Abnormal psychology : leading researcher perspectives [3rd edition.] 9781743764763, 1743764766

Table of contents :
contents in brief
contents in full
lecture2
lecture3
lecture4
CH5 somatic and dissociative disorders
Dissociative disorders
CH9 personality disorder

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II Reprinted 2015 (twice) Copyright© 2014 McGraw-Hill Education (Australia) Pty Limited Additional owners of copyright are acknowledged in on-page credits. Every effort has been made to trace and acknowledge copyrighted material. The authors and publishers tender their apologies should any infringement have occurred. Reproduction and communication for educational purposes The Australian Copyright Act 1968 (the Act) allows a maximum of one chapter or 10% of the pages of this work, whichever is the greater, to be reproduced and/or communicated by any educational institution for its educational purposes provided that the institution (or the body that administers it) has sent a Statutory Educational notice to Copyright Agency Limited (CAL) and been granted a licence. For details of statutory educational and other copyright licences contact: Copyright Agency Limited, Level 15, 233 Castlereagh Street, Sydney NSW 2000. Telephone: (02) 9394 7600. Website: www.copyright.com.au Reproduction and communication for other purposes Apart from any fair dealing for the purposes of study, research, criticism or review, as permitted under the Act, no part of this publication may be reproduced, distributed or transmitted in any form or by any means, or stored in a database or retrieval system, without the written permission of McGraw-Hill Education (Australia) Pty Ltd including, but not limited to, any network or other electronic storage.

Enquiries should be made to the publisher via www.mcgraw-hill.com.au or marked for the attention of the permissions editor at the address below. National Library of Australia Cataloguing-in-Publication Data Title: Abnormal psychology : leading researcher perspectives / edited by Elizabeth Rieger. Edition: 3rd edition. 9781743078020(paperback) ISBN: Notes: Includes index. Subjects: Psychology, Pathological. Psychology, Pathological-Case studies. Psychiatry. Clinical psychology. Other Authors/Contributors: Rieger, Elizabeth, editor. Dewey Number: 616.89

Published in Australia by McGraw-Hill Education (Australia) Pty Ltd Level 2, 82 Waterloo Road, North Ryde NSW 2113 Publisher: Robert Ashworth Product developer: Samantha Allemann Senior production editor: Yani Silvana Permissions editor: Haidi Bernhardt Copyeditor: Jess Ni Chuinn Proofreader: Gillian Armitage Indexer: Shelley Barons Design coordinator: Dominic Giustarini Cover design: Ami-Lou Sharpe Internal Design: Lauren Statham, Alice Graphics Typeset in 10/14pt Minion Pro by Laserwords Private Ltd, India Printed in China on 70 gsm matt art by CTPS

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1

Chapter 1

Conceptual issues in abnormal psychology

Chapter 2

Anxiety, obsessive-compulsive and trauma-related disorders

43

Chapter 3

Mood disorders

89

Chapter 4

Psychotic disorders

133

Chapter 5

Somatic and dissociative disorders

173

Chapter 6

Eating disorders

216

Chapter 7

Addictive disorders

263

Chapter 8

Sexual and relationship problems

310

Chapter 9

Personality disorders

351

Chapter 10

Disorders of childhood

401

Chapter 11

Ageing and psychological disorders

447

Chapter 12

Health psychology

492

vi

Contents in full Acknowledgments

xii

Preface

xiii

About the editor

xiv

Contributing authors

xv xx

Text at a glance

xxii

Digital resources

Chapter 1 Conceptual issues in abnormal psychology

1

2

The humanistic perspective

26

3

The sociocultural perspective

29

Abnormality

3

An integrative approach

29

Mental disorder

5

The classification and diagnosis of mental disorders Advantages and disadvantages of diagnosis

7

The development of the DSM system of classification and diagnosis

ABNORMAL PSYCHOLOGY: AN AUSTRALASIAN FOCUS The definitions of abnormal behaviour and mental disorder

Perspectives on the classification, causation and treatment of mental disorders The biological perspective

7

Psychological perspectives

12

Summary

29 31

32 39

The psychoanalytic perspective

13

Key terms

39

The behavioural perspective

19

Review questions

40

The cognitive perspective

22

References

40

The cognitive-behavioural perspective

25

Chapter 2 Anxiety, obsessive-compulsive and trauma-related disorders ANXIETY DISORDERS: AN AUSTRALASIAN FOCUS

44

The nature of fear and anxiety disorders Specific phobias The diagnosis of specific phobias The epidemiology of specific phobias

CASE STUDY: SPECIFIC PHOBIA The aetiology of specific phobias The treatment of specific phobias Panic disorder and agoraphobia

