groups, or a vague "they." The mechanis1n of control is sometimes sp elled out-for example, hypnotism, extrasensory perception, or influencing machines such as a television set or an X-ray device.

People with schizophrenia or other p sychot ic disorders tend to perceive tl1ings different ly tha11 others do. (Shutterstock)

Delusions ofreference are false beliefs that events, people, or things in the immediate environment h ave a sp ecial and unique significance for the individual. For example, a p er son m ay b elieve that graffiti refers sp ecifically to t he private events of an indiv idual's life or that a song broadcast on the radio was m eant to send a sp ecific m essage to the p erson alon e.

Persecutory delusions concern the theme of being plotted against, attacked, cheated, threatened, or persecuted in some way by other various p eople or groups, such as neighbors, competitors, bosses, politicians, or the FBI. People holding such beliefs may find confirmation in seeing a group of people laughing among tl1em selves or in the frow n of a passing pedestrian.

Somatic delusions are false convictions that con cern the body. Examples include the belief that one is chan ging sexes or is pregnant or that internal organs are rotting.

Thought broadcasting delusions involve the belief that others can hear or receive one's thoughts.

Thought insertion delusions con cern the belief tl1at so1ne external person or agency is inserting thoughts into one's consciousness. In some cases, the delusion involves receiving special broadcasts through a sp ecial receiver implanted within the brain.

These categories of delusions are organized co11ceptually and are not mutually exclusive. Persecutory delusions, for example, could b e mood congruent with depression while also being bizarre.

10.lb

Hallucination Se11sation or perception in tl1e absence of an exter11al source Illus ion 111e incorrect perception of sensory sti1nuli

Disturbances in Sensation and Perception

Psychotic individuals often report perceptual distortions. The world may seem flat, unreal, or remote; objects may seem unusually large or sm all; or time may seem to pass witl1 unusual slown ess or rapidity. One patient described how other p eople appeared distorted: "People look confusing. ... They look almost like they'r e m ad e up .. . like they're real people ... and people I know, but they have masks on or they're disguising themselves. It's like a big play" (Freedm an & Chapman, 1973, p. 52). Even more dramatic than p er ceptual distortions are false sensory exp erien ces called hallucinations. The person hears voices, sees visions, smells odors, or has sensations of touch for which there are no identifiable external stimuli. Halluci11ations must be distinguished from illusions, in which an actu al sensor y stimulus is perceived incorrectly. (In the dark bedroom, clothes hanging in the closest m ay b e misperceived as a lurking killer, but this is not hallucinatory.) Hallucinations also are distinguish ed from tl1e strange sensory exp eriences that are som etimes associated with falling asleep, dreaming, or awakening.

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Hallucinations can involve any sensory systcrn: •

In auditory hallucinatio,u. the person hears voices tha t may condemn, praise. direct. or accuse. lhcy may be identified with a specific agent, such as God. the devil. parents. past acquaintances, or unspecified ·others." \Viii le experiencing a hallucination. the person may or may not i·calizc it is unreal: often. it may seem to come from nn external source. 'Ote individual may listen passively to the voices. act upon their c.omrnands, or talk back to them- arguing. pleading, or cursing them. Interestingly. brain imabringstudies have s hown that individuals experiencing auditory hallucinations display activation in the expressive. rather than receptive. language areas of the brain (Cleghorn ct al.. 1992): in rnany ways. auditory hallucinations appear to involve faulty interpretation and monitoring of self-talk (Allen. Aleman. & McGu ire. 2007).

Visual hallucinations can include lights. moving objects, places. and people. In some cases, they may appear as cartoon objects or as unformed images.

Guslatoryhalluciua.tions involve the perception ofa taste, such as blood. f\,lost often. the taste is unpleasanL

Olfactory hallucinations invohrc odors. usually unpleasant. such a.s decaying matter or burning hair or rubber.

Somatic hallucinations concern false sensations experienced as coming from inside t he body. such as e lectricity or pressure.

1fJclile hallucinations concern the false feeling of being touched or having something just beneath the s kin. s uch as splinters or crawling insects.

Andreu Yates. convicted in 2002 of murdering her fh·e children. was later fou nd not gullty by reason of 1ru.anily. She reportedly suffered from auditory hallucinations. CAP Pbolo,'St.tv-e l'..du:,U

Hallucinations can also be considered as mood congruent or mood incongruent. Any type of hallucination can occur in psychotic individuals. but certain types may be more comm.on in some d isorders. For example. the hallucinations rnost commonly reported in sc.hizophrcnia arc auditory. alt hough othc.r types can also occur. Drug-induced psychoses can involve strong. visual hallucinations. Tactile hallucinations may be more typical of drug withdrawal. Damage to any sensory areas of the brain could result in hallucinatory res ponses involving those arc.as. Gustatory and olfactory hallucinations may often be more characteristic of medical cond it ions or localized brain impairments. such as temporal lobe epilepsy. than of schizophrenia {American Psychiatric Association, 2000).

10.1c Disturbances in Motor Behavior Psychotic persons may seem unresponsive to others and engage in strange. stereotyped gestures. postures. or facial grimaces, referred to as catatonia. OccasionaUy, t hey may cease bodily mo\'Cment.~ altogether in catatonic immobility (stupor). or they may become wildly excited, at the otl1cr extreme. and move violently or unpredictably in catatonic e.xcitcment. Sometimes. a waxy flexibility is present, in which a catatonic person can be molded jnto a posture that may be rigid I)' maintained over long periods. Other forms of catatonic behavior indudeapparently motiveless resistance to instructions or attempt.~ to be moved. stupor. refusal to speak (mutis m). and echopraxia, in whic.h a person imitates the mO\rcments of others. Some become unable (or unwilling) to d.rcss, undress. feed themselves. or attend to their toileting needs. Ordinary inhibitions may be lost so that they urinate, defecate. or masturbate in public.

Catatonia Unusual movement or immobiHty associated with psychosis Mutism

Refusal to speak Ecbopraxia Repetitively imitating the movements of others

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Catatonia can occur within several disorders. The DSM-5 has added it as a specifier, defined by the presence of at least three catatonic symptoms: other p sychotic disorders, other m ental disorders, and other medical conditions. For example, cat atonia can be a characteristic of schizophrenia or other psychotic disorders, major depressive disorder, or bipolar disorder; it can also occur with head injuries and neurological diseases. In these conditions, the appropriate DSM-5 diagnosis would be catatonia associated with another m ental disorder, catatonic disorder due to another medical condition, or unspecified catatonia (when the underlying condition is unclear).

10.ld

Emotional Disturbance

Frequently, the em otional state in psychotic conditions is described as shallow, flattened, or blunted. Affective flattening is characterized by a lack of range of emotions. The lack of enjoyment in all aspects of life that often characterizes the schizophrenic person is sometimes referred to as anhedonia. In some psycl1oses, emotions are expressed inappropriately. People m ay laugh, cry, giggle, or rage with no clear relationship to events in the social environment.

10.1 e

Social Withdrawal

Schizophrenic individuals tend to avoid close interpersonal relationships, spend much of their time alone, and retreat more and more into their own fantasy world. The withdrawal is both physical and psychological. Their unintelligible speech and inappropriate emotio11al expression can keep them as psychologically distant from others as would miles of physical space. There 1nay be confusion about personal identity, gender, and sense of self that add to disrupted social relationships. In addition, volition (or goal-directed behavior) seem s impaired, so that work a11d self-care responsibilities are not con1pleted, further isolating the individual from others.

10.2 Diagnosis of Psychotic Disorders Affective flattening Lack of range of emotions Anhedonia

Loss of interest or pleasure in all aspects of life

Table 10-1

Although the psychotic disorders are discussed together in the DSM-5, there is no assumption that these disorders share a common cause, a common pathway, or even a common fundamental set of symptoms. Psychotic symptoms can appear briefly (transiently) during periods of stress in individuals wl10 l1ave ma11y different conditions and do not, i11 themselves, verify the presence of a psychotic disorder. The symptom patterns and degree of impairment differ within the psychotic disorders as well. The main psychotic disorders are summarized in Table 10-1. Not listed in Table 10-1 is schizotypal personality disorder (refer to Chapter 8), wl1ich the DSM-5 co11siders within the schizophrenia spectrum but also describes among the personality disorders (American

DSM-5 Psychotic Disorders

Disorder

Key Symptoms

Minimum Duration Required for Diagnosis

Sex Ratio

Schizopl1renia

Delusions, hallucinations, disordered speech and behavior

6 montl1s

More com1no11 a1nong males

Schizopl1reniform disorder

Same as schizophrenia, but duration less than 6 months

1 montl1

Slightly more common among males

Schizoaffective disorder

Mood episode a11d halluci11ations/ delusions occurring togetl1er

2 weeks

More common amo11g females

Brief psychotic disorder

Delusions, hallucinations, disorganized speech but duration less than 1 month

1 day

More common among females

Delusional disorder

Nonbizarre delusions witl1out other symptoms

1 month

Equal

Source: A1nerican Psychiatric Association, 2013.

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257

Psychiatric Association, 2013). The distinction among schizopl1renia, schizophreniform disorder, and brief psycl1otic disorder is one of duration. The involvement of significant mood components distinguishes schizoaffective disorder. In delusional disorder, the psychotic symptoms are largely limited to delusions, and, in that sense, individuals m ay show less overall impairment in daily living. Many medical conditions ca11 also produce psycl1otic symptoms. Neurolog ical conditions (such as epilepsy and multiple sclerosis), endocrine disorders (including hypothyroidism), metabolic conditions, fever, and nearly any other disorder with central nervous system involvement could be responsible for p sychotic states. In addition, a variet y of legal and illegal substances can produce hallucinations, delusions, verbal incoherence, and other psychotic behavior as a direct result of use or upo11 abrupt withdrawal. The appropriate diagnostic categories for these Because a variety of legal and illegal substances can produce conditions are "p sychotic disorder due to another m edical h allucinations, delusions, and other psychot ic behavior, they 1nust be considered wl1en atte1npti11g to diagnose a psycl1otic condition" and "substance/m edication induced psychotic disorder. (Psilocybe.tampanensis.t"vo by Workman, available u nder a disorder," respectively. Creative Con1mons Attribut ion License CC BY SA 3.0 at https://con1mons. ,vi kimed ia.org/\viki/ F ile: Psi lacybe.ta1npanensis.two .j pg)

10.2a Schizophrenia Probably no mental disorder has received as much attention within the professional literature as schizophrenia. The disorder represents a puzzle that has so far defied solution, despite the focused effort of medical and psychological science. Much important knowledge has been gained, yet much more information is needed to understand this extreme condition.

History of the Diagnosis As noted i11 Cl1apter 2, Kraepelin used the term dementia praecox to refer to a syndrome that involved an early, usually gradual onset and a progressive deterioration of mental functioning. Bleuler (1950) introduced the term schizophrenia Can schizophrenia be in 1911 to refer to essentially the sam e pattern of reliably diagnosed? psychological symptoms. He drew upon the Greek words for "split mind" to refer to a split bet ween thought processes and emotions or to a gener al disorganization in thought and behavior. This kind of splitting is not the sam e as that in the dissociation reactions offugue, amnesia, or multiple personality. In those conditions, tl1e split is between different states of consciousness (or different selves) rather than between thought and emotion. Bleuler did not believe that schizophrenia necessarily began in childhood or adolescence or that it necessarily progressed to an irreversible dem entia. Europea11 and American psychiatrists diverged in their diagnostic practices witl1 respect to schizophrenia. The Europeans stayed rather close to Kraepelin's original concept and tended not to give this diagnosis to individuals who abruptly developed acute schizophreniclike symptoms but who then recovered from the episode within a few months. European psychiatrists were also more inclined to diagnose patients as manic-depressive (or bipolar) who would have been diagnosed schizophrenic in the United States. U.S. psychiatrists, on the other hand, were more influenced by Bleuler; thus, they did not insist on a chronic course of the disorder. Further, their approach explicitly stated that the diagnosis of manic-depressive disorder should be made only if tl1e diagnosis of schizophrenia had definitely been ruled out. A demonstration ofhow the diagnosis of schizophrenia increased from the 1930s to the 1950s in the United States is provided by Kuriansky, Deming, and Gurland (1974), who showed that only 28% of the patients at the New York State Psychiatric Institute were diagnosed schizophrenic between 1932 and 1941, co1npared ,-vith an astounding 77% between 1947 and 1956.

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Aficr 1980. some of these differences began to disappear. By employing t he more precise

d iagnostic system of DSM~JJ/. the number of people diagnosed wit h schizophrenia in the United States was cut in half: Acute schizophrcnic~likc episodes lasting fewer than 6 months

were classified as schizophreniform disorders, while those with strong mood components were more likely diagnosed with schizoaffective disorder.111ose who m.ight have been labeled with ·simple schizophrenia" or · latent schizophrenia" in the DSA1-JJ \...·ere likely, instead, to be

DSM-5

Diagnostic Criteria for Schizophrenia

295.90 (F20.9) Sch;rophren;a A. Two (or more) of the following. each pre-s ent for n significant proportion of lime during a 1-monlh period (or Jes.,; if successfuUy treated). At least one of these must be (I). (2), or (3,): J. Delusions.

2. Hallucinations. 3. Disorganized speech (e.g.• frequent derailment o r incoherence). 4. Grossly disorgani:r.ed orcalatonic behavior. 5. Negative symptoms (Le.. diminished emotional expres.sion or a\'olilion). B. Forasigni6canl portion of the time since lheonsetof the disturbance. level of fonctionlng in one or more mujorareas. such as work. interpersonal relations. or .self~care. L,; markedly below the level achieved prior to lhe on.set (or when the onset i.s in childhood or adolescence. there is failure to achieve expected le,·el of interpersonal. acudt."lTiic., or occupational functioning).

C. Continuous signs of the disturbance persist for at least 6 months. This 6-monlh period must include at least I month of symptoms (or Jes,.,; if succe.ssfuUy t reated) that meet Criterion A (i.e.. actlve-phase .symptoms) and may include periods of pmdromaJ or residual symptoms. During these prodromaJ or re.siduaJ periods. the .signs of the di.sturhance may be manifested only by negati\'e.i.1'Tnptoms or by two or more symptoms listed in Criterion A present in an a ttenuated form (e.g.. odd beliefs. unusual perceptual experience-s). D. Schiz.oaffc.,ctive djsorder and depre.ssi\' Were

Necesary. What 1hey Demonstrated and Failed to Demon!llrate," by S.S. Kety et al. 1916, Sc/1/zophrtn la Bl1/leti1t. 2. pp. 413-·12$.

lhe rc.suJts of these adoption studies a:rc difficult to expla in by environmental fac tors. since the early removal of the child from the biological fami ly should prevent the. psychologicaJ transmission of the d isorder from the biologic.al parents. It would be necessary to show that

the adoptive environments of the experimental children were more pathology inductive than those of the control children. and there was no reason to suspect that might be the case. Many adoption and family studies tend to show that a greater-than-expected proportion of biological parents or otlu:-r relatives ofschizophrenic child rcn have schizophrenia spectrum disorders such as schizotypal personality disorder and schiwaffcctivc djsorder: the evidence is more limited for schizoid, pamnoid. and avoidant pcrsonaHtydisordcrs {American Psychiatric Association. 2000). All of tl>.is suggests the possibi1ity that some aspect of the genetic disposition to schizophrenia may. in weaker form. manifest itself in these djversc disturbances. In summary. both the twin studies and the adoption studies indicate that genetic factors contribute substantially to the development of schizophrenia. although estimates of tJ-1e degree of influence have moderated somewhat over the past few decades.Ongoing research is attempting What non genetic factors seem to identify specific chromosomes or genes that could to contribute to psychosi.s? be rc-sponsible for increased risk for the d isorder.

Genetic Linkage Studies Tracing the disorder within a pedigree and deciphering ONA segments that may affect the production ofvarious neurotransmitters arc among the techniques

employed to search for the genes thataffcctschizophrcn.ia. Many studies ha\·e been conducted in this endeavor. and 111.any more are undcn'lay. Researchers looking for marker genes have irnplicated multiple sites on at least 10 chromosomes: incre.asingly. the developing vi.cw is that the disorder is very complex genetically. In fact. no single gene has been consistentJy as.sociated with increased risk for schizophrenia. despite intensive research (Tandon. Kcshavcn, & Nasrallah. 2008). According to one estimate, of the 325 possible dopamine• related polymorphisms that are candidates in Caucasian r isk, only 19 have been evaluated in methodologically appropriate ways: satisfactory conclusions about their involvement arc still elusive (Talkowski ct al.. 2007). Genome studies have also revealed smaJJ but significant

genetic overlap bcl:\\"ecn schizophrenia and other major mental disorders- notably. depression. bipolar disorder. a utism. and attention-deficit/hyperactivity disorder (Smoller et al. 2013). At present, the most accurate description of research is that the genetic mechanisms producing schizophrenia arc unknown but probably involve a broad spectrum of both common and uncommon aUcles, each contributing to a smaUdegree (American Psychiatric Association, 2013). For perspective on the djfficulty of genetic research into the disorder. Cromwell (1993) noted thal 89% of schizophrenics have no known relative with schizophrenia.

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Neuroc/Jemistry One possibHjty is that genetic influences impact t he risk of schizophrenia by modifying biochemical processes in the central nervous system. especia lly tJ1osc related to neurotrans.. mission (sec Figure 10-3). This idea of a biochemical imbalance in psychopathology has an

Schizophrenia and Psychotic Disorders

Figure 10·3

Release of Neurotransmitters

Molecules ofchemic.al neurotransmitters, such asdopami1\C and norepinephrinc, arc released at tJ1e nerve endjng. travel across the synaptic cleft, attach t hemselves to receptor sites on a succeeding neuron. and thus activate an cJectrical impulse that travels aJong that neuron. Afier pcrfonning this function. most ncu.rotransm ittcr molecules. including those ofdopamj ne and norcpinephrinc. arc released and re-absorbed in the original nerve ending. Copyright© BVT Publb•hi ng

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old and honorable tradition that goes back to Grecian theories of-humors" in the blood and more recently to Kraepclin. who believed that dementia praecox was probably caused by toxic substances secreted from the sc.x glands. 'Ole fact that certain chemicaJs. such as hallucinatory and stimulant drugs. can produce strikingcha.ngcs in mental experiences that resemble the schizophrenic reaction lends credence to the hypothesis that. in schizophrenia.

267

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Chapter 10 Abnormal Psychology

tJ-1e body may be producing its own toxic substances. 1l1e search for that toxin included the taraxei11 hypothesis, which proposed that copper proteins in the bJood of schizophrcn~ ics p roduced a toxin that interfered with normal bra.in function. Kidney dial}1sis was used as a treatment for schizophrenia until 1977, under the assumption. that the toxin could he removed. Others proposed that a naturally produced psychedelic substance was overabun~ dant in lhe brain of schizophrenics. A~cr 50 years of work. one of t he most consistently s upportc-d What is the dopamine findings has been evidence implicating the role of hypothesis? e.xccssive activation of neuronal tracts that use the neurotransmitter dopamine. 11,~ dopamine hypothesis. which proposed that schizophrenia resulted fron1 a relative. excess ofdopamine activity in tJtc braio. was an outgrowth of the attempt to explai n the action of the anti psychotic medications that began appearing in the l950s.Although the drugs from the phcnothiazine class. with the first product marketed as 'ntorazi neo-. were originally used for tranquilizing properties prior to surgery, they were inadvertently determined to reduce several signs ofpsychosis including delusions. catatonia. and. to a lesser extent, hallucinations. Research into their mechanism of action indicated that they a ppeared to block dopamine receptor sites on post.c;ynaptic neurons in brain networks now thought to participate in attentional. motivational. and emotionaJ activities. 'fhe drugs were assumed to be effective because they counteracted the cause of schizophrenia- that is. too much dopamin ergic activ ity. Severa] lines of evidence support the dopamine hypothesis. First. among the frequent side effects of heavy and prolonged use of phenothiazincs for schizophrenia are symptoms resembling Parkinson's disease: rhythmic t remors accompanied hy difficulty in controlling body movements. fOte dopamine tract has been shown to degenerate in Parkinson's disease. and the d isease can be successfully treated with L-dopa. an amino acid that rc-plcnish cs tlte available supply ofdopamine. The 2001 fi lm A BC(tubful Mwd is lou.o;ely based on the lire ofJohn furbes Nash Jr- a genius tltus. the phenothiazincs. in all likelihood. arc in sornc way reducing matluunalician. The film shows how Na.sh activity in dopamine neurons and mimicking. in part. the symptoms of d eveloped paranoid schirophrenia as a young Parkinson's disease. m an und endured t he loss und burden thnt his condition brought lo hi!. wife and friends. 1J1c dopamine hypothesis also receives support from research with (Jflhn fotbc, N.uh,Jr. b\• Economldonm1, av1ul.11ble under amphetamine drugs.1hese stimulant drugs produce two cff'ect.s related a Cri,ahvc-Common, AttnbuOOnl.ic~ns.c, ct' BfSA ;UI 1d httJ>$://C'ClfflmoM.wdrimc:di.a.CK1'.. ,._,fld/File:.fnh n_ Finb~_ to schizophrenia: (I) In large and continuing doses. amphetamines elicit N"~h._Jr-,pg} a psychosis that can be indistinguishable from acute paranoid schizop hrenia (2) 1n very small doses. they exacerbate certain symptoms of schizophrenic patients. f"inally. tbe phenothiazines have a calming effect on amphetamine psychosis (Snyder. 1974). l'his evidence provides a strong, though indirect. indication that some k ind of ovc.r activation or dopaminergic neurons is associated with schizophrenia. At first. it was assumed that the disorder involved excessive p roduction of dopamine. but f urthcr research cast doubt on this possibility. Post. !,;-ink. Carpenter Jr.. and Goodwin (1975}. for example. found no difference in levcls ofhomovanillic acid (one of the substances resulting when dopamine is mctaboliz.cd) in the ccrebrospinal fluid of acute schizophrenics and various comparison groups. findings of this kind led investigators (Bacop oulos. Spokes. Bird . & Roth. l979: Post ct al .. 19'75) to suspect that ovcrsensiti\fity in the dopamine receptors. rather than excessive amounts. may account for the inferred unusual degree of activation in the dopamincrgic neurons. More recent work suggests that an excess of particu Jar types of dopamine receptors. called 02 receptors. arc present in the brains of schizophrenics (Abi;Oargham. 2004). As promising as the dopamine hypothesis is in explaining schizophrenia. there arc data that do not appear to support it. For one third of schizophrenics. dopamine-blocking drugs arc unhelpful. For those who do respond. it may take weeks to show improvement. evc.n

Schizophrenia and Psychotic Disorders

though the receptors arc blocked almost immediately. Other neurotransmitters have also been implicated. includingglutamate (which may a]ter dopamine transmission), serotonin. and t he inhibitory transmitter GABA (Goff & Coyle. 2001). Newer antipsychotic drugs may on ly weakly block dopamine and have most ofthcir effects on these other neurotransmitters. yet t hey seem to be about equally effective as the original phc.notlliazines. 111e dopamine hypothesis is now considered a part of the neurochemicaJ description of schizophrenia- but it is not the entire story.

Neuroanatomy '01e brains ofschizophrenic patients reveal no specific anatomical deviations or lesions t hat consistently distinguish tJ1em from the brains of normals. However.evidence collected over the past SO years docs suggest some possible impairment in brain functioning in schizophrenia. Ricks and Namcche (1966), for example. found e\•idencc for Msoft signs- of neurological impairment (abnormaJ speech. abnormal gait. poor c-0ordination, impaired attention span. and hyperactivity) when U-1ey examined guidance clinic records ofadolcs.cents who were subsequently hospitn.Jired for schizophrenia.Subsequently. EEG studies (e.g.. ltil. 19n)

suggested higher incidence of abnormal brain wave patterns among schizophrenics. along witJ1 evidence that points to dysfunction in the left hemisphere of the brain in samples of schizophrenic patients (Buchsbaum. 1977). None ofthes.c findings in small groups of subjects was consistent enough to b-c useful in diagnosis. With improvement in brain imaging. research turned to CAT. PET. Mfll. andjlvLRI scanning to identify difforcnces

, •

between schizophrenic and normal brains. with mixed results. Some proportion of schizophrenics. variously estimated at between 25% and 60%, show evidence of Improvements in brain imaging led re.searchers to use CAT. enlarged brain ventricles. Unfortunately. brain ventricle P£T. MRI. and/MRI .scanning in tln:ir al tempts lo identify differences between schizophrenic and normal brains. Some enlargement is not unique to schizophrenia: it a lso schizophrenics s how evidence of e nlarged brain ventricles.. occurs in several other conditions. including chronic flStac:kl alcoholism. Huntington's disca~e. and AJzheimer's disease. Enlat'g:cmc.nt may also not correlate well with psychotic symptoms. sometimes appeari ng in the well twin or the healthy siblings of schizophrenics (Staal ct al.. 2001).

Other neurological reports suggest that some schizophrenics shm-..• ccrebraJ atrophy (Keller ct al. 2003). decrease in the size of the thalamus (Staa l ct al.. 2001). and reduction in the si1..c of the hippocampus (Velakoulis ct al.. 2006). Special caution is needed in interpreting the resu lts. both because of concerns over the vaHd ity ofjMRI studies in general (sec Chapter 4) and because brai n changes are known to result from prolonged use of neuroleptic. medications. such as t he phenothiazincs. which might be confused for separate evidence of the disorder. Torrey (2002) concJuded that evidence for brain abnormalities is strong and not related to medication use. However. no anatomical marker specific to schizophrenia or necc$sary for its occurrence is known.

10.3b The Search for Neurobehavioral Markers Since the 1930s. researchers have employed t he techniques of experimental psychology to ascertain differences between schizophrenic and normal subjects on common cognitive tasks such as memory. reaction time. and attention. Over the years. a vast literature has accumulated. Although numerous ncurobehavioral deficits have been identified in schizophrenic samples, the severity ofeach has varied widely. It was hoped that these deficits

2 69

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Chapter 10 Abnormal Psychology

might serve as rnarkers for the disordc.r (endophenotypcs). valuable as risk indicators either in predicting onset or prognosis of the disorder or in identifying neurological facets that may identify genetic foundations of schizophrenic functioning. Shakow (1962) was among the first to report large dfffcrcnccs in a simple reactiou--t imc experiment. Reaction time was measured when a subject was asked to lift a finger fron1 a telegraph key as soon as a light came on. Schizophrenics were markedly slov.1 cr on this task

than normals, with process schizophrenics showing greater impairment U1an reactive or paranoid schizophrenics. Numerous subsequent studies found similar results. Asarnow. Steffy.

MacCrimm.on. and Cleghorn (1977) reported that foster children whose biological mothers were schizophrenic showed greater deficit.~ in paying attention than various comparison groups. Attentional dysfunction can a]so be observed in sch izophrenics whether t hey arc on or off medication (Finkelstein, Cannon. Gur. Gur. & Moberg. l997).1J1esc results suggest that attention deficit might be a useful marker for schizophrenia. A common interpretation of these findings is that schizophrenics become distracted by inclcvant stimuli, either from the external environment or from their own thought processes. An unusual susceptibility to distraction by irrelevant stimuli might be a basic feature in the schizophrenia-prone individual. present before the full.blown disorder develops and after recovery from an acute phase of the disorde,r. However. despite consistent evidence of attention problems. the nature of the deficit is still not well understood (Gold & 11,aker. 2002).

111c.re are other possible ncuropsychological markers for schizophrenia as well. \Vorking memory deficits may be a useful indicator(Barch. 2005). perhaps related to attention deficit. Errors in smooth pursuit eye movements have been noted for some time (e.g.. Holzman & Levy. 1977); schizophrenics tend to track a moving target with frequent inlcrruptions and numerous rapid movements. Tltere also appears to be an association between impaired eye tracking and schizotypal features in community samples. suggesting lhe measure could be valuable as an cndophenotypc for liability to schizophrenia (Lenzenwegcr & O'DriscoU. 2006}. Some evidence suggests t hat the impairment is evident in fam ily members. However. Boudct and his colleagues (2005)

-

Since genetic makeup is p recisely tl1e same in discordant monozygolic twins. different environmental influences must accoun t for the development o f schizophrenia in one twin and not nnolher. (Shutt.intock)

found eye-tracking impairment in schizophrenics but not in their first-degree relatives. thus calling its usefu lness as a liability marker into question. Finally. it is important to note that some schizophrenic patients show no obvious evidence of these or other endophenotypes. Palmer and h is colleagues ( 1997) found that almost 30% of schizophrenics given a comprehensive

neuropsychological evaluation produced normal profiles that could not be dfatinguishcd from a control group by experienced ncuropsychologists.111e rneasures employed inc.ludcd verbal and cognitive ability. attention. memory. sensory function. and motor skills. Research continues to be brisk in this area. but. to date. the marker candidates are not uscful for diagnosis or identification of at-r isk individuals.

10.3c Environmental Factors Endopbcnotypc Observable trait Lhat can serve as

a biomarker for a disorder

111c strongest evidence for an cnvironmentaJ influence in the etiology of schizophrenia is the fact that concordance rates for identical twins are much less than 100%. Since genetic makeup is precisely the same in discordant monozygotic twins. different environmental influences must account for the difference. Jt does not ncccssarHy follow. however. that t he environmental influences arc psychological or sociaJ in nature. ·me hiologicaJ context. such as different intrauterine environments. birth complic.ations. or subsequent d iscascs. might contribute to the development of schizophrenia in one twin and not the other.

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One research strategy that seems promising is tJ-1e study of identical twins that arc discordant for schizophrenia. Environmental factors should be highlighted in the situation in which one identical h\1in becomes schizophrenic and the other docs not. because the two individuals begin life with exactly the same genetic disposjtions. Some ear,Jy studies found e\•idencc suggesting that the twin who became schizophrenic had CX']>Cricnccd more central nervous system illnesses. suffc.1·ed from more complicatjons or asphyxias at birth, or had a lighter birth weight (Pollin & Stabcnau. 1968). These observations we.re. expanded in subsequent years, consistently implicating the prenatal and perinatal period as important. Schizophrenia appears to be more common in those whose mothers had viral infections during the second trimester of pregnancy {Brown et aL 2000): perhaps relatedly. more schizophrenics are born during the winter and spring months (Davies. \Vclham, Chant. Torrey. & McGrath. 2003). after the peak of seasonal virus such as cold and influenza. In addition. Buka and h is colleagues (2008) reported t hat offspring of mothers who were infected with herpes simplex virus at the end of pregnancy were at increased risk for later development of schizophrenia. Certainly. the find ings ofltigher concordance rates in monochorionic than dichorionic MZ t\\fins hr Davis et al. (1995) arc also consistent with a viral risk hypothesis. These observations point to the importance of early developmental factors in the complex etiological picture of the disorder. More generally. a variety of birth factors associate wilh schiz.o phrcnia. McN'eil. CantorGraae. and Ismail (2000) noted that obstetric complications. reduced head circumference., and minor physica1 abnormalities of the head and limbs are a ll significantly associated with offspring who later became schizophrenic. These findings arc supported by a meta• analysis of population-based studjes by Cannon.Jones. a nd Murray (2002), confirming that com.plicatfons during pregnancy. complications during delivery. and abnonnal fetal growth and development arc.risk factors associated with schizophrcnia.1herc is also newer evidence from a populatjon ..based study in Denmark that viral or bacteria l infectjon durjng childhood. serjous enough to warrant hospitalization. is associated wi th a 50% increase in the likelihood of developing schizophrenia (Lowry. 2013). '!he related possibility that schizophrenia reflects an in flammatory resp onse in the brain has attracted increasing interest. fueled in part by reports that the addjtion of anti-inflammatory drugs such as aspirin to antipsychotic med ication may improve clinical outcome (Sommer ct al.. 2014}. Other reports have suggested links between schizophrenia and lead exposure., vitamin 0 deficiency, and excessive glutamate metabolism in the brain (Stetka & Correll. 2014). Outside of early childhood. increasing attention is being given to adolescent devclopmcnL t>oor academic achievement and social adjustment in the adolescent years precede onset of schizophrenia. Some data implicate cannabis use as a r isk factor for schizophrenia: Use in adolescence was associated with some increase in incidence (e.g.• Tandon ct al., 2008). Later studies. however. have disputed these results. find ing no d ifference in risk to relatives of schizophrenics who use or do not use cannabis (Proa!. Fleming. Galvez-Buccollini. & Del isi. 2.014).

10.3d Psychosocial Factors Because schizophrenia was known earJy in the h istory of psychology, much attention was historically afforded to finding possible psychological causes oftJ1c condition. c.spcciaUy in the mother-child or family relationship. Psychoanalytic t heory long held that schizophrenia reflected a weak ego t hat could no longer contajn the expression of ordinarily unconscious id impulses. lhc combination of weak ego and fixations at the oral stage led to a regression to this early level of dcvcJopment. Schizophrenic p,c.rsons we.re also said to have withdrawn their libidinal attachments from other people and turned tJlis energy inward on thcmselvcs.1hus. they would become detached from other people and autistically preoccupied with their own inner world. Howeve,r. these views sti mulated little research. and schizophrenics were rarely targets for psychoanalysis.

Viral risk bypoth.,sis "lheory that schizophrenia may be cru.tscd in utero bv viral infection of the mother

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Chapter 10 Abnormal Psychology

Family Influences Schi.zophrenogenlc Mothers

Nco-Freud.i an writers on schizophrenia, less tied to the concepts of orthodox psycboanaJytic theory, stressed the importance of the early relationship with the rnothcr (see. e.g.. Sullivan, 1953). In fact. certain mothers thought to have special ~talent"' for producing schizophrenic offspring were called schizoph,-cnogenic. 'rite central feature of the schizophrcnogcnic mother is extreme ovcrprotcctiven.ess and intrusiveness. 111is ~engulfing,. mother infantilizcs the child, tells the child what to think or foci. and. in general. prevents the child from growing up as a separate person with a sense of personal identity and autonomy. The lack of separation between the mother and child is thought to reflect the mother's perception of the child as an extension of hersclf.111e child c.annot escape this relationship and contribute~~. in a way. to jts continuation, Several early studje.,; found that. relative to mothers of normal offspring. mothers of schizophrenics answered The lack of separation behveen the mother and child 1s thought to reflect th e mother"s perception of the c h ild as questionnaire iterns about child-rearing attitudes in a a n extension ofhC!rself. Some early t.heories suggested that direction more consistent with overcontrolling. intrusive exlTema overprotecth-ene!ls a nd inlrusi\•enes..1o may contribute behavior (e.g.. Ma1'k. 1953). Further. studies that measured to tl1e development of i.ch1zophrt.-nta. tiS-1oclt) children's perceptions of maternal behavior seemed to consistently show that children with schizophrenia perceive their mothers as being intrusively 0\1ercontrolling (e.g.. Heilbrun Jr.. 1960: McKinley. 1963). Of course, having a seriously disturbed child may elicit more overprotective responses from a mother. confounding the direction of causality. In the early 1950s. Murray Bowen was one of the first researchers to conduct systematic dinical studies in which he and his staff directly obsenred the interaction of families that included a schizophrenic son or daughter. Beginning at the Menninger Clinic and continuing later at the National Institute of Mental Health in Bethesda. Maryland. he brought the mothers and families of schizophrenic young adults to live on the grounds in cottages or in special apartments on the hospital wards. On the basis of his observations. Bowen (1978) described a phenomenon that he called the transfer ofanxiety. 1be mothe1·. for example. would become anxious and then focus her thinking on the sickness of her child. repeatedly verbalizing how disturbed the child was. Soon the mother's anxiety would be less. but the patient's psychotic symptoms would be worse. In other less cornmon instances, the son or daughter would make positive steps toward recovery. and the mother would show increasing signs of anxiety. perhaps taking to her bed with some kind of physical illness. More generally, Bowen proposed that when one member in an m·erly attached relationship functioned at a level less than the person's capacity. the other individual functioned in an overadcquatc fashion. As with anxiety. the roles of underadequate and overadequate would occasionally be exchangOO. ()\rcrt schizophrenic. symptoms might then he one manifestation of underadequate fa nctioning.