43

CASE STUDY: PANIC DISORDER AND AGORAPHOBIA

53

45

The aetiology of panic disorder and agoraphobia

54

49

The treatment of panic disorder and agoraphobia

55

49 49 50

Social anxiety disorder The diagnosis of social anxiety disorder The epidemiology of social anxiety disorder

57 57 57

CASE STUDY: SOCIAL ANXIETY DISORDER

57

51

The aetiology of social anxiety disorder

52

The treatment of social anxiety disorder

58 59

50

The diagnosis of panic disorder and agoraphobia

52

The epidemiology of panic disorder and agoraphobia

53

Generalised anxiety disorder (GAD) The diagnosis of generalised anxiety disorder

60 60

Contents in full

61

CASE STUDY: GENERALISED ANXIETY DISORDER The epidemiology of generalised anxiety disoocfer ~

The aetiology of generalised anxiety disorder The treatment of generalised anxiety disorder

62 62 65

vii

The aetiology of posttraumatic stress disorder

74 74 74 76

Posttraumatic stress disorder (PTSD) The diagnosis of posttraumatic stress disorder The epidemiology of posttraumatic stress disorder The treatment of posttraumatic stress disorder

77

The diagnosis of obsessive-compulsive disorder

67 67

CASE STUDY: P0STTRAUMATIC STRESS DISORDER

79

CASE STUDY: OBSESSIVE-COMPULSIVE DISORDER

70

Summary

71 71 72

Key terms Review questions

80 83 83

References

84

Obsessive-compulsive disorder (OCD)

The epidemiology of obsessive-compulsive disorder The aetiology of obsessive-compulsive disorder The treatment of obsessive-compulsive disorder

89

Chapter3 Mood disorders MOOD DISORDERS: AN AUSTRALASIAN FOCUS Unipolar depression Historical and current approaches to the classification of unipolar depression The epidemiology of unipolar depression Problems associated with unipolar depression The aetiology of unipolar depression The treatment of unipolar depression CASE STUDY: THE SYMPTOMS OF MAJOR DEPRESSIVE DISORDER Bipolar disorder The history of bipolar disorder

90

The diagnosis of bipolar disorders

91

The epidemiology of bipolar disorder Problems associated with bipolar disorder

91 94 96 97 103 107

108 108

Bipolar disorder and creativity The aetiology of bipolar disorder The treatment of bipolar disorder CASE STUDY: TREATMENT Of BJ POLAR DISORDER

124

Summary

125

Key terms Review questions

126 126

References

127

133

Chapter 4 Psychotic disorders PSYCHOTIC DISORDERS: AN AUSTRALASIAN FOCUS The definition and symptoms of psychosis Hallucinations Delusions

I

Disorganised thinking Grossly disorganised behaviour Negative symptoms The diagnosis of psychotic disorders: core and associated features Core features Associated features Historical and current conceptualisations of psychotic disorders Historical developments Ongoing controversies The epidemiology of psychotic disorders Prevalence and age of onset The course of psychotic disorders The aetiology of psychosis Vulnerability factors: biological

109 112 112 115 116 119

Symptom-specific aetiological factors: delusions

153 156 156 157

Symptom-specific aetiological factors: thought disorder

157

134

Vulnerability factors: psychosocial

135 135 136 138 139 139

Triggering factors Symptom-specific aetiological factors: hallucinations

The treatment of psychotic disorders Prodromal phase interventions

140 140 142

Acute phase interventions Interventions to prevent relapse Interventions for enduring psychosis The consumer recovery model

146 146 146

Limitations of current treatment approaches CASE STUD\'; FROM PRODR0MAL PHASE TO EARL¥ RECOVERY

147 147 147

Summary

151 151

References

Key terms Review questions

158 158 160 162 163 164 164 165

167 168 168 169

viii

Contents in full

173

Chapter 5 Somatic and dissociative di~orders SOMATIC AND DISSOCIATIVE DISORDERS: AN AUSTRALASIAN FOCUS

Dissociative disorders 174

The definition of somatic disorders, dissociative disorders and related terms

175

Historical approaches to somatic and dissociative . disorders

176

Somatic symptom and related disorders The diagnosis of somatic symptom and related disorders