Fc1111ily Dy11a111ics 1he phenomenon of the transfer

The phenomenon of the tnmsfor of an.:uety was just one aspect of the kind of family relationships tlml existed in enmeshed families-that ls. those I.hat were too closely knit in an emotionaJ sense. (iSlod:)

of anxiety was just one aspect or the kind of family relationships that existed in enmeshed families (those that were too closely knit in an emotional sense). Lidz. Ficek. and Cornelison (1965). who conducted intensive studies of the families of 17 schizophrenic patients. found ~whole family" psychopathology in all of them. ,-he mothers were seen as unstable, strange persons who had difficulties

Schizophrenia and Psychotic Disorders

setting boundaries between themselves and the disturbed child. ·me fathers tended to be either aggres.c;ivc and paranoid or pa.~sive and ineffectual. Although none ofthe parents had been hospitalized. in 60% of the families. at least one parent was considered to be virtual ly psychotic or paranoid: in the remaining families. one or botJl parents m.aintained a precarious adjustment involving considerable distortion of reality. Generational boundaries were always breached, either because one parent acted like a rival sibling or because a parent used a child as an ernotional replacement for a spouse. Marital problems were present in most farnilics. and the remaining famiJies showed a pattern called marital skew. jn which the serious psychopathology of the dominant parent \'las passively accepted by the other. Lidz especiaJly emphasized the transmis.~ion of irrationality that occurred in such a family. in which members deny and distort the obvious interpretations of experiences: act as though certain disturbing situations did not exist: talk to each other in vague. amorphous. or fragmented ways: and are impervious to the child·s own feelings and dcsires.1l1c effects of these family patterns on the child were t hought to include the production of schizophrenic symptoms.

NO LOIT£RING 71,e Double Bind Bateson. Jackson. Haley. and \Veakland {1956) proposed that one kind ofparent~child interaction is especially important in the development of schizophrenia- the double bind.1hc double bind arises when (I) the child is emotionally dependent upon the parent, making HO Em it extremely irnportan.t for him or her to understand communications accurately and respond appropriately: and (2) the parent expresses t\'io contradictory messages. The content of what tJ1e parent says may be the opposite oft he message contained in tone of voice or facial expression. or the content itself may simpl)• consist of two incompatible mcs.~age$. "£he child cannot comrnenton the incongruous messages. withdraw from the situation. or ignore the messages. Caught in a bind from which there is no escape. the chHd uses ..crazy.. thinking and actions to cope with this intolerable situation. The double bind (COJl';\'riytlO BVT Publi.dun.!l,I 11w double bind notion thus proposed that psychotic symptoms were a form of adaptation to an impossible situation. \-Vorking f:rom a similar perspective. Laing and Esterson (1971) studied the familie~~ of 11 schizophrenic women. In each case. they felt there was strong evidence that famil y environment could account for the patient's schizophrenic behavior.111eir basic thesis was that the behavior and thought processes of people diagnosed as schizophrenic. indeed.seem c.razy outside of the fam ily context. but when seen from the family perspective.. they arc not crazy or irrational at all. In fact. such behavior is just how a person might rationally re.act to such an environment. 1),c reports of Bate.son and

his colleagues (1956). Bowen (1978). Laing and E.sterson (1971). and a number of other authors seem to make a plausible case for family determinants of schizophrenia. ~these hypothesized family influences could be conceptualized within tlle framework of social learning theory. Parents might mode) and perhaps reinforce disturbed communication and peculiar ideas and then punish attempts at interpersonal intimacy. ·straight.. communication. and developing a distinct identity- ultimately. forcing the child to withdraw in order to escape tllis aversive experience.

Co11/rolled Resellrch 011 Family Correllites Although these sorts of theories (the double bind. the schizophrcnogcnic motJ1er. the transmission of irrational ity) and other family• oriented views of the origins ofschizophren ia initially seemed useful. controlled research has provided only partial support for these views. Some researchers sought clues in information about family characteristics obtained before the- child was diagnosed as schizophrenic. McCord. Porta. and McCord {1962) made use of an extensive body of information that had been gathered on a large sample of boys as part of a delinquency prevention study.

27J

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Chapter 10 Abnormal Psychology

Later. 12 of these boys became psychotic. and their family backgrounds were compared with a group closely matched on such variables as socioeconomic c.lass and ethnic background of parents. presence of psychoses or neuroses in parents. neurological signs and glandular imbalances. and race. 1:hc comparison showed that a higher percentage of mothers of the psychotic sons we.r e rated as ovcrcontrolling (67%) than we.re motJ1ers of the control group (8%). Although based on a small sarnple. the results appeared consistent with the schizophrcnogcnic mother hypothesis. In asimilar study. \Varingand Ricks(l965)compared recordsof50childrcn who had been treated at the Judge Baker Guidance Center in Boston and who later became schizophrenic as adults with records of a control group of children who were also treated at the center but who did not become schizophrenic. The h'lo groups were matched on age. sex. IQ. presenting symptoms. socioeconomic class. and ethnic background. Like others, \.Varingand Ricks found a higher proportion ofpsychotic parents in the schizophrenic group than in the control group. Absence of disturbed family environment was characteristic of 48% of the nonschizophrenic control families, whereas alJ of the families of schizophrerucs were identified as disturbed. A related findjng was that the.re were no healthy marriages in tJ1e schizophrenic groups as compared with 15% healthy rnarriagcs in the control group. 111esc data provided support to the idea that future schizophrenics grow up in severely disturbed fam.Hy environments; otJ1er researchers. however. reached different conclusions. For example, Jacob (1975) surveyed the research based on direct observation of family interaction and found no consistent evidence that families ofschizophrenics were djfferent from normal control families in the amount of conflict, expression of positive or negative emotion. or relative dominance of father and mother. Even in supportive studies, no one pattern of family interaction was related to the subsequent development of schizophrenia. 'Jbe reports of communication disturbance in the families of schizophrenics arc. of course, consistent with the psychological transm is.~ion of this disturbance. However. these results arc equally consistent with genetic transmission. Parents who are not overtly schizophrenic themselves but carry a genetic disposition to schizophrenia may manifest their ~schizotypar tendency in the form of somewhat impaired communication skills. '!'he basic d isposition to become schizophrenic. however, may be transmitted through the genes rather than through mystifying communication. Assessing communication deviance in the adoptive parents of children who become schizophrenic is one test of these two alternative theories. If psychological transmission is important. then these adoptive parents should show more disturbances in communication than adoptive parents of children who do not become schizophrenic. In two studies designed to test this hypothesis. one supported it (Wynne. Singer. & Toohey. 1976). and the otlwr did not (Wender. Rosenthal Rainer. Greenhill. & Sarlin. 1977). Since that time, the overall adoption research seems to provide more evidence for genetic transmission than for the influence of pathological families.

Recent Research on Fan1ily Influences At the same time. research has provided

Expressed emotion (EE) Vv'ithin family dynatnics. the expression of criticism. hostility. and emotion.al ovcrinvolvement

strong data that family interactions contribute to the reappearance of symptoms following improvement. if not to their initial onset. Brown (1959) noted that after discharge from treatment.schizophrenics who had only limited subsequent contact witJ1 relatives did better than those who spent more time with their fam ilies. Over tJ1e next 20 years, he refined his explanation for this difference in outcome by proposing that expressed emotion (EE) in the family home was the important factor. Expre,~scd emotion consists ofcriticism. hostility, and emotional ovcrinvolvcment (intrusiYeness). \>Vhcn CE levels in the family were high. patients were more prone to relapse. Manystudie,~havcsubscquentlyconfirmcd that high££ situations do lead to reappearance or worsening of psychotic symptoms. Level~ of EE can also be used to predict relapse (Butzlaff& Hooley. 1998). In addition. the effect of close family contact on a schizophrenic person interacts with the emotional climate of the family: Patient.,; who have more than 35 contact hours per week with the family have the highest risk of relapse in high £E. frunilies but have the lowest re.lapse risk in low EE families (Beggin.gton & Kuipers, 1994).

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ll1e effect of EE on relapse mighL explain certain cultu.raJ differences in outcome in

schizophrenia. As a general rule. those indjviduals with schizophrenia in the developing world tend to have a more acute course and a better outcome than schizophrenics in the industriaJized world. such as the United States (American Psychiatric Association. 2000). Jenkins and Karno (1992) noted that higher !eve.ls of family EE arc present among British and Anglo-American cultures. with lower EE levels in Mexican and Indian cultures. Family levels of EE might c.~plain some of the differences in relapse across various cultures.

Cultural Influences Schizophrenia apparently exists in all cultures. from the most Hprimitivc- to the most ·advanced..,. Global incidence appears to be up to 0.7%ofthc population (American Psychiatric Association. 2013}. However. the incidence rates and character of the symptoms vary widely from culture to culture. Murphy (1968). for example. J'eportcd unusually high incidence rates of schizophrenia in several subcultures. Tamil Indians living in Singapore showed a higher rate than their Chinese and Malay counterparts: Irish Catholics in southern Ireland had higher rates than Catholics living in England. Differences of this kind could conceivably reflect differences in the genetic makeup of the populations. although that seems unlikely with large populations that have not been isolated. Murphy then compared ratc.s of schizophrenia in three ~traditional" French Canadian communities with rates in otJlc.r French Canadian communities in which traditions we.re changing and had less hold. The prevalcJlcc of schizophrenia in women was found to be extremely high in the traditional communities and was especially apparent in two subgroups of women: married women over age 35 and young unmarried women. Schizophrenia was almost nonexistent among younger married women in traditional settings. Murphy (1968) s uggested that the unusual prevalence of schizophrenia among the young single and older married women might be explained by cultural factors.1he tradition.al communities cons·idcrcd the ideal woman as one who gets married early; has many children: and is hardworking, patient. and submissive to her husband. 111c idea of an independent career for women. outside of religious orders. was only just beginning to be accepted as a possibility. For some women. according to Murphy. the conflict between satisfying the expectation of the community and pursuing interests of their own became sufficiently acute to precipitate the schizophrenic reactions- reactions th.at tended to occur either at the time the women were entering the marriageable age or later as their children were growing up and the satisfactions derived from the fam ily were diminishing. It is also known that there are differences in the onset. symptom presentation. and course or schizophrenia across different cultures (American Psychiatric Association. 2013). ln an early examination of the differences. Murphy. Wittkower, fried. and Ellenberger (1963) surveyed psychiatrists in 27 countries representing the major regions of the world. collecting information about schizophrenic patients they had seen. Eastern religious such as Hinduism. Budd hism. and Shinto pro mole a more passive acceptance

including ethnic and religious background and the frequency ofvarious of fate a nd an emotional detachment from life. symptoms. Social and emotional withdrawal. auditory hallucinations. f,Stockl delusions, and flatness of affect were broadly seen among patients. Other fcatu1·es. however, varied markedly in the different cultures. for example. t\V'o kinds of delusions showed an especially strong relationship to the world's religions- delusions with religious content and delusions ofdestruction. 1l1c highest percentage of religious delusions was found for Roman Catholics; the lowest. forJudaism and Buddhism. Murphy and his colleagues (196:i) proposed that religious delusions and delusions of destruction were positively correlated with the extent to which religions induce a sense of

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Chapter 10 Abnormal Psychology

guilt. They also suggested that Eastern religions, such as t he Hindu, Buddhist. and Shinto types. promote a more passive acceptance of fate and an emotional detachment from life. Consistent with the latter point was the finding that social and emotional withdrawal occurred most frequently as a symptom among the Japanese and Okinawans. The authors noted that the low frequencies of religious delusions and delusions of destruction among the Jewish schizophren ics were inconsistent with their gcnc-raJ interpretation. but they were unable to offer any alternative explanation.

Socioeconomic Influences 1t has long been known that rates of schizophrenia arc highest in the

lowest socioeconomic social classes. It is aJso well established that risk of schizophrenia is higher for those raised in u1·ban environments (Pederson • & Mortensen. 2001).1\,.•o fundamentally different hypotheses ha,•c been proposed for such social influences: (J) 1l1e stresses associated with t he extremes of sociaJ disorganization, poverty. and harshness found in the lowe.o;t socioeconomic level (and urban slums) are a cause or partial cause of schizophrenia. (2) Schizophrenic or schizophrenia..prone individuals tend to drift into these slum areas because t hey arc unable to fun ction effectively in the rest of sodety. Studies dating back several decades have supported both positions. In support of the-drift" hypothesis. Gerard and I-louston (1953) fou nd that the e.x cess of schizophrenics from slum areas resu lted almost entirely from young schizophrenics who had left home and rented rooms in rundown sections o(town. Goldberg and Morrison (1963) obtained information on the occupations of t he fathers of male schiz.oph renics Ratt-s of schiimph renia are higher wncmg those in England and \iVnlcs. 1·hcy found that although the occupations of in lower socioeconom ic classes and urban areas. l~tod:) schizophrenic sons were concentrated in the lowest social class. the occupations of the fathers were not. implying a downward drift on the part of the sons. Turner and \Vagenfcld (1967) reported similar results. However. Brenner (J973) presented data showing a strong relationship between times of economic hardship and first•admission rates to mental hospitals (including schizophrenia) in New Yorkstntc. with evidence extending back to 1841. Furthermore.in the 1841- 19J5data. the relationship was much higher for farmers. laborers. and salesmen than for individuals in more economicallysecure professions, such as lawyers and doctors.1hc stress of an economic downturn should fall most heavily on the former groups. Corrclational findings. of course. arc subject to many interpretations. One possibiJity is that du.ring times of relative prosperity. individuals who are already schizophrenic arc supported and cared for by re.latives. ln hard times. however. the rclatives find they can no longc.r provide for such persons and commit them to a mentaJ hospital. thus increasing the first-admission rates. Brenner. however. offered several bits of evidence against such an interpretation. First admissions of patients who a.re totaJly dependent on others were not more affected by economic changes than were admissions ofindividuals who had some savings and at least marginal capacity for earning a living.Second. admissions to private hospitals showed a similar relationshil>to economic cycles. The cost of private hospitalization is considera bly higher than the cost of keeping the patjcnt at home. 'lltird, hospitalization rates for t he criminally insane showed the same relationship. In these cases. t he commLc;sion of a crime triggered hospitalization. not t he need of a family to cconomizf Depressive 01sordft PersJst.ent Depressive ~sorder (Oysth)'mia)

Orsruptive Mood Oysregulation Oisorder PremcnstruaJ Oysphonc Disorder Other Oepressive Oisorders

113 Causal Factors in Depressive Disorders ............ .. _298 Bmlogical Components Psychosocial Components

11.4 Treatment of Depressive Disorders ...... ........ - 305 Btological Treatments Psychological Treatments Other Treatments for Oeprewon

Summary or Treatment fcx Umpolar OepressiOn

11.5 Bipolar Mood Disorders •.•...........311 Btpolar I0 1sorde, Btpolar II Disorder Cydothymic 01sorder O ther 8ipob.r 01sordeu

11.6 Causal Factors in Bipolar Disorders .. ......... ..... .... 313 11.7 Treatment of Bipolar Disorders ..... 313 Med,catK>O Psychosoaal Treatments

11.8 Suicide ....................... .. ............ 315 l)sycho&ogical Correlates R.isk factOf'S Su,cide Preven oon

CHAPTER OPENER Q UESTIONS What a re mood episodes, and how are they used diagnostically? What a re the causes of the depressive d isorders! How are mood disorders different from normal variations in mood? How common are mood disorders?

Do mood disorders improve

without treatment? Does medication work better than psychotherapy for depression? Is mania treated differently than depression? How common is suicide?

Who is at greatest risk?

Mood Disorders and Suicide O

ur life experiences typicall)' involve subjcctfrc foe.lings and emotions that serve, in part, to provide us with feedback about the outcomes of our efforts. Success. progress. frustration, and failure usually are accompanied by different emotions. ranging from joy and euphoria. to a sense of satisfaction and wcJJ.. being. to irritability. anger, sadness. or despair. Emotions a.re clearly adaptive for all species that display them (Darwin. 1873/ 1955). However. high levels of emotionality in humans can become maJadaptivc. causing major problems in social. occupational. and interpersonal functioning, as wel l as significantly increasing the risk of attempted or completed suicide. The mood d isordcrs describe conditions in which the intensity of emotion and affect create significant problems for indi\liduals and tJ1e people around them. Disturbances in mood have long been recognized as disabling. For example. melancholia (a particu larly deep depression) formed one of the four humors of early Greek medicine (Chapter 2). Mood disorders (also sometimes called affective disorders) are among the most common diagnoses in the DSM-5, where t hey arc broad ly classed as depressive disorders and as bipolar and related disorders. They include the widest range of affect. from those who find nothing what.,;oever pleasurable in life- to those who seek as much immediate gratification as possible.

11.1 Diagnosis of M ood Disorders 11.1a Mood Episodes In the DSM•S. the mood disorders arc largely defined by various combinations of mood episodes that function somewhat like diagnostic building blocks. These components include the major depressive episode. t he manic episode. and the hypomanic episode. 111ey do not constitute diagnoses in themselves. but their What are mood episodes, and presence or absence i,; essential in most mood how are they used diagnostically? disorder diagnoses.

llelancboUa Particularly deep level of depression characteri1.ed by absence af mtercst or pleasure in all things. changes in sleep.

changes Ill weight. and/ or excessive guill

Ma1or Depressive Episode 'llte criteria for a major depressive episode are shown in DSM.s: Criteria for a. Major Depressive Episodc.111c episode involves a 2•wcck period of nearly constant depressive symptomatology: sadness. loss of interest or pleasure. changes in weight. changc.s in sleep. loss of energy. agitated or slow movement, difficulty concentrating, guilt. and/or thoughts ordeath. Obviously. many ln a m11Jor dcpr· wak ing ear1ynnd being unable to return to sleep.

people experience occasional depressed mood. including some of these symptoms. A major depressive episode is distinguished IShuUCDtud:) by its du ration (nearlyconstant for 2 weeks). the degree ofdist urbance (at le.a.st five ofthcsymptoms arc present). and the impairment t hat it causes in life. To be considered part of a major depressive episode. the symptoms must represent a change from previous functioning (American Psychiatric Association. 2013). 219

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~·l ost comrnon ly, the depressive episode imrohrcs loss ofintercst or plea.~urc in activities that used to be enjoyable. Appetite is nearly always affected: most often. it is reduccd1 though some people increase their food intake. \Veight may change in accordance with the alteration in eating patterns. Similarly, sleep is usually disturbed. either in terms of insomnia or by waking early and being unable to return to sleep. Others. however. increase their sleep du.ration. People feel fatigued. tired. and find common tasks exhausting. Concentration is difficult. and thinking may seem to be slowed: tasks that are intellectually demanding arc not completed or attempted. Sufferers may be preoccupied with personal faiJurc and blame themselves for any nonpositive event they encounter: the sense of guilt and worthlessness can combine with feelings ofhopclc$S1less and helplessness and e.xtcnd to thoughts of suicide and death. During a major depressive episode., some people n1ay experience psychotic symptoms. Ga ill may be of delusional proportions. s uch as feeling responsible for global problems or natural disasters. \r\1hen psychotic features arc prescnL the additional symptoms they produce arc not included in the identification of the episode. For example. an individual may hold tJ1c delusion that falling asleep will cause other people to die: any resulting loss of sleep would not be counted as evidence of meeting the diagnostic criterion of insomnia because the sleep disturbance is caused by the delusion itself. The presence ofpsychotic symptoms in a major depressive episode requires differentiation from schizoaffcctive disorder. in which psychotic symptoms arc also present in the absence of the mood episode. A distinction must be made between a major depressive episode and the normal depressive sympton1s associated with bereavement. As discussed in Chapter 5, the normaJ

DSM-5

Cr iteria fo r a Major Depressive Episode

~fajor Depressive.Episode A. Pive {or more) of the following symptoms have been pre.sent during the same 2-week period and represent a change from

previous functioning: at least one of the symptom.sis either (1} depressed mood or (2) loss of interest or plea.sure. Nole: Do not include symptoms that are clearly attributable to another medical condition. L Depressed mood most of the day. nearly every day. as indicated by either subjective report (e.g.. feels sad or empty) or observations made by others (e.g .. appears tearful}. (Note: In children and adolescent.s. can be irritable mood.) 2. Markedly diminished interest or pleasure in all. or almost all. aclivities mo.st of the day. nearly every day (as indicated by either subjective aC!count or observation). 3. Significant weight los.s when not dieting or weight gain (e.s- a change of more than 5% ofhody weight in a month). or decrease or increa.w in appetite nea.rly every day. {Note: In children. consider failure lo make expected weight gahL) 4. Insomnia or hypersomni.a nearly e,•ery day. 5. Psychomotor agitation or retardation nearly every day (obi.ervable by others: not merely subjective feelings of re..'itlessness or being slowed down). 6. Fatigue or loss of energy nearly every da)'· 7. Feelings of worthlessness orexce.'iSive or lnappropriale guHt (which may be delusional) nearly everyday (nol merely self. reproach or guilt about being: sick). 8. Diminished abilil)' to think or concentrate. or indecisiveness. nearly twt-ry day (either by subjective account or as observed by others}. 9. Recurrent tJ1oughl'.s of deatl1 (not just fear of dying). recurrent suicidal ide-.ttion without specific plan. or asufoide attempt or a.specific plan for committing.suicide. B. The symptoms cause clinically .significant distress or impairment in social. occupational. w· other important areas of functioning.

C. The episode is not att:ributahle to the direct physiological effect of a substance or another medical condilion. Note: Responses to a significant Joss (e.g.. berean1me.nt. financiaJ ruin. losses from a natural disaster. a serious medical i.llness o r disability) may include the fo·eling.s of intense s.adness. rumination about the loss. insomnja. poor appetite. and weight loss noted in Criterion A. which may resemble a depressiYe episode. Although such symptoms may be understandab)e or considered appropriate to the loss. the presence of a majordepres.-.i\'e episode in addition to lhe normal response lo a significnnt los..'i should also be carefully considered. This decision inevitably requires the exerdse of clinical j udgment based on the individuat·s hi.story and the cuJturaJ norm.s for the expression ofdistre.'is tn the contad ofloss. Source: Reprln1ed "'' Ith perml!islon from the Diagmmit:and Statia.tlco/Matrualo/Mentol Dl.1ordns. 5th ed. (Copyright 2013). American Psychiatric Association.

Mood Diso(ders and Suicide

291

grief reaction following death of a loved one generally does not include a strong sense of worthlessness. su icidal ideation. psychosis. or extreme impairtnent. as is shown in major depressive episodes. As suc.h. in the DSM.JV. a major depressive episode was not d.iagnosed i f the depressive symptoms could be better accounted for by bereavement. 'lhe DSM...S discontinued this practice of"'bereavemcnt exclusion'" because bereavement often extends more than a year and can itself serve as a trig_~c.r for a major depressive episode. 1he issue for the dinician wou ld be to distinguish normal gricffrorn a grief.related dcpression. 111c DSM,5 notes. for instance. that depression usually involves a loss of interest in almost aJI things. while those in grief may stiU experience positive emotions. such as fond memories (American Psychiatric Association. 2013).

Mame Episode 1he key feature of a manic episode is a d istinct period (at least I week in duration, unless the person has already requjrcd hospitalization) or expansive. c.lcvated. or irritable mood. In many ways. the manic episode (DSM-5: Diagnostic Criteria for a Manic Episode) L~ nearly the opposite of a major depressive episode. 1l1e elevated mood is usuaJ ly experienced as enjoyable or euphoric: to observers who know the person. it .s eems excessively so. \Vhen mood is expansive. the individual may seem overly enthusiastic and intrusive in social interactions. Irritability is a lso common. perhaps related to a blocki ng of the person's wishes. and frequently there are rnood s,'t'ings between irritabil.ity and euphoria (American Psychiatric Association. 2013). Duri ng manic episodes. people show evidence of grandiose or inflated self-estcem. littJc need for sleep. pressured speech. Aight of ideas. and distractihility. 111cy perform several activities at once a.nd seek out pleasurable activities that pro\•idc immediate gratification. without regard for consequences. 1l1ey arc usuaUy very sociable and. frequently. sexually indjscri mina.tc. However. the excessive social involvement typical ly becomes demanding

DS'M-5

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Diagnostlc Criteria fo r a Manic Episode

Manic Episode A. A distinct period of abnormally and persistently ehH,aled. expansive. o r irrituhle mood and ahnonnnJly and persistently increased goal-directed acli-vity or energy. lasting al least l week and present most ofthe day, nearly every day (or any duration if hospitalization is necessary). B. During the period of mood dj.st urbance and increased energy or activity. lhree {or mo.re) of the following symptoms have persisted {four iJlhe mood is only irritable) are present to a significant degree and represent a noticeable change from usual behttYior: I. Inflated se)f.esteem or grandiosity. 2. Decniased need for sJeep (e.g.. feels rested after only 3 hours of sleep).

3. More talkative than usual or pressure to keep tuJkjng. 4. Flight of ideas o r subjecti\re experience lhat thoughts arc racing. 5. OistractibiUty (i.e., attention too euiJy drawn to unimportant or irrelevant external stimuli), as reported or observed. 6. Increase in goal-directed activity (either socially. at work or school.or sexually) or psychomotor agitation (i.e.• purposeless non•goaJ-direcled activity). 7. Exc:essive invoh'ement in activities lhat halo'e a high potential for painful consequences (e.g.. engaging in unrestrained buying sprees. sexual indiscretions. or foolish business investment.-,). C. the mood disturbance. is sufficienll)' severe lo cause marked impairment in socinJ or occupational functioning or to necessitate hospitu.li7..alion to prevent harm to self or ot.hers. or there are psychotic features.

0 . 'The episode is not attributable to the physiological efl8ct of a substance (e.g.. a drug of abuse, a medication. other treatment) or another medic:aJ condition. Nc,te: A full manic episode that emerges during antidepressant treatment (e.g. medication. eJectroconvulsive therapy) but persi.sL-. at a fully srndromnl level beyond the physiological effect ofthal treatment is sufficient evidence for a manic episode and. therefore. a bipolar 1 diagnosi.s. Source: Reprinted wllh ~nnls !llon from the Diag,tost/c and Sta.rlst lcal Ma,wai o/Memal Disorders. Sthed.{Copyrlght 2013). Ame.rlc:an P!l)'Chiatrlc AS!IOCl.atlon.

2,

Chapter 11

Abnormal Psychology

and domineering. Angry outbursts and hostility may be part of the nearly constant Oow of verbal output, some of which is so tangentiaJ as to be incoherent. Consider figu re J 1--1.. which shows a letter written after a patient in a manic state was involuntarily hospitalized. lhe manic pc.rson·s demeanor is typicaJ ly flamboyant or dramatic. and judgment is poor: illegal activities and arrest arc not uncommon. Shopping sprees may occur. in which an individual may squander life savings or purchase large quantities of unneeded items without t he ability to pay. Sometimes. manic individuals become a&:,trf'cssivc and assaultive and increase their use of alcohol or drugs. Manic episodes typically begin rapidly and may follow exposure to stresso1·s. 111c syrnptoms build quickly and usually escalate over several days. TI1ey tend to be briefer than major depressive episodes. but can last several weeks.

Figure 11· 1 Letter Sent by a Patient in a Manic Episode Source: Court.esyofOr.Charles L)'On11.

Mood Disorde,s and Suicide

Hypomanic Episode '£he remain ing mood episode in the DSM-5 concen,s symptoms that arc similar to. but less severe than, a manic episodc.111c criteria identifying a hypomanic episode arc displayed in DS/d..S: Diagnostic Criteria for a Hypomanic Episode. At least three syrnptoms of elevated, expansive, or irritable mood are required. lasting at lea~t4 days: no psychotic symptoms arc allowed by the d iagnostic criteria. A variety of manic-like activities may occur. but they are less bizarre aud more organized than those within a manic episode. In addition. impairment resulting from the episode is minirnal. and hospitalization is not required. Nonetheless. the episode represents a change in functioning that is observable by other people. Hypomanic episodes tend to begin abruptly and may last from weeks to months: frequently. a major depressive episode eithc.r precedes or follows the experience. Up to 15%ofsufferers eventually develop a manic episode as well (American Psychiatric Association, 2013). 1be DSM-JV included a mixed cpisodeinvolvingalternation between a major depressive episode and a manic episode nearly evc.ry day during a l•wcck period. 1l1is wa~ removed in the DSM-5 and replaced with the specifier-with mixed features,- which can be added to manic or hypomanic episodes. to indicate that depressive features arc also present. or to depressive episodes. to indicate involvement of manic or hypomanic features. These three mood episodes arc combined in various ways to describe the DSM•S mood disorders. summarized in Table 11 · 1. As can be seen. the presence of any manic episode results in the diagnosis of bipolar I disorder. A major depressive episode can occur in major depressive disorder. in bipolar I or U disorder. or in persistent depressive disorder. Cyclothymic disorder involves less severe depressive states: a hypomanic episode characterizes bipolar Il disorder and, to a lesser extent. cyclothymic disorder.

DSM-5

Diagnostic Criteria for a Hypo manic Episode

Hypomanic Episode A. A distinct period of abnormally and pe:rsistent.lyelevnted. expansive. or irritable mood and abnormally and persistently increased ac:Uvily or energy. lasting at least 4 consecutive days and present most of the day. nearly every day.

8. During the period of mood disbtrbance and increased energy and acti"vity. three (or more} of the following symptom.-. (four if the mood i.s only irritable) have persisted. represent a noticeable change from usual behavior. and have been present to a significant degree,; I. In Ruled self-esteem or grandiosity. 2. Decrea.c;ed need for sleep (e.g.. feeJs rested after only 3 hours of sleep). 3. More talkative than usual or pressure to keep talking.. 4. Plight of ideas or subjectiYe experience that thoughts are racing.. S. Distractibility (Le.. attention loo easily drawn lo unimportant or irrele\'ant external stimuli). as reported or obsened. 6. Increase in goal-directed activity (either socially. at work or school. or sexually) or psychomolor agit.alion. 7. ExcessiYe invol\'ement in activities that hm·e a high pote.nliaJ for painful consequences (e.g.. engaging in unrestrained buying sprees. sexual indb;cretions. or foolish business investments). C. The episode is assocmted wilh an unequivocaJ change in functioning that i.s uncharacteristic of the individunJ when not symptomatic. D. The disturbance in mood and the c:hange in func tioning are observable by others.

£. The episode is not SC\•ere enough to cause marked impairment in social or occupalionaJ functioning. or to necessitate hospitaJjzution. Tf there are psychotic features. the episode is., by definition. manic.

F. The epjsode is not attributable to the physiological effects ora substance{e.g.. a drug orabuse. a.medication, other treatment). Note: A full hypomanic episode that emerges duringanUdepressanl treatment (e.g., medication. e.lectroconvulsive therapy) but persjsts at a fully t.-yndromaJ leYel beyond the physiological effecl of that treatment is sufficient evidence for a hypomanic episode diagnosis. However. caution is indic-ated so that one or two symptoms (particularly increased irritohility. edginess or agitation following antidepressant use) are not taken as sufficient for diagnosis of a hypomanic episode, nor necessarily indicative of a bipolar diathesis. Source: Reprinted with perrnis!tlon from the Dlagmutlc at1d Statlstlcnl Mmwol of.M ental Disorder&, Slh ed. {Copyright 2013). American Psychiatric Aslloclatlon.

293

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Chap ter 11

Abnormal Psychology

lhc-se conditions occur at relatively high rates in the population. Kessler. Berglund. and their colleagues (2005) indicated that Ii fctimc. prevalence for any mood disorder is 20.8%. Sex ratios for the unipolar (depressed) conditions are decidedly higher for females. by a factor of2 or 3 tim.es tbe rates for males. Sex ratios arc approximately equal for bipolar I disot'der and cyclothymic disorder: however. it is expected that more boys than girls will receive the. diagnosis of disruptive mood dysrcgulation disorder (American Psychiatric Association, 2013). Ofcourse, premenstrua l dysphoricdisorder is only diagnosed in females.

Table 11-1

DSM-5 Depressive and Bipolar Disorders

Disorder

Key Symptoms

Minimum Duration Required for Diagnosis

Sex ftatio

Major depressive disorder

Presence of major depressive episode

2 v.'eeks

More common among females

Per.sislent depressive d1sorder (dysthymia)

Pers:L~te.nt depressed mood. usually including major depressi\1e !:!pisode

2 years

More common among fe'males

Premenstrual dysphoric disorder

Mood lab.ility and mitability during mosl menses

l year

None

Disruptive mood dysreguJation disordec

llefore age 10. recurrenl 5e\'ere temper outbursts

3 or more times per week. for 12 months

Moreoommon among males

Bipolar I disorder

Presence of man1e episode

I ,..-eek.

Equal

Bipolar II disorder

Major depressive episode plus hypomank episode

2weeks

More common among females

Cyclothymic disorder

Rec.'Urrent depression and hypomania. w1thout major depressive or manic epi!mdes

2 years

Equal

Source: American Psychiatric Aiisoclation. 2013.

Diagnostic reliability varies among the mood disorders. Brown and his colleagues (2001) reported good to excelleotreUability when agenc.ral mood disorder was the principal DSM-IV diagnosis (up to .72}and good reliability for the speci6cdiagnosis of major depressive disorder. 1lie reliability for dysthymic clisorder(.22) was poor. however. In the DSM-5 field trial Cl.

(/)

..c ......

5

C'CI Cl>

Cl

All * NOTES: API

Non-Hispanic Non-Hispanic white black

Hispanic*

API

AIAN *

=Asian Pacific Islander; AIAN =American Indian or Alaska Native.

11.Sa Psychological Correlates Many investigators have tried to determine the type of p erson ality traits or life exp erien ces associated with individuals who attempt suicide. For example, Paykel, Prusoff, and Myers (1975) compared reports of stressful life events during the 6-month period preceding a suicide attempt for 53 individuals wl10 attempted suicide with those of 53 depressive control patients who h ad not att empted suicide; participants were m atched individually for age, sex, marital statu s, and race. Data were also obtained on a match ed sa1nple from the general population. Those wl10 had attempted suicide reported 4.0 times as many stressful life events as did individuals in the general population sample and 1.5 times as many as in the depressed sample. Som e of the sp ecific life events that were significantly different in frequency are shown in Table 11-5. These results suggest that two ge11eral t ypes of events were present more often in the lives of the suicide attempters: interper sonal conflicts (as suggest ed b y "arguments with spouse'' a nd "new p erson in the home") and serious illness in a close family member or themselves. Baechler (1979) studied 127 cases of suicide and proposed that suicidal acts could be grouped into four categories according to their meaning to the person: (1) For many, perhaps most, suicide represents a n escap e from a n intolerable situation . The p erson may be experiencing inten se shame, guilt, fear, or physical p ain and sees suicide as the only way out. (2) For som e individuals, the m ain n1otive for suicide is aggressio11-to seek ven gean ce on others, to make them feel remorse. (3) Others commit suicide as an act of sacrifice or in relation to some higher values. The immolations of Buddhist monks, or devout suicide bombers, would be examples. (4) Finally, there are suicides performed in the context of games or to undergo an ordeal in order to prove oneself. Russia11 roulette is an example of the former. These categories may not capture all the variatio11s in suicidal motivation, but they do serve to remind us that p eople commit s uicide for a variety of reasons.

Mood Disorders and Suicide

Table 11-5

Frequency of Stressful Events Preceding Suicide Attempts Suicide Attempts (N = 53)

Depressives (N = 53)

General Pop11lation (N = 53)

Serious argument ,ivith spouse

19

8

New person in home

11

4

Engagement

7

4

Serious illness of close family member

17

7

4

Serious personal physical illness

15

5

1

Event

Data source: "Suicide Attempts and Recent Life Events," by E. S. Paykel et al., 1975, Archives ofGeneral Psychiatry, 32, pp. 327-333.

11.Sb

Risk Factors

A variety of risk factors for suicide have been identified. The most widely supported indicators for inpatients are similar to those for tl1e general public (Cassells, Paterson, Dowding, & Morrison, 2005), including the following: •

Previous suicide attempt: This is the strongest single predictor of suicidal activity.

Contemplated method at hand: Those who h ave planned the m ethod of suicide a11d have the means or materials needed to carry it out are at highest risk.

Male gender: Males are much more likely to succeed at suicide, compared to females.

Hopelessness: A hopeless attitude is related to lifetime risk of suicide.

Diagnosis of mood disorder or schizophrenia: Along with a11orexia n ervosa, epilepsy, personality disorder, and obsessive-compulsive disorder, these conditions are associated witl1 increased risk of successful suicide.

Previous psychiatric admissions: Especially if there have been multiple admissions.

Other conditions increasing the risk for suicide include the presen ce of alcohol or drugs, because substances can reduce ability to inhibit self-damaging impulses. Functional physical and psychological lin1itations, resulting from chronic health proble1ns, are also significantly associated with increased risk (Kaplan, McFarland, Huguet, & Newsom, 2007). Data from the National Comorbidity Study, taken fro1n a r epresentative sample of nearly 8,100 respondents, indicat ed that the people most likely to attempt suicide were males with fewer years of education, living i11 tl1e wester11 or southwest ern United States, and without active religious affiliation (Nock & Kessler, 2006). Other predictors included psychiatric disorders, substance abuse or dependence, mania (which increased risk ninefold), and a history of multiple- (but not single-) episode rapes or sexua l molestations. Interestingly, the risk for suicide is higher among fem ale physicians than among females i11 the ge11eral populatio11, based on a study of doctors in England and Wales (Hawton, Clements, Sakarovitch, Simkin, & Deeks, 2001). The risk is also increased for mothers who were infected with Toxoplasma gondii, a parasite common in cats, n ear the time of giving birth (Pedersen, Mortensen, Norgaard-Pedersen, & Postolacl1e, 2012). Goldstein, Bridge, a11d Brent (2008) fou11d that adolescents who completed suicide were more likely to have displayed a sleep disturban ce (including insomnia) within a week of the suicide tha n control subjects, suggesting that sleep problem s may serve as an effective warning sign.

317

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Chapter 11

Abnormal Psychology

11.Sc Suicide Prevention ln assessing suicide potential. protective factors arc considered as well. family support. employment. significant relations hips (including marriage), having future plans. and being in treatment- all serve to reduce the risk of

completed suicide (Sanchez, 2001). A person is usually intensely suicidal for only a short period; i f that time can he gapped by the support ofothers and by resorting to remaining

strengths. the suicidal crisis can pass. Suicide prevention is one important goal of crisis intervention in community mental health scr,,;cc.s. *l'he aim is to help a person contemplating suicide to consider other alternatives and to direct the person to resources for psychotherapeutic or other forms of help. A common model of crisis intervention (e.g.• Slaikcu. 1990) involves first making psycho]ogical contact w ith the person, actively listening and exploring the A sign ad\'i.sing of Lhe phone number for a smcide-pre\'enbon hotlin e is dimensions of the problcrn. and hc.lping with sh own o n the Auroro Br id1,"8 in Seattle. Washington. The signs. along with solutions to immediate jssucs covering the telephone call boxes. were p ut up man effort to reduce the number of next twelve hours or so. At times of imminent people who jump to their deaths from the bridge. danger, actions might be nec.c-s.o;ary without the (Suicidchatbne ,_ign an G\V M'°1nori.al 8nd~by Cumulu•Cloud11. ll'l'a.ilnblc undtt a CR-•til'e Con1man• AU r1buhim l.lC'Jl!n.:t. CC B \' SA :Li at http$.//c:om.mon11:,nlmncdl11...wivwiki/ pcrson·s consent (such as protecti\1e custody). Filc:S11idde_ lwt lu,e_, i~n_on_GW_ M~moria.l_ Bridm:_ :!..jH,I If the person can be supported and assisted through the brief period in which risk of suicide is highest. then additional resources can come into play to work on the longer•tcrm issues. such as relationships. unemployment. and heaJtJ1 problems. Many suicides cannot be prevented. Howe\'Cr. the availability of rapid•response crisis intervention services saves many lives each year.

319

Chapter Review TO SUM UP ... •

Mood episodes include the major depressive episode, the manic episode, and the hypomanic episode. Mood disorders are diagnosed, in large part, by the presence or absence of these components.

The depressive disorders include major depressive disorder, persistent depressive disorder, disruptive mood dysregulation disorder, and premenstrual dysphoric disorder. They are characterized, in general, by depressive or irritable mood and loss of pleasure in activities.

The bipolar disorders include bipolar I disorder, bipolar II disorder, and cyclothymic disorder. They are characterized by increased activity and talkativeness, inflated self-esteem, decreased need for sleep, and elated or expansive mood, sometimes alternating with depression.

Episodic mood disorders are characterized by a tendency toward spontaneous recovery and recurrences.

There is evidence of genetic involvement in the development of mood disorders. The genetic factor appears to have a much greater influence in the bipolar conditions than in the unipolar conditions.

Effective antidepressant and antimanic medications began to appear in the 1950s. Newer medications may not be more effective, but they do have milder side effects.

Explanations for the mode of action of antidepressant medications led to the hypothesis that depression is caused by a relative depletion of neurotransmitters such as NE and 5-HT. The evidence for this theory is inconsistent.

A variety of theories exist concerning the psychological causes of depression, including intrapsychic aggression turned inward, disrupted maternal-child relationship, reduced rate ofreinforcement, effect of uncontrollable stressors, and depressive attributional cognitive style. Effective psychotherapies have developed that include behavioral therapy, cognitive therapy, and interpersonal therapy.

In treatment of unipolar depression, medications and psychotherapies can produce approximately equal results. Risk of relapse appears to be less for psychotherapy than for pharmacotherapy.

ECT is effective for short-term relief of serious depression. It may also produce some memory loss, and relapse rate is high.

Lithium is effective in treating bipolar affective disorders. It reduces active manic symptoms and decreases risk of suicide. However, treatment compliance is a problem.

320

Psychotherapy may be useful as an adjunct to mood-stabilizing medication in bipolar I disorder.

People with mood disorders, as well as other mental disorders, are at increased risk for suicide.

Males are much more likely to commit suicide than females, although females make more attempts. The highest risk groups for suicide in the United States are older white males and younger American Indian/Alaskan Native males.

KEY TERMS Attribution model of depression 304 Automatic thoughts Bipolar

Melancholia 303

311

Introjection

Monoamine hypothesis of depression 298 Phototherapy

Chronotherapy

310

310

Transcranial magnetic stimulation (TMS) 308

301

Learned helplessness

289

304

QUESTIONS FOR STUDY •

Compare unipolar and bipolar mood disorders in terms of their incidence, gender ratio, genetic loading, and effective treatment.

Give examples of the internal, global, and stable attributions that characterize depressive thinking.

You are interviewing a patient who has attempted suicide. Describe three factors that might lead you to worry about increased risk of completing suicide and three factors that might lead you to conclude that risk is lower for completed suicide.

321

POP QUIZ 1.

The depressive episode includes all of the following except - - - - -· A. distractibility B. sleep disturbance C. fatigue D. indecisiveness

2.

The key feature of a manic episode is a distinct p eriod (at least - - - - -) of expansive, elevated, or irritable mood. A. 1 week B. 2 weeks C. 4 days D. 5 days

3.

The hypomanic episode cannot include which symptom? A. inflated self-esteem B. distractibility C. decreased need for sleep D. delusional grandiosity

4.

The presence of a manic episode results in the DSM-5 diagnosis of _ _ _ _ _ _ A. bipolar I disorder B. bipolar II disorder C. major depressive disorder D. cyclothymic disorder

5.

If echolalia, echopraxia, or disturbances in motor activity are dominant among the depressive symptoms, which specifier applies? A. "with melancholic features " B. "with catatonic features" C. "with p eripartum onset" D. "with a seasonal pattern"

6.

Temper outbursts in disruptive mood dysregulation disorder must persist for •

A. 1 montl1

B. 6 months C. 1 year D. 2 years

32.2

7.

'lhe prevalence of premenstrual dysphoric disorder is close to _ _ _ __ ofworncn. A. 1% B. 6%

C. 10\11\

0. 20% 8.

Learned helplessness is the theory that depression is caused by a lack of connec.t ion between responses and their outcome. which was proposed by A. Seligman B. 'Beck C. Freud D. Skinner

9.

Lithium is recommended for which disorder?

A. bipolar I disorder B. bipolar LI d;sordcr C. cyclothymic disorder

0. major depressive d isorder 10. Which class of antidepressants shows lower discontinuation rates due to intolerance and is generally the 6rst•linc medical treatment for depression? A. tricyclics

B. TPAs C. MAO-ls 0. SSR ls

I1. \\fhich of these disorders is most common? A. bipolar ( disorder B. bipolar II disorder C. cyclothymic dL~ordcr 0. major depressive d isorder 12. \Vhich disorder shows an equal sex ratio? A. B. C. 0.

major depressive disorder

disruptive mood dysrcgulation disorder bipolar I disorder bipolar II djsordcr

13. One of the most reliable sleep disturbances associated with depressiou is A. B. C. D.

shorter latency to REM longer latency to R£M early evening awakening late evening awakening

323

14. The attributional style of depressed individuals is charact erized by a tendency

to m ake _ _ _ _ _ attributions for negative events. A. B. C. D.

internal, stable, specific external, unstable, global internal, unstable, specific internal, stable, global

15. Among adolescents, those who completed suicide were more likely to have displayed a/an _ _ _ _ _ wit hin a week of the suicide, suggesting that it may serve a s an effective warning sign. A. eating disturbance

B. motor disturbance C. sleep disturba11ce D. visual disturbance

Additional study resources are available at www.BVTLab.com.

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CHAPTER OVERVIEW 12.1 Substance Use Disorders ..... ... ..... 326 12.2 Substance•lnduced Disorders .. .. .. 328 $ubstance Intoxication $ubstance WithdrawaJ

12.3 Develop ment of Substance

Use Disorders .. , .. ... . ,.,, .... . ,., .. .330 Causal Factors for $ubscanc:e Oependence Biological Components

Psychosocial Components Summary

12.4 Develo pment of Substance· Induced Disorders ..... .. .. .. .... ... 339 Alcohol-Induced 01sorders Stimulant-Induced. 01SOfders Caffe1ne•lnduced Disorders

Cannab1s•lnduced Disorders Cocaine-Induced 0 1sorden Halluanogen-lnduced Disorders Inhalant-Induced O,csorders Tobacco-Induced Disorders Op101d--lnduced Disorders Sedative-, Hypnoc:ic-. or Anxiolync-lnduced 0tSOfders

12.5 Treatment ofSubstance•Related Disorders ..... ... ... ...... ...... .... ... 346 Bmlogical Treatments PS)'chok,gical Treatments

12.6 Gambling Disorder ..... .. ............ . 353 Causal Factors Treatments for Gambling Disorder

CHAPTER OPENER QUESTIONS How do substance use and substance-induced d isorders d iffer?

How common are substance-related disorders? What is the difference between dependence and abuse?

Is one born an addict? What is withdrawal? What is tolerance?

What d isorders are t riggered by chro nic drug use? Which treatments are effective for

substance use disorders?

Substance-Related and Addictive Disorders A

Guatemalan, when asked why he drank so much of the local beverage (aguardiente). replied: ..A man must sometimes take a rest from his memory... The need to forget our cares seems to be uuivcrsal; in almost all cu ltures throughout re.corded history. one way of achieving this has been by using substances that have psychoactive properties - that is. they can modify mood, perception. or brain function. The Greek historian Herodotus wrote ofScythians reaching certain pleasurable states by casting hemp seeds over open fires and inhaJi11g the vapors. The Aztecs described. in great detail. their ritual drugs: teona,ui.catl(psilocybin), pcyotl (pcy6tc). ololiuqui {morning glory seeds). picie.tl. and toloalZin. In many South American cou ntrie-s. away from the cities. indi\•iduals prepare a potent hallucinogenic drink from the plant Banisteriopsis caapi. which they call ayalwasc.a or caapi. Inhabitants of the South Pacific Islands use a drug called kava: people in the East Indian archipelago ingest nutmeg: people of the \!Vest Indies use cohoba snuff; both the Siberians and the Norsemen swallowed smaJI amounts of the potentially deadly Amanita muscaria, or ny agaric mushroom, which reportedly passes through the kidneys uncha..nged so that one could drink one's own urine (or a friend's) and regain the effect. Finally. fruits or vegetables fermented into some variant ofalcohol are probably among the earHcst known intoxic.ants, The drug that has been used most effectively as an analgesic (pain reducer) throughout the centuries is opium. Both the Egyptians and the Persians used it medicinally. and the Greek physician Theophrastus mentioned its cffccti\•eness as a sleep inducer and pain reliever. In addition. opium became the standard therapeutic agent for cough and hysteria. Despite its wide medicinal use, however, its potentiaJ for producing psychological and physiological dependency was unnoticed by the mcdjcaJ profession. In fact. addiction to opium did not become widespread until the British East India Company imported the drug on a large scale into Europe during the 19th century (Maurer & Vogel, 1954). Over the centuries, human beings have used an impressive number of substances to alter Lhinking. mood. and perception. Some of these substances have been used in religion or medical treatment. and others. with Jess official sanction. in an attempt to attain a degree of euphoria. AJmostevery society appears to allow. if not directly employ. one or more mind• alteringsubstanc:es for certain segments of the population. In U.S. culture today1 use of legal and illegal substances is a leading social and health problem that is implicated in a large proportion of crime. occupational and interpersonal dysfunction, disease. disability, and death each year. Yet nearly all of these impacts might be pre\1entable if we can understand how substance use begins, how it is maintained. and how it can be treated.

l'sycboactlve Altenng mood. perception. or brain function Analgesic A drug U,at reduces pain Addiction

Chronic pattern of habitual maladaptive behavior, often experienced as compulsive and uncontrollable. that tends to provide immediate gratification

Substance involvement ranges fronl occasional intake to a complete dependency on and compuJsive use of drugs Lhat literally destroy the person's life. Although the term addiction is widely used to describe particuJarlychronic patterns of substance use. the DSM-5 docs not include the word in its d iagnostic terminology "'because of its uncertain definition and its potentially negative connotation" (American Psychiatric Association. 2013. p. 485). Curiously. the DSM•S nonetheless names the general category of these conditions '"Substance-related and Addictive Disorders." In the nomenclature of the DSl•1•5. substance-related disorders arc divided into substance use disorders (which describe the pathological pattern of How do substance use behaviors related to tJ1c use ofa substance) and substancc•induced disorders and substance-induced (which include the results of substance use- intoxication. withdrawal. and disorders differ? induced mental disorders). In revising these classifications. the DSl11f.5 abandoned tho distinction, fundamentaJ in DSM-IV. between substance dependence and substance abuse. Instead. the behaviors to which these terms referred arc incorporated into the criteria for substance use disorders. 325

326

Chapter 12 Abnormal Psychology

12.1 Substance Use Disorders 111.egcncraJ criteria used for diagnosing substance use disorders are summariz-ed in Table 12· 1 General Diagnos tic Criteria ror Substance Use Disorders. '01e D,W ~S considers the symptoms to be loosely organized into four general clusters: impaired control over use ofthe s ubstance:

1·otera.uce Need for increasing amounts of a substance to have the desired effect

\Vltbdrawal A specific psychological and phystological reaction to discontinuation of a

substance

social impairments that rcsuJt fro,u use: risky use How common are substance~ of the substance: and pharmacolog ical critc.riarelated disorders? namely. tolerance and withdrawal. 'l'olerance is a need for increasing amounts of a substance in order to have the desired effect or the diminution of effects produced by taking the same amount of the drug. \\1itbdrawal is a specific psychological and physiological reaction to disoontinuation of a substance: taking the substance can relieve the effects ofwithdrawaJ. Neither tolerance nor withd.rawaJ is required for the diagnosis of a substance use disorder: indeed . not all s ubstances (e.g .. phencyclidinc rPCPJ and other hallucinogens and inhalants) are associated with \ofithdrawal. ln fact, tolerance and withdrawal symptoms that occur during -appropriate mc-dical treatment with prescrjbcd medications ... are spccificall)r not counted when diagnosing a substance use disorder" (Arnerican Psychiatric Association. 2013. p. 484). In general, at least two of the criteria for substance use disorders occurring wit hin a 12 -month period are needed t o meet the c:ritcria for a diagnosis. Severity of the disorder is specified jn terms of how many symptoms arc present: *i\•1ild" severity is indicated by h vo to three symptoms: .. Mode.rate.~ by four to five symptorns; and -sc\•crc."' by six or more.symptoms. Other course speci fiers allow one to distingujsh whctJ1cr the disorder is in early or s ust ained rcmissfon: in a controlled environment (where the substance is unavailable}. or on maintenance therapy. me.a.ningsymptorns arc controlled b)•an agonist drug (a chemical that acts on the same receptors and. in effect, substitutes for t he drug. as methadone docs for heroini 1·hc diagnostic criteria for alcohol use disorder arc shown in DSM•S: Diagnostic Criteria for Alcohol Use Disorder. In form and content, these criteria are almost identical t o those for any other substance. with a few minor substancc•spccific alterations. Typically. the person continues to use the substance even while knowing t hat a persistent physical or p sychological problem is being caused or made worse. 1l1c pattern of use produces significant social or

Table 12-1

DSM-5 General Diagnostic Criteria for Substance Use Disorders

Symptoms of impaired contr.ol Use of substance in la rger amounts or over longer period than intended Persistent desire or al tempt.s to cul down or regulate use. often unsuccessfully Much hmespenl acquiring a n d using thesubslance. or recovering from its effect.ral Approach.~ by S. T. Higgins et al.. 1993. 1/Je American j,mma/ efPr.ychlntry. /5,(). pp. i63-769.

100

• Behavioral 0 Standard

80

~

"E , 60

-c0

t

40

" & 20 0 2

4

6

8

10 12 14 16 Weeks of treatment

18

20

22

24

100

Behavioral

~ "E

-,

80

■ Standard

60

~

C

~ &

4-0

20 0

I 2 3 4

s

6 7

8 9 1011 12 13 14 lS 16 1718 1920 2122 2324 Weeks of continuous abstinence

Cognitive-Behavioral TI1erapy Multicomponent cognitive-behavior therapy involves the combination of skiUs training. stress management. identification of high•risk situations. relapse prevention. and cogn itive: restructuring. 'Otis approach has been well established for smoking CC$Sation and appears helpful for cocaine dependence as well (Chambless ct al.. 1998). When combined with cornmunity reinforcement and behavioral marital therapy. its use appears very promising in treatment of alcohol dependence (Finney & Moos. 2002). A novel study by Clifascfi. Bernstein. Mantonakis. and Lofm, (2013) attempted to modify drinking preference by implanting false taste•aversion memories. Participants who received the suggestion that t hey had bcc.orne sick after drinking rum or vodka before age 16 became more confident that the suggestion was true and subsequently reported reduced preference for that particular beverage. Possibly. the induction of false memories could be a useful adjunct in U1crapy for substance use disorders.

Substance-Related and Addictive Disorders

12.6 Gambling Disorder Unlike the conditions we ha\·e considered tlms far in the chapter.gambling dL~order resembles an addiction without a substance. During the development of the DSM-5. proposals were made to include a categoryof .. behavioral a ddictions., to include uncontrolled Internet use. compulsive pornography use. shopping addict.ion, and possjbly several other non-substance• related disorders. Eventually, these planswe,r cshclvcd until further research could accumulate about the addictive nature of people's involvement with these pleasurable activities. Grunbling disorder rernains t he only ~addictive'" behavior to earn inclusion into the DS.1W~S. In gambling disorder (see Table 12..s). individuals repcatedJy engage in gambling t hat is persistent and maladaptive. as evidenced by preoccupation with gambling: unsuccessful attempts to e ither stop or control gambling: and interpersonal. occupational. and social disruption resulting from Lhe activity. 111c individual frequently-chases- losses over the long term and may commit crimes or lie to family membc.rs to get money as the 6.na.nciaJ situation worsens. Many individuals seek excitement through gambling. and larger bets may be needed to achieve the same level of excitement ovc.r time. Others. however. gamble to escape problems or to relieve unpleasant moods (such as guilt or depression). Toe prevalence of gambling disorder (called pathological gambling in the DSM-IV) may be increasing a.~ more opportunities for legal gambling become available. lt may affect as much as 7%ofthepopulation within certain areas such as Australia (American t>sychiatric Association. 2000): a comrnonly accepted figu re for t he general U.S. population is about 3%, although DSM:.S reduces tJ1e estimate for gambling disorder to no more t han l% Ii fetimc risk in the general population. 1l1e condition appears to be 3 times more common among males. who tend to have adolescent onset and gamble for excitement females have later onset and tend to gamble for escape. Pathological gamblers arc often highly competitive

Table 12· 5

Summary of DSM-5 Diagnostic Criteria for Gambling Disorder

Ongoing prob1ematk: gambling behavior that causes person lo experienves himself to poit.c;ess great mtcgnl)' ;U1d Ion, for l11e people he encounters. tr«rm Gump by2d Amon1 U•. 1wAibbll' undc-r .a CrNlin:CommQQS .-\ttributfon l. ,ec:nlll'. CC Dl:' SJ\ l.Ocin Wild.med.ea Commoiu.l

364

Chapter 13 Abnormal Psychology

dressing. with extended training and frequent reminde.rs. As adults, tJ-1cy are unlikety to achieve complete independence but can contribute to their own support in the protective environment ofs heltered work conditions.

Severe Intellectual Disability People with severe intellectual disability make up about 3.5% of those with intellectual development disorder. Impaired development is apparent in infancy or early childhood in the form of poor motor development, minirnal speech. and. fairly often. the prescnccofphysic.aJ

deformities. ,.hey do not profit as much from training as the moderately disabled do; however. as they get o lder. many can learn to taJk in sim.plc words and phrases and learn elementary health and grooming habits. 'Otey remain dependent on others in problem~solving and personal Those wilh intellectual dis.ability require assistance in ar eas of ind ependent fun ctioning. (AP Pbnt.u/Ca,olyn Wterl hygiene areas. requiring support and assistance at all times. As adults. t hey rnay learn to perform certain routine tasks and develop recreational interests: in .general. however. they require complete supervision and economic support. Maladaptive behavior becomes increasingly problematic.

Profound Intellectual Disability 111e smallest group with intellectual disability (about l.5% ofthc total) is profoundlydisahled. Extreme deficits in both intellectual a nd sensorimotor functions are a pparent early in life. Conceptual abilities arc limited largely to the physical world. Some limited goals of habit training may be achieved in the older child. but usually those with profound intc.llectual disability will require tota.1 care for the re.~t of their lives. Many have physical or sensory dysfunctions that further restrict their capacity to walk or othenri~e cope with environmental demands. Still. these indivjduals can initiate and respond socially and can enjoy relationships with others.

Causal Factors in Intellectual Disability Pbenylketonuria

A variety of factors arc linked to intellectual disability. inc.luding heredity. problems in

(PKU) Rare single-gene recessive metabolic disorder that results in intellectual disability

1z, 0

>,

lnteOectual

Disability Due to

~

Heredity

Organic Defect

,~

~

embryonic devefopmcnt. environmental influen ces. oU-lCr rnentaJ disorders. pregnancy or perinatal problems. and acquired medicaJ conditions. No specific causal factors arc identified in 30%-40% of the cases (American Psychiatric Association. 2000). lngene.ral. specific organic factors arc more likely to be associawd with profound and severe Jcvds of disability. Zigler (1967) suggested tJ1at if the distribution of JQ scores were plotted from a sample of the totaJ populatio11. including U1osc in institutions for people with intellectua.J disability. it would form t he usual beJl..shaped normal curve except at the. very low end. where there tends to be a bump (see J~igure 13·2).

"'

' - -=-- -'---''---'--"---__J 100 130 70

IQ

Figure 13·2

Distribution of IQ Scores

The distribution oflQ scores showing the subdistribution thought to reflect individuals whose intcllectua I disability resu lts from specific organic defect.

At the gene level. numerous recessive inherited conditfons arc associated with intellectual disability. One of the best )01own of the recessive syndromes is phcnylkctonuria (PKU). an inherited error in protein metabolism. T he genetic site associ ated with l>KU is located on chromosome 12. ln PKU. the individual lacks liver enzymes necessary to convert the amino acid phenylalanine. which is found in many foods. into another amino acid. tyronine. As a resu lt . phenylalanine accumulates and is converted

Neurodevelopmental and Disruptive Disorders

into phcnylpyruvic acid and other abnormal metabolites that cause brain damage, hyperactivity, and seizures. Newborns arc routinely screened for PKU by blood tesLOpulation (An1crican Psychiat1·ic Association. 2013).

13.1c

Developmental Coordination Disorder

'lhc ncurodcvelopmental disorders also include a set of motor disorders or conditions in which a deficit in motor coordination or delay in meeting motor development milestones interferes with ac.ademic or daily life. These include developmental coordination disorder. stereotypic movement disorder, and the tic disorders. Poor motor coordination may be indicated by clu msincss. dropping things. bclow~avcragc sports skills, or poor handwriting. Delays may occur in walking. sitting. or crawling. 'fhe clumsint'ss of developmental coordination disorder is not due to a physical disability such as cerebral palsy or muscular dystrophy. nor is it characteristic of the motor difficulties associ .. atcd with intellectual disability. Instead. the ability to execute coordinated motor skills is below that expected by the person·s age. For the diagnosis to qualify, the motor deficiencies must be severe enough to interfere with the normal aclivities of daily living. 1J1c IJSM•5 reports the prevalence at between 5% and 6% of children ages 5 - 1J (American Psychiatric Association, 2013). Little information is available on causal factors or treatments for those with developmental coordination disorder. and in some cases it persists into adulthood.

Neurodevelopmental and Disruptive Disorders

13.1d Stereotypic Movement Disorder rvtotorbchavior that is nonfunctional and repetitive is the key feature ofstereotypic movement disorder. Alt hough such simple movemc.n ts arc rather common in children, the disorder's diagnostic criteria require that the stereotypic movements interfere with normal social or academic activities and have the potential to cause setf~injury. ?\"iovements consist of body rocking, hand waving. or shaking: however. all types of movements rnay be involved. Some repetitive activities arc also physically damaging: Eye poking. head banging. face slapping. and sclf•bit:ingcan cause serious injury and may persist for years. Risk factors may include social isolation or environmental stress. Some ncurogcnetic conditions such as Rctfs syndrome also contribute to stereotypic movement disorder (A1ncrican Psychiatric Association. 2013). t>rcvaJcnce may be between 10%-15% of those with intcUc.ctual disability who a.re living in residential facilities. AIU1ough there may be gender differences in the e.~pression of particular symptoms (e.g.. self-biting may be more common among females than males with the disorder). the overall gcndc.r ratio appears to be equaJ (American Psych iatr-ic Association. 2000). 11reatment information is lirnited for non~tic movernent disorders. However. there is substantial literature supporting behavioral methods that provide a,1ersivc consequences contingent on self-injurious acts. while simultaneouslyshaping competing responses (Matson & LoVulJo, 2008). A.utipsychotic medication has not been particularly effective apart from tranquilization: however. small case reports have indicated that the opiate receptor site blocker naJtrcxone has been useful for some individuals with self-injurious behavior (Symons ct al.. 2001).

13.1e Tic Disorders TI1c lJSM-5motor disorders category includes three disorders in,rolving verbal lies. motor tic.,;. or a combination of the two. Tics arc sudden.stereotyped motor movements or vocalizations that are rapid. recurrent. nonrhythmic, and experienced as irresistible. Simple motor tics include eye blinking. facial grimacing, and neck jerking: U1cy may last less than a second. Complex motor tics. which tend to last at least several seconds, can include hand gestures, squatting, twirling, retracing onc.'.s steps. smelling objects, jumping. or making obscene gestures. Simple vocal tics may involve clearing U1e throat. grunting. or snorting. Complex vocal tics include words: phrases: changes in the volume. emphasis. or pitch of language; and coprolalia. verbal obscenities or social ly unacceptable verbalizations. Tics often occur in bouts. separated by minutes or hours. which may vary in intensity and frequency across different contexts and settings. They can be temporarily suppressed with varying degrees of success in certai n circumstances. such as at school or when a person is engaged in directed activity; they usually cease during sleep.

Tourette's Disorder In Tourctte's disorder. both multiple motor and vocal tics have persisted for at least a year. Symptoms must have begun hefore the age of 18, and the tics. which tY]>ically happen many times each day. cannot be attributable to a gcneraJ medical condition or a substance. Tics usuall)Tbegin by age 6 and can wax and wane in a course that tends to diminish in severity as the person age..,; into adulthood (American Psychiatric Association. 2013). In fewer than JO% of persons, c-0prolalia occurs: more often. however. vocal tics consist of coughing, barking. or grunting. About halfof the cases begin with a simple motor tic such as blinking (American Psychiatric Association, 2000).

'fie

Involuntary muscular

twitching. usu.ally in the facial muscles Coprolalia Verbal obscemties or socially unacceptable verbaJizations. often emitted as voc.a.1 tics

J71

J72

Chapter 13 Abnormal Psychology

Persons with Tourcue·s disorder often feel discomfort, shame. or social embarrassment over their condition, especially if they arc older; impairment in fu nctioning is not arnong the diagnostic criteria for this condition. Obsessions or cornpulsions may be present. About one half of people w ith 1'o urctte's disorder also have ADHO. and the stimulants used to treat ADHD have been associated in some studies \\11t h increased tic incidence a nd severity (l>idsosny & Virani. 2006). Toureuc·s disorder also may co~occur with obsessh1c--compulsive disorder. 'the diagnosis is given to males between 2 and 5 times more often than to fomaJc-s. It is a rare condition with an upper prevalence estimate of about 8 school•agcd children per l.000 (American Psychiatric Association. 2013). There appears to be a substantial genetic component Lo the d isorder. a lt hough t he mechanism is unknown: some individuals w ith Tourettc·s disorder show no evidence of familial pattern. M'cdic.ations. including older and newer antipsychotic drugs (e.g. haloperidol and r ispc.ridonc). arc useful in treatment but have significant side effects. includjng weight gain (Swain. Scahill. Lomhroso. King. & Leckman. 2007). Behavioral techniques. including habit reversal therapy(involvingawareness;: trainh1g and competing response training) and exposure and response prevention. have been proposed for inclusion among the well-established psychothe.r apies (Cook & Blacher. 2007). A randomized controlled trial found behavior therapy to be as effective as antipsychotic medications for treating Tourctte's disorder in children {Pfacentini ct al.. 2010).

Persistent (Chronic) Motor or Vocal Tic Disorder and Prov1s1onal ric Disorder Persistent (chronic) motor or vocal tic disorder involves e ither vocal tics or motor tics. but not botJ1. ltdiffcrs in t his way from Tourctte·s disorder. which requires the presence of each at some point. Like Tou.rette's disorder. symptoms must pc.r sisl for a year a.nd have onset before age 18. In provisional t ic d isorder, sing le or multiple vocal or motor tics occur but have persisted for fcv,,er tha.n 12 months.

13.1f Language Disorder

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resources available for this chapter.

l~our specific disorders of expressive or rece ptive language are classified by the DS.M•5: language disorder. speech sound disorder. childhood-onset fluency disorder (or stuttering). and social (pragmatic) communication disorder. Although the 1JSA1•1V noted that these disorders were more common among ma les. the DSM•S indicates that sex ratios are unclear. All of these communication djsorders also appear to aggregate within fam iHcs. although specific genetic. neurological. or environmental causes are unknown. Language disorder involves language use a.nd acquisition that is substantia lly below that cxp-ccted from an indjvidua l's chronological age. •n1c language impairments arc not due to intellectual disability t o auditory or visual impairment. or to a motor dysfunction. Expressively. this is shown by limited vocabulary. word recaU difficulty. shortened or overly simplistic sentences. errors in verb tense. or a deficiency of understandable discourse. Receptive communication may a lso be affected. involv ing difficulties unde.rstandingwords or sentcnc.cs orparticuJar types of word phrases (such as-if•thc.n" statc.mcnts). As a result ofthis comprehension deficit. it may appear as if the person has not heard or attended to a comment or question: he or she may seem shy or confused or g ive inappropriate or tangential responses to questions. All language modalities may be involved: Expression of written language. spoken language. and sign language can be impaired. The course is variable. although some difficul• ties tend to persist into adulthood: t hose with receptive language deficits appear to have a poorer prognosis {American Psychiatric Association. 2013).

Neurodevelopmental and Disruptive Disorders

13.1g Speech Sound Disorder Speech sound disorder is an articulation disorder in which persons fail to use the speech sounds that arc normal for their developmental level. OifficulLies may occur in knowledge of the correct phonological sounds or in the motor coordination required for speaking (which invoh1es movements of the jaw, mouth. lips. and tongue. as well as controlled airflow). For cxomplc. sounds moy be difficult to produce (th. ch). substituted for one onothcr(t fork). or omitted. Lisping is also common. Speech therapy is hclpfu.J. and articuJation tends to improve over time. However. if language disorder is also present. the prognosis is less optimistic (American Psychiatric Association, 2013).