178 178

The diagnosis of dissociative disorders

195 196

The epidemiology of dissociative disorders

198

The aetiology of dissociative disorders

200

The treatment of dissociative disorders

203

CASE STUDY:THE RECOVERED MEMORY/FALSE MEMORY DEBATE

204

CASE STUDY: DISSOCIATIVE IDENTITY DISORDER

208

182

Summary

209

The aetiology of somatic symptom and related disorders

184

Key terms

209

The treatment of somatic symptom and related disorders

189

Review questions

210

193

References

210

The epidemiology of somatic symptom and related disorders

CASE STUDY: SOMATIC SYMPTOM DISORDER

216

Chapter 6 Eating disorders EATING DISORDERS: AN AUSTRALASIAN FOCUS

217

Historical and current approaches to the diagnosis of eating disorders

218

The epidemiology of binge eating disorder

245

Anorexia nervosa

218

The aetiology of binge eating disorder

246

Bulimia nervosa

219

The treatment of binge eating disorder

248

Binge eating disorder

220

Other OSM-5 feeding or eating disorders

221

Anorexia nervosa The epidemiology of anorexia nervosa The aetiology of anorexia nervosa The treatment of anorexia nervosa CASE STUDY: ANOREXIA NERVOSA Bulimia nervosa

222 222 224 230 235 237

The epidemiology of bulimia nervosa

237

The aetiology of bulimia nervosa

238

The treatment of bulimia nervosa

240

CASE STUDY: BULIMIA NERVOSA

244

Binge eating disorder

245

CASE STUDY: BINGE EATING DISORDER

251

General topics in eating disorders

252

Current challenges and controversies

252

Eating disorder organisations

256

Summary

257

Key terms

258

Review questions

258

References

258

Chapter 7 Addictive disorders ADDICTIVE BEHAVIOURS: AN AUSTRALASIAN FOCUS Substance use disorders The diagnosis of substance use disorders CASE STUDY: SEVERE ALCOHOL USE DISORDER CASE STUDY: CANNABIS WITHDRAWAL The epidemiology of substance use disorders CASE STUDY: STIMULANT-INDUCED PSYCHOTIC DISORDER

263 264

Gambling disorder

284

265

Types of gamblers

286

265

Historical approaches to gambling and problem gambling

286

The diagnosis of gambling disorder

287

The epidemiology of problem gambling

290

The aetiology of gambling disorder

292

266 268 269 271

The aetiology of substance use disorders

274

The treatment of substance use disorders

280

CASE STUDY: A BEHAVIOURALLY CONDITIONED PROBLEM GAMBLER The treatment of gambling disorder

298 299

CASE STUDY: COGNITIVE THERAPY FOR A PROBLEM GAMBLER 302

Contents in full

ix

Summary

304

Review questions

305

Key terms

304

References

305

Chapter 8 Sexual and relationship problems SEXUAL AND RELATIONSHIP PROBLEMS: AN, AUSTRALASIAN FOCUS

Sexual problems: sexual dysfunctions The definition of sexual dysfunction The conceptualisation of sexual dysfunctions The aetiology of sexual dysfunction The treatment of sexual dysfunction

The aetiology of paraphilic disorders 311

312 312 315 316 319

CASE STUDY: A MALE WITH ERECTILE DISORDER

325

Sexual problems: the paraphilic disorders Historical and current approaches to understanding paraphilias

326

The diagnosis of paraphilic disorders

310

326 327

330 330

The treatment of paraphilic disorders Relationship problems Historical and current approaches to understanding relationship problems The aetiology of relationship problems A developmental perspective on relationship problems The treatment of relationship problems

344

Key terms

344

Review questions

345

References

345

The definition of personality and personality disorder Personality

354 354 354

Personality disorder CASE STUDY: PERSONALITY DISORDER

355

The diagnosis of personality disorder The Cluster A personality disorders

355 357

CASE STUDY: SCHIZOTYPAL PERSONALITY DISORDER

357

The Cluster B personality disorders CASE STUDY: ANTJSOCIAL PERSONALITY DISORDER

Understanding psychopathy The Cluster C personality disorders CASE STUDY: OBSESSIVE-COMPULSIVE PERSONALITY DISORDER

The epidemiology of personality disorders General models of the aetiology and treatment of personality disorders CASE STUDY: COGNITIVE ANALYTIC THERAPY

351

, 352

331 332 340 340

Summary

Chapter 9 Personality disorders PERSONALITY DISORDERS: AN AUSTRALASIAN FOCUS

331

I

.

The aetiology and treatment of sp~cific personality ~ .) disorders . Aetiology of the Cluster A perso ~c;il.i~y cJ ismders: schizoid, schizotypal and paranoi~ ersonality dis , rders Treatment of the Cluster A pe son-a l~ty disorders: schizoid, schizotypal and paranoid personality disorders Current challenges and controversies Are personality disorders better represented by dimensions or categories?

373 373 374 386 386

What is the role of culture in the development of personality disorders?

390

360 360

Are there real gender differences in the prevalence of certain personality disorders or do such differences represent diagnostic biases?

392

361

Can the impact of personality disorders be reduced through prevention and early intervention programs?

393

358 359

362

Summary

394

Key terms

395

363

Review questions

395

371

References

396

401

Chapter 10 Disorders of childhood DISORDERS OF CHILDHOOD: AN AUSTRALASIAN FOCUS

402

Psychological and behavioural disorders in children Myths, realities and research challenges

403 403

Historical and current approaches to the understandi ng and classification of childhood disorders

405

Neurodevelopmental disorders

408

X

Contents in full

The diagnosis and epidemiology of attention-deficit/ hyperactivity disorder

,

408

The aetiology of separation anxiety disorder

431

The treatment of separation anxiety disorder

432

The aetiology of attention-deficit/ hyperactivity disorder

409

The diagnosis and epidemiology of selective mutism

433

Specific learning disorder

411

The aetiology of selective mutism

434

Autism spectrum disorder

413

The treatment of selective mutism

434

Intellectual disability

415

Externalising disorders The diagnosis and epidemiology of oppositiona l' defiant disorder

418

Elimination disorders The diagnosis and epidemiology of enuresis

435 435

The aetiology of enuresis

435

418

The treatment of enuresis

436

The aetiology of oppositional defiant disorder

419

The diagnosis and epidemiology of encopresis

437

The diagnosis and epidemiology of conduct disorder

421

The aetiology of encopresis

437

The aetiology of conduct disorder

421

The treatment of encopresis

437

The treatment and prevention of externalising disorders

423

CASE STUDY: PARENT MANAGEMENT TRAINING FOR OPPOSITIONAL DEFIANT DISORDER Internalising disorders The diagnosis and epidemiology of separation anxiety disorder

428 430

Summary

438

Key terms

439

Review questions

439

References

440

431

Chapter 11 Ageing and psychological disorders AGEING AND PSYCHOLOGICAL DISORDERS: AN AUSTRALASIAN FOCUS 448 Ageing The demographics and epidemiology of ageing

449 449

Historical overview of the psychology of ageing

452

Normal ageing processes: cognitive, emotional and social functioning

454

Psychological disorders in later life: the dementias The definition of dementia and recent DSM-5 changes

461 461

Alzheimer's disease

462

Vascular dementia

464

Other forms of dementia and related disorders

465

The assessment, treatment and prevention of dementia

466

Psych o logical disorders in later life: depression and anxiety Depression Anxiety disorders

471 471

447 Life events associated with later life: retirement, grandparenting, driving cessation and bereavement Retirement CASE STUDY: DEPRESSION

476 476 478

Grandparenting

479

Driving cessation

480

Bereavement

481

Positive or successful ageing

482

Ageing organisations and resources in Australia ' and New Zea.land

483

Summary

484

Key terms

484

Review questions

484

References

485

473

Chapter 12 Health psychology

492

HEALTH PSYCHOLOGY: AN AUSTRALASIAN FOCUS

493

The definition of health and health behaviour

494

Models of health behaviour The health belief model

496 496

Protection motivation theory

499

The theory of reasoned action and the theory of planned behaviour

500

Interventions based on health behaviour models The relationship between stress and disease Definitions of stress Evidence of the impact of stress on health Communicating with patients about health, risk, disease and treatment Shared decision making and patient-centred care

506 509 509 512 515 516

The stages of change model

501

Risk communication

518

Self regulation theory

504

Interventions to increase the accuracy of risk perception

519

Contents in full

xi

Quality of life and adjustment to chronic disease "'' Coping with and adjustment to disease Interventions to promote adjustment to illness'E>'

521 522 523

Summary Key terms

528

Review questions

529

CASE STUDY: A WOMAN WITH CANCER

526

References

529

Glossary Index

528

534 543

t

r !

xii

Acknowledgments Teamwork has been an essential part of the creation of this important book. We are very proud to acknowledge the contributions made by the esteemed author team; without their experience and passion this text would not have been possible. Peter McEvoy wishes to acknowledge Professor Andrew Page for his contribution to Chapter 2 of the first and second edition. Thank you also to John McDowall for his work on the accompanying digital resources (Power Point® slides and testbank).

REVIEWERS We owe special thanks to the distinguished colleagues and peers who provided research and review feedback for the third edition of this book. Many of the improvements in the book are due to their feedback. We sincerely appreciate the time and effort contributed by the following academics: • Gavin Beccaria, University of Southern Queensland • Mark Boschen, Griffith University • Pia Broderick, Murdoch University • Marie Caltabiano, James Cook University • James Donnelly, Southern Cross University • Jessica Grisham, University of New South Wales • Tanya Hanstock, University of New England • Simon Knowles, Swinburne University • Jennifer Loh, Edith Cowan University • · John McDowall, Victoria University of Wellington

• • • • • • • • • •

Jim Malcolm, University of Western Sydney Kimberley Norris, University of Tasmania Jay Richards, University of Newcastle Julia Rucklidge, University of Canterbury Rachael Sharman, University of the Sunshine Coast Rebecca Sng, University of Wollongong Mark Symmons, Monash University Joanne Taylor, Massey University Lucia Vardanega, University of Western Sydney Tom Whelan, Australian Catholic University.