13.1 h Childhood-Onset Fluency Disorder (Stuttering) Childhood-onset fluency disorder (stuttering) is a disturbance in speech fluency typically charactc.rized by speech blocks. repetitions of words or syllables, and prolongations of speech sounds. Approximately 1% of all children are pc.rsistent stutterers; another 4%- 5% show transitory stuttering when young. but outgrow it in time (Arncrican Psychiatric Association, 2000). Children with the condition often find the dysfunction embarrassing, and they may avoid speaking opportunities or limit speech to short. simpJc utterances. '01e difficulties increase under conditions of stress or anxiety. Stuttering aJmost aJways starts before Do we know what causes the age 7. but it can be coded for adult onset: stuttering? Can we help the usually. the onset is graduaJ (American Psychiatric person who stutters to speak Association, 20l3). In families in which the father in a normal way? has a history of stuttering. IO% of daughters and 20% of sons also stutter (American Psychiatric Association. 2000). Stuttering has received perhaps rnore historical attention from psychologists than the other communication disorders. Psychodynamic theorists emphasized the symbolic meaning of stuttering: One psychoanalytic scholar suggested that stuttering stems from conflict around the expression of anal-sadistic impulses (Fenichel. 1945}. Speaking became associated with the utterance ofobscene, especially anal. words and the expression of verbal aggl'ession. The same motives which in childhood were directed against pleasurable playing ·w ith feces make their appearance again in the form of inhibitions or prohibitions of the pleasure of playing with words. 'lbc c.xpulsion and retention of feces, and actually the retention of words. just a.s previously the retention of feces. may either be the reassurance against possible loss or a pleasurable auto-erotic activity. One may speak in stuttering. of a displacerncnt upwards of the functions of the anal sphincters. (pp. 311- 312) Other less complex psychologicaJ theories tended to emphasize factors that create anxiety or concern about speoking properly [Bloodstein. l975;Johnson 1959; Sheehon. l975~ Consistent with an anxiety or tension theory, Lanyon(l978)suggestcd that the stuttering act is preceded and accompanied by a physical struggle to speak. (t can involve excessive muscle tension. e~~pcci.aJly in speech•rclatc-d areas. along with breathing irrcguJarjties and a variety of extraneous body movements. According to Lanyon. the stuttered word appears to be the end point of a chain of events. of which the initial event appears to be the perception that a disruption in flucnc.y is about to occur.1his perception has become conditioned to elicit the physical struggle that eventuates in the stuttered response.

J7J

374

Chapter 13 Abnormal Psychology

Treatment for Stuttering Half or more of the individuals who begin to stutter will rccovcr,'lith l.ittJc or no professional help: this is especially true for t he younger child (\Vi ngatc. 1976). According to t he DSM-5. 65%- 85% ofstutterers recover from the dysOuency (American Psychiatric Association. 2013). Stutterers themselves are usually aware of circumstances in which thcjrdysflucncydisappcars or is greatly diminished. Blood stein (1949) found that at least 90% of the stutterers sampled reported substantial rcductjon in stuttering when reading in chorus. speaking to an animaJ

or to an infant. singing. swearing. speaking to a rhythmic swing of the arm or tapping of the foot. or imitating a regional or foreign d ialect. A number of techniques. some similar to those reported above by stutterers. have been shown to reduce stuttering. although generalization to more normal ways ofspeaking outside of the clinic can be a problem. One technique that has been found to consistently produce an immcd.iate reduction in stuttering is delayed auditory feedback. \Vhcn nonstuttercrs talk while hearing their own speech played back through earphones with about a 1/IO•sccond delay. they tend to show marked

disruptions in speech similar to stuttering. Paradoxically. when a stuttercr's speech is delayed in this fashion. the stuttering is almost completcJy suppressed. Another example is rhythmic cuing. in which the person is asked to speak in a rhythmical. singsong fashion. usually with the aid of a rnetronomc. \Vingate (1976) suggested that t he important common factor in these and other procedures found to reduce stuttering is a slowing down of speech that permits a deliberate substitution of a nonstuttercd utterance. In later research. \>Vagaman. Miltenberger. and The Delayed Auditory Feedback (OAF) device alJows the speaker lo hear his or he r own voice wilh a lime de.lay. which help.sstul terers to speak more clearl)'· tA P Phc,t.u/Sc,utl1 Bend 1'nbnne. c; ~.i;s,.,•,crc.i:l

Arndorfer (1993) trained eight child"ren to detect any instance of stuttering. to regulate breathing from the diaphragm. and to exhale s lightly before beginn ing

to speak. Subjects practiced speaking during natural exhalation. beginning with short conversational phrases. lf a stutter occurred. subjects stopped speaking imrnediatcly and reinstated the breathing technique. Parents as.,;isted in practice. kept records of progress. and offered social praise. Improvement was significant and sustained for all children outside of the treatment setting. Both parents and speech pathologists reported that the child.ren's speech was unimpaired and natural after treatment (sec Figure 13·6).

13.1i Social (Pragmatic) Communication Disorder New to the /JSJ\i/~5is social (pragmatic) cornmunication disorder. a condition in which basic practical social communication skills- such as greetings. taking turns in conversation. asking forcla1·ificat.ions. or matching speech styles to the context of the listencr(for example. playground versus classroom)- are impaired. Children with this condition have difficulty telling stories. making inferences. clistinguishing humor. and understanding common metaphors, resulting in social and academic difficulties. Social (prag1uatic) communication disorder is not due to intellectual deficiency, autism spectrum disorder. or other mental disorders: however. it does occuJ' more commonly in families that have histories of autism. communication disorders. or learning disorders (American Psychiatric Association. 2013).

13.1j Autism Spectrum Disorder One particularly controversial change made during the development of the DSM·S involves the decision to combine four of DSM 1V's pervasive developmental disorders into a single. spectrum diagnosis. 1hc-se conditions included autistic disorder. Asperger's disorder (in 4

Neurodevelopmental and Disruptive Disorders

Figure 13-6

Behavioral Treatment for St.uttering

Percentage of stuttered words in four subjccts.1]1c arrows represent treatment sessions. 111e squares are generalization probes. Data s ource: "An.al)·sl4 o r a Si mplified 'ITeat ment for Stuttering In Children: b)' J. R. Wagaman rinted with pemil,sion from the Diagmmk ond Star/.fJica/MmwaloJMmtal Disordera.. 6th ed. {Copyrighl2013). American Psrchlatrlc A!lsociatkm.

Neurodevelopmental and Disruptive Disorders

387

Causal Factors of Conduct Disorder Conduct disorder tends to rw1 in families and is more like]y when parents or siblings have antisocial personality disorder or conduct disorder. substance use disorder. mood dL,;ordcrs. or AOHO. Other predisposing factors include parental rejection or neglect, use of harsh discipline. physical or sexual abuse. lack ofsupervision. peer rejection. below-normal IQ, and early institutional living. Both genetic and environmental factors arc t hough t to be involved in its development (American Psychiatric Association. 2013}. Granicand Patterson (2006) described a behavioral model of antisocial behavior. emphasizing the dynamic interplay Certain behavjors consistent with conduct disorder are between parents and U1c child. Based on coercion theory. t he serio us rule \'iolations. social deviancy. and aggression. model proposes that parents and children train each other, Smoking. sexual nclivil-y. and usc ofille_gnl substances arc through ongoing dynamic responding. in ways that increase common a nd begin 11t a young age. (iStQck) aggressive and oppositional behavior by the adolescent. In one example interaction. a p arent may request compliance from an adolescent engaged in an inappropriate activity. 1-bc adolescent then responds coercively. escalating tJ1c problem behavior to the point that the parent. frustrated. withdraws. The child senses the parent"s acquiescence and reduces the problem activity. 1he child's cscaJation of misbehavior is reinforced by the wit hdrawal of parental demands for compliance.. while lhe parental withdrawal is thus reinforced by the temporary improvement in bchavior.1bc cumulative effect of many such exchanges over many situations is to produce more coercive behavior on t he part of the adolescent and less monitoring and discipline on the part of the parents. Inept discipline and monitoring from parents. together with rejection by normal peers and increasing adolescent commitment to deviant peer groups. further contribute to the development of antisocial behavior and delinquency.

Treatn1e11t for Conduct Disorder Behavioral techniques have been effectively employed for the treatment of anti social and oppositional conduct in children and adolescc.nts. One key part of the interventions is training of parents in behavior management skills. a]ong with training both parents and children in problem-solving a pproaches. Especially when instituted in families early after t he onset of conduct disorder iu young children. child training (e.g.• modeling p roblem solving . social skil ls, and coping with stressful situations) and parent training (e.g .. modeling of parent ing skills and solutions for interpersonal problems) arc effective in significantly reducing problem behaviors. Improvements have been maintained at l•ycar follow-up (Kazdin. 1998: WebsterStratton & Hammond. 1997). Both parent training a nd comrnunity-hased prevention programs have been shown to be effective (American Psychologica] Association. 2006; Parmer. Compton. Burns. & Robertson. 2002). However. t here arc concerns that group-based treatments can have ia trogenic effects- that is. group treatments may result in in creased rather than decreased problem beh avior by inadvertently reinforcing de,•iant values. increasing contact with peers who model inappropriate behaviors, and nonnalizing skewed perceptions about the prc,•alence of delinquent activities. Several reports of increased deviancy in delinquent or at•risk youth undergoing peer-group treatment formats in community or school setting are a,1ailablc. inc.l uding some evidence of increased likelihood or substance use following participation in Drug Abuse Resistance Education (DA RE) programs {Rhule, 2005). It is important to be aware of these possibilities in order to modify programs and dcli,•crymcthods that present such risks.

Chapter 13 Abnormal Psychology

13.2c

Intermittent Explosive Disorder

Intermittent explosive d isorder describes recurrent outburst.~ ofverbal or physical aggressive• ncss involving failure to rc$ist aggressive impuJscs.111c aggression may include destruction

of property. physical attacks that injure others. or verbal threats of assault. Outbursts are not preplanned and arc not attempts to achieve any clear objective such as intimidation. 1J1ey arc sometimes accompanied by strong emolions. such a.s rage. grossly out of proportion to any provocation or precipitating stress. 1J1csc episodes arc often very distressing to t he indjvidual and t heir consequences can involve loss of employment. interpersonal difficuJ. tics. divorce. legal problems. or serious injur ies. 'lhe diagnosis cannot be given before age 6. Onset of the condition is usually in late childhood (American Psychiat ric.Associatfon, 2013). Because aggressive acts may occur in many mental disorders. careful diagnosis is

required to rule out alternative conditions tJ1at can account for the behavior. such as antisociaJ or o ther personality disorders. conduct disorder. ADH"O, or manic episodes. Most people w ith intermittent explosive disorder also have other disorders (Coccaro & Danehy. 2006). complicating t he diagnostic process. Similarly. t he djagnosis requires t hat t he aggression not be explainable by the effects or a substance or a general medical condition (such as head trauma). 111ose with intermittent explosive disorder may have childhood histories of tantrums and sometimes experience mood. anxiety, or substance use disorders or other impulse• control conditions. Data fro m a representative sample. of more than 9,000 adults found lifetime pre\ralence rates of7.3%of the population. with average onset at age 14. and (for those affected} a lifetime average of 43 attacks (Kessler ct aL 2006}. There is limited information on the etiology or treatment of intermittent explosive disorder. although som.e evidence exists supporting t he effectiveness ofrcJaxation training, cognitive-behavioral therapy. and SSR I antidepressants in reducing aggressive behavior and improving affect (Coccaro & Danehy. 2006).

Some authorities complained that the diag nostic reliability and validity o f the intermittent explosive disorder diagnosis was poor because many impulsively aggressive persons would not be captured within the DSW1 JV criteria for the disorder. whicb required a sense ofincrc.asing tension, relieved by t he outburst. Coccaro. Kavous.1,i, Berman. and Lish (1998) proposed a set of revised diagnostic criteria that include rate (twice per week) and duration (J month) criteria. together with removing the rule out regarding other conditions (like antisocial personality disorder) that might better explain the aggrcssion.111esc new criteria we.re tested on a group of 188 personality...disordcred individuals and were found to have good intcr•ratcr reliability and construct validity: they were subsequently incorporated into the DSM-5. 4

4

13.2d

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Kleptomania

Kleptomania involves an impulsi\'e urge to steal items that are not needed either (or personal use or for t hejr value. 111e theft is not driven by a nger or a sense of vengcanc.c. nor is it in response to delusions or hallucinations. In kleptomania. the person experiences a growing sense of tension before stealing. which is replaced by pleasure and rclicf after the t heft occurs. Items are stolen impulsively. w ith little prcplanning. and hold little value to the individual. who subsequently may discard t hem or give them m..•ay to others. People with this disorder know tJ1at the t heft is wrong, and they may fear being caught and arrested: they often feel guilty afterward. However, stealing may be chronic and contjnue for years. despite a series of arrests and convictions. Kleptomania may occur in a significant minority of shoplifters. but its prevalence in the general population is less than 1%. 11uee fourt hs of those with kleptomania are female (American Psychiatric Association. 2013).

Neurodevelopmental and Disruptive Disorders

As with intermittent explosive disorder, kleptomania must be distinguished from stealing that can occur in the context of conduct disorder. antisocial personality disorder. or a manic episode. Comorbid conditions most often include major depressive disorder. anxiety and eating ilisorders. and other impulse-control djsordcrs. Compulsive buying may be present as well (American Psychiatric Association. 2013).111cre is a high rate of hoarding of items by tJ1osc with kleptomania. bat often individuals report amnesia for the theft event (Grant. 2006).11,c condition usually begins by adolescence. Little is known about etiology or effective t herapy. Most indjviduals report shoplifting for 10 or more years before entering treatment. Some positive reports involving naltre.xone (an opiate-receptor blocker) for reducing urges to steal have been reported. but overal l data are mixed: no pharmacological treatment is supported by controlled studies. Similarly. there arc case reports suggesting co,·crt sens:itization and exposure and response prevention have been effective behavioral interventions. but no well-controlled studies have been published (Grant. 2006).

13.2e Pyromania Pyromania involves muJtiple episodes of jntentionaJ fire setting. 111e urge to start a fire is accompanied by increasing tension or arousal. and pleasure or relief accompanies the fire and its aftermath. Individuals w ith pyroman ia do not set fires for monetary gain. to conceal a crime. as expressions of anger or vengeance, or for sodal or politic.a..J reasons. Fire setting is also not a result of impaired judgment. such as t hat associated with intoxication, limited intellectual functioning. or dementia. Instead. individuals with pyromania arc fascinated by fire and arc attracted to and curious aboul all aspects of fire. includ ing firefighting paraphernalia. fire alarms, and firefig htjng. Some people with lhc disorder affiliate themselves with local fire department.~ and may actually become firefighters in order to be close to their source of fascination. Although pyromania is an impulse•control disorder. fires arc not often set on impu lse but rather after advanc.c preparation that may be considerable. Howe,•er. the person is frequently indifferent to the possible loss of li fe or destruction of property that may result. ·the condition is more common among males with poor social skills or learning difficulties: in juveniles it is associated with conduct d isorder a nd ADHD (American Psychiatric Association. 2000). ll is also common for fire•settcrs to have a history of alcohol use disorder. (t.s prevalence is unknown in the popuJation, but 3.3% of fire-setters in t he cri minal Individuals with pyromania a.re fascinated by. attracted to. justice system may qualify for the diagnosis (American an d curious about all aspects of fire. Pyromania involves multiple episodes or inten tional fi re selling. fShu:Hrutockl Psychiatric Association. 2013). Classic psychoanalytic theory considered pyromania to be a symbolic sexual act: Freud considered it the equivalent of masturbation. Occasional case studies have reported sexual arousal in both male and female arsonists, suggesting that pyromania. sometimes occurs in the context of fetishism (e.g .. Balachandra & 5',-.,aminath. 2002). Others have prop osed that it is a form of communication. aggression, or self-destructiveness by juveniles with limited socia l skills: suicidal thoughts or acts are very common among arsonists (Lejoyeux. McLaughlin. & Ades. 2006). A few case studies have reported positive outcomes with behavioral interventions such as aversion therapy. However. very littJc systematic work is available on the etiology or treatment of pyromania.

Jlt

390

Chapter Review TO SUM UP ... •

1hc ncurodevclopmcntaJ disorders involve dysfunctions relating to the developmental p rocess. The disruptive. impulsc--control. and con.duct d isorders involve deficient self-control of emotions and behavior.

lntcllcctuaJ disability is significantly bcJow average intclloctuaJ functioning. combined with impairment in adaptive skills. Its causes include genetics. embryological errors. prenatal or postnatal conditions or injuries, environmental restrictions. or any conditions that prevent normal brain development.

Although medications arc commonly used in treating symptoms related to intc.llcctual disability and autism spectrum disorder. there is little evidence for their effectiveness. (ntcnsivc behavioral intervention is helpful in treating many children with autistic disorder, especially if intervention begins at very young ages and includes parents as therapists.

Severa) communication disorders may have onset during childhood or adolc-scence. and may impair acadernic and social functioning. 1l1esc conditions tend to improve as individuals get older.

Tic disorders involve sudden. rapid motor movement.~ or vocalizations t hat are experienced as irresistible.

111c most comrnon childhood disordc.r s irwolvc disruptive behavior such as that seen in ADH 0. conduct disorder. and oppositiona.l defiant disorder. Although both genetic and cnvironmc.ntal factors arc involved in the development of these disorders. their specific causes arc unknown.

ADHO is controlled by stimulant medication and behavioral therapy during the short term. However. there is no evidence that medications have long-term value for ADH 0. and stimulants appear to inhibit physical growth. Behavior therapy and family therapy have been demonstrated as effective in treating conduct disorder and oppositional defiant disorder.

Conduct disorder is a dJsruptivc condition t hat involves violations of rules and the rights of others. lt is a prerequisite for later development of antisocial personality disorder.

There is much overlap and comorbidity among A OHO. oppositional defiant disorder. and conduct disorder.

Both kleptomania and pyromania are impulse.oeontrol disorders in which rising tension is relieved by the impulsive act.

391

KEY TERMS Amniocentesis

Coprolalia

365

J>rcmaturity 367

371

Down syndrome

Phcnylkctonuria (J'KU) 364

365

Savant syndrome 377

Encephalitis 367

Stimulus oversclcctivity 378

Fragile X syndrome 365

lbcory of mind

IQ 362

1'ic

Meningitis

378

37 J

367

QUESTIONS FOR STUDY •

Identify three p.rcvcntablc causes of intellectual disability.

Discuss contro\•ersic$ involved in the diagnosis and treatment of ADH D.

Distinguish the symptoms of two cornmon djsordcrs from two uncommon or rare djsorders described in the chapter.

Describe the disorders in this chapter in which crirninal behavior may be present.

POP QUIZ 1.

111c specifiers for intellectual disability (mild. moderate. severe. profound) arc based on which of the following? A. IQscorcs B. degree onmpairment in adaptive functioning C. the number of symptoms that occur D. the number of settings in which tJ1c disability is apparent

2.

A standard score on intelligence test has a mean of _ _ _ _ _ and a standard deviation of _ _ _ _ __ A.100 / 15 8 . JOO / 50 C. 50 / 15

0. 50 / 5

392

3.

Among chHd.rcn, the most frequent psychological referral to mental hca.JtJ1 facilit ies occurs for which disorder?

A. Af>HO B. oppositional defiant d isordcr

C. conduct disorder 0. stuttering 4.

How do psychostimulant drugs affect normal children? A. 11u:y induce a period of depression. B. 'TI1cy increase energy but decrease alertness. C. 111cy improve attention and decrease motor activity. 0. 1l1cy have no observable effects on normal children.

5.

______ associated with intellectual disability. is also called trisomy 21. A. Fragile X syndrome

ll. PKU C. Rctt's disorder D. Oown syndrome 6.

The wide availability of _ _ _ _ _ has led to the virtual climination of cretinism in the VVcstern ,-.,orld.

A. lithium

B.

iodized salt

C. MMRvaccinc

0. folic acid 7.

Harry is given a series of tests. His reading and writing results are significantl)r below those predicted by his intelligence and education. He would most likely be diagnosed as havjng _ _ _ _ __ A. intellectual d isability

B. Af>HD C. language disorder

0. specific learning disorder

S.

In families in which the father has a history of stuttering. _ _ _ _ _ of daughters and ______ of sons also stutter. A. 20% / 40% B. 20% / 30% C. 10%/ 30% 0. JO%/ 20%

9.

\Vhnt is savant performance? A. extreme sociability

B. an exceptional skill in a specific area C. self-injurious behavior

0. very high IQ

393

10. \Vhid1 of the following disorders is more likely to involve coprolalia? A. language disorder 8. conduct disorder C. Tourctte's disorder

0. Rct.t's disorder 11. Brain growth may be unusually rapid for the first2- 3 years in children with A. autism spectrum disorder B. fragile X syndrome C. stereotypic rnovcmcnt disorder 0. ADHO

l2. Delayed auditory feedback helps reduce _ _ _ __ A. language disorder

B. childhood~onset fluency d isorder C. social (pragmatic) c-0mmunication disorder D. speech sound disorder 13. Tim has been diagnosed as having oppositional defiant disorder. Vince has been dfagnoscd as having conduct d.isordcr. \1/hat is the rnajor difference bcnvecn these two boys? A. Tint is older than Vince. B. Compared to Tim, Vince has a much better prognosis. C. Vince has en.gaged in more serious forms of rule violations than has Tim. D. 111ey demonstrate the same symptoms. but 'l'im is more likely to be intellectually disabled. 14. \Vh ich of the followingdisordc.rs is more common among females? A. conduct d isorder B. pyromania C. autism spectrum disorder 0. kleptomania

15. Although considered an impu lse-control disorder. _ _ _ _ _ actuaUy includes planning and preparation for the act. A. kleptomania 8. pyromania C. intermittent explosive disorder D. none of the above

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CHAPTER OVERVIEW 14.1 Feeding and Eating Disorders ... ....395 Anorexia Nervosa Bulimia Nerwsa Btnge--Eating 0 1sorder

Avoedam/t{estncdvc food Intake Dts0edl!'r Pica Rumination Otsorder

14.2 Overview of Sleep•Wake Disorders ...... ... .....405 14.3 Dyssomnias ............................. .407 Insomnia Oi.Sorder

Hypersomnolence Disorder Narcolti»y

Brcalhrng,R.elated. Sleep Otwrders Cucadian Rhythm Sleep-Wake 01SOCde.rs Re,tloss legs Syndrome Substance/Medauon-lnduced Sleep Orso,der

14.4 Parasomnias .... ......... .. ..... .. ...... .412 Non•RapKI Eye Movement Sleep Arousal 01sorders N,ghtmare Orsorder Rapid Eye MOYemen l Sleep Behavior Disorder

14.S Elimination Disorders ............. ... .415 l:ncoprl!'SG

£nures1s

CHAPTER OPENER QUESTIONS What is the relationship among eating d isorders, culture, and gender1 How are anorexia nervosa and bulimia nervos.a

different? Which is easier to treat?

What are parasomnias and dyssomnias? What are the most common

sleep disorders? Can someone fall asleep in the middle or a conversation? Do people sleepwalk because they are dreaming? Do some people act out their d reams' What t reatments are effective for elimination disorders?

Eating, Sleep, and Elimination Disorders T

he dysfw1ctions examined in this c hapter involve basic biological processes necessary for human lire: eating. sleeping. and elituinatin gwastc. Many of the conditions involve t he patterning of the activ ity. altJ1ough symptoms ofexcess and deficiency arc diagnostic.1'hc largest category- the slccp•wakcdisordcrs- conccn1s dissatisfaction with t he quality. timing. or amount of sleep. The smaJlest classification- the elimination disordersconsists only of two conditions involvin g inappropriate toileting. \Ve begin with the feeding aud eating disorders.

14.1 Feeding and Eating Disorders Among the feeding and eating disorders arc conditions t hat can seriously impair physical and psychological health. They involve patterns of altered consumption. some of which affect the absorption of nutricnL~. J)ica and rumination disorder were moved fro m -Conditions first d iagnosed in infancy. childhood. or adolescence" in the DSA1-JVto join anorexia nervosa, buli• utia nervosa. and binge-eating disorder (a formerly What is the relationship provisional diagnosis), as well as a new conditionamong eating disorders, cu.Jture. avoidant/restrictive food intake disorder- in defin• and gender? ing this category. 'lbc various feeding and eating disorders are displayed in Table 14•1. 1he feeding and eating disorders do not include obesity. which is not c urrently listed as a mental disorder. According to the DSM-5. "Obesity (excess body fa t) results from the Jong-tenn excess of energy inta ke relative to energy expendit ure. A range of genetic. physi• ologicaJ. behavioral, a nd environmental factors that vary across individuals contributes to the development of obesity; thus, obesity is not considered a mental disorder" (American Psychiatric Association. 2013. p. 329). However. since all the fJS;\1-5 conditions considered in this text develop from a range orgenetic. physiological, behavioral and e nvironmental factors.H that distinction is less than clear. Presumably. the rnore pertinent issue would be that obesity is defined not in terms of t he behavior t ha t produces il but rather in terms of its product- excess body fat.1l1is is rather analogous to the relationship betwc-cn smoking (the beha,r:ior) and lu ng cancer (its product).

Table 14-1

DSM-$ Feeding and Eating Disorders Minimum D u ration

Disorde r

Key Symptoms

Required for Diagnosis

Sex Rulio

None

More common among females

Anorexia nervosa

Low \-..-eight with restriction of energy intake, plus mtense fear of gammg we1ght

BuUmia ner-..·osa

Recurrent binges with c:Ompensutory behtwiors

3 months

More common i n females

Binge-aating disorder

Recurrent binges without c:ompensalory behaviors

3months

Morec()mmon in females

A,•oidant/ restricbve food intaka disorder

Persistent faUure to meet nutritional needs

Pica

Eating oonf0d substanc:~

Rumination db,order

Repeated regurgitation

Source: American Psyc:hlnttlc Association, 2013.

or food

Nona

fVestcrn industrialized nations where food is plentiful. It appears to be linked to cultural views about beauty and thinness and driven by widespread Anorexia appears to be Linked to culturaJ views about media representations of increasingly thin models and beauty and thinness. and driven by wide.,;-pread media repre.scntnlions ofincrea..•dngl)' thin models as images of actors as images of pcrfcction.1lte influence of culture can perfec.1ion in fushion. {SbuU.t'rd«.kl be seen in the fact that immigrants· ris k for the disorder increases as they become more enmeshed in American life (American Psychiatric Association. 2013). Lucas. Beard. O'Fallon. and Kurland {1991) reported that the prevalence of anorexia ncrvosa over a 50•year period in Minnesota. from 1935 to 1984, rose linearly among females ages l5 to 24. with incidence increasing 36%cvery 5 years during that period. In the same period, incidence of the disorder did not change formal cs or older females. Overall. female rates were nearly J2 times higher than male rates of anorexia nervosa during 1980- 1984. Since that time. the rate of increase has slowed . Amenorrhea Lifetime prevalence rates are about 0.9~ for women and 0.3% for men (Hudson ct aL 2007). Absence of Male cases tend to be associated with homosexuality (Russell & Keel. 2002). 1hose at high· menstruation in a est risk arc white females ages 15- 24: in contrast. anorexia nervosa appears to be extremely woman of reproductive rare among African Amc.rican females (Hock. 2006). One possible explanation for such racial age disparity is that risk for the disorder is greater among tJ1osc of higher socioeconomic status Purging (Striegel-Moore & Bulik. 2007). A compensatory Anorexia nervosa commonly occurs in conjunction with other mental disorders. In a activity intended to sample of 101 adolescent females in treatment for anorexia nen•os~ more than 73% were reverse the effects diagnosed with at least one other disorder- most often. mood or anxiety disorders. 111c of eating. usually hinge•eating/ purging type is associated with significantly greater risk of substance use involving se!f•induccd disorders than the restrictfog type (Salbach-Andrae ct al.. 2008). The binge-eating/ purging vomiting or use of t)1>e is also linked to signjficantly greater likelihood of suicide attempts (Bulik et al.. 2008). laxative~ 4

Eating, Sleep, and Elimination Disorders

399

Causal Factors the etiology of anorexia ncrvosa remains unknown. Psychoanalytic writers proposed that individuals with anorexia. when faced with tJ1c anxiety•arousing prospect of genital scxuaHty at adolescence. regress to already-- cxisting oral fixations. Deufal of eating is thought to reflect deniaJ of sexuality or. even more specifically in some cases. gu ilt over the unconscious wish to be impregnated tluough the mouth. Family•systcms LhcrapisLi; have emphasized con Oicts around issues of independence and changing from child hood to adult ways. Anorexic children a re likely to appear in families that arc excessively enmeshed. en1otionally. have overprotective parents. and lack effective ways of directly resolving conflicts.11rns. the anorexic girl Cer tajn athletes. especinlly those in\'olvcd in aesthetic may be seen as asserting her independence in the only way performa nce (such as fig ure skating o r gymnastics) or those she can- by refusing to cat. emphnsiz.mg a sped fie weight (such us Judo or wrestling). are at high er risk for eating disorders. (Shuttc·ntod:l Biological and cultural influences interact i n the development of the disorder. Anorexia ncrvosa runs in families. and concordance rates arc higher in MZ than DZ twins (American Psychiatric Association. 2013). Concordance has been reported as high as 55% for MZ twins versus 5% for OZ twins (Fairburn & Harrison. 2003). suggesting substantial genetic contribution to risk for the disorder. Offspring of mothers with anorexia ncrvosa arc at high risk for the disorder as well (Striegel-Moore & Bulik. 2007). However. its strong association with cu ltural portrayals of beauty in terms of thinness a]so indicates important contributions fmm environmental factors. which may e.xplain the significant variations in prevalence among different ages. ethnic groups. and sexuaJ orientations. As noted above. homosexual orientation is a significant risk factor for eating disorders in males. Greater emphasis on physical attractive• ness among gay men places them. like heterosexual women. at higher risk for attitudes and behaviors related to eating disorders (Siever, 1994). Among heterosexual adolescent males. the factors increasing t he r isk of eating disorders similarly involve low sclf~esteem and peer pressure to lose weight. although body-image issues tend to involve male pursuit not of thinness but of muscularity (Ricciardelli & McCabe, 2004). Certain athletes. es1,ccially t hose involved in aesthetic pcrfonuance (such as figure skating or gymnastics) or those empha• sizing a specific weight (such as judo or wrestling). arc at higher risk for eating disorders (Sundgot-Borgen. 1994). An interesting behavioral perspective of anorexia ncrvosa comes from studies showing that if a rat is placed on food restriction and presented with a running whe-cJ. it increases activity levels and further lowers food consumption: tJ1is '"activit y anorexia- can result in selr•starvation unless the study is terminated {Epling. Pierce. & Stefan. 1983).' Jhe increase in activity after food restriction could have evolutionary value. as it increases migration and foraging for food in animals. Female rats experiencing activity anorex.ia become hypo• the.rm ic. as food intake is insufficient to meet metabolic demands. and their ovulatory cycle is suppresscd.1.hcir weight loss can be halted if activity is prevented or if the animals arc kept warm. Bergh and her colleagues (2013) proposed that similar events happen in human females: As t he person reduces food intake. there is widespread disruption of t he HPA axis: hypothermia and amenorrhea develop: and the dopamincrgic reward system is activated. making food restriction and increased activity rewarding. Anorexia then deveJops from the reinforcing effects provided by further food restriction and increased activity. and it is maintained by conditioning to the situations that originally were associated with t he rewardFlashcards are avaBable ing value ofeating less than before. In this view. it is disordered eating that causes anorexia fo, this chapter at rather than underlying pathological processes. www.BVTLab.com.

BVT Lob

400

Chapter 14 Aooormal Psychology

Treatment for Anorexia Nervosa

Binge eaUng

f:atJng much larger amounts of food than normaJ within a given time

..

Outcome of treatment for anorexia ncrvosa did not improve much t h roughout the 20U1 century: Stcinhauscn (2002) reported that even after 1950. mortality remained significantly high (ranging up to 22% in some studic.s), and less than half of patients fully recovered. More recently. some p romising results have been reported for a particular form of conjoint family therapy for adolescents. in which parents are coached in how to assume control over the anorexic child's eating and weight. External controls arc then gradually reduc.cd as the child compl ies wit h parental authority so that increasing autonomy is linked with improved eating patterns (\Vilson. Grilo. & Vitousck, 2007). However. this approach is less beneficial with older persons or if the disorder has persisted beyond a few years. ~fcdic.ations arc rarely used as the sole therapeutic approach. and there is no clear evidence that antidepressants, which are widely prescribed for the condition. have any value over placebo (\1/ilson ct aL, 2007). No drug has been found to promote wejght gain for these patients (Fairburn & Harrison. 2003). Inpatient treatment, which a llows for close monitoring. nutritional counseling. and specific behavioral contingencies. can be effective in restoring bodyweight. However. the addition of medication does not add to outcome expectations. and -al present. there is no sp ecific role for pharmacology in tJ1c treatment of anorexia nervosa(\r\'ilson et al.. 2007. p. 577). In a smaU randomized controlled trial. repetitive transc.ra.niaJ magnetic stimulation (rT~,AS) was moderately effective in reducing the urge lo restrict levels of feeling full and levels of feeling fat. compared with sham r'l'MS (McClelland ct al.. 2016). Additiona.J studies involving multiple sessions and larger samples arc planned to replicate the.,;e results and determine the efficacy of rTMS and the time course of its effects on anorexia. One prom ising therapy approach is based on the activity anorexia model pre,s cntcd earl ier. ln this inpatient program (Bergh. Eklund. £riks.,;on. Lindberg. & SOderstcn. 1996). anorexic patients cat meals from a plate that has been placed on a baJanc.cso that the weight of remaining food can be recorded by computer. Each minute:, a 0 - 10 scale appears on a monitor, a.Bowing the patient to rate satiety. During each meal the computer ca.Jculates t he rate of food intake and level ofsatiation and displays these curves on the monitor. along with normal eating curves for that food. 1-'o regulate the eating pattern. the patient is encouraged to match the curves for normal eating and satiety rates. Patients arc also provided thermal blankets and warm rooms. and their physical activity is restricted. As the eating pattern is regulated and normalized . patients are encouraged to resume normal social interactions. In an evaluation of 1.428 patients w ith anorexia nervosa or bulimia nervosa treated over an 18-ycar period at six centers in Swc-den. the Netherlands. Australia. and the United States. 75%achieved remission after a median of J2.5 months of treatment. and only 1096 had relapsed after 5 years (Bergh ct al, 2013) .

14.lb

ln bolh anorexia ner vosa and bulimia nen osn. se.lf-evaJualion is u nduJy inOuenced by body weight o r shapc.11Sloct) 1

Bulimia Nervosa

l hc condition known as bulimia nervosa (see DS.41•5: Diagnostic Criteria for Bulimia Ncrvosa) differs substantially from anorexia ncrvosa. Lnstcad of weight loss and strict control of eating associated w it h a sense of achievement. bulimia nervosa involves a sense of lack of control related to recurrent episodes of eating la.rge quantities offood . 'fhe binge episode is then foJlowed by some attempt to compensate, such as purging. fasting. or excessive exercise. Like anorexia nervosa. t hose with bu Iimia nervosa fear gaining weight. arc dissatisfied with their bodic~~- and base their self• evaluation on weight and body shape. Binge eating involves amounts of food largc.r than others would normally cat in a given t ime. lt usually includes h igh~catorie foods su ch as cookies, cakes. and ice cream: Fairburn and Harrison (2003) estimated

Eating, Sleep, and El imination Disorders

Diagnostic Criteria for Bulimia Nervosa 307.51 (F50.2) Bulimia Nervosa A. Recurrent episodes of binge eating. An episode of binge eating is characterized by botl1 of the following: 1. Eating, in a discrete period of time (e.g., within any 2-hour period), an amount of food tl1at is definitely larger than wl1at most individuals would eat in a similar period of time under similar circ1unstances. 2. A sense of lack of control over eating during the episode (e.g., a feeling that one cannot stop eating or control what or how much one is eating). B. Recurrent inappropriate co1npensatory behaviors in order to prevent weight gain, such as self-induced vomiting, misuse of laxatives, diuretics, or other 1nedications; fasting; or excessive exercise. C. The binge eating and inappropriate compensatory behaviors both occur, on average, at least once a week for 3 montl1s. D. Self-evaluation is unduly influenced by body shape and weight. E. The disturbance does not occur exclusively during episodes of anorexia nervosa. Specify if: In partial remission: After full criteria for bulimia nervosa were previously met, some, but not all, of the criteria have been met for a sustai11ed period of time. In full remission: After full criteria for bulimia nervosa were previously met, no11e of the criteria have been met for a sustained period of time. Specify current severity: The minimum level of severity is based on tl1e frequency of inappropriate compensatory behaviors (see below). The level of severity may be increased to reflect other symptoms a11d the degree of functional disability. Mild: An average of 1-3 episodes of inappropriate compensatory behaviors per week. Moderate: An average of 4-7 episodes of inappropriate compe11satory behaviors per week. Severe: An average of 8-13 episodes of inappropriate compensatory behaviors per week. Extreme: An average of 14 or more episodes of inappropriate compensatory bel1aviors per week. Source: Reprinted with permission fron1 the Diagnostic and Statistical Manual of1vlental Disorders, 5th ed. (Copyright 2013). American Psychiatric Association.

that between 1,000 and 2,000 food calories are typically consumed during the binge event. Binge eating usually takes place rapidly, in secret, and continues until the individual becomes uncomfortably full. The person often reports feeling out of control during a binge event, although he or she is able to stop the act if suddenly interrupted by others. Once the binge eating concludes, the person may employ several techniques to compensate for the binge in order to avoid weight gai11. Most commonly vomiting is self-induced, often by use of fingers or instruments to trigger a gag reflex; one third of those with bulimia nervosa also use laxatives to compensate for binge eating (American Psychiatric Association, 2013). Nonpurging methods include fasting for a day or more or excessive exercise. Bulimia nervosa is more common than anorexia nervosa, affecting up to 1.5% of females; the female-to-male ratio is 10:1 (American Psychiatric Association, 2013). Most receiving the diagnosis are white. Onset is usually 5 years later than that for anorexia nervosa, and average duration of the disorder is much longer-about 8.3 years (Hudson et al., 2007)-although over the longer term, symptoms tend to diminish (American Psychiatric Association, 2013). Unlike anorexia nervosa, which tends to occur a1nong individuals of higher socioeconomic status, bulimia nervosa is not related to SES (Striegel-Moore & Bulik, 2007). The purging behavior is associated with several negative physical consequences, including disturbed electrolyte balance, extensive dental erosion, stomach problems, and diarrhea. Dependence on laxatives for bowel movements may develop in those wl10 use that technique for purging. Bulimia nervosa is often associated with mood disorders, and up to one third of sufferers also have substance use disorders, usually involving alcohol or stimulants (American Psychiatric Association, 2013).

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Causal Factors Risk for bulimia ncrvosa is elevated among victims of childhood physical or sexual abuse

(American Psychiatric Association, 2013). Data suggest familial aggregation in buJimia nervosa, and some studies have suggested heritability estimates between .50 and .83 (Striegel•

Moore & Bulik. 2007). However. clinical studies showing :i5% concordance in ~AZ twins versus 30% concordance in DZ twins seem to indicate a weaker genetic link than for anorexia ncrvosa (Fairburn & Harrison, 2003}.

llte cultural fac tors affecting one:,; tendency to rcJatc body image to sc)f..cstccm in bulimia nervosa arc assumed to be similar to those for anorexia nervosa. At least among college students. exposure to mass media (especially magazines) t hat promote thin .. beauty jdeals is associated with increased likelihood of diso.r dercd eating (Harrison & Cantor. 1997). Stice (2001) outlined one pathway by which this may occu r in vulnerable individuals: Exposure to thinne~o;s,. promoting media, particularly in young people who value appearance highly, leads to acceptance (internalization) of these ideals of beauty. Together with a social pressure to be thin. these internalized ideals of beauty lead to dissatisfaction witJ1 one·s appearance. Because these ideals arc unattainable for nearly everyone. negative se(f..affect develops_ leading to d icting and restrict ion. thereby increasing t he chance that bingcing will occur in response to severe hunger.

I

Treatments for Bu/1m1a Nervosa A greater number ofcontrolled interventions have been conducted with bulimia ncrvosa than with anorexia ncrvosa. and the outcome data arc more promising. with evidence s upporting the use of both medications a nd psychotherapy. Antidepressant medications produce greater improvements in both binge eating and purging than placebos (Wilson & Fairburn. 2002). 1hey a lso improve mood and tend to work rapidly. However. medications are not associated with sustained improvement or with effect sizes equal to those of cognitive-behavioral therapies (Fairburn & Harrison. 2003). Among psychotherapies. interpersonal therapy focuses on how the Bulitnla nervosu. more common lhun nnor€!x.ia person's relationships with other people contribute to the eating disorder. ncrvosa. affects about 1.5% of females. !iStockl '£his treatment has s ho,,;n some evidence of effectiveness but rcqujrcs furll1er evaluation (Wilson etal.. 2007).1hcidentificd treatment ofchoice for bulimia ncrvosa is cognitive...behavioraJ t herapy. under which about half of patients cease binge eating and purging. and many report improvement in deprcs.o;ive symptoms and se)f.. esteem (\Vilson & Fairburn. 2002., Wilson ctal., 2.007). One example of a comprehc.nsive CBT intervention for bulimia ncrvosa comes from SpangJcr (1999). 111c 20-wcek program begins by estabJishinga regular eating pattern. First. a detailed food record is kept in which t he person records each instance of food consump• tion. includ.ing what and how much is eaten. time of day, and context. foods and situations that the client l'eports as .. low risk~ and -rugh r isk"' for binge eating arc identified. t hen, t he client begins a defined schedule of normal eating. involving three meals and two snacks per day. so t ha t the person iseatingsomethingcvery3- 4 hours. Many bulimics fear t hat eating on a regular basis w ill result in weight gain. However. their practice of restriction actually le-ads to increased hunger. setting the stage for binge c.ating. Regular eating patterns re.duce binge events. A list of pleasant activities (bathing. phone conversations, gardening) is compiled with the instruction that t he client must engage in one immediately after finishing a normal meal to reduce the opportunity and t he temptation to engage in compensatory acts. The person is instructed to ea.tat specified t imes. whether hungry or not. followed immediately by a

Eating, Sleep, and Elimination Disorders

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pleasant activity (rather than remaining in the kitchen area). As a normal pattern of eating is resumed. the client experiences less hunger and therefore fewer urges to binge and less temptation to purge after normaJ portions. \Vcekly weighing reveals that resumptfon of a regular eating schedule produces little. if any. weight gain, removing a source ofanxiety about normal eating patterns. An cducationaJ component adds information about nutrition and contradicts commonly held false beliefs about vomiting (wh.ich docs not expel the majority of calorics consumed) and laxative use (which expels even fewer calorics). Next, the therapy begins a process to counter the cognitive componcmts of bulimia nervosa by attempting to modify tl1e client's beliefs about body shape. and ,1i•eight. body dissatisfaction. and bingcing.1l1rough example giving and standard cognitive disputation. the importance ofphysicaJ appearance to self-esteem and self.worth is c hallenged. Food tolerance is increased with the gradual addition of some -high-r isk" foods to the daily diet. 1his shows the client t hat normaJ portions of forbidden foods can be consumed without a binge ensu ing. Homework assignments might include activities to reveal the body, such as swimmjng. as a way to reduce the importance of concerns about appearance and to promote normal exercise. Stress~reduction and problcm,solvingskills arc also taught as alternatives to binge eating during times of stress. Finally. a relapse prevention component is added. '01e client lists a set of clues or markers. such as changes in eating pattern or the presence of certain moods. which might increase t he chance of relapse. Then. a plan is drawn up for the client to follow if the clues or markers a ppear. including activities in which to engage or family or friends to contact. Spangler (1999) reported improvement that persists during long..term follow-up for clients using interventions of this type.

14.1c Binge-Eating Disorder 1l1e diagnostic criteria for binge-eating disorder include recurrent episodes of binge eating associated with both a sense of lack of control and rapid consumption. Other symptoms arc eating until uncomfortably full. eating large amounts when not hungry, eating alone because of embarrassment about eating patterns. and guilt after overeating. Binge-eating disorder requires that binges average at least once a week for a 3•month period, a nd they must be associated with marked distress. Binges are not accompanied by compensatory behaviors (as in bulimia nervosa); as such. lhe condRion is frequently associated ,\Tith varying degrees of obesity (American 'P sychiatric Association. 2013). Most people showing this condition have long histories ofunsuccessful djeting. The eating pattern tends to be chronic and is often associated with depression. anxiety, and negative self-image. Unlike anorexia ncrvosa and bulimia nervosa.. which tend to have onset during adolescence. binge-eating disorder may notappc.ar until well into adulthood. Although some earlier stud.ies suggested that binge-eating djsorder is more common among white p eople than other ethnic groups (Brody ct al.. 1994). later studies reported t hat t he condit ion is not linked to racial/ethnic status (Striegel-Moore & Bulik. 2007). Nationally. representative data show higher Ufetime incidence among women (3.5%) U1an men (2.0%). which is a significant but less ex.tremegendcrd iffcrence than those of other eating disorders (Hudson ct al .. 2007). 1l1e DSAl~S provides 12-rnonth prevalence rates at 1.6% for adult females and 0.8% for adult males (American Psychiatric Association. 2013). ln a sample of pc,rsons witl1 eating disorders. binge-eating disorder was twice as common as bulimia ncnrosa (Kutlcsic ct al.. 1998). Some evidence suggests that. like those with other eating disorders. persons ,\Tith binge• eating disorder may harbor dysfunctional attitudes about body shape and size that excessively influence self-evaluation (Hrabosky. Mashcb. \Vhitc. & Grilo. 2009). Although not all binge caters engage in such overvaluation. t hose who do show higher levels of disordered eating and depression (Grilo ct al.. 2008). Binge..eatingdisorder appears to be different from a related pattern of disordered eating called night eating syndrome. in which individuals consume more than half of their daily calories in late-night binges.Subjects with e ither condition show greater depressive symptomatology than a comparison group. but those with binge-eating

Night eating syndrome Eating pattern in which individuals consume more than half their daily calorics in lnte• night binges

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disorder engage in more bingcing episocfos and fee l less c.ontrol over eating (Allison. Grilo. Masheb. & Stunkard. 2005). ln the DSM-5. night eating syndrome would be d iagnosed within the category ~other specified feeding or eating disorder." Treatments for b.ingc•eatingdisorder include antidepressant medications and psycho• therapy. Cognitive-behavior therapy is generally associated with h igh treatment completion rates. remission ofbingc eating in. more than half of subjects.and improvement inaccompa• nying depression. Antidepressant medications arc superior to placebo in reducing bingcing and in weight loss: however. relapse rates are high, and discontinuation of treatment remains problematic (\'l'ilson et al .. 2007). Those who respond rapidly to either type o[treatment (that is. those who show a two-thirds reduction in b inge eating within 4 weeks) arc more likely to show remission of the disorder and greater weight loss (Grilo, Mashcb. & \Vilson. 2006}.

14.ld Avoidant/Restrictive Food Intake Disorder 1]1ose with avoidant)restrictivc food intake disorder do not eat enough food to meet their energy or nutritional needs. A significant weight loss, nutritional deficiency. dependence on supplemental focdjng. or marked interference in normal functioning is needed for the diagnosis. Like anorexia ncrvosa. this disorder is associated with malnutrition that can be Ii fc threatening. Unlike anorexia. the lack of appetite or avoidance of food does not involve body shape or image. 1l1c condition cannot be associated with lack of available food. gastrointestinal disorders. or a general medical condition. nor docs it occur exclusively during anorexia or bulimia. 111e new DSM~Sdiagnosis replaced the DSM-fV condition -reeding disorder of infancy or early childhood." which required childhood onset. l.nfant feeding disorders may account for half of hospital admissions for .. fai lure to thrive.' which itself may have community incidence- of 3% and appears to be equally prevalent in males and females (American Ps:ychiatr'ic Association. 2000).111e avoidance or restrict.ion of food might be attributable to Pavlovian conditioning. in the sense that an aversive experience (such as vomiting or choking) may be paired with particular food -related stimuH. Then. the avoidance of food may emerge as an anticipatory conditioned response. sometimes termcdfw1ctional dysphagia (American Psychiatric Association. 2013).

14.le Pica Pica essentially involves t he persistent (at least J month) eating ofnon•nutritive. nonfood substances such as soil. paint. c loth. string, chalk. and pebblcs.1he substances eaten tend to vary with age. with younger children more Iikcly to eat paint or plaster, hair, and cloth. whereas older children arc more likely to consume pebbles. animal droppings. sand. and leaves. The eating of these substances must be inappropriate to developmental level (very young children normally put almost anything into tbeir mouths). and it must not be a culturally sanctioned practice. A variety of physical and medical complications can develop among ind ividuals with pica. Some materials eaten may be toxic or may cause gastrointestinal problems. including infections. perforations, and blockages.1'ypicall)'. the condition remits after several months or a few years. Pica is more commonly found in association with intellectual cLisabilit.y. where its incidence can be as high as 15% (Americ.an Psychiatric Association. 2000). It is also sometimes seen in females during pregnancy (American Psychiatric Association. 2013). Ferreri. Tamm. and \!Vier (2006) describe an intervention for pica involving a 4-year• old autistic boy who had engaged in toy pica durjng the previous year. 1l1e boy would place various plastic toys into his moutb. sucking on and chewing the edges until pieces could be bittc.n off and swallowed. He became aggressive when attempts were made to remove the toys. 'the treatment program involved djpping the toys into tapioca pudding. which the boy d is liked, before they were made available to h im. Pica ceased a lmost immediately and did not recur after the tapioca dipping was discontinued. 1he boy contiuued to use the toys during normal play, however.

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14.1f

405

Rumination Disorder

Ln rumination disorder. individuals repeatedly re.g urgitatc their food. There is no nausea associated with the process. lhe material is then either discarded or. more commonly, rcchcwed or reswallowed. The condjtion must persist for a month and not be associa ted with a general medjcaJ condition or neurodcvelopmental disorder. nor does it occur as part of anorexic or bulimic patterns. Rumination disorder usually occurs in infants. with onset before I year of age. Some older individuals. especially those with intc-Jlectual disability. may also show the condition. f\!lalnutrition and weight loss arc associated difficulties; it can be fatal in infants if untreated. Humination disorder appears to be rare (American Psychiatric Association. 2013). Most interventions for rumination disorder have come from the behavioral perspective. Earlier studjcs employed aversive techniques to punish rumination activities. For example., Cunn ingham and Linscheid (1976) applied brief, mild electric s hocks contingent on rumination to a 9-month•old infant suffering from malnutrition and weight loss. Rumination was suppressed quickly and effectively. with significant weight gain occurring within da)rs. (nan ABAB reversal dcsign.Sajwaj, Libet. and Agras (1974) demonstrated the effectiveness of lemon juice. squirted into the mouth contingent on rumination. in a 6 -month~old infant with the disorder: however. more recent interventions have moved away from punishment techniques in favor of alternative behavioral approaches. A review of 21 studies published between 1987 and 2010 (Lang ct al.. 2011) found the most common treatments for subjects with intellectual disabilities involved diet manipulation (su ch as pacing the presentation of food, increasing food quantity. or changing the food's texture). sensory-based interventions (such as providing a lternative t hings to chew). and use of socially me.d inted rcinforccrs (such as attention and praise contingent on rumination-free periods). Only two of the reviewed studies employed punishment (i.e., contingent mouthwash or sour drinks). Overall. behavioral interventions have produced effective and durable treatments for rumination disorder.

14.2 Overview of Sleep-Wake Disorders Humans spend about a third of t heir lives in s leep. However. the DSA1 system did not identify a separate c lassification of sleep disorders until the DSM-IV. and these mental disorders remained less familiar to many clinicians than other d iagnoses. 'l11e category was reworked in the DSM-5 as the s leep-wake disorders. with the intention of making t he classifications useful both to mental health profcs.~ionals and to general n1edicaJ practitioners. Consequently. the conditions include a wider range ofsupporting biological validators than are fou nd c-lsewhere in the rnanual. ln some instances. formal sleep studies (polysomnograpby) arc required for diagnostic determination. Optimal sleep is consid11rcd to be restful and refreshing under most circumstances. with good sleep continuity(fcw periods sp-c.nt in wakefulness). efficiency (most relative time in bed spent asleep). and short latency (the number of minutes required to fall asleep). Disturbances of sleep in theDSM-/Vwcre described in broad terms as the dyssonu1ias (conditions involving abnormal sleep amount. quality. or timing) and the parasomuias (concerned with abnormal events or beha\•iors involving the sleep cycle or sleep-wake transitions). Although that distinction What are parasomnias is no longer central to the DSM•S organization. the and dyssomnias? tem1s retain their descriptive value in discussing the sleep-wake djsorders (sec Table 14•2).

Polyson1nograpb)~ Using a polygraph to make a continuous record during sleep of multiple physiolog1caJ variables (such as breatlting. heart rate. EEG. eye movemenls. and muscle contractions)

Dyssomnia Sleep disorder that is concerned with abnormal sleep amount. quaJity. or liming

Parasorunia Sleep disorder that is concerned with abnormal events or behaviors involving the sleep cycle or sleep• wake transitions

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Table 14-2

DSM·S Sleep-Wake Disorders

Key Symptoms

Disorder

Minimum Duration Required for Diagnosis

Sex Ralio

lnsomnia disorder

Dissatisfacbon with sleep amount or quality

3 monUu

More common among females

Hypersomnolence dtsorder

Excessive sleepiness despite getting at le-dst 7 hours .sleep

3 months

Equal

Naroolepsy

Recummt irrepressible need to sleep

3 months

Slightly more common among ma1es

Obstructive sleep apnea hypopnea

NoctumaJ breathing pauses: due to obstruction

None

b.fore common among males

Central sleep apnea

NoctumaJ breathing pauses not due to obstruction

None

More co mmon in males

Sleep•relat·e d

Decrea.o;ed respiration with elevated carbon dioxide

None

Unclear

Persistent sleep d isruption due to misaHgnment of circadian rhythm and s leep-wake schedule

None

Un dear

Non-rapkl eye mo1,--ement sleep arousaJ disordea

Repea.ted part1aJ wakening wllh sleepwalking or nighl

None

Unclear

Nightmare disorder

Repeated distressmg nightmares

None

More common among females

Rapid •l"'

Repeated arousaJ with complex acti\•ityduring REM sleep

None

More common among

Frequent urges to mO\·e legs. especially at night

3 monUu

hyJ)OVentdation

leveJs Circadian rhythm

sleeJMva.ke disorders

movement (REM) sleep behavior disorder

Restless legs syndrome

terrors

maJes

More common among females

Source: American Psychiatric Assoclatkm.2bl3.

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People with sleep-wake disorders can have significant life impairment. similar in degree to chronic health cond.itions like diabetes. heart disease, or arthritis (Sateia& Nowell, 2004). Often. the symptoms presented by people with sleep disorders resemble those of other mental disorders (panic, anxiety. and depression) and may be mis identified as a result. Correct diagnosis may be difficult rcqu.iringcxtensivc info nnation about history and evaluation in a s]ecp laboratory. Nonetheless. structured interviews using DSA1-JJI-R criteria produced good to cxccllent inter•rate.r agreement across different disorders. with h ighest agreement on insomnia and hypersomnia: the only category with poor reliability was circadian rhythm sleep disorder (Schramm ct al., 1993). Sleep-wake disorders were not assessed in U1c DSM-5 field tria.ls. Many people experience periodic sleep disruption or unusual sleep experiences but raroly seek treatment for the condition. Because sleep patterns are so variable and symptoms arc so common. the prevalence of most sleep disorde,r s is uncertain. Diagnoses of t hese condi• t ions should be restricted to t hose indjviduals for whom the sleep disturbances produce significant distress or impairment in important areas of fu nctioning. Sleep problems are notable a mong the elderly. with a lmost 50% complaining about c hronic sleep difficulties (Cooke. & Ancoli-lsracl. 2006). It is likely U1at these conditions arc undcrdiagnosed among the general population.

Eating, Sleep, and Elimination Disorders

14.3 Dyssomnias 11lc dyssomnias arc disorders in which disturbances are evident in the amount or sleep, the quality of sleep, or the timing of sleep. In the DSJ\1.5. these disorders include insomnia disorder. hypersomnolencc disorder. narcolepsy. breathing-re.lated sleep disorders. c ircadian rhythm sleep-wake disorders, and restless legs syndrome.

14.3a Insomnia Disorder In insomnia disorder. individuals have difficulty faUing asleep or remaining asleep. or they arc unable to get back to sleep after early-morningwakening.11ley commonly cornplain that the sleep they achieve is nonresloralive- that is. restless and of poor quality. Daytime fatigue is often problematic as a result. To qualify for diagnosis. the sleep disturbance cannot be due to the effects of a substance: if there is a coexisting general medical condition or another mental disorder. it docs not adequately explain tl1e sleep impairment. Insomnia disorder must persist for at least 3 months. occur 3 nights per week. and cause significant distress or impairment in functioning. lt can be specified as being comorbid with nonsleep mental disorders, other medical disorders. or other sleep disorders. Specifiers are also provided to indicate ifthe condition is episodic (1- 3 mont hs of symptoms). persistent (more than 3 months ofsymptoms). or recurrent (two or more episodes within a year). Ct is the most prevalent sleep disorder. with a t hird of adults complaining about What are the most common insornnia: perhaps 10% of the population would sleep disorders? meet the diagnostic criteria for im:omnia disorder (American Psychiatric Association. 2013). People with insomnia often find themselves trapped in a vicious cycle. in which d.istrMs at not being able to sleep increases their level of arousal. which in turn makes sleeping less probable. Often. t hey acquire maladaptive sleep habits. such as napping during the day. that add further to the disturbance. ln their attempt to bring on sleep. they rnay use rnedications or a lcohol to induce dro,,.,sincss. followed later by stimulantdrugs to combat fatigue the next morning. As a result. substance dependence may develop. Other conditions associated with insomnia include rnood and anxiety disorders (American Psychiatric Association, 2000). Nearly J in 5 people who consult a physician indkatc that insomnia is problematic (Vgontzas & Kales. 1999). Onset is rare in childhood or adolescence. Insomnia increases with age. affccting25% of the elderly population. Generally. youngc.r people report prob~ lems falling asleep. whereas oldc.r people experience 1nore difficulty remaining asleep. 11le disorder occurs rnorc. often in women: for them. first onset is often reported following the birth of a child or an.er mcnopause.1hc course is variable. but more than half of people with chronic complaints of insomnia continue to experience symptoms for more than a year (American Psychiatric Association. 20J3). Sleep restriction can cause a variety of neurobchavjoral symptoms. including memory impairment. depressed mood. and lapses of conccntration.11lcse effects accumulate across several days of sleep restriction unti l they equal the approximate deficits associated with 3 days oftota.J sleep deprivation (Banks & Dinges. 2007). Insomnia disorder rnay also be related to a range of serious rnedical conditions. including hypertension. heart disease, and conditions involving mus.cu Jar or skeletal pain.

Causal Factors Problems with d isrupted sleep run in fam ilies. but the genetic contributions to insomnia disorder arc unclcar(American Psychiatric Association. 2013). Many physical and mcdkal conditions can precipitate the condition: -primary" insomnia (not related to other condi• tions or causes) makes up only about 15% of chronic insomnia cases (Sateia & Nowell. 2004}.

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Psychological distress is the most common cause of primary insomnia (Vgontzas & Kales, 1999). Development may be.g in with any specific event or strcssor that disrupts sleep.

If the disruption continues. the person becomes frustrated. anxious. and concerned about his or her inability to sleep. increasing thc.ir emotional arousal and ful'ther interfering with sleep. (ndividuals often attcnlpt lo force sleep by l'Cmaining in bed longer. but that serves to associate the bed with arousal and wakcfulncss.1he resulting conditioning of arousal is evident, as people may sleep better when not trying to s leep (for example. when watchingTV) or when they arc in different sleep environments (sucl1 as a hotel).

Treatments for Insomnia Disorder Benzodiazcpines a.re widely used to promote s leep. but they arc not recomrncndcd for long.. term use. Antidepressants may also be helpful. However. pharmacothc.rapy for insomnia degrades over t ime (Vgontzas & Kales, 1999). 1ltc naturally occurring hormone melatonin has been shown in randomized controlled triaJs to improve sleep in chronic insomniacs. with few side effects and no withdrawal symptoms after discontinuation (Lemoine. Nir. Laudon. & Zisapel. 2007). Nonpharmaco)ogical interventions include stimulus control (for e.xamplc. restricting use of bedroom to slccp-rcJated activities only). s leep restriction via a regular slcep-wakcschedulcwi.thout napping. relaxation training, and control ofstimulants such as caffeine. Elegular exercise. not close to bedtime. is also helpful. Cognitivc..bchaviora.J treatment including several oftht'-se components can be robust. effective. and durable (Sateia & Nowell. 2004).

14.3b Hypersomnolence Disorder Hypersomnolcnce disorder consists ofexcessive s leepiness despite receiving at least 7 hours of sleep during the main slee1>period. 11lose with the condjtion may sleep for more than 9 hours without finding s leep refreshing and then ha\'Cdifficulty awakening. Daytime naps arc not experienced as restorative or refreshing. Unintentional s leep may occur. especially when the person is in low•stimulation or inactive situations. Individuals struggle to remain alert. but efficiency. concentration. and memory are typically impaired, as arc social and occupational fu.nclions. Specifiers for the condition include como.rbidity w iU1 another menta.1 disorder. medical condition. or sleep disorder: duration specifiers for acute (less than 1 month). subacute (1- 3 months) and persistent (more than 3 months): and severity indicators for rnild (alc-rtness difficulties 1- 2 days per week). moderate (alertness difficulties 3- 4 days per week). and sc,•erc (aJertne.o;s difficultie.o; 5- 7 days per week) (American Psychiatric Association. 2013). Ouringonc type of rccu rrcnt h)1lersomnolencc disorder (called KJc.ine- Lcvin syndrome). individuals may spend as much as 20 hours per day in bed (American Psychiatric Association. 2000). For some people experiencing recurrent hypersomnolence. the s leepiness is associated \\lith disinltibit ion of sc.xuality, compulsive overeating, or impulsJ\rc behavior. Mood disorders and substance dependence (related to stirnulant use) may be more common among those with hypcrsomnolenc.cdisordcr, but much is unlo1own aboutcomorbidity\'lith othc.rdisorders. The prevalence for males and females is approximately equal. Hypcrsomnolcnce runs in families. but its causes arc not clear. Onset is usually bet ween age.,; 15 and 30. and the course tc.nds to be chron ic and stable. sornctimcs for decades . Its incidence is about 1% in the popu lation. but as many as 1096 ofindividuals presenting at sleep clinics complain ofhypersomnolcnce (American Psychiatric Association. 2013). Treatment usually includes stimulant drug.~.

14.3c Narcolepsy People ,vit h narcolepsy experience repeated. irrepressible sleep or the ncc-d for sleep. occur~ ring a.t least three times per week for at least 3 months.111eslecp is unintended and may occur in inappropriate situations. such as when driving a car, attending a meeting, or engaging in a conversation. In addition to sleep attacks. the diagnosis of narcolcpsy requires either

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cataplexy (sudden loss of muscle control without loss of consciousness). a deficiency of hypocretin (a h)•pothalamic ncurotransrnitter associated with arousal) measured in the cerebrospinaJ fluid. or short latency (15 minutes or less) to rapid eye movement (REl\t) sleep. Between 20%and 60% cxpericnroslccp paralysis (being awake but unable to move or speak during the s lcep•wake transition). A significant proportion of sufferers aJso experience REM s leep intrusions. which produce vivid dreamlike imagery just as one. is falling asleep (hypnagogic hallucinations) or just after awakeni ng(hyp11opompichallucinations). REM intru• sion irnagery may be visual. aud itory. or kinetic. often incorporating components fron1 the surrounding environment- for example. a person may sec movement within a picture hang• ingon the wall. REM intrusion and its sleep paralysis sometimes combine into frjghtening experiences of being unable to move while unusual events are unfolding. However. hypnagogic and hypnopompic hallucinations occur in about t5% orthe general population. and up to 50% have experienced sleep paralysis: t ints. U1esc RE.M-rclatcd symptoms are not unique to the disorder (Arn.crican Psychiatric Association. 2000). Cataplcxy is often precipitated by strong Can someone fall asleep in emotions s uch as anger. laughter. or surprise. the middle of a conversation? Cataplc.xy occurs outside of sleep attacks and can range from subtle signs that may not be obvious to others {such as drooping eyelids or a sagging jaw) to dropping items and fall ing to the ground. In children. cataplcxy may involve grimaces or jaw opening with tongue thrusting- these symptoms have been called ~cataplcctic faces." full consciousness is maintained during the episode. which typically lasts only a fmY" seconds or minutes. 111ose with narcolepsy typically experience sleepiness daily. and some may take voluntary naps in an attempt to manage sleepiness. However. involuntary episodes can present serious risk of harm to oneself or others: 1\v-o thirds of those with narcolepsy have fa llen asleep while driving (Aldrich. 1992). Social activities may be curtailed out of fear of sleep attacks or of emotional arousal that rnay precipitate an episode of cataple.-xy (in fact. joking and lauglting are the most typical triggers for cataplexy). Affected individuals may also have a history of mood or anxiety disorders. as well as obesity. Narcolcpsy is quite rare (0.04%of t he population or less) and may be slightly more common among males (American Psychiatric Association. 2013).

Causal Factors Narcolcpsy is a serious problem that persists throughout life. Pc.011lc with narcolcpsy are often overweight or obese and have elevated risk for type ll diabetes. though t heir eating patterns are not abnormal when compared to controls (Dahmen. B.c,cht. Engel. l homrnes. & Tonn. 2008). Up to one half of first-degree rc.lativcs of those with narcolepsy also show sympton1s of s leepiness. and up to 15% have the disorder. suggesting a strong genetic co1\lri• bution (American Psychiatric Association. 2000). 'l'he risk of narcolepsy among first•degrce rcJativcs of those with the disorclcrwascalculated to be 75 times higher t han t he risk in the general population (Ohayon & Okun. 2006). However. MZ twins have high nonconcordancc rates (Vgontz.as & KaJes. 1999). jndic.ating unknown environmental contributions to the disorde-r. Because of an association with a specific pattern of human leukocyte antigen (HLA) response. some have proposed that narcolepsymay arise as part of an autoimmune condition (Ern1an. 2006). although many in the popula t ion s hare similar HLA patterns without narco .. lcpsy. Manipulation of genl?s controlling production ofhypocretin can produce narc.oll?ptic states in dogs and mice. and there is a deficiency of hypocretin in the spinal fluid of some narcolcptics (Nishi no. Ripley. Overccm. Lammers. & Mignot. 2000). lncrcasingly, it appears that narcolepsy may be due to an autoimmunc ..rclated loss of neurons in the hypothalainus that produce hypocrctin (Dauvilliers. Arnulf. & Mignot. 2007). As noted above. a hypocretin deficiency now satisfies one of the criteria for narcolepsy in the DSA1•5.

Cntaplcxy Sudden Joss of mu sell? control without loss of consciousness

Rapid eye move.men! (REM) sleep Sleep phase that im•olvcs rapid eye movements. often associated with vivid dreaming

Sleep paralysis Being awake but unable to move just at the junction ofsleep and

\,:akc.fulness

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Chapter 14 Aooormal Psychology

Treatment of Narco/epsy 111crapcutic naps for 10- 60 minutes daily may be of benefit in managing the cond.ition. Stimulant drugs arc typically used to stave off sleep attacks; mcthylphcnidatc is the preferred drug for preventing s leep onset (Vgontzas & Kales. 1999). Antidepressant medications may help reduce cataplcxy in patients with narcolepsy.

14.3d Breathing-Related Sleep Disorders 1-he central feature of a brcathing.. rclated sleep disorder is sleep disruption (leading to e.xccssive sleepiness or insomnia) caused by a breathing difficulty. Most often. the breath· ing difficulty is sleep apnca. in which breathing ceases during sleep. E.,;;scntially. the sleeping individual stops breatlting, begins to su ffocatc.. and then rouses from sleep briefly to gasp for breath. In addition to apnca. hypopn ea (a reduction in airflow, related to unusually slow or shallow breathing) and b ypove.utilation (abnormal blood levels of oxygen and carbon dioxide) also constitute the respiratory events that may disturb sleep in these conditions. ~rhese ventilation cycles may occur more than 15 times per hour. so that the. indhridual pa1'tia1ly awakens from sleep hundreds of t imes throughout the night. As a re.suit. sleep is not expc• rienccd as rcstfu l or restorative. and symptoms similar to those of insomnia are evident (poor concentration. irritability. mood distur• hanccs, and memory disturbances). -'tlte most common form of breathing-related sleep disorder is obstructive sleep apnea hypopnea. involving repeated obstructions of Tua nasal continuous posill\'e airway pr essure (nCPAP) is used to treat. seve re sleep apnea by the upper airway. accompanied by loud snoring.111c DSM•S diagnosis d elivering n continuous Oow of air to the nostrils requires at least five apneas or hypopneas per hour of sleep, verified through a nose mask. (iStac:k} by polysomnography, that result in nocturnal breathing disturbance or daytime fatigue. or evidence of 15 or more apneas or hypopneas per hour of sleep, regard less of resu lting symptoms. Jt c.an be specified according to severity. based on the degree of reduced blood oxygen saturation. Obstructive sleep apnca is more common in overweight indivjduals. for whom soft tissues in the neck can block the airway: Sleep apne.a those with lal'ge necks (over 16- 17 inches) are at greater r isk. In less obese persons, obstrucFrequent ccs.satton of t ions can be related to tonsil size. abnormal growths. or nasal airway obstruction. breathing during sleep People with breath ing•rclatcd sleep disorders (as well as those with hypersomnolcnce. Hy1,op11ea disorder) often experience a dull headache on awakening, sometimes accompanied by sleep Reduction in airflow. drunkenness (difficu lty wakening. confusion. and inappropriate bcha\'ior: also called sleep related to unusually inertia). 1hey often are excessively sleepy during the day and may i1woluntal'ily fall asleep slow or shallow at inappropriate times in extreme cases. simi lar to those with narcolepsy. Naps arc usually breathing not refreshing. Mood and anxiety disorders arc often associated with breathing-related sleep d isordcrs. Hypoventllallon Obstructive sleep apnea hypopnea is more common among midd le•agcd. overweight Decreased level of males and in children with enlarged tonsils (who. unlikeadults.maynotsnorc). Jt occurs in up oxygen and increased level of carbon dioxide to 15%oftheadult population. with h igher rates (more than 20Citi) among the clderly(Amcrican in the blood Psychiatric Association, 2013). Interestingly, sleep-disordered breathing is significantly less common in childl'en who were breastfed for at least 2 months (Montgomery-Downs. Crabtree. Sleep drunke.n1rn·ss Sans Capdcvila. & Gozal 2007). Obstructive sleep apnea hypopnca tends to have a gradual Difficulty awakening onset and a chronic course. and it can contribute to premature death by heart arrhythmia or from sleep. often cardiovascular disease. \iVeight loss and continuous positive ain\1ay pressure or other tech• including confusion niques to keep the airway open are the most effective treatments (Vgontzas & Kales. 1999). and inappropriate A much rarer breathing-related sleep disorder is central sleep apnea. in which there are behavior: also known as sleep inertia five or more apneas per hour ofsleep not related to obstruction. Snoring is much less common

Eating, Sleep, and Elimination Disorders

in this condition.111e periodic breathing pattern that occurs in central sleep apnca can he s ubtypcd as idiopathic. comorbid with opioid use (which impact.c; respiratory rhythm). or related to Cheyne- Stokes respiration. an increasing/decreasing air--intakc pattern that is tied to the development of heart failure.. It appears most often in users oflong,.acting opioids, such as methadone. and in association with renal failure or stroke {American Psychiatric Association. 2013). Slccp,rclated hypoventilation need not involve apncas but rather shallow or dec.r eascd breathing that leads to elevated levels or carbon dioxide (CO,) levels in the blood. Sufferers complain of frequent wakening. sleepiness. insomnia. and headaches. 111e condition is thought to be uncommon but may be increasing related to rising obesity and chronic obstructive pulmonary disease (COJ>O) rates (American Psychiatric Association. 2013).