PUBLISHERS Our thanks and acknowledgement go to the McGraw-Hill Education Australia team. The publication of a work of this scope and innovation would not have been possible without them. We appreciate the work of our publisher Robert Ashworth, for his vision and faith in this project, and our product developer Samantha Allemann, for her organisational skills and enthusiasm for the project. Our thanks to senior production editor Yani Silvana for her methodical project management during production; Dominic Giustarini, our design coordinator; the digital team Marisa Rey Bulen and Belinda Lum; our copyeditor, Jess Ni Chuinn, and marketing manager, Sarah Long.

xiii

_,,.

The field of abnormal psychology is well served by several competent textbooks-so much so that in my first years of teaching in the area I was not immediately aware of the need for an innovative approach. Indeed, this impetus was initially provided through feedback from my students, who expressed their frustration with the lack of local content in the available texts, most of which were American, so that the content tended to distance them from, rather than more fully engage them with, the material. Having thus been encouraged to take a closer look at the range of available texts, I became aware of the additional need to have specialists presenting the current body of knowledge in their respective areas of expertise if students were to be provided with material that accurately reflects contemporary theorising and research. Both of these innovative aspects of the book- that is, the local content and reliance on specialist authorsrequire some elaboration. The local content is most obviously reflected in the selection of authors from Australia and New Zealand; the inclusion of research from this region when such studies constitute the best exemplars in the field; the presentation of topics of regional relevance (such as a relatively extensive section on pathological gambling given the prevalence of gambling and problem gambling in Australia and New Zealand); and the application of concepts using regional examples, most notably in the 'Australasian Focus' pieces that introduce each chapter. While these sections refer predominantly to Australian people and governmental policies, this material was selected so as to be highly recognisable and pertinent in the New Zealand context as well. Clearly abnormal psychology is an international discipline, the knowledge base of which is informed by theoretical and empirical work worldwide. Yet, by presenting this information in a manner that is also sensitive to the reader's cultural context, this text aims to generate maximum relevance and hence interest and engagement on the part of the reader. Indeed, approximately 80 per cent of students in an undergraduate abnormal psychology course that I taught stated that they appreciated the inclusion oflocal content in the first edition of this book. We have therefore sought to expand this aspect of the book in this third edition by including new Australasian Focus pieces at the beginning of each chapter. Aside from its Australian and New Zealand content, this book is noteworthy for the high calibre of its authors. The c~hapters have been written by eminent researchers and practitioners who continue to make a significant contribution to understanding the disorders in which they have expertise. As such, they are ideally placed to impart to the reader highly contemporary perspectives on the various disorders. While it is common practice for undergraduate students to be availed only of textbooks written by generalists, the use of specialist authors is intended to present readers with the most current scholarship from the time of their earliest engagement with the subject matter of abnormal psychology. Given our commitment to currency, we have introduced this third edition of the book only three years after the previous edition so that readers can be acquainted with the most recent research across the various domains of abnormal psychology, while also anticipating future challenges and innovations. Thus, while the book received its initial inspiration from students, its state-of-the-art approach aims, in turn, to inspire the next generation ofleading researchers and clinicians by informing them of the limits of what is currently known and what remains to be understood in the field of abnormal psychology.

Elizabeth Rieger

xiv

is an Associate Professor and clinical psychologist in the Research School of Psychology at the Australian National University where she conducts research, teaching and clinical work. In her research she specialises in eating disorders and obesity, having completed her PhD on anorexia nervosa at The University of Sydney and a postdoctoral fellowship at the Centre for Eating and Weight Disorders of the University of California, San Diego and San Diego State University. She has published widely on both eating disorders and obesity, including the motivational, cognitive and interpersonal aspects of these conditions and their effective treatments. She has taught undergraduate courses on abnormal psychology and health psychology, and postgraduate courses on eating and weight disorders, motivational interviewing, cognitive behaviour therapy and interpersonal psychotherapy. She has 20 years' experience as a clinical psychologist during which time she has worked in a diverse range of public and private settings. She is a member of the Eating Disorders Research Society, the Australian and New Zealand Academy of Eating Disorders, the College of Clinical Psychologists of the Australian Psychological Society, the Australian Clinical Psychology Association and an Editorial Board member of the Journal of Eating Disorders.