14.3e Circadian Rhythm Sleep-Wake Disorders Circadian rhythm sleep•wake disorders involve a persistent sleep disturbance due to a mismatch between the person's internal 24-hour sleep-wake cycle (the circadian sleep• wake pattern) and the schedule required by the person's environment. As a result of the mismatch in cycles. affected people us11ally experience insomnia at some times of the day and sleepiness at other time$. with significant distress or impairment of functioning evident (for example. falling asleep at inappropriate times). In some types of circadian rhythm sleep-wake disorders. an individual may foci ~locked in" to a cycle of unusually late sleep and awakening. unable to adjust the cycle to an earlier one such as that re quired for a job (de.laycd sleep phase typc). ln other cases. people may experience earlier sleep onset and awakening, with the inability to adjust to the conventional later sleep and wake times (advanced sleep phase type). 'the condition may be generated by certain work schedules. especially night shifts (shift work type). or it may appear as a lack of di,;-ccrniblc slecp•wake rhythm. with sleep rragmented into at least three different periods during the day (irregular sleep-wake type}. ln another pattern (non-24..hour slcep..wake type). the sleep phase gradually increases and drifts out of24•hour alignment. so that sleep time moves into daytime hours. This subtype is particularly common in blind or visually handicapped persons. for whom the incidence approaches 50% (American Psychiatric Association. 2013). Persons diagnosed with the delayed sleep phase type of the disorder typically have great difficulty shifting t he slecp,wake cycle forward. but once sleep is initiated. it is normal. 1hey feel continually sleep-depri\lcd due to the need to maintain social or occupational obliga• lions, except on weekends or during vacations, when they tend to shift back to a later cycle. Shifi work type may be most common among those on n ig lll•shift or rotating-shift schedules:: shorter sJcc.p duration and more frequent awakenings arc often accompanied by difficulties pertain ing to family demands and environmental disturbances during sleep times {such as traffic noises and tclephoncs). ln addition to sleep disruption, other symptoms associated witb circadian rhythm slecp,wake disorders include headache. fatigue. impai red coord ination. decreased appetite. and indigestion. All forms of the d isorder produce difficulties in concen• tration and memory. attention, and performance: depressive symptoms arc not uncommon. lite severity of the sleep disruption appears to increase with age. Some forms (e.g., shift work type) show reversal of symptoms with schedule changes, while the delayed sleep phase type may last for decades. The prevalence of circadian rhythm sleep-wake disorders is unknown. More U1an 7% of adolescents may experience delayed sleep phase type. and more than 10% ofn ight•shift workers may experience shift work type. Some t)'pes appear to aggregate within families (American Psychiatric Association. 2013). Melatonin. which is secreted by the pineal g land a nd helps re.g ulatc sleep-wake eye.le. rhythm. appears to be beneficial in treatment ofcircadian rhythm sleep-wake disorders (l>andi•Pcrumal. Srinivasan. Spence. & Cardinali. 2007).

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Chapter 14 Aooormal Psychology

14.3f Restless Legs Syndrome Restless legs syndrome was also elevated to a dyssomnia from provisional status in the DSM-IV. It involves frequent urges to move the legs. especially when resting. in order to relieve unpleasant sensations such as itclting. burning. or tingling. 'lbc u_rgcs arc worse in the evening or night and are partly or totally relieved by movement. 1he urges may interfere

with sleep onset or sleep continuity, producing daytime fatigue or sleepiness. Symptoms must occur three times per week for 3 months to qualify for the diagnosis. Between 2.0% and 7.2% of the popula.tion may be affected (American Psychiatric Association. 2013). Other l.imb movement conditions may occur rhythmically during non-REM sleep. inducing briefarousals that degrade t he quality of sleep. Sleep-related limb movement disorders. including restless legs syndrome. increase with age (Cooke& Ancoli-lsrcal. 2006}. The incidence increases up to about age 60. wjth the disorder more prevalent in fcrnales, especially during pregnancy (Arnerican Psychiatric Association, 2013).

14.3g Substance/Medication-Induced Sleep Disorder Finally, the DS1l1-S provides the category ·substance/ medication-induced sleep disorder" to describe the many sleep dyssomnias t ha t can be caused by substance use. intoxication. or withdrawal. A large array of substances. inc1uding caffeine. alcohol. tobacco. sedat ives. and opioids. arc associated with sleep dysfunctions: those with parasomnias and older individuals who take multiple medications may be at greater risk. \Vomcn seem more susceptible to substa.ncc/ medication•induccd sleep problems than men. given the same amount and dura• tion of consumption (American t>sychiatricAssociation. 2013).

14.4 Parasomnias 111c parasornnias are sleep disorders that involve abnormal activities or psychological/ physiological events that occur dur ing sleep or during the transi tion from sleep to wakefuJ. ne-ss. ln t he DSM#S. those disorders include non -rapid eye movement sleep arousal disorders. nightmare disorder. and rapid eye movement sleep behavior disorder.

14.4a Non-Rapid Eye Movement Sleep Arousal Disorders 111e non-REM sleep arousal disorders involve incomplete awakening from sleep. accom• panied by sleepwalking or sleep terrors (sec Table 14--3). 111e DS:.'1-5 diagnostic category is a combination of two separate DSM.JV disorders- sleepwalking disorder and sleep terror disorder. Usually. U1c incomplete awakening occurs in t he first third of the sleep episode and tends to be brief (fewer than 10 minutes). although longer (up to 1 hour) events may occur. Typically. in thcslccpwalkingtypc. thccye.'iare opcn.1hc event may begin simply and become progressively more complex, including getting out of bed and leaving the room. Sleep terrors in\•olve a strong sense of dread and a compulsion to escape . but the person usually docs not wake completely and returns to sleep. In both types of episodes. persons do not remember the event t he next morning. Sleepwalking involves repeated episodes of complex motor activities that begin during slow~wave non•REM sleep. Depending on the severity. the motor activities can range from s'itting up in bed to carrying on conversations. Sleepwalking mny begin s imply and become progre..o;sh.-ely more eating food, leaving a building. or even operating ntachin• complex. indudingg.ett.ing out of bed and leaving the room. {iStod::) cry. Episodes us ually terminate with return to fuU sleep

Eating, Sleep, and Elimination Disorders

Table 14-3

Summary of DSM-5 Diagnostic Criteria for Non-Rapid Eye Movement Sleep Arousal Disorders

Ongoing experiences of not fuUy awakening while sleeping (often in the first third of a major period ofsJeep). aJong with either: -SleepwaJkmg [duringsJeep. frequent experience of nsmg from bed and walking. displaying a blank. staring face. mostly unable lo respond t() other's efforts t() communicate. and requiring great difficulty to he wakened] -Sleq> terrors (frequent abrupt terror arousals from sleep: episodes often start with a scream of panic, accompanied by intense fear and signs of autonomic arousal (e.g.. rapid breathing. sweating. mydriasis. tachycardia): mostly unable to respond to other's efforts to provide comfort during an episode] Person cannot recall the episodes (amnesia). Little ,f any dream imagery 1s recalled. CHnica.1.ly significant distress or impalnnenl in lmportanl areas of functioning (e.g.. social. oc:cupational) are caused by Lhe symptoms. Symptoms cannot be attributed to the physiological e ffect of a substance or methc:ation. Episodes c annot be explained better by coexisting mental and medJcal disorders..

Specify if: -With sleep-related eating: -With sleep-related sexual beha\'lor (sexsomnla) Source: Amer.Can Psychlatrk As!!oclatfon. 2013.

(sometimes in new or unfamiliar locations). (fawakcned (which is difficuJt).theslccpwalker is typically confused for several minutes and docs not report dreaming or awareness of the event. During a s leepwalking episode, the individual commonly has a blank face and is rcla • tivcly unresponsive to attempts to communicate or be awakened by others. 'fhe person may talk or even ansi.-vcr questions, but a genuine dialogue is usually not established. Although their eyes are typically open. sleepwalkers may be clumsy (Plante & Winkelman. 2006). Some inju re themselves by walking into walls or falling Do people sleepwalk because through windows. Occasionally, s leepwalkers may they are dreaming? strike out at others, particularly if sleep terrors are also present. 111cre have been reports of complex sexual or violent behaviors, including homicide and rape, occurring during episodes ofsleepwalking (Cartwright. 2004; Rosenfeld & Elhajjar. J998). Actually, a fuU range of directed sexual activities with oneself or partners (sexomuia) has been reported in s leeping individuals: such activitic~o;; indude masturbation. fondling, sexual verbalizations, and intercourse, with complete amnesia for the episodes reported after awakening the next morning. These types of complex acts are not limited to sleepwalking: they have also occurred within other parasomnias such as REM sleep behavior d isordc.r (discussed below) and confused arousals associated w ith sleep apnea (Schenck. Arnulf. & Mahowald. 2007). Although traditionally considered extremely rare. sleep•rclatcd violence may b-c greatly w1derreportcd. with as much as 2% of the population enacting some form of violence during s leep (Lettieri & Williams. 201 1). However. the majority of such cases occur in young to middle -aged men with a h istory of s leepwalking (Plante & 'Winkelm an. 2006). Slecp~relatcd eating may also occur du ring slecpwaJki ng episodes. especially ruuong femaJcs. with varying degrees of amnesia. Inappropriate. foods may be consumed at t hese times as wcl l (American Psychiatric Association. 2013). In sleep terrors. indjviduals awake from s leep abruptly, usually with a cry or pa.nick")' scream. 'Ibey show intense fear and autonom.ic arousal. such as rapid heartbeat. rapid breathing. pupil dilation (m ydriasis). and sweating: they are generally unresponsive to efforts by others to awaken the.m. 'tbcy may actively resist attempts to comfort or hold them by swingjng. punching. or rising from the bed and fleeing: t hese acts can result i n physicaJ injury lo themselves or others. In most episodes. individuals do not fulJy awaken and return to sleep.

Sexomnla Sexual nclivilics during sleep without conscious awareness

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Chapter 14 Aooormal Psychology

However. if fully wakened. they do not recall dreaming. apart from fragmented images and a sense of terror. The next morning. there is amnesia for the episode. which usually docs not occur more than once in a night. Episodes recur after several days or weeks and arc made more likely by fatigue. stress. and alcohol or sedative use.

Usually. noo~R£M sleep arousal disorders begin before age l2 and resolve du ring adolescence and thereafter. declining from an incidence of perhaps 5% among children to less than l% in adults (American Psychiatric Association. 2013}. Much is unknown about the causes or treatments for the condition. ln one study involving three boys with histories of recurrent sleep terrors. scheduled awakenings 30 minutes before expected occurrence of sleep terrors ,,•ere effective in reducing their frequency (Durand & :.l indcll. 1999). Especially in adults. sleep terror is related to higher incidence ofgeneral psychopathology. including PTSD. mood and anx.iety disorders, and some personalitydisorde.rs. A family history of sleepwalking or sleep terrors is present in up to 8096 of cases (American Psychiatric Association, 2013).

14.4b Nightmare Disorder 111ose with njghtmarc disorder repeatedly experience frightening dreams that resu lt in awakening. lndjviduals rapidly become alert and oriented after waking and can recall the nightmares in detajl. Most often, the nightmares involve threats to the person·s safety. security. or self-esteem: these intense dreams (or the sleep disruptions they produce) cause significant distress or impairment for tJ1c ind.ividual. 1he dreams in nightmare diso.r der usually last longer than lO minutes and happen during R.£r-.,1sleep, which increases in the second halfof the Do some people act out night. 'lhe nightmares often are lengthy. elaborate. their dreams? and terrifying and may recur several times jn a night. Themes about attack. injury. pursuit. and personaJ failure or embarrassment are typical. Upon awakening, the person 1uay be anxious and fearful and can recall the sequence and imagery of the dream in detail. TI1e most common impact of recurrent nightmare.,; is subjective distress: some individuals may avoid sleeping. and daytime functioning may then be impaired as a result of sleepiness. Nightmare disorder most often occurs in children who have been exposed to severe psychosociaJ stressors. ·me dreams usua.11)' begin between 3- 6 years of age and increase in prevalence and severity into early adulthood Females experience nightmare disorder up to 2 times as often as males (American Psychiatric Association. 2013). Depression, substance use disorders, and personality disorders may be associated with the condition. Prs·o is accompanied by nightmares nearly 5 times more often than any other disorder. and some consider ·PTSo a prcd.isposing factor for nightmare disorder (Plante & \tVinkclman, 2006). The incidence of n ightmare disorder is unknown. although 50% ofadults experience occasiona1 nightmares, and up to half of children ages 3-5 experience nightmares severe enough to disturb parents (American Psychiatric Association. 2000).

14.4c Rapid Eye Movement Sleep Behavior Disorder

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A provisionaJ condjtion in the DS!lf-lV. rapid eye movement sleep behavior disorder was e levated to a parasomnia in the DSM-5. ltconsists of complex motor activity or vocalizatfons that occur during REM sleep and are associated wiU1 vivid dreaming. Normally. skeletal muscles arc paralyzed during REM sleep: in those with REM sleep behavior disorder. that paralysis is absent, alJowing people to essentially act out their dreams. Violent activities such as punching and kicking sometimes occur du ring episodes: emotion~ladcn. loud shouting may be present during the episode. 111e condition may precede or accompany the development of some neurodcgcnerativc conditions. including Parkinson's disease, and it may be more likely in children with autism. Its prevalence is about 0.5% of the population (American Psychiatric Association. 2013), though it is more common in the elderly- especially men

Eating, Sleep, and Elimination Disorders

(Cooke & Ancoli~lsrael. 2006). ·n1.e disorder appears to have. good inter-rater reliability (about .65) when assessed among patient.~ with Parkinson's disease (Scaglione et al.. 2004). lt can also be induced by a variety of medications. including antidepressants. However. its causes remain uncertain. lt is most commonJy treated with benzodiazepine medications (Thomas. Bonanni. & Onofrj. 2007)

14.5 Elimination Disorders Only two elimination disorders arc listed within the DSM-5. Both must be distinguished from developmentally appropriate deficiencies in toileting abilities in the youngest children. 1lms. the.~e a.re not diagnosed until after the normal period for attaining continence.

14.Sa Encopresis Encopresis involves repeated passage of feces by a person age 4 or older into inappropriate places, such as into clothing or onto the floor. Events- which are usually. but not always, involuntary- must occur at least once a month for at least 3 months and are not due to general medical conditions (other than constipation and its mechanisms) or to use of laxatives. Usually the pattern in cncopresis consists ofconstipation (which can develop in response to anxiety or othc.r psychological states). followed by impaction. further retention. and overflow incontinence. lhccondition is often associated with embarrassment. social ostracism. and avoidance of social situations. Encopresis may affect 1% of 5-year-olds. and it is more common among males. If events arc voluntary or intentional. t he disorder may be associated with conduct disorder or oppositional defiant disorder {Amc.rican Psychiatric Association. 2000). 1here are no known pharmacological interventions for encopresis at present (At>A \Vorking Group on Psychotropic Medications for Children and Adolescents. 2006). Treatment m.ay involve high-fiber diets. use of laxatives. relaxation training. and bchavioraJ interventions that shape and support regular patterns oftoileting. Combinations of behavior techniques with d iet and education appear to be helpful (Mikkelsen. 2001).

14.Sb Enuresis Enuresis is repeated void.ing of urine into bed or clothes. during day or night. in children age 5 years or older (by which age bladder control would ord inarily have been acquired). 1he condition is not due to a general medical condition and must occur at least twice a week for 3 months.111.c diagnosis can be sub typed as nocturna.J. diurnal, or both. Although few consider enuresis in itself to represent a serious disorder. for the young child. it c.an be a source of intense psychological discomfort. resulting from the jeers and taunts of unsympathetic peers and the obvious irritation of parents and others who have to cope with frequent changes of bedding. Children may avoid certain activities. such as sleeping at a friend's house., because of the potential embarrassment.

Causal Factors Most children with enuresis become continent by adolescence. 1he prevalence of the disorder may ho Jo% among 5-year-olds. but it falls to hair or that by age IO; about I% of cases continue into adu lthood.111.e condition has strong familial patterns: Offspring ofan enurctic parent have 5- 7 times the risk of the general ('>Opulation for developing enuresis. and 75% of children with the disorder have a fi rst~de.grcc relative who was affected (American Psychiatric Association. 2000). Several contributing factors have been proposed for enuresis. including bladder d)•sfunction. insufficient bladder capacities. disturbance of biological rhythms. poor toilet training. and psychological stress. Psychodynamic theorists

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Chapter 14 Aooormal Psychology

considered the meaning of the symptom in terms What treatments are effective of intrapsychic conflicts that have their origins in for elimination disorders? disturbed family relationships. Wetting the bed may be seen. for example., as an unconscious expression of hostility toward a parent, a stubborn refusal to accommodate the parent's demand for more age..appropriatc behavior. or a wish to remain infantile.

Treatrnent of Enuresis Ora l medications such as antidepressants and desmoprcssin (a synthetic urine suppressor) are more effective than placebo in reducing enuresis. but relapse is likely when medication is discontinued (Mikkelsen. 2001). Behavioral approaches have involved attempts to condition children to respond to the sensation of a full bladder: the effectiveness ofsuch approaches is well validated (Chambless ctal. l998).111ebcll and pad metl1od. the best known technique, was developed more than 75 years ago and is based on a Pavlo,rian conditioning model. Urination is an automatic reflex response to a distended bladder. As they grow older. most children learn to inhibit this reflexive response. even while sleeping, and learn to make the response at the right tirne and place. for the child with nocturnal enuresis. this control is established by conditioning the response of awakening to the stimulus of a full bladder. 1bc procedure itself is quite simple. The child sleeps on a pad t hat. when moistened by urine, cornplctcs an electric circuit. triggering a bell to sound (the unconditioned stimulus). which causes the child to awaken (thee unconditioned response). After a few such pairings. the conditioned response (waking up) is triggered by stimuli that predict the bell- that is, by bladder distension (the conditioned stimulus). According to Mikkelsen (20Cll), the bell and pad device is t he only treatment that is associated with generalized improvement aftc.r the treatment is withdrawn: although it is the mostcost~effcctivc intervention. it remains underused. It is effective in 75% of cases: compared to medication. it has low risk and high benefit (APA Working Group on Psychotropic Mcdicatfons for Children and Adolescents, 2006}.

4 17

Chapter Review TO SUM UP ... •

Anorexia nervosa is a form of self-starvation rela ted to strict control of eating. fear of gaining weight. and disturbed body image. It is associated with belownormal body weight and serious physical and medical effects, including death.

Bulim ia ncrvosa is a loss of control over food intake that occurs in binges. 1·hc person e ither purges the food or engages in excessive exercise or fasting to compensate for binge eating.

Both anorexia nervosa and bulimia ncrvosa involve sclf•cvaluation that is too strongly connected to body shape and weight. 111cy arc much more common among young white fem a.Jes. \Vhcn they occur among males. the eating disorders arc likely to be associated with homoscxuaLity or \\Tith sports that emphasize aesthetic performance or weight limits.

Bingc...cating disorder involves repeated food binges without compensatory activities. (tis much rnore common than the other eating disorders and may affect males and females equally.

Effective treatments for eating djsordcrs include cognitivc•bchavioral interventions and (to a lesser extent) antidcprcs.~ant mc-dications.

111cre arc two general classes ofslccp •wake disorders: dyssomnias (with abnormaJities in amount. quality. or timing of sleep) and parasomnias {,-.'1th abnormaJ behavioral or physiological events occurring during sleep or in the transition between s leep and wakefulness).

Insomnia disorder is the most common dyssomnia.. indicated by d.ifficulty falling asleep or staying asleep. Its like lihood increa..,;cs with age. Other dyssomnias include conditions of excessive or unexpected s leep. breathing• related s leep disorders. and circadian rhythm s leep disorder.

Effective treatments incJude cognitive-behavioral thcrapie~o;; and melatonin for insomnia. stimulant drugs for hypcrsomnolence disorder and narcolcpsy. and positive ain'la)' pressure for breathing•related slccp~wake disorder.

Among the parasomnias. nightmare disorder aud R..EM sleep behavior disorder occur during REM sleep. whereas s leep terrors and s leepwa lking occur during

non-REM sleep. •

Enuresis and encoprcsis arc-disorders involving inappropriate elimination. Enuresis is often effectively treated with the bell and pad method.

418

KEY TERMS Amenorrhea 398

Polysonmography 405

Binge eating 400

Purging 398

Cataplcxy 409

Rapid eye movement (REM) sleep 409

Dyssomnia 405 Hypopnea 410

Scxomnia

413

Hypoventilation 410

Sleep apnea

Night eating syndrome 403

Sleep drunkenness 410

1>arasomnia

Sleep paralysis 409

405

410

QUESTIONS FOR STUDY •

Speculate on reasons a norexia ncrvosa has a much shorter average duration than other t'ating disorders.

Describe binge eating. and describe t he disorders in which it occurs.

Discuss the role of REM sleep in various para~omnias.

Distinguish nightmares front sleep terrors.

Describe how the bell and pad rncthod works.

POP QUIZ l.

Which of the following docs pica involve? A. regurgitating and rcchcwing food B. eatingofnon•nutritivc substances C. eating unusually large amounts of food

0. purging 2.

Lifetime prcva.Jcncc rates of anorcx:ia ncrvosa currently arc about _ _ _ __ of females. A. 15% B. 10% C. 5%

D. 1%

419

3.

\Vhid1 of the following arc at h ighcst risk for anorexia nc.rvosa? A. Caucasian women age 15- 24 8. African American women age 13 - 18 C. Hispanic women age 17- 24 0. Caucasian women age 11- 16

4.

\Vhich of the following statements is true about eating disorders? A. Bulimics maintain bclow•avcragc body weight. B. Anorexics do not engage in bingeing/purging eating patterns. C. Bulimia ncrvosa is not related to socioeconomic status. 0. Mortality rates are similar for bulimia.and anorexia.

5.

_ _ _ _ _ arc sleep disorders concerned with abnonnal sleep amount., quality, or timing. whereas _ _ _ _ _ arc sleep disorders concerned with abnormal events or behaviors involving the sleep cycle or sleep..wakc transitions. A. Hyposomnias / parasomnias 8. Endosomnias / dyssomnias C. Dyssomnias / parasomnias D. J>arasomnias / dyssom nias

6.

\\/hid, could not happen duringcataplexy? A. sleepwalking 8. falling C. being aware of surround.in~ D. feeling e1notional distress

7.

Nightmare disorder generally has a(n) _ _ _ _ _ onset. A. childhood

8. adolescent C. young adulthood D. midlife 8.

Jack's repeated. irresistible attacks of unintended sleep started to affect his work and famiJy life.Jack went to his doctor. who ordered a sleep study that diagnosed Jack with _ _ _ __ A. central sleep apnea 8. narcolcpsy C. hypcrs.omnolcnce.disorder D. circadian rhythm slecp•wake disorder

9.

Many people experience the sensation of falling out of bed or falling down the stairs as they arc starting to fall asleep. This is known as ______ A. hypnopompic hallucinations

8. cataplcxy C. sleep drunkenness D. hypnagogic hallucinations

420

JO. _ _ _ _ _ is unusually slow or shallow breathing and may disturb sleep in

breathing-re.l ated sleep disorder.

A. Sleep drunkenness B. Oyssomnia C. Sleep apuea D. Hypopnea

I I. Melatonin. secreted by the pineal gland. helps regu late the sleep-wake cycle and appears beneficial in the treatment of _ _ _ _ __

A. hypcrsomnolcncc d isorder B. central sleep apnca

C. nightmare disorder 0. circadian rhythm sleep-wake disorder 12. Sleepwalking involves repeated episodes of complex motor activit ies that begin during _ _ _ __ A. the first stages of sleep B. tJ,e later stages or sleep C. slow-wave REM sleep

0. slow-wave non•.R..EM sleep

t:t \Vhich of the following normally occurs during REi,t sl~p? A. Skeletal muscles arc paralyzed. B. Cataplcxy occurs.

C. 'TI1c eyes arc nearly motion.le-ss. 0. Sleep apnca occurs. 14. _Enuresis cannot be diagnosed until age _ _ _ _ __ A. I year

8. 3 years C. 5 years 0. 7 years 15. 1hc bell and pad device is used to treat _ _ _ _ __ A. pica

B. enu resis

C. rumination disorder

D. cncopresis

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CHAPTER OVERVIEW 15.1 Compromised Brain Function ..... .423 15.2 Delirium ..... ... ................. .. ..... . .425 Substance Intoxication Oelinum Substance Withdlawal Delirium Medouon•lnduced Oelirlum Delirium Due to Another Medical CondJtion Oeftrium Oue to Multiple Euologies

15.3 Major and Mild Neurocognitive Oisorders ... ... .. .429 Neurocogmtive Oisorder Oue to Alzheimer's Disease Vascular Neurocognitive Disorder Frontotemporal Neurocognitive Olsorde, Neurocognitive Oisorde, Ouc to HIV lnfocuon Neurocognitive 0 1sorder Due to TraumatK Brain Injury Substance-/Medicabon• Induced Neuroc:og.nltive Oisorder Other Causal Diseases forNeurocognitive Disorder Neurocognitive Disorder Due t.o Another Medical Condition

r

CHAPTER OPENER QUESTIONS What is delirium' Can younger people show the symptoms of delirium? What causes neurocogniti~ disorders? Is dementia permanent? Can it be prevented? What treatments are effective for t he

neurocognitive di.sorders? How are the memory impafrments of dementia

and amnesia different'

Neurocognitive Disorders T

he physiological basis of many of the disorders discussed up to this point remains unclear and sometimes controvcrsiaJ. As we have seen. some of the sleep-wake disorders generally include within their definition specific measurements from sleep studies or bjochemicaJ assessments. For most other DSM conditions. however. the undcrJ~-.-ing physiological causes have not been unequivocally identified. and diagnosis cannot be confirmed by physiological assessments. for the mental disorders considered in this chapter. the situation is decidedly different. Delirium, dementia. and the amncstic disorders were categorized as ..organic mental disorders" in the DSA1-JJI. rencc.ting their evident connoction to brain pathology. That nomenclature was climinatcd in the DSA/./V due to the growing recognition that all mental disorders have organic or physiological components. The disorders included under the DSM-5 classification ofneurocognitivc disorders arc unique in the extent to which tJ1eir biologicaJ etiology can be demonstrated.

Ncuroc~crnitivc disorders a.re conditions in which impairment was not present during the developmental period. and so tJ1ey represent declines in cognitive abilities. In the DSM•IV. it was important to distinguish these conditions- alJ of which involve some degree of memory dysfunction- from the effects of normal aging. As poople become older. cognitive abilities such as memory and complex pro blem solving generally become less efficient. Some people can become easily confused or lost or forget about where important items arc kept. 1'he DSA(./Vprovidcd a nondisordc.r listing- '"agc•rclatcd cognitive decline"- to describe the occasional need for clinic.aJ attention by people whose difficu lties were within nonnal limits for persons ofsimilar years. 'rhe/JSJW•S. instead. includes these symptoms under the new diagnosis of mild ncurocognitive disorder- a decision that has raised some concern about overdiagnosis, However. as we will sec. the dysfunctions considered here arc quite common among the aging population.

15.1 Compromised Brain Function Many pathological conditions of the brain arc more common in older persons. 'J'hc prevalence of dementia. for example. is highest in those over age 85 (Americ.an Psychiatric Association. 2000). However. compromise of brain function (and t he psychological effects it entails) can occur at any age. resulting from factors such as disease. injury. tumor. inflammation of the brain (encephalitis). or a drug or toxin. Some of tJ1cse conditions arc progressive, with continuing decline in cognitive function for the remainder of life. Others are transient and may resolve rapidly and completely. If the underlying organic cause is resolved. the c.ognitive decline may cease or reverse its course.. As an illustration of the range ofthe psychological consequences ofbrain infection. consider the example of the syndrome knowu a.,; general paresis. As noted in Chapter 2. the discovery that genera.J paresis is caused by a syphilitic infection was a landmark in the development of the organic view ofpsrchopathology. Only a small proportion of individuals (less than 5%) who contract syphilis and fail to get treatment ultimately develop the symptoms ofgeneral paresis. Once the initial physica1 signs of infection (chancre. skin rash) subside. a lengthy latc.ncyperiod sets in. during which the infecting spirochetes may invade the heart. spinal cord. brain. or other organs. Ancr this .latency period. which can last 10- 30 years. overt symptoms of neurosyphilis may begin to appear: failure of the pupil of the eye to contract to light. failure of 0U1cr reflexes such as the lmcc•jcrk rcOc.x. sluned speech. and shaky handwriting. Behavioral changes also occur. often quite slowly. Individuals are likely to become more irritable and have periods of depression or confusion. As t he disease progresses. they may become neglectful of dress and forgctfuJ of social amenities: they may also lose ordinary inhibitions jn t he expression of

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Figure

15 ·1

Cortical Areas of the Brain

CorticaJ areas of the left hemisphere ofthe brain. with shaded areas showing more specialized sections: Broca's area and \Vernickc's area arc involved in the product ion and understanding of language: the angular gyrus mediates between visual and audnory infonnation. Source: Adapted from "Spedalb.atlons oftbe Human Bra.I n.~ by N. Ge~hwlnd. 19i 9.S.C/e ,.,ijicAmerlt:a11. 2JIJ. pp. 180-199.

Frontal lobe

Motor cortex

Somatosen.sory area

Parietal lobe

Angular gyrus

Temporal lobe

Broca's aphasia Language disturbance

involving slow. cffortful articulation that conveys little expressive information

\\'ernickc"s aphasia Language disturbance

in,•olving profound deficit in speech comprehension and iluent expressive speech conveying little information

Neglccl syndrome A spatial disorder involving inattention Lo the left visual field due to damage to th c right pa rie ta! Jobe of the brain: also caUed hemineglect or

1.mila1eral inatle.ntion

WernidceS

P.rimary visual area

area

aggressive or sexual impulses. In some cases. grandiose delusions of great power or wealth develop: in other cases. there is simply a progressive dementia or paralysis. Eventually. widespread brain destruction occurs, accompanied by progressive dementia and paralysis. lhe nature of the psychological impainnent produced by brain dysfunction is related to the area of the brain affected. Although the degree oflocali.zation ofparticu.larcognitivc and cmotionaJ activities has often been overstated (Kagan. 2007). some broad psychological functions are integrated in specific parts of the brain. For example. general auditory. visual. and spatial orientation is greatly impacted by damage to particular ar·c.as of the cortex (Figure 15· 1). Sensorimotor integration related to the sense of touch is richly innervated along the somatosensory cortc.x. and sensation and motor control for different areas of the body and head arc mapped onto confined cortical re,g ions. Specific language difficulties can be produced by damage to Broca,s area (Broca•s aph asia involves effortful. slow articulation with little infonnation included) or \Vernickc·s area (\ Vcrnicke's aph asia involves Ouent speech thal conveys lit t ic meaning. as well as a profound deficit in speech comprehension). A type of spatial dysfunction is caused by damage to the right parietal lobe of the brain. which controls the left visual field because. the optic nerves cross ovcr.1he impairment. called n eglect syndrome. is one in which the left visual field seems to be ignored (sec Figure 15-2). An interesting distinction is apparent between those who experience neglect syndrome (also called hemineglect or unilateral inattention) because of damage to the left hemisphere. as opposed to damage to the right hemisphere. Damage to the right parietal lobe. producing the spatial neglect illustrated in Figure 15~2. is frequently accompan ied by relative unconcern on the part of the patient. who may consider the condition amusing and seem unaware of its seriousness. Patients with left•hemisphcrc damage. in contrast. tend to sho,,1 strong depressive reactions to their conditions (Ogden. 2005). lhc djffercnt psychological impairments produced by brain damage can be assessed and quantified through various neuropsychologic.aJ test batteries and mental status examinations. 111esc assessments may involve tasks of verbal or visual memory and can incJude visual

Neurocognitive Disorders

425

reproduction of standardized complex figures or freehand drawings. like the clock and Hower in Figure 15·2. 'Ole accuracy and organization of these reproductions can provide important information about the affected brain areas. Other assessments aim to measure executive control (counting to to. reciting the alphabet. oaming as man)' animals as possible in a m inute). short-term memory (recalling a Ustof digits or pictures following a short delay). visual and auditory recognition (identifying a target stimu lus in a list). and the ability to acquire new information (such as learning pairs of words. with one word then serving as a prornpl to recall the other). 1be result.,; from these types of assessments aid in differential diagnosis of the cognitive disorders. lhe reliability of organic mental d isorders in the DSJW•lll ficld trials was good. witb overall kappa values showing highest consistency for the diagnosis of dementia. Later reviews (V\folfs. Dirksen. Severens. & Verhey. 2006) also indicated good agreement on the dementia category. but not on various dementia subtypes with different etiologies. For example. the DSM-IVcriteria showed better reliability and validity for dementia of the Alzheimer's type t han for vascular dementia (Hogen1orst. Bandelow. Combri nck. Irani. & Smith. 2003). 'the DSM-5 field trials found test-retest reliability to be ·good" (pooled kappa of .46) for mild neurocognitivedisorder and ''very good" for major ncurocogniti,•c disorder (pooled kappa of .78). but reliability was ·questionable" (kappa = .36) for mild traumatic brain injury (Regier ct al .. 2013). Reliability estimates arc harder to find for delirium and amnestic disorders: one reason may be that amnesia can occur in the absence of any biological evidence. as in dissociative amnesia and other dissociative disorders. The issue is further complicated by the high base rate of mali ngering of amnesia after mi ld head injury (Larrabee. 2004). Dementia also is more chronic and global in its impact and more consistently observable, in that sense, lending itself to agreement in di~"llosis. Figure 15-2 Neglect Syndrome Due to Damage In the rnultiaxial structure of the DSM.JV. the mcntaJ of the Right Parietal Lobe disorder (e.g.. dementia. delirium. or amnestic disorder) was listed on Axis I based on diagnostic criteria that identify jts Examples of neglect on a drawing test. psychologicaJ and behavioral characteristics. such as memory or Source: Adapted from 1he Me11/a/ Staw.r Examlnatimt in Neurolt>gy. by R. L. Strub and F. W. Black. 1917. PhHadelµhia.. PA: language disturbancc.1he physical disturbance (e.g.. Alzhcimcr·s F.A. Davis. disease) that causes the mental dis.order was separately coded on Axis JU as the associated medical condition. 11\e DSM-5 no longer makes such distinctions: The physical disease is coded along with the mental disorder.

15.2

Delirium

1l1econdition now known as delirium has been recognized for thousands of YL"ars. Hippocrates wrote in 500 BCE of phrenitis (one of several rnore or Jess equivalent terms). describing a mental disorder tJ1at re~,;ulted from poisoning. head injury. or fever. Historically. delirium was associated with incurable madness. poor prognosis. and death. By the 19th century. it was understood to have several ca.uses. including What is delirium? alcohol. and was seen as a serious but often transient condition from wh ich full recovery could occur (Adamjs, Treloar. Martin. & MacDonald. 2007). It was know11 as -acute brain syndrome'' in J)S)H.J and has also been called ~acute c.onfusional state."" "toxic psychosis.Hand "metabolic encephalopathy" (American J>sychiatric Association. l980).

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As currently defined (sec DSM-.S: Diagnostic Criteria. for Ocliriurn). delirium is a change

in consciousness that can involve disorientation. impairment of memory (usually recent). illusions or hallucinations. and reduced attention to the surrounding world. lt develops rapid.Jyand can nuctuatc in severity throughout the day. By definition. there must be evidence that the disturbance is related to a specific physiological ca.use. such as a medical condition.

a medication, or a substance. Delirium involves a rcfativcly brief, but global. cognitive impairment of attention and awareness. Delirious indi\1iduals often arc not oriented to place or t:imc·- for example. believing themscJvcs to be at home rather than in the hospital or confusing day for night.1hcy

Delirium

Rapidly developing change in consciousness that im•olvcs impairment in memory and cognition and rtiduced attention

to surroundings

DSM-5

are easily distracted. and their rapidly shifting attention may make conversation difficult or impossible. There is frequently disruption of the sleep•wakc cycle. ranging from hypersomnia to insomnia; sometimes a reduced wakefulness or "clouded consciousness'" dominates. Motor activity can vacil late.shifting between hyperactivity and lethargy (American Psych iatric Association. 2000). 'fhc course fluctuates during the day, typically becoming worse at night as externaJ stimuli that provide orienting information become less available (Amc.r ican ·Psychiatric Association. 2013).

Diagnostic Criteria for Delirium

Delirium A. A disturbance in attention (i.e.. reduced ability tu direct. focu.,;, sustain. and shifi-allention) and awareness (reduced orientation lo the environment}. B. The dislu rbance develop.,; O\'er a short period of lime (usually hours to u rew days), represent..s a change &om baseline attention and awareness. and tends to Ruchmte in severity during the course or a day. C. An addiUonnJ disturbance in cognition (e.g.. memory deficit. disorientalion. language. visuospatial ability, or perception). D. The disturbances in Criteria A and Care not better explained by nnother preexisting, established. or evolving neurocognitive disorder and do not occ:ur in the context of n severely reduced level of arousal. such a.s comn. E. There is evidence from the history. physical examination. or laboratory findings thnt the disturbance is a direct physiological consequence of another medical conditi.on. substnnoe intoxication or withdrawal {i.e.. due to a drug of abuse or to a medication). or exposure toa toxin. or is due lo multiple etiologi~. Specifywhelher: Substance intoxkaUon delirium: This diagnosis should be made instead of substance intoxicalion when the symptoms in Criteria A and C predominate in the clinical picture and when they are sufficienll)' se-,·ere to warrant clinical attention. Substance withdrawal delirium: This diagno..o;is should be made instead of .substance withdrawal when the .symptoms in Criteria A and C predominate in lhecUnicaJ picture and when lhey are sufficiently severe lo warrant cllnical attention. Medicalion•induced delirium: This dingnosls applies when the .symptoms in Criteria A and C arise as side effects of a medication taken as prescribed. Delirium due tu another medical condition: There is e'\'idencefrom the history. physical examination. or laboratory findings lhat the di.sturbance is attribulabl~ lo the physiological consequences of another medical condition. Delirium due to multipleetio1ogies! There is evidence from the history. physical examination. or laboratory findings that the disturbance has more than one etiology (e.g.. more than one etiological medical condition. another medical condition plus substance intoxication or medication side effects). Specify if, Acute: Lasting a few hour.s or days. Pen.is tent: Lasting weeks or months. Specifyif, Hypemctive: The individual bas a hyperactive level of psychomotor activity I hat may be accompanied by mood )ability. agitation. and/o r refusal tu cooperate with medical care. Hypoactive: The indh•idual ha.s a hypoacti\·e level ofp.sychomolor activity that may be accompanied by sluggishness and lethargy that approaches stupor. !vlixed level of activity: The individual ha.s a normal level of psychomotor activit )' e\'Em though attention and nwnrene.ss are disturbed. Also includes indh•iduals whose activity level rapidly Ructt1ates. Coding Note: Please see the Appendix.. pg. 472 for the appropriate codes used for Delirium. Source: Reprfoted with perml!lslon from the DJogmmit: tmd Sta1isJlt:1ll Mtmuafo/Me1ua/ Di~orders.. Sth ed•• (Copyright 2013). American Piirchlatric AsJiodatlon.

Neurocognitive Disorders Shifting emotional disturbances are typical. includ ingcxt.rcme$ such as euphoria. anger. and depression. Fear is commonly present and sometimes leads to attempts to flee or to attack others perceived to be threatening. People who have experienced states of delirium later report having felt confused. anxious. and afraid. Visual hallucinations, especially of animals or people. are common and. together wiU1 delusions. arc the mostsignificantsourccs of fear and anx_iety (O'Malley. Leonard. Meagher. & O"Keeffe, 2008). Speech disruptions in delirium can include articulation difficulties. inability to name objects, rambling and incoherent verbalizations. repetition. or difficulty understanding words.Writing ability may be impaired as wc11.111esc emotionaJ. perceptual. and speech disturbances can resemble other psychotic conditions such as schizophrenia. except for their fragmented and fluctuating presentation. Delirium usually follows an acute course. developing witJ1in hours or days and most often resolving within weeks or. more rarely. months. lt can. nonetheless. become chronic jf supe.rimpos.cd onto a prc,cxisting major ncurocogWtivc disorder (see below): it can progress to stupor. coma. and death for those whose underlying cause remains unrecognized or untreated. Its prc.scncc is associated with increased risk of mortality: Nearly40% die within a year of diagnosis.At any one time, delirium may affect between 1% and 2% of the general population: its inc.idence increases. with age. such that nearly one seventh of those over age 85 are affected. More than half of hospitalized patients display delirium. and s:1% of people develop the condition at the end of life (American Psychiatric Association. 2013). Delirium can occur in all ages. and childr·c n (perhaps due to their developing physiology) are at increased risk. especially during iUnesses involving fever. 'Jhe cognitive signs of the disorder may be difficu lt to identify in children. and the child's behavior may be misinterpreted as uncoopcrativencss (American Psyc hiatric Association. 2000). 111e cJderly arc particularly su sceptible to multiple influences that can combine to produce the condition. In frail geriatric groups. at least 250 different contributing factors to delirium have been identified. the most common of which are infections, adverse metabolic events. and adverse medication effects (Laurila. Can younger people show the Laakkonen. Tilvis. & Pitkala. 2008). In addition symptoms of delirium? to advancing age. other risk factors include male gender. alcohol abuse, deme ntia. and sensory impairment (Bourne. Tahir. Borthwick. & Sampson. 2008}. Delirium can be caused by exposure to toxins (including fuel. solvents, insecticides. and carbon monoxide) and by medications. drugs or drug abuse. physical damage to tJ1e brain. and a host of other event.~. 111e DSJ\tf.s organizes delirium diagnoses according to etiology: substance intoxication delirium. substance withdrawaJ delirium. medication .. induced delirium. delirium due to another medical condition, or delirium due lo muJtiple etiologies. 111e diagnosis can be specified as acute (lasting a few hours or days) or persistent (lasting weeks or months): it is also based on the level of psychomotor activity involved (hyperactive. hypoactive, or mixed). 111e hyperactive subtype appears more commonly when delirium is associated with medication side effects and drug withdrawal (American Psychiatric Association. 2013).

15.2a

Substance Intoxication Delirium

Each intoxicating substance produces a characteristic pattern of behavioral disturbances, according to the drug's pharmacolog)'. Jfthe reaction following drug ingestion is signifi .. cantly diffel'ent from ~normal" intoxication. resulting in cognitive impaim1c.nt t hat is excessive and serious enough to warrant clinical attention. then a substance-..induced deliriu1n (e.g.. alcohol intoxication delirium) may be diagnosed. lo addition to aJcohol, intoxication deUrium is associated with amphetamines. cannabis. cocaine. hallucinogens. opiates. PCP. sedati ves. anxiolytics. or combinations of drugs and substances. In most conditions. the delirium resolves within a few hours or days as the intoxication dissipates (American Psychiatric Association. 2000}.

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15.2b Substance Withdrawal Delirium Some substances capable ofcausing withdrawal can produce substance withdrawal dc-l irium.

involving cognitive disturbances in excess of those normally accompanying withdrawal and serious enough to warrant clinical attention. Substance withdrawal delirium develops as tissue concentration of a drug changes following cessat ion or sharp reduction in us.c. A wc11-known example. described in Chapter 12. is alcohol withdrawal delirium (formerly called delirium tremens). which can include agitated behavior and vivid visuaJ. tactile. and auditory

halluc.inations. beginning a couple days after reduction or cessation of drinking. Alcohol withdrawal delirium occurs in less than 5% of those hospitalized for alcohol dependence and usually runs its course in a few days (American Psychiatric Association. 2000). Substance withdrawal delirium has also been identified for the sedative. hypnotic. or anxiolytic cl.rugs. In some longcr-actingsubstanccs. withdrawal delirium can persist for weeks before resolving.

15.2c Medication-Induced Delirium Many mcd.ications- including anesthetics. analgesics. antihistamines, mus cle relaxants. heart medications. and some psychotropic medications such as lithium- or their s ide effects can cause dclirium. Medication-induced delirium usually develops in close accordance to the rate of drug distribut ion in the bloodstream. often witMn minutes for rapid•actingsubstances or over longc-r courses (hours} for drugs that have longer haJf.Jives. lts duration can be affected by rate of both drug absorption and metabolism. as we.LI as by drug interactions (American Psychiatric Association. 2000). Especially among the c.lderly, polyphannacy is a major risk factor for substance-•induced delirium: Almost 44% of frail geriatric patients in an inves .. tigation of delirium prevalence were receiving more than eight regular tncdications daily (Laurila ct al.. 2008).

15.2d Delirium Due to Another Medical Condition Delirium can develop in the context of a wide range of medical conditions. Specific lesions or tumors of tJ1c brain, especially in the parietal or occipital lobe. can produce delirium. as can many djsturbances of the central nervous system. metabolic disorders. heart condit ions. or systemic illnesses. Delirium may occur in connection with high fevers. encephalitis, fluid imbalances, dehydration. and certain severe vitarnin or mineraJ dcficienc ics. Jt may develop postoperatively or in association with hypoxia, s hock. or head injury.1l1c specific medical condition (such as an infection of the brajn, a stroke. low blood s ugar. or a tumor) is noted in the diagnosis (e.g.. delirium due to head trauma). Because many of the med ical conditions that cause delirium can be treated. delirium due to a general medical condition is frequently resolved rather quickly by interventions for the.underlying medical issue.

15.2e Delirium Due to Multiple Etiologies

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If more than one specific physical factor is known to be involved in the cause of the delirimn. delirium due to multiple etiologies can be diagnosed. For example, delirium might result from the combined effects of a liver djseasc and substance withdrawal. frequently in the elderly population. medication s ide cffc-cts interact with physical disorders. both of which contribute to delirium. However. the multitude ofpotential triggers of delirium can also produce a variety of different presentations. -other s pecified deliriurn~ describes those cases of delirium not fitting into the above categories, s uch as delirium that is produced by sensory deprivation. or those that do not meet full diagnostic criteria for the condition.

Neurocognitive Disorders

Treat1ne11t for Delirium Most people recover full y from deli riun1 whether or not they receive treatment. but int ervention shortens the course of disturbance (American Psychiatric Association, 2013). Treatment of the florid and often psychotic symptoms of the disturbance frequently involves sedation. usuaUy via low-dose antipsychotic medjcation. Some attempts have been made to prevent the development of delirium in h igh-risk cases through the prophylactic use of antipsychotics or bcnz.odiazepincs (Bourne et al.. 2008). Of course, careful review of causal factors is important prior to preventative attempts because the medications may themselves contribute to the development of delirium.

15.3

Major and Mild Neurocognitive Disorders

'£he cognitive disturbance associated witJl neurocognitivc disorders involves decline in one or more cognitive domains. rn contrast to delirium. mild and major ncurocognitive disorders may have a gradual. slow onset and more frequently What causes neurocognltive have a chronic course. disorders? In the DSM-IV. major ncurocognitive djsorder was known as dementia. It always involves a memory deficit. most apparent in recent memory and the retention of new learning. For example., a person may lose recently handled items. forget activities that are in progress. or be unable to recall a list of words given moments before. The demented person may become easily lost when walking in Wlfam iliar settings. \>Vhcn dementia is advanced. memory impainnent extends beyond recent evenu, and people may forget important personal information (such as occupation or even name). Although dementia remains a useful term. the DSA(.5 diagnosis of major neurocogniti.ve disorder was broadened to include the memory impairments known as amnestic disorders. Is dementia permanent? Ncurocognitive disorders ared.iagnoscd on the Can it be prevented? basis of a decline in functioning in at least one of s ix cognitive domains: a.

Contplex attention is the ability to attend to sustained1 multiple. or selective aspects of an activity. It is demonstrated when a person can remain on task, ignore distractions. and divide attention between two or more thing.~.

b.

Executive function is the ability to plan tasks, make decisions, manipulate information. solve problems based on feedback. apply complex and cffortful solutions. and shift between concepts.

c.

lenn1ing and memory involve several memory abilities such as short•term recalJ. delayed recall. cued recall. and recognition, as well as the abi lity to learn new things.

d.

language involves expressive abilities s uch as naming. word finding. grammar and syntax. and receptive understanding.

c.

Perceptua/.motor abilities include the ability to navigate: to use tools or devices: and to imitate. d.raw. or copy.

f.

Social cognition includes the ability to detect and recognize emotion in others or to understand another person's point of view.

A variety of neuropsychological tesu. such as the Halstead ..Reitan Ncuropsychological Battery, include specific tasks to mea~urc relative functioning in these areas. Together with intc.lligence tests and memory instruments. like the V\'echsler Memory Scale, they provide a rather thorough ind icator of cognitive decline and provide the type of documentation required within the diagnosis.

Dementia Global development ofmulllple cognitive arning and memory. Language. perceptual-motor. or social cognjtion) based on: L Concern of the individual. a knowledgeable informant. or the clinician that there has been a significanl decline in cognitive function and 2. A substantia) impajnnent in cogniti\'e performance. preforably documented by sl.andardjzed neuropsychoJogicnl testing or, in its absence. another quuli.fied cJinicaJ assessmenL 8. The cognitive deficits interfere with independence in everyday activities (i.e .. al a minimwn. requiring assistance with complex instrumental nctivitjes of daily living such as paying bills or managing medications). C. The cognitive deficits do not occ~ur exclusively in the context or a delirium. D. The cognitive deficits are not better explained by another me.nta) disorder {e.g.• major depres..o;ive disorder. schizophrenia).

Specify whether due to: AJz.heimer·s disease Lewy body djsease Traumatic brajn injury HN in(ec-tion Parldnson·s dj.sease Another mediClll condition Unspecified

Fronlotemporal lobar degeneration Vascular disease Substance/ medication use Prion disea,s e Huntington's disease Multiple etiologies

Specify Without behavioral dtsturbance: If the cognitive disturbance is not accompanied by any signi.ficant behnvioraJ disturbance Wllh behavioral dist u rhance: (.specify disturbance): Jf the cognitive disturbance is accompanied b)' n cl inicalJy sign ificanl behavioral disturbance (e.g.. psychotic,i.')'mptoms. mood disturbance. agitation. apathy. or other behnviom.J symptoms. Specify current severity: Mild: Difficulties with instrumental activities of daily living (e.g.. housework. managing mone)'). Moderate: Difficulties with basic activities of daily Living (e.g.. feeding. dres.o;ing). Severe: fully dependent. Coding Note: PJease see the Appendix, pg. 472 for the appropriate codes used for Major Neurocogniti1-·e Disorder. Source: Reprhued with perml!islon from the Dlognostle OJ1d StatisJlcol Mamwlo/Mmtal D'Uorders. 5th ed. (Copyrlghl 2013). American Psychiatric Assodatk>n.

Neurocognitive Diso rders

Apraxia is manifested by impaired ability to execute motor activities, altl1ough motor function is intact. For example, individuals may not be able to demonstrate how to comb their hair or brush their teeth or how to wave good-bye, although they are physically capable of making those movements. As a result, normal self-care abilities such as dressing and grooming are often disrupted. Agnosia is failure to recognize objects or people that were formerly familiar to the perso11. Co1nmo11 items such as car keys or pencils might 11ot be identified or labeled verbally. In severe cases of dementia, individuals may not recognize close friends, family members, or even themselves in a mirror. Disturbances in executive function involve impairments in the ability to plan and execute actions. Abstract thinking is deficient, and serial tasks such as counting or reciti11g familiar sequences (e.g., the alphabet) are impaired. Individuals with disturbed executive function might not recognize error or resist a temptation; they have difficulty with sequences of actions that have not been well practiced. As the condition progresses, these impairme11ts become more obvious. Individuals may show early symptoms of difficulty with financial issues or with shopping, progressing to problems in daily activities such as dressing, bathing, and eating. They may also lose the ability to use common tools such as telephones. They almost always have impaired judgment and poor insight and may u11derestimate tl1e dangers of certai11 activities, such as driving. Delusions (often persecutory) and hallucinations (often visual) can occur; depending on the causal factor, additional delirium may also be present. In fact, it can be quite difficult to distinguish dementia from delirium in the elderly; the t,-vo disorders co-occur in the majority of hospitalized older patie11ts (Blazer & van Nieuwenhuizen, 2012). However, the dementia must be separable from the effects of any preexisting delirium before the diagnosis can be applied. The prevalence of dementia increases rapidly with age, such that 30% of people 85 years of age and older are affected (American Psycl1iatric Association, 2013). Ma11y physical co11ditions are known to cause dementia; any condition that is associated with physical damage or deterioration of the brain can be involved. The DSM-5 diagnosis lists several of the most typical associated conditions witl1in the diagnostic criteria, but the list is not exhaustive. Recently, the link between midlife obesity and later dementia has become apparent (Loef & Walach, 2013). Some of the conditions are described in more detail below.

431

Apraxia

I1npaired ability to execute 1notor activities, altl1ough motor functions are intact Agnosia

Failure to recognize familiar objects or people Disturbance in executive function An impairment in the ability to plan and execute actions

15.3a Neurocognitive Disorder Due to Alzheimer's Disease Neurocognitive disorder due to Alzheimer's disease, also called dementia of the Alzheimer's type (DAT), is the most common form of dementia (see Table 15-1); its prevalence is increasing as the population ages, and its numbers are expected to triple by 2050 (Caselli, Beach, Yaari, & Reiman, 2006). Alzheimer's disease accounts for up to 60% of all cases of dementia (Blennow, de Leon, & Zetterberg, 2006). It rarely develops before age 50, but then increases dramatically with age, such that 10% of those in their seventh decade and more than one fourth in later decades show tl1e disorder. Alzheimer's disease causes a progressive and irreversible dementia that gradually worsens as brain deterioration proceeds, with death occurring, on average, 10 years after diagnosis (American Psychiatric Association, 2013).

A 1nale patient with Alzheimer's rests on l1is bed. Due to his loss of short-term memory, l1e relies 011 sticky notes to remi11d hi1n l1ow his clothes are organized. (Getty Images/John Livzey)

4J

Chapter IS

Abnormal Psychology

Table 15-1

Summary of DSM-5 Diagnostic Criteria for Major or Mild Neurocognitive Disorder Due to Alzheimer's Disease

Along with meeting the criteria for major or mikl neurocognitive disorder. there is evidence of jn_n1TYcs.,;ion of Alzheimer's disease as seen. in brain slides showing increased cortical atrophy. enlarged ventricles. and hippoc.ampal shr inkage: (a) the brain of patient with preclinical Alzhcimcr·s disease (b) the brain affected by mild to

moderatcAlz.hcirncr's disease. and (c) a severely affected brain. Source: lllustrationscaurtesy or the National lnstitut..e on Aging/National Institutes ofHealth. {a)

Cerebr.11 Comix

(b) Cortical Shrinkage

(c)

Extreme Shrinkaee of Cerebral Cone

'

"

Causal Factors Alzheimer's disease occurs in both familial and sporadic forms. 'Titc familial form is rare. with prevalence below 1% (Bien.now ct al.. 2006). 1l1is form has onset before age 65 and is most closely associated with prcscnilin l and prcscnilin 2 genes (see Figure J5-7). Several known genetic mechanisms that contribute to the sporadic form of Alzhci mer·s disease. but most cases seem to be associated with the apo)ipoprotein £ (APOE) site on chromos.ome 19 (Blcnnow et al .. 2006: Caselli ct al.. 2006). It is not known specifically how mutations at this site increase risk for OAT, but forms of this gene may be ass.ociated with enhanced bcta•amyloid deposition (Caselli et al.. 2006). However. the association of APOE with DA1' is not exclusive. and APO£ genetic testing is not yet useful in confirming risk for developing the condition. In t he case of the sporadic form of Alzheimer's disease. it appears likely that APOE and several other genes may be invoh1cd. each of which confers some risk in complex inter• action with cnvironrnental factors still to be cnu rncratcd (Blennow ct al.. 2006). A recent report that found that magnetite nanoparticlcs. possibly released during industrial combus• t ion. arc accumulating in brain tissue is concerning because magnetite is toxic to the brain and may cause neu rodegenerativc changes such as those that produce Alzheimer's disease (Ma.her etal.. 2016). Magnetite is also a common a ir pollutant. illustrating the possibility that environmental neurocognit ivc hazards are widespread. Certain psychotropic medications

Figure 15-6 Progressive Reduction in Brain Activity in Alzheimer's Disease (a) Localized reduction in preclinical Alzheimer's disease: {b) spreading inactivation in mild to moderate Alzheimer's disease: and (c) widespread metabolic reduction in severe Alzheimer's disca,;e. Source: IUus trations: rourtesy or the National lns1itule or Aging/Natklnal Instil ute!I of Hea.1th.

(a)

(b)

(c)

Neurocognitive Disorders have aJso been implicated: A Canadian study of J,796 persons diagnosed with Alzheimer"s disease. as compared with 7.184 matched controls. found that use ofbenzodiazcpines for more than 6 months was associated with an 84% increased risk of developing Alzhc.imer's disease. suggesting that extended benzodiazcpinc use may a.~ , promote t he development of the disorder (de Gage ct a l., 2014). Neither of these studies demonstrates causality. however. Several mutations ofa bcta-amyloid precursor gene.APP. on chromo~ sorne 21 have also been linked to Alzheimer's disease (Le ndon, Ashal l, Ctwomow,me l4 & Goate. 1997). 1·his may explain the relationship hetwoon Alz heimer's 0 disease and Down syndrome. caused by trisomy of chromosome: 21: Chr01"1'10SOff11C 19 Alzheimer's disease is aJmost im•ariantly present in people with Down Chrom~me21 syndrome after age 45 (\Villcrman & Cohen. 1990).

Treatment for Neurocogn1t.Jve Disorder Due to Alzhein1er's Disease

• •

It is not yet possible to stop or reverse the course of Alzheimer·s djscasc or its accompanyi ng dementia. At pre.,;:ent, treatment ror ncurocognitive APO! ll.l disorder due to Al.zhcimcr·s disease is focused on techniques to slow the PS> advancement of the deterioration and to improve U1c qua lity of life of patients. lt is known that destruction ofcholincrgic neurons in t he basal forebrain reduces levels of acctylcholine (ACh) in the brain and interferes with t he functioning of the h ippocampus and other areas important to memory.1licACh depiction m ight be a ddressed by use of cholinesterase inhibitors. which slow the breakdown of ACb in the synapse. causing levels of t he neurotransmitter to decline less stceply.11uee cholinestc-rasc Figure 15-7 Genes Associated with inhibitors are current ly available: donepczil (sold as Aricept• ). Alzheimer's Disease rivastigmjne (Exelon•). and galantaminc (Reminyl•). ·n1esc drugs can Source: Adapted from "E.rplorlng the FJiolOg)' of produce modest but measurable effects on cognition, t ranslating into Al1.helmer Disease Using Molttular Genetlclt.-by delayed worsening or temporary slight improvements in some cases C. I.. Lendon et al. 1991.JOrder. (Quttn V1ctorl11or 1he Alabama Supreme Court, in Parso11s v. State (1887), expanded the En~l:md b1· Alcunder Mth•d It' od pnulimg ( uu:;). from conditions under which the insanity defense might be acceptable. It ruled Wikimfflia Cuenmm.u.) that even if a person committing a criminal act could tell right from wrong. that person might. be not guilty by reason of insanity if a pathological drive or impulse that the incLividua l could not control had compelled the crime. In this irresistible impulse ruJc., the criminal act could be seen as t he product of t he mental disorder rath er than t he person who could uot resist acting. The irresistible impulse rule is sometimes referred to as the -police officer over t he shoulder" rule, suggesting that a trulr unprevent able act would have been comm itted even if a police officer were looking over the defendant's shoulder at th e McNaughton role timc.1hc effect of this. and similar rulings. was to provide a defense for ..crimes of p..'ts.-;ion" Legal guideline Lhat or ~temporary insanity"- if the irresistible impulse was a momentary one. Ofcourse. a major insanity concerns an problem with t his standard is t he difficulty in distinguishing impulses that a person cannot individual's inability to control from impulses that a person simply does not control. distinguish nght from By the mid-20th century, the psychiatric profession had become more and more critical of wrong in committing the crime these approaches. t he McNaughton rule, they believed. was based on a conception of people as rational beings who made free choices informed by conscious considerations. Modern Irresistible impulse psychiatry. influenced by Freud and other adherents of the psychodynamic movement, role however. preferred a model that induded irrational and unconscious. as well as conscious. Legal guideline Lhat determinants or behavior. The psychiatrists argued that it was difficult for t hem to testify as insanit \t concerns a to whether a defendant knew right from wrong but that they could bring their expertise to pcrson·s inabilit}• to bear on whether the accused was s uffer ing from a mental disturbance. In 1959.Judge David L resist committing the Bazclon of the U.S. Court of Appeals. acknowledging these points. wrote an opinion in tJ1c crime

,.......,.,,,._

--~,.,,-"", ..,_...,,.

45

Chapter 16 Aooormal Psychology

Durham case that formu lated a third test of criminal responsibility.111c Durham, ruJc held that an accused person is not criminalJy responsible ifit is shown that the un1awfo1 act was the product of a mental disease or defect. In Judge Bazelon·s view. however. the Durham rule never accomplished its intended goal: 13 years later. in 1972. he favored its abandonment (Bazclon, 1974i 1l1e basic probll?m. accord• ing to Bazelon. is t hat when psychiatrists testify, they limit t hcmsel\•cs to conclusions (for example, U1at the defendant is Mmcntally ill H) without providing the jury with undc.rstandablc evidence to support their conclusion or, for that matter, illuminating what the term mental/y ill means in a g iven case. Psychiatric testimony, according to Bazelon. should be s ubmitted to the same scrutiny and C.\'.amination as any other kind of opinion presented in court. lt is not clear what a Mproduct of a mental disorder- is. whereas it is clear t hat expert psychiatric witnesses d isagree about their opinions in such cases. Further. the Durham ruJc did not address the issue.,; of -right from wrong'" or of irresistible impulse., allowing defendants to claim that simply carrying the diagnosis of any disorder recognized by mental health profcs,. sionaJs could be the-cause"" of any criminal action they committed. In light oftJlc persisting criticism and d_issat• Can a person be insane but isfac.tion w ith definitions of insanity to that competent? Incompetent but point. the- American Law Institute (American Law sane? Institute. 1962) issued a more comprehensive stan• dard in its Model Penal Code. 1J,e ALI standard stated the following: 1.

A person is not responsible for criminal conduct if at t he time of such conduct. as a result of mental disease or defect. he lacks the substantial capadt)· either to appreciate the criminality (wrongfulness) of his conduct or to con.form his conduct to the requirements of the la,v.

2.

As used in this Article. the terms -mental disease or defect" do not include an abnormality manifested only by repeated criminal or otherwise antisocial conduct. (American .Law Institute. 1962, pp. 61 - 62}

It is apparent that this standard incorporates components of each of the earlier rulings but also appears to exclude soc.iopathic behavior. conduct disorder, and antisocial personality D1u·l1a1n rule disorder from the conditions that qualify for the insanity defense. Later rulings determined Legal guideline that that voluntary use ofdrugs or alcohol could not serve to create a "temporary insanity" defense insanity concerns for a crime under the ALI s tandard.Some legal experts (e.g.. \Vinick. 1995) have suggested that the extent to which there arc also good reasons to cxcfude personality disorders. impulse control disorders. and the criminal act was most psychosexual paraphilias from mcctingthC! legal requirements ormental disease." either a product of mentaJ for t he insanity defense or for civil commitment. because their physical status as -illnesses.. disorder is questionable. (That legal argument perhaps incorrectly presumes that the .. illness.. status of other DSM conditions has been physically established.) Most states adopted the ALI standard as a framework for insanity cases. If the capacity to intend to commit a crime (i.e.. criminal intent) is diminished by a mentaJ disorder. a defendant could be found not gu ilty of the crime. However. diminished capacity argumenu have continued to be controversial. \1/hc.n John Hinckley Jr. wounded President Ronald Reagan in an assassination attempt in 1981. he had carried a diagnosis of schizophrenia for scveraJ yea.rs and had been obsessed , ..ith the actress Jodi Foster. to whom he had been mailing love letters. He explained that he s hot t he president in an attempt to impress f'ostcr so that she would then return his love. A jury found Hinckley not guilty by reason of insanity, accepting the argument John HinckleyJr.. who shot .President Ronald Reagan in t hat schizophrenia had diminished his capacity to understand the 1981. was found by a jury lo be nut guilty by reason of insanity. (AP P11aao/ban Vucril wrongfulness of the act or to conform to the law.

Legal, Ethic•~ and Professional Issues in Abnormal Psychology

Public criticism of the Hinckley ruling, together with grO\•\ting dissatisfaction with other verdicts. eventually led to the federal Insanity Defense Refom1 Act. passed by the U.S. Congress in 1984. describing the insanity standard for all federal courts to apply. Largely on the recommendation of the American Psychiatric Association (J983). the act limited

the volitional component of conforming conduct to the law and partially returned to the McNaughton standard:~ person charged with a criminal offense shou.ld be found not guilty by reason of ins.unity if it is shown that as a result of mental disease or mental retardation. he was unable to appreciate the wrongfu lness of his conduct at the time of his offense... 1hc insanity defense frequently evokes skeptical reactions in people who wonder whether it is just a strategy that clever lawyers use to get guilty clients acquittcd. lhis skepticism is not helped much by the fact t hat one psychiatric ..expert" may testify that a defendant was insanc a t the time of a crime and another psychiatric expert may testify that the defendant ,,,as sane. As one psychiatrist experienced in legal testimony put it. ..Attorneys for the prosecution and defense will consult privately with as many potential psychiatric witnc.~scs as necessary (when they can afford it) until they find one or h\TO whose opinion they deem useful to their side" (Lunde, 1975). Among t he widely cove.red trials invoking the insanity defense was t hat ofJames Holmes. who o pened fire in a crowded movie-theater in Aurora. Colorado. in July 2012. during a m idnight showi ng of t he Batman fi lm 1he Dark Knight Rises. Holmes had become increasingly ,....-ithdrawn and scJf..absorbcd in the months before the killings. He was failing in his graduate neuroscience program. and in March 2012, he told a campus psychiatrist that he was t hinking about killing people. Shortly before the s hootings. Holmes mailed a notebook to the psychiatrist that included both psychotic ramblings and apparently measured planning of the massacre. although s he d id not sec the notebook until after the killings. He booby•trappcd his apartn1ent with homemade grenades and 10 gallons of gasoline and then calmly entered the theater. heavily armed and fu lly body-armored. with bl'ight orange hair. According to some witnesses. he announced ...1am t he Joker:· (a statement he later repeated to the police) ru1d fired a weapon into thcair(Frosch &Johnson, 2012). He then attacked the 400 moviegoers from t he front of the theater. throwing tear gas grenades and fir ing with an AR•l5 automatic r ifle. a Glock pistol. and a shotgun, reloading and continuing until his weapons jammed. By then. he had killed 12 people and injured 70 in one of the worst mass shootings in U.S. history. Holmes was quickly apprehended outside the theater without resistance. He later told a psychiatrist that he was on a mis.~ion and that he accumulated one Cl'edit for each life he took. adding to his own life capital by killing (ff Neill. Cabrera. & Weisfeldt, 2015). Once the prosecution announced it would scc.k the death penalty. Hohnes's defense team entered a pica of not gui lty by reason of insanity. (In Colorado. un like other states . the burden is on the prosecution to prove that t he defendant is sane rather than on the defense to prove that the defendant is insane.) During the trial, the prosecution produced two psychiatrists who had evaluated Hohncs: One diagnosed him with schi2otypa.J pc-rsonalitydisorder. and the other testified that Holmes suffered from schizoaffective disorder. However. both believed him. to be sane. llle defense clai med that 20 doctors w ho had seen Holmes in custody had declared h im to be suffering from schizophrenia (Gurman, 2015). although none were called to testify. Instead. the defense presented videos of Holmes acting strangely. slamming his head against t he wall of a holding ccl l. and covering h is head ,....-ith blankets and sheets while naked in a hospital bed. 1l1c notebook that Holmes had sent to the campus psychiatrist was entered into the triaJ record. with both sides anticipating that its contents would support their case. ln the end. it proved that Holmes's acts were deliberate and premeditated. A~er 12 hours of jury deliberation. Holmes was convicted of murder. attempted murder. and possession of explosives: he was sentenced to 12 lifc terms w ithout parole. plus 3.318 years.