I

xv

Contributing authors Maree Abbott is a Senior Lecturer and the Postgraduate Co-ordinator for the Doctorate of Clinical Psychology/ Master of Science degree in the School of Psychology at The University of Sydney and a practising clinical psychologist. Maree teaches on the Doctorate of Clinical Psychology program in the areas of psychopathology and the assessment and treatment of adult psychological disorders, in addition to conducting clinical and research supervision. Prior to this appointment, Maree was based at Macquarie University as the Royce Abbey Postdoctoral Fellow. Her research focuses on further understanding the nature and treatment of child and adult anxiety disorders, particularly social phobia and generalised anxiety disorder. She is a registered clinical psychologist and has served on the Executiv~ of the Australian Psychological Society College of Clinical Psychologists in New South Wales and currently chairs the Membership Committee for the Australian Clinical Psychology Association. Jillian Ball was a senior clinical psychologist at the Prince Henry and Prince of Wales Hospitals for 25 years. She also held the position of conjoint lecturer at the University of NSW during this time, a position she has held since 1986. Her major research interests include the evaluation of clinical programs for depression, bipolar disorder and eating disorders. She is particularly i~terested in studying the mechanisms of change in cognitive therapy and schema therapy, and how experiential techniques can be used to facilitate change. Jillian has published widely in international journals and co-authored three popular self help books including the bestseller Beating the Blues. She also runs an extensive private practice in Sydney. Alex Blaszczynski is a Professor of Clinical Psychology and Director of the Gambling Treatment & Research Clinic at the School of Psychology, University of Sydney. He is a clinical psychologist with extensive experience in treating individuals with pathological gambling and other impulse control disorders. His

research interests are directed toward the development of a conceptual Pathway Model of Problem Gambling, the role of the personality trait of impulsivity, treatment outcomes and their predictors, and the effectiveness of warning signs on electronic gaming machines as harm minimisation strategies. Alexander has investigated the association between pathological gambling and crime, and with co-authors has developed a model for casino self-exclusion. Richard Bryant is a Scientia Professor of Psychology, ARC Laureate Fellow, and Director of the Traumatic Stress Clinic at the University of New South Wales. His research has included conducting prospective studies of posttraumatic stress responses, developing the first assessment measures of acute stress disorder, implementing controlled treatment trials of acute stress disorder and investigating the biological and cognitive factors that influence psychological adaptation after trauma. He has published more than 380 peer-reviewed journal articles and co-authored the leading text on acute stress disorder. His assessment and treaFIT}ent protocols are currently being employed by many civilian and military agencies around the world, including those coordinating mental health projects in the wake of terrorist and natural disaster events. Richard is a Fellow of the Australian Psychological Society and the Australian Academy of Social Sciences in Australia. Phyllis Butow is a Professor, and National Health and Medical Research Council Senior Principal Research Fellow, in the School of Psychology, University of Sydney. She co-directs the Centre for Medical Psychology and Evidence-based Medicine (CeMPED), a very active research group, and chairs the Australian Psycho-Oncology Co-operative Research Group (PoCoG). Phyllis has worked for over 20 years in the area of Psycho-Oncology and has developed an international reputation in this and the area of health communication. She and her team run a Master of Health Psychology at The University of Sydney. Phyllis

xvi

Contributing authors

,

has published more than 350 articles in peer-reviewed journals and her work has been translated into health communication modules for oncology professionals' guidelines and practice. David Clarke is Professor of Psychological Medicine at Monash University. He works at the interface between psychiatry and physical medicine, as a consultationliaison psychiatrist at Monash Medical Centre. He is Clinical Director of Consultation-Liaison and Primary Care Psychiatry at Monash Health in Melbourne and teaches psychiatry at undergraduate and postgraduate levels, with his main interests being depression and somatisation. He has been the recipient of a number of research grants from the NHMRC, with research focusing on the nature of distress and depression in the medically ill, demoralisation as a concept and a particular form of depression, the use of psychotherapy in the medically ill, and the nature of psychiatric presentations and pathways to care for people in the general medical and primary care settings. He has published more than 100 articles in scientific journals and presents his work regularly at conferences. David Gleaves is Professor of Psychology (Clinical) at the University of South Australia in Adelaide. He has worked in the areas of dissociative and eating disorders for approximately 25 years and has produced over 115 scholarly publications in these and related areas. He previously received both the Morton Prince Award for Scientific Achievement and the Pierre Janet Award for Writing Excellence from the International Society for the Study of Trauma & Dissociation. He is or has been a member of the editorial board of several journals including Journal of Abnormal Psychology, Journal of Clinical Psychology, Journal of Child Sexual Abuse, and Journal of Trauma & • Dissociation. He is also a registered clinical psychologist and a full member of both the Australian Psychological Society (and the APS College of Clinical Psychologists) and the American Psychological Association. John Gleeson is a Professor of Psychology at the Australian Catholic University. Previously he was an Associate Professor who held a joint appointment between the North Western Mental Health Program, a program of Melbourne Health, and the Psychology Department ofthe University of Melbourne. His research interests include cognitive behaviour therapy (CBT) for first-episode psychosis and psychological treatments for the complex behavioural problems associated with psychosis. He has taught psychological assessment