4SJ

454

Chapter 16 Aooormal Psychology

A few pages from the nolcbookjames Holmes mailed to his psycbmlnst jusl before attacking moviegoers to Aurora. Culorodo. in 2012. (Ca lorado Ju(htia! Di:rpart ment I

Actually. the insanity defense is rarely used in the United States and is even more rarely successful: most such defendants are found sane by juries. In general, only a smal l percentage of those raLliing the insanitydc-fcnsc- oftcn less U1an 12%-are judged by forensic

psychologists as meeting the requirements for insanity. though there is much variability between evaluators {Murrie & \Varren. 2005). Some other high-profi le cases involving successfu I and unsuccessful use of the insanity defense arc shown in 1'able 16-1. As is the case in cva1uations ofcompetency, sanityexamjnations must deal with the issues of correct d iagnosis and of accurately distinguishing actual from feigned symptoms. \rVhen the defendant purportedly suffers from intellectual disability. that determination can be difficult. Ofcourse. someone with significant intcllcctuaJ deficits could not -rake good" on an intclligence test: yet, someone with average or above intelligence could attempt to -rake bad.~ 1l1is becomes important in the light of a U.S. Supreme Court ruling (Atkins v. Virginia. 2002) prohibiting the execution of intellectually disabled defendants. The ruling is interesting because it specifies the presence of a cond ition. ratJ-1cr than a dimi nished capacity, in asSC$Sing legal responsibility (Bonnie. 2004). Unfortunately, standardized intelligence tests are not very sensitive to malingering~although neuropsychological assessments may be better in that regard. they arc not specific to intellectual disability (Graue ct al.. 2007}. Shandera and her coJlcagues (2010) adntinistercd the \rVcchslcr Adult Intelligence Scale. as well as a series of 10 common neurological screening devices. to 24 adults: with intellectua l disability. t hey also adm inistered the tests to :~s matched community volw1.teers- JO of whom answered items honestly. while tJ1.e other 25 were instructed to foign intellectual disability. Of the 11 indicators commonly used to detect neurological or intellectual feigning. only one (the Test of Memory Malingering) s howed adequate specificity detecting feigned intellectual disability. In general. the newer neurological screens were ineffective in distinguishing those with

actual intellectual disability from those pretencling to have intellectual disability. The authors concluded that there is a need for a new approach for detecting intentional falsification of low intelligence. In the past. the result has been Uttledifferent for defendants whether they were found sane or insane. ln the former case. they spent many years in prison: in the lattcrcas.c. they spent.on average. about the same number of years confined to a mental hospital {Lunde. 1975). Daniel McNaughton. though found -not guilty.- spent the last 22 years of his life in an institution for the criminally insane. where he received essentially no treatment.John Hinckley Jr. remained under the supervision of St. Eli7.abcth's Hospital until 2016. which was 35 years after his attack on Reagan. though he bad been allowed furloughs and home visits w itJ1. hjs parents since

Legal, Ethic•~and Professional Issues in Abnormal Psychology

Table 16-1

45S

Some Famous Cases Involving the Defense of •Noc Guilty by Reason of Insanity" Case

Outcome

J9n! Francine Hughes poured gasoUne over her husband. whUe he ,vas drunk and asleep. and set him on are. She claimed she wa.;; ool responsible due to years of beatings and threau.

Nol gwlty by reason of insanity

1979~ Kenneth Bianchi claimed he had multiple personaltty djsorder and. therefore. wa.s not responsible for a se-ries of murders and ropes In the "HdJside"Slrangler~ case.

Guilty

1981:John HinckleyJr.attempted to ass.assmate President Ronald Reagan in order to impress actres,..rivilcged communication

Durham rule

Sanity 450

452

460

Treatment guardian 450

Institutionalization 459 Irresistible impulse rule

451

451

QUESTIONS FOR STUDY •

Describe the type of inforrnation that a court might need in order to decide on the issue of insanity.

A psychologist is obligated to protect patient confidentiality except under certain circumstances. Describe several of these limits to confidentiality.

Discuss how a patient has both a right to treatment and a right to refuse treatment.

POP QUIZ 1.

To which of the following docs competency refer? A. one·s ability to succeed ata task B. one·s current mental state C. one·s legal responsibi lity for criminal acts 0. onc·s ability to understand legal charges and assist in own defense

2.

Sanity refers to which of the following? A. one·s ability to succeed at a task 8. one's current mental state C. onc·s legal responsibility for criminal acts D. onc·s ability to u ndcrstand legal charges and assist in own defense

3.

In legal terms. ·competency., is to -sanity" as _ _ _ _ __ A. -tria l - is to -crime" B. "crime-is to-trial"" C. -private- is to -public"' 0. "public., is to ··private"

466

4.

'llte _ _ _ _ _ is a le.gal guideline that describes insan ity in terms of an individual's inability to distinguish right from wrong.

A. irresistible impulse rule B. Durham rule C. -police officer over the shoulder'" rule D. McNaughton rule

5.

\Vho makes the determination of whether a defendant is competent to stand trial? A. the judge B. the qualified mental examiner C. the plaintiffs lawyer 0. the defendant's lawyer

6.

According to the Model Penal Code, which diagnosis would probably be disqualified for a ..not guilty by reason of insanity" plea?

A. antisocial personality disorder B. major depressive d isorder C. sexua] sadism disorder 0. major neurocognith'e disorder 7.

A person with a mental d isordcrcouJd be civilly committed ifhc or she were A. refusing rnedication B. dangerous to self or others C. delusionaJ

0. abusingdrugs 8.

A main issue in 11'),'all v.Stickney(1971) concerned the right to _ _ _ _ __ A. refuse treatment

B. be free of mental disorder C. rccei\'e trcatrncnt D. trial by jury

9.

Overall. the prevalence of violence among those with mental disorders is _ _ _ _ _ those without a mental disorder. A. lower than

B. equal to C. 2 times as high as 0. 5 times as high as

10. A U.S. Supreme Court ruling (Atkins v. Virginia. 2002) prohibits execution of those who are _ _ _ _ __ A. intellectually disabled B. personality disordered C. psychotic 0. severely depressed

467

11. \Vhid1 defendant was found not guilty by reason of insanjty? A. 8. C. 0.

John Hinckley Jr. David Berkowitz (·Son of Sam·) Lee Boyd Malvo Anders Behring Brcivik

12. \Vhich of the following is one outcome of the de.institutionalization movement? A. More patients arc able to receive treatment. B. Fewer patients arc treated with medications. C. More patients are involved with the penal system. 0. Fewer patients show signs of serious mental disorders. 13. All of the following are limitations on confidentiality except ______ A. child abuse

8. imminent danger to self or others C. abuse of the elderly D. criminal activity 14. A clear impl ication of the Tarasoff decision is that the therapist should do which of the following? A. inform t he police when a client has admitt~d child abuse 8. warn the authorities when a dient threatens suicide C. begin commitment proceedings ifa client appears dangerous D. warn a person whom the client has spccificaUy th.r eatcned to harm 15. Currently, most psychotropic medjcations are prescribed by ______ A. psychiatrists B. nonpsychiatricphysicians C. clinical psychologists

D. psychiatric nurse practitioners

Additional study resources are available at www.BVTLab.com.

a·sr a·M a ·r. , :ri1 v ·tt v ·or a·& :J's a·L v·9 v·~ a·~ v·& ;r i 0 ·1 Sll3,\\St-'V

468

DSM-5 Classification Neurodevelopmental Disorders Intellectual Disabilities 317

315.8

:119

(_._) lntellectuaJ Disability (F70) Mild {F71) Moderate Sm,er e (F72) (F73) Profound (F88) Global Developmental Delay (F79) Unspecified Intellectual Disability

Communication Disorders 315.32 315.39 315.35 315.39 307.9

{f80.2) {FSO.O) (FS0.8 l) (FS0.82) {FS0.9)

Language Disorder Speech Sound Disorder ChiJdhood•Onset Fluency Disorder SocinJ (Pragmatic) Communication Disorder Unspecified Communication Disorder

Autism Spectrum Disorder 21)9.00 (FS-4.0)

Autism Spectrum Oisonler

Actencion-Deficit/Hyperaccive Disorder _ ._

(_._)

Att.e.ntion•Deficit/Hyperactive Oisonler

Spwf.hvhetber, 314.0 J {F90.2) 314.00 (f90.0) 314.0 J {F90.I) 314.0 1 (f90.2) 314.01 (F90.9)

Combined presentation Pn.-dominunt:Jy inattenth·e presentation PredominantJy hyperactive/ impulsive presentation Other specified Attention-Deficit/ Hyperacth'lty Disorder Unspecified Attention-Deficit/ Jlypemctivity Disorder

Specific learning Disorder _ ._

L._) Specific Learning OisonJer Spe9

(G47.09) (G:17.00) (G47. 19) (Ci47. 10) (G47.8) (G47.9)

Disorder Stx:cifr whether: {fSl.3) Sleepwnlking type (F5 1A) Sleep terror type ~ightmare Di.sorder Rapid Eye Movement Sleep Behavior Disorder Restless Leg,y.20 13.01.017 Cuccaro. F.. F.. & Dan ehy. ~1. (2006). lntermillent explosive disorder. ln E. Hollander. & D. J. Stein (Ed s.). CJinical manual ofimpulse-control disorders (pp. l 9-37). Arlington. VA: American Psychiatric Publishing. Coccarn. F.. F.. Ka,•m Lo;si. R.j.. Berman. M. £.. & Lish.j. D. ( 1998}. Intermittent explosi\'e disorder-re,'lsc.-d: Developmenl reliability. and \lalidity of rese·u ch criteria. Comprchcu.vilte f'>;ychil.erone acetate with seven pedophiles. C,madianJounwl ufPs)'t:hiatry. 37( IO). 687-693. Cornell. 0. G .. & Hawk. G. L ( 1989). ClinkaJ presentation of malingerers diagnosed by experienced forensic psychologists. Law and lluman Behavior. /3(4). 375-383. Cornn'e. ~,L fl. & Glea\'es. D. H. (2001 ). Body dysmorphic disorder: A review of conceptualizations. assessment. and treatment strategies. Clinical Psyt:hnlogy RcvieH~ 2/(6). 949-'JiO. Coli:raux,j. (2005). keoent developments in research and treatment for social phobia {sodnl anxiety disorder). Currcut Opinion in Aychiatry. 18(1). 51-54. Couturier.j. L. {2005). £fficncy of rapid-rate repetitive Lranscranial magnetic stimulation in the treatment of depression: A systematfo re\'iew and meta-analysis. Joumal of'Aychia1ry & Neuroscience.. .l0(2). 83--90. Coyne.j. C. {1976). Depression and llle respon.se of others. Joumal ,ifAb,wrmal Psrchol.ogy. B5(2). 186- 193. http:// pi.1·cnet.apa.orsfdoi/ l 0.1037/0021-84.1X.85..2.1$6 Craighead.\\~E.• Ha.rt. A 8.. Craighead. L W. & Ilardi. S. S. {.2002). Psycho.wcial t.reabnents for Major Oepressi\'e Disorders. In P. E.. Nathan &j. M. Gorman (Eds.). A guide to trcotme11ts I.hat work (2nd ed .. pp. .245-261}. New York. NY: Oxford University Press. Craighead. \11 E.. Milclowitz. 0.J .. Frank. E_ & 1-\tjk. F. C. (2002). Psycho.,;ocinl treatmcnl-. fo r bipolar disorders.. In P. F.. Nathan &J. M. Gonnan (Eds.).Aguidc totreatmenls that 1t'Orl. {2nd eress. Crils-Christoph. P.. & Barber.J. P. (2002). Psychosocial treatments for personality disorders. ln P. E. Nathan & J. M. Gom1an (Eds.). A guide lo lreatme11ts that wtJrk (2nd ed.. pp. 6 11-62:3). New York. NY: Ox.ford Unh.·ersUy Press. Cromwell. R. L {l 993). Searching for the o rigins of schizophrenla. Psychol.ogical Science. 4(5). 276-279. Cuijpers.. P.. van Strahm. A.. & Warmerdum. I.. (2007). Behavioral activation treabnents of depression; A mel'aanalysjs, Clinical Psy,:hology Review. 2;(3). 3 18-326. https://doi.org/ JO. IO l6/ j.cpr.2006.1 I .00 I Cunningham. C. £.. & Linscheid.1'. R. (1976). Elimination of chronic infant ruminating by electric .shock. Behavior 1/1crupy. 7(2). 231-234. doi,IO. JOJ6/S0005-7894(76)80280.8 Curtin. S. C .. \Varner. M.. & Hedegaard. H.(2016. April. 22). Increase in suicide in the United States. 1999-20 14. NaUonal Centerfor llcallh Slalistics. 241. Retrieved from https:/ / www.cdc.go\'/ nchs/ proclucts/ databriefs/ db241.htm

D Dahan. C.. Vieta. f_ Mackin. P.. & Young. A. H'. (2005). Hypothnlamic-pituitnry-ad.renal axis and bipolar disorders.. Psychiatric Cli11ic.,· rif/1.'orih America, 2,S'(.2). 469-480. https:// doi.org/10. 1016/ j.psc.2005.01.00.5 Dahl. A. A. ( 1993). The personality dJ.sorders. A critical review of family. twin. nnd adoption studjes.j,mma/ of

Personality Disorders. Suppl/. 86--99. Dahlstrom. W. G.• Welsh. G. S~ & Dahlstrom.LE. {1975).

An AIMPI ha11dhook.• Vol. IL &sea.rd, applicalian,,;. Minneapolis. M i~ : University of Minnesota Press. Dahmen.N.. BechLJ.. Engel.A. Thommes. M.. & Tonn. P. (2008}. 1>re\'nlence of eating disorders and ea.ting attacks in narcolepi.1•. /1.'europsyvhiatric Disease and TreotJ,ier,t. 4( I). 257-261. Dalenberg. C.J.. Brand. 8. L.. Gleaves. 0 . H.. Oorahy. M.J .• Loewenstein. R.J., Cardefm....Spiegel. D. (2012). EvnJuation of the evidence for the trauma and fantn.-.:y models of dissodnUon. Psychological Bulletin. 138{3). 550-588. dol:10.1037/ a0027447 Darwin. C. ( 1873/ 1955). 1hc exprcssitm ofemotions in man and ,mimal~. New York. NY: Philosophical Library. DauviJJiers. Y.• Amulf. L. & Mignot. E.. (2007). Narcolepsy with cataplexy. 1he Lancet. 369(%60). 499-51 1. doi,I0.1016/

S0140.6736(07)602'17-2 Davidson.J. R. (2004). Use ofbenzodiozepine.s in Social Anxiety Disorders.. Generalized Anxiety Disorder. and Posttrnumalic Stress Disorder. Journal ofClinical P>ychiatry. 65(Suppl 5). 29-3.1. Davidson. P.R .• & Pnrker. K. H. (2001). Eye Movement Desensitization and Reprocessing (£MOR}: A metaanalysis. )ourunl ofCAm:.ulting aud Cllnical A~ho/tJgy~ 69(2~ 305-316. Davidson. R.J- Pi?.zagalH. 0 .. Mlschke.J. B.. & Putnam. K. (2002). Depre.o;sion: Perspectives from affective neuroscience. A,r,rual Review o/Psycl,olttgy. 5..1. 545-574. 10. J 146/ a.nnure\'.psych.53.10090 L 135148 Davies. G .. \Velham.J .. Chant. 0 .. Torrey.£. F'.. & McGraill.J. (2003). A systematic review and meta-analysis of northern hemii.--pheresea.son of birth studies in schizophrenia.

Sd,izophrmia Bullcliu. 2~3). 587-593. Davis. A. S. (2008). Children with Down syndrome: Implications for assessment and intc~r\'ention in the school. Sch1wl Psyr:hologyQuartcrly. 23(2). 271-281. Oavis.J. 0 .. Phelps.j. A.. & Bmr:ha. H. S. ( 1995). Prenatal development of monozygotic hi.ins and concordance for schizophrenia Schizophrenia Bulletin. 2/(3), 357-366. Davis. Vi. M_ & Smith. S . G. (1979i Role of conditioned reinforce.rs in the initiation. maintenance, and extinction of drug-seeking be:ha\'ior. 7Jre Pal'l0Yi.m1 Joumal ofBi"logical Scicnr.e.-.. J1(4). 222-2.%. doi:10.1007/ BF0:!000316 Dawson. G.. Rogers. S.. ~ifun.son.J .. Smith. M.. V/inter.J_ Greenson.J .....Varley.j. (2010). Randomi.z.ed. controlled trial of an early intervention for toddlers with autism: The Early Start Denver Model. Pediatric.,;, J25f, 1). 17-2:t de Gage. S. B.. l\tforide. Y.• Ducrnet. T .. Kurth. T.. Verdoux. H.. Toumier. M.... ...Begaud. 8. (2014). Benzodiazepine use and risk of AJzheimer's disea.o;e: Case-control study. British Medicalj,mmal. 349. hltp.s!// doi.org/JO. I 136/bmj.g5205

499

Dell. P. f . ( 1998). Axis lJ pathology in outpatients with dissociative identity disorders. 1heftmmal a/Nervous and Mental Disease. 186(6). 352-3:,6. De.LrOs.s.o. B~ Altamura. A. C.. AJJen. A_ ~tfnmzzili. D.• & Hollander. E:. (2006). Epidemiologic and c linical updates on impulse control disorders: A critical review. European Archive.~ ofPsyc.hiharma.cologic treatment of body dy.smorphic disorder. /'rimaryPsychi J--U9. Hummelstein. P.. Pietrow.sl--y. R.. Merbach. M .• & Brahler.£. (2005). Psychogenic urinary retention {'paruresis'):

Diagnosis and epidemiology in representative male samples. Psychotherapy and Psychosomatics.. 74(5). 308-314. https,//doi.org/ I0. 1109/ 000086322 Handen, B. L.. Johnson. C. R.. & Lubet.sky. M. (2004). Efficacy of methylphenidate among chiJdren with autism and :,,Jmploms of uttention•deficit hyperactivity disorder. jounwl ofAutism and Developmental Db;orders, .1(.{3). 245-255. Hare. R. D. ( I96aa). Acquisitions and generalization of a conditioned•fear response in psychopathic and nonpsychopathic criminals. 71teJoumal ofPsychofogy: lnlerdisdpli.uaryo.nd Applied. 59(2). 367-!HO. http:// dx.doi.org/ JO. 1080/ 00223980. 1%5.1054462..; Hare. R. D. ( I 96f)b). Te.mpornJ gradient of rear arousal in psychopaths. Jou.ma/ ofAbnormal Psyt:hychfolry. 147(4). 470-476. doi:IO. l 176/ ajp.147.4.470 4

509

Lund e. D. T. {1975). Murdtr and madnes.,;.. Stanford. CA: Stanford University Press.. Luria. A. R. ( 1982). J.anguagc and cognition. •'{ew York. NY:

Wiley. Lykken. 0. T. ( 1957). Ast:udy of anxiety in the sociopalhic

personality.Journal oftlbnom,al ,md Social Psychology. 55( I ). 6-Hl. h ttp,//psycneLnpa.o rg/doi/lO.I037/ h0047232 Lynn. S.J~ Lilienfeld. S. 0., Merckelbach. H~ Giesbrecht T .• McNally. R.J .. Lofius. E. F.•... Malnktaris. A. (2014~ The trauma mode) of dis..'iOCia.tion: Inconvenient truth.sand stubborn fiction..,;. Comment o n Dalenberg elal. (2.012i Psychulogfr:a/ BulleJin. /40(3). 896-9 10. doi, 10.1037/ n0035570 Lyons.. C. A {1991). Stimulus control-application : Smoking. ln W. lshaq {Ed.). Human l,ehavior in today$ world(pp.

217-230). New York.NY: Praeger. Lyons. C. A (2002. May). PnthologicnJ sambling. impulse control. and the uddiction.s.. Paper session presented at the meeting of the As$0Cia1iou for Behavi\vs. F. £•. Barnes. D. E•. Yaffe. K•. & Bmyne, C. (2014). Potential for primary preYention of Al-~heimer's disease: An anaJysis of population-based data. 1he Lm1a:I Ncurafogy. 1.1(8). 788-794. doi:J0.1016/ S1474-

4422(14)70 136-X

512

Noves. R.. Holt. C. S.. Happel. R. L Kathol. R. G.. & Yagla. S.J. ~ {1997). A fnmjJy study of hypochondrias-is. 1he]ouma/ nf Nerw,us and Me11UJ.I Disease. 185. 223-2.~2.

0 Ohler.

M~ (L973}. Systematic desensitization in .sexual

disorders. Jounw/ ofBchaliior 11,cmpy and Experimental Psyc/,;a1ry, 4(2). 93- 101. htlps,// doi.org/l0.1016/00057916(73)90051-7 O"Orien. C. P.. & McKay.). R. (2002~ Pharmacological treatments for .sub.o;tance use disorders. In P. £. Nathan & J. M. Gonnan (£ds.). A guide to trealnumls that n'Ork (2nd ed .. pp. 12::;- 156). New York. NY: Oxford Uni\'ersity Press. Odeh. M. S~ Ze.is.s. R. A.. & Huss. M. T. (2006). Cues they use: Clinjcians· endorsement of risk c ues in p redjctions of dangerousness. Bchaadnra/ Scicuces & lhe I.am 24(2). 93- 101. https,/ / doi.org/ 10.1002/bsl.672 Ogden.]. A. (2005). Pmclured minds: A case-sl.ud_rapproach Ii> c/iJtical m:umpsyclwlogy(2nd ed.). New York. NY: Oxford Universjty Press. Ohayon. M. 1\.L & Okun. M. L (2006). Occurrence of sleep disorders in tl1e families of narcoleptic p.a.Uent.s.

Ncuro/ractical approar:h,:s (pp. 107-119). New York. NY: Oxford University f>res.s. Okie, A (2010). A Rood of opioid,;, a rising tide or deaths.. 11,c New England journal aJAfedicine. 363. 1981-198:,.

doi:10. 1056/NEJMplOI 1512 O'Malley. G_ Leonard. M_ Meagher. D.• & O'Keeffe. S. T. {2008). The delirium experience: A review. A Joumal of Psyc:hosomaJ.ic Research. 65{3). 223-228. doi:10.1016/j.

jpsychores.2008.05.017 OmaJu, B. I.. OeKosky. S. T .. Hamilton. R. L.. Minster. R. L. Kam ooh. M.1.. Shalcir. A. M.. & Wecht. C.H. (2006). Chronic truumatic enc.ephaJopathy in a National Footbnl.l Le-"Sue player: Part JI. Neuros.urgcry. 59(5). I 086-1092.

doi: 10. 1227/01.NEU.0000245601.6945 1.27 OmaJu. B. L DeKosJ...1•. S. ' f_ Minster. R. L. Kamboh. M. L. Hamilton. R. L. & WechL C.H. {2005). Chronic truumatic encephnJopathy in a National F'ootball League player. Neurosurgery. .57( l~ 128- 134. O'Neill.A.. Cabrera. A.. & \VeLo;feldt. S. (20 15.June JO}. A look inside the ·broken' mind orJames Holmes. CNN. Retrieved from http://www.cnn.com/20 15/ 06/ 05/ us/ jnmes-holmes• theater-shooting-trial/ index.html Ost.1..-G_ & Hugdahl. K. {J981). Acquisition or phobias and anxiety response patterns i n clinical patients. !Jehavio11r Research and 1hc.mpy. /9(5). 439-447. htlps://doi.

org/ I0. JO 16/ 0005-7967(8 1)90134-0 Ouj. U. (2009). Pseudocyesis in a. rum! southeast Nigerian communlty. Joumal ofObstetrics and Gym:cology Re.search.

34(5). 6"0-665. doi, 10.1 11 L/j. 1447-0756.2008.00997.x OvemUer. j. B.. &: Seligman. M. R. ( 1967). Effects or inescapab1e shock upon subsequent escape and avoidance learning. Journal ofComparative and Physfological Psyclmlogy. 63( I).

23-33.

.p

Pllez.-Blnrrina. M.. Luciano. C. Gutierrez-Martfne7_ O_ Valdhia. S.• Ortega..J .. & Rodriquez-Valverde. M. (2008). 'The role of values with personal examples in altering the functions or pain: Comparison behveen acceptance-based and cog.nith,.e-control-based protocols. Behaviour &search and Therapy. 46(1~ 84-97. https://doi.org/l0.1016/j.

b rat.2007. 10.()(IS Pago.in. D- de Queiroz.. V~ Pinj, S_ & Cassa.no. G. 8. (2004). Efficacy orECT in depression: A meta-analytic review. 11ic

JuumnlofiJCT.2'1,)). 13-20. Pallanti.J\.. & Rossi. N. 8. (2006}. Pathological gambling. In E. HolJander & 0.J. Stein (Eds..). Oinical mamwl ef impulse-amtrol dlsarden;{pp. 25.1-289). Ar lington. VA! .American Psychiatric Publishing. Palmer. B. W.. Heaton. R. K.. PauJsen.J .. Kuck.J.• Braff. 0 •. Harris. M.j. ....Jeste. D. V. (19'17). J.s it possible to be schizophrenic yet neuropsychologica.Uy normal? Neuropsyd,ology. I 1(3). 437-446. Pandl-Pemmal. S. R.. Srinh•asan. V.. Spence. D. W.. & Cardinali. 0. P. (2007). Roles or the melatonin system in t:he control ofsleep: 1l1erdpeutic implications. CJ,lS Drug.,;.

21( 12~ 995- 1018. Paris.J. ( 1999). Borderline personality disorder. lo

T. ~lillon. P.H. Blaney. & R. 0. D•v;s. Oxford textbook of psyd,opathou,gy (pp.1>28-652~ New York. NY, Oxfonl Universitv Press. Parry-Jones.\\~L Santer•\\~ststrate.. H. C.. & Crawley. R. C. ( 1970). Behaviour therapy in a case of hysterical bJindness.. Bdwviour Research and 1hcrupy. 8(1). 79-85. Paul. G. L.. & Lentz.. R. j. (19n}. />,,;ydm.wciaJ treahnent ,if chronic mentalpatients.: Milieu versus social learning progm,ns. Cambridge. MA: l-tarvard Unh·ersity Press. Paulose-Ram. R., Safrnn. ~,f. A.. Jona.-.. B. S .. Gu. Q.. & Orwig. D. (2007). Trends in p.sychotropk medication use among U.S. adulls. Pham,acocpidcmiologyand Drug Safety. /(,(5),

560-570. htlps://doi.org/l0.1002/ pds. 1367 Pavlov. I. P. ( J 928). l..cclure.,; rm conditimu:d reflexes: Twe11tyfivc years ofobjcdivc study ,ifthe higher nervous activity (bchm•iour) ofanimal.,;. New York. NY: International Publishers. Paykel. F.. S.. Prus.off. 8. A.. & Myers..j. K. (1975). Suicide attempts and recent life m·enlo;.Archfres ,ifGcuerol PsJ~hiatry. :J2(3). 327-33-3. Pavne.J. L.. Potash.). 8.. & DePnulo. J. R.. Jr. (2005). Recent · finding on the t,-enetic basis or hipolo.r disorder. A.ychiaUic Clinics ,ifNorth America. 28. 481-498. https:/ /

doi .org/ l 0.10J6/j.psc.2005.01.003 Pedersen. M. G.. Mortensen. P.13.. Norgaard-Pedersen. B.. & Postolnclte.1'. 1'. (2012). Toxoplasma gondii infection and self.directed violence in mothers. Archives of Gcm:ml Psychiatry. 69(1 1). 1123--1 130. doi.:-10.1001/ archgenpsychiatry.2012.668 Pederson. C. 8 .. & Mortensen, P. B. (2.001 ). £vidence or a dose-response relationship between urbanidty during upbringing and schizophrenia risk Archives o/Gettcral

PsJ~hit,try. 581_ I I~ 1039- I046.

5 13

Peele. S. (2007}. Addiction as disea.o;e: Policy. e pidemiology. and treabnenl consequences of a had idea. In J. £. Henning.field.

RB. Santora.& \V. K. Bickel. Addiclim1 trcaimcnl: Science and policyfor Jlu: lwenty--fin;t ccnlury(J,p. J 53-J.64). Baltimore. MD:Johns Hopkins Uni\'crsity Pre.ss. Pl!re2.Cruelj. (1976). Conditioning of striatal dopamine metabolism with methadone. morphine or hulbocapnin e as an unconditioned stimuJus.. 1hc Pavlovianjoumal of Biological Science. //(4). 2:37-250. Penone. M. (20 11 . Nmrember 30). lnspector highlights psych drug use among elderly. Yalu,o! News. Retrieved from https://www.yuhoo.com/ news/ inspeclor-highlight.s psych-drug-among-e ldcrly- I90217832.html

Peter.son. ~•l. J.. & Benca. R. M. (2006). Sleep in mood disorder:,;.. Psydiialric Clinics ofNorth America. 21..(4). 1009-1032.

http,// dx.doi .o rg/ I 0.10 I 6/j.psc.2006.09.003 Petry. N. M.• & Roll,J. M. {2006). Cognitive-behavioraJ treatments for pathological gambling. Ln P. M. Gheni. C. A. Lyom. M. R. Dixon. & G. R. \Nilson (£ychology. JJI. 390-395. Rofl?. Y. (2008). Does repres.o;jo n exist? Memory. pathogenic:. unconscious and clinical evidence. Review ofGeneral Ps)~holugy. 12(1 ). 63-85. doi: IO. I 037/ !089-2680.12.1.63

515

Rogeherg. 0 . (2013). Correlutions between cannabis use and JQ change in the Dunedin cohor t are consistent with confounding from .socioeconomic sta.tus. /-'roceed;ngs ofthe l\'aJional Acadcmyo/Scicncc~\ J JO( I l). 4251-4254. doi:IO. 1073/ pnas.12l56781 10 Rogers. C. R.. ( 1961). On l,ca1ming a person. Boston• .MA: Roughton Mifflin.

Rogers. M. p_ Reich. P-St:rom. T. 8_ & Carpenter. C. B. (1976). Behaviorally conditioned immunosuppression: Replication of a recent study. Psydwsamtdk Medic;ne. 38(6). 447-451. Roger.s. S. j.. Vlsmara. L_ Wagner. A. L. McCormick. C., Young, G.. Ou.muff. S. (2014). Autism treatment in the first year ornfo: A pilot study of infant start. a parentimplemented intervention for symptomatic infants. jounu,l ,ifAutism and Dei,c/opmmlal Disorders, 44( 12). 2981-2995. https,/ / doi.orgl I0.1 007/s l OS00-014-2:!m-y Rohan, K.j.. Roecklein. K. A . Lacy. T.j.. & Vacek. R i\•L {2009). Winter depression rt.'Currence one year after cognitivebehaviora l therapy. light therapy. or combination tre-.thnenl behavior 11tcrapy. 40(3). 225-2:.18. doi:10. 1016/ j. belh.2008.06.004 Rollin. H. R. (2000). Psychiatry in 200I>. A bird·s -eye \'lew. Ayr:h;atric.Bulletin. 24{ I). l 1-15. doi: 10. 1192/pb.24. l.11 Rosen. G. ( 1968). 1l·tad11e.,;s in sodeJ_y: Chaplen; in thchi.-.lon·ca.1 sociology ofmental illne.s~·. Chicago. IL: University of Chicago Press. Rosenfeld. D.S .. & Elhajjar. A.J. ( 1998). Sleepsex: A variant of sleepwalking. Archfres o/Se.nwl lkhmdor. 27{3). 2.69-278. Rosenhan. D. L ( 1973). On being sane in insane places. Science. 17!(4070). 250-2::;8. Rosenthal. D.• Wender. P. H.. Kety. S. S.. Schulsinger. f:. WeJne.r.J .. & Rieder. R. 0. (1975). Parent-child relationships nnd psychopathologicnl disorder in the child. Archii-es ofGeneral Psychia1ry. 32(4). 466-476. doi: I 0. 100 I / archpsyc. 1975.0 I 760220078009 Rosenthnl. R.J. ( 199'2}. Pathological gambling. Psychiatric Annal.< 22(2). 72-78. doH0.3928/ 0048-5713-19920WJ-09 Rowhmd. D. L (2007). V/i!J medical solutions lo sexua1 problems make s.exological care and science obsolete? Journal ofSex & Marital 11wmpy. 33(5). 385-397. https:/ / doi.org/ IO. JOS0/009262307014 77022 Rowhmd. D. L &: Burek. M. {2007). Trends in research on premature ejnculatfon over the past 25 years. Journal of Sexual Medicine. 4(5). 1454- 1461. https://doi.org/ 10. 111l / j. I743-6 109.2007.00S52.x Roy-Byrne. P. P.. & Cowley, D.S. (2002). Pha.nnacologica.l treahnents for panic disorder. generalized anxiety disorder, specific: phobia. and social anxiety disorder. In P. £. Nnthan & J. M.. Gorman. A guide to tn:almcnls that work (2nd ed.. pp. 337-365). New York. NY: Oxford University P ress. Roy-Byrne. P. P.. Cm.ske. M. G.• & Stein.1\.1. 8. (2006). Pnnic Disorder. 1hcLancet. 368(9540). 1023-1032. ht:tps://doL orgi I0.10 16/80140.6736(06)69418-X Runyon. R. P-& Haber.A. ( 1971}. Pundamcnlalsofhelwvioral .\tati.-.tics (2nd ed.). Reading. MA: Addj.son-\Ve.sJey. Russell. C.J_ & Keel. P. K. (2002). Homosexuality as a specific risk factor for eating disorders in men. luiernali1111al Journal 44). -437. Sie\rer. LJ .. & Davis. K. L (2004). The pathophysiolobty of schizophrenia di.sorders: Perspecti\'e-s from the .spectrum. 1J1eAmerica11)ournal ofPs)'t:hiatry. /6/(3).398-41:-1. https://doi.org/10.1176/ uppi.ajp. 16 1.3.398

t,,

517

Sien:r. M. D. ( 1994). Sexual orientation and !,1ender as factors in .socioculturally acquired vulnembility to body dissatisfaction and ellting disorders. Journal

FAQs

What are the 4 D's in abnormal psychology? ›

Psychologists often classify behavior as abnormal using 4 D's: deviance, distress, dysfunction, and danger. Providing a straightforward definition of abnormality is tricky because abnormality is relative, but the definition has several primary characteristics.

What are the perspectives of abnormal psychology? ›

Psychologists often look at abnormal behaviors through a number of different perspectives including the psychoanalytic, behavioral, cognitive, and medical approaches. Such perspectives can influence how a condition is treated, but therapists also often draw on techniques from multiple approaches.

What is the Somatogenic perspective of abnormal psychology? ›

The somatogenic perspective of abnormal psychology is the theory that abnormal behavior has a physical cause. Most often, theorists of this perspective believe that some physical disorder of the brain is causing the abnormal behavior, as opposed to a purely psychological cause.

What is abnormal psychology called now? ›

Psychopathology is a similar term to abnormal psychology, but has more of an implication of an underlying pathology (disease process), and as such, is a term more commonly used in the medical specialty known as psychiatry.

What are the 4 definitions of abnormality? ›

WHAT YOU NEED TO KNOW. Definitions of Abnormality: Statistical Infrequency, Deviation from Social Norms, Failure to Function Adequately, Deviation from Ideal Mental Health.

What are the 3 D's of diagnosing mental disorders? ›

Mental disorders are hard to define. Most definitions include the “3 Ds”: Dysfunction, distress (or impairment), and deviance.

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