and CBT within the postgraduate clinical psychology professional training program at the University of Melbourne. He edited the first treatment handbook of psychological interventions for early psychosis, which includes contributions from Europe, North America, Australia and Scandinavia. He has more than 10 years' experience in providing clinical supervision to clinical psychologists and has provided training workshops nationally and internationally on CBT for psychosis. Together with colleagues from Orygen Youth Health Research Centre and the University of Melbourne he has recently pioneered moderated online social therapy for first-episode psychosis-therapeutic online social networking fully integrated with online expert and peer moderation with online interactive therapy in a single application. Phillipa Hay is a Professor and Foundation Chair of Mental Health at the School of Medicine, University of Western Sydney and Adjunct Professor of Psychiatry at James Cook University. She has been researching and working in the area of eating disorders for two decades since completing her postgraduate training in psychiatry and has two higher research degrees in the area. She completed her DPhil under the supervision of Professor Christopher Fairburn at the University of Oxford. She has written more than 150 research articles, book chapters and other publications on eating disorders and related topics, and has been invited to present her research at meetings in the United States, Europe and South America. She ·i~ co-Editor-in-Chief of the Journal of Eating Disorders, a past President of the Australian and New Zealand Academy for Eating Disorders and serves at a senior level on education and scientific committees of the Royal Australian and New Zealand College of Psychiatrists, the Australian Medical Council and the international Academy for Eating Disorders. Carol Hulbert is an Associate Professor in the School of Psychological Sciences at the University of Melbourne and also holds the position of Director of the Clinical Psychology Program. She is a clinical psychologist and clinical researcher with extensive experience in mental health services. She has worked as a clinician, manager and regional senior psychologist in public mental health. Her program development experience includes involvement in the setting up of the Early Psychosis Prevention and Intervention Centre (EPPIC) and the establishment of the Spectrum Personality Disorder

Contributing authors

Service of Victoria. Her research interests include social cognition and social functioning in bottlerline personality disorder, the aetiology and psych~logical treatment of personality disorder, and the role of trauma in outcomes for early psychosis. Martina Jovev is currently a psychologist at Orygen Youth Health Clinical Program and a Res€arch Fellow at Orygen Research Centre in Melbourne. Since completing her PhD, she has been an investigator on projects in the emerging borderline personality disorder (BPD) in young people and has collaborated with leading researchers in the field of neuroimaging and youth mental health at the Melbourne Neuropsychiatry Centre (MNC) and Orygen Research Centre (ORC) to conduct pioneering work on the relationship between brain development and environment in risk for personality dysfunction in adolescence. Dr Jovev's previous research has examined processing of psychosocial threat in young people with BPD symptoms. She is also a co-investigator on several large clinical projects in the field of BPD in young people, including a randomised controlled trial of cognitive analytic therapy in emerging BPD, screening for BPD in youth, emerging BPD and psychosis, sexual and reproductive health in youth with BPD. She has published multiple articles in the area of cognitive biases in BPD and is a co-author on several papers published in prestigious international peer-reviewed journals, such as Psychiatry Research: Neuroimaging and Journal of Clinical Psychiatry. Dr Jovev has presented her work at numerous major national and international conferences, including the International Society for the Study of Personality Disorders Congress. Marita McCabe is a Professor of Psychology at Deakin University, Mel~ourne. She has conducted research on a broad range of topics in the area of human sexuality for the past 30 years. In particular, she has studied the aetiology and treatment of sexual dysfunction. This research has involved the evaluation of cognitive behaviour therapy programs for male and female sexual dysfunction, which in recent years have been successfully converted to be delivered via the internet. Marita is on the editorial board of a number of journals and has supervised many doctoral students who have completed their theses in the area of human sexuality. Louise McCutcheon is a senior clinical psychologist and joint founder of the Helping Young People Early (HYPE) program, an early intervention program for

borderline personality disorder in youth at Orygen Youth Health (OYH) in Melbourne. She coordinated the clinical program for 11 years and has been an investigator on various research projects including two randomised controlled trials of interventions in the clinic. Her current role in the program includes clinical, research and training functions; and she coordinates service development programs for mental health clinicians working with personality disorders and other complex problems, and in cognitive analytic therapy. Peter McEvoy is an Associate Professor of Clinical Psychology in the School of Psychology and Speech Pathology at Curtin University, and a Senior Clinical Psychologist at the Centre for Clinical Interventions, Perth. Peter previously worked at the Anxiety Disorders Clinic at St Vincent's Hospital in Sydney. He has extensive clinical experience providing evidence-supported group and individual treatments for emotional disorders. His research interests are broad and include treatment outcome evaluations, transdiagnostic approaches to conceptualising and treating emotional disorders, the use of imagery in psychotherapy, repetitive negative thinking, mechanisms of behavioural and cognitive change, and the epidemiology of mental disorders. Peter is on the editorial board of the Journal of Anxiety Disorders, regularly provides training and supervision to health professionals, and lectures in the Masters of Clinical Psychology program at Curtin University. Catharine McNab is a Senior Clinical Psycho!ogist in the Orygen Youth Health Clinical Program in Melbourne. Her clinical experience has focused on mental illness in adolescents and young adults, most recently in indicated prevention and early intervention for borderline personality disorder in young people. She consults with and provides training to medical and allied health staff about effective collaboration with young people with these difficulties, particularly in acute service settings. Her research interests include examining the experiences of families of people with early-onset mental illness and identifying what the consequences of appropriately supporting families might be, both for families and patients. Vijaya Manicavasagar is a senior clinical psychologist and Associate Professor within the Black Dog Institute, School of Psychiatry at the University of New South Wales. As the Director of Psychological Services she is responsible for overseeing activities that involve

xvii

xviii

Contributing authors

psychological expertise including professional education programs for psychgfugists, allied health professionals and youth wi rkers, supervising clinical and research initiatives as well as leading the development of a range of online programs including the youth positive psychology website called Bite Back. In addition, she is the Clinical Director for the Psychology Clinic at the Biack Dog Institute and is involved in a number of research projects focusing on mood disorders and resilience-building interventions including the Headstrong national program for schools. Ross Menzies is Associate Professor of Psychology in the discipline of Behavioural and Community Health Sciences at The University of Sydney. In 1991 he was appointed founding Director of the Anxiety Disorders Clinic, Faculty of Health Sciences, University of Sydney, a post he continues to hold. He is the past NSW and National President of the Australian Association for Cognitive and Behaviour Therapy (AACBT). He is the President and Chair of 2016 World Congress of Behavioural and Cognitive Therapies (WCBCT) and is Editor of Australia's national CBT scientific journal, Behaviour Change. Ross holds numerous national competitive grants in the area of anxiety. He has produced more than 150 international journal papers, books and book chapters and is regularly invited to speak at conferences and leading universities and institutions around the world. Philip Mitchell is Scientia Professor, Head of the School of Psychiatry at the University of New South Wales. His research and clinical interests are in bipolar disorder and depression, with particular focus on youth at high genetic risk of bipolar disorder, the molecular genetics of bipolar disorder, transcranial magnetic stimulation (TMS) for depression, and the pharmacological and psychological treatment of bipolar disorder and depression. Philip has published (in conjunction with colleagues) more than 400 papers and chapters on these topics. In 2002 he was awarded the Senior Research Award of the Royal Australian and New Zealand College of Psychiatrists. In 2004 he received the Founders Medal of the Australasian Society for Psychiatry Research. In the 2010 Australia Day honours list Professor Mitchell was appointed a Member of the Order of Australia. He is a Visiting Professor at Harbin Medical University in China and Guest Professor at Shanghai Jiao Tong University in China. He is also Chairman of the Australasian Society for Bipolar and Depressive Disorders.

Alina Morawska completed her PhD in Clinical Psychology at the University of Queensland in 2004, for which she received the Australian Psychological Society's Excellent PhD Thesis in Psychology Award. Alina is the Deputy Director (Research) at the Parenting and Family Support Centre, University of Queensland. Her research interests are in the area of prevention and early intervention of child behavioural and emotional problems, particularly for chronic childhood conditions and she has published more than 45 articles and book chapters. She is a Director of the Australian Association for Cognitive and Behaviour Therapy Ltd. Alina is also a Training Consultant for Triple P International, conducting training for allied health professionals in the delivery of Triple P-Positive Parenting Program. Richard O'Kearney is Associate Professor in the Department of Psychology at the Australian National University. His research includes evaluation of interventions and prevention programs for depression in the community and schools, as well as work on the development of emotional regulation abilities in children and adolescents. He has published applied and basic research in OCD and PTSD. As a member of the Cochrane Collaboration, Richard has been actively involved in the dissemination of the evidence base for interventions in mental health and has authored and co-authored several systematic reviews. He also practises as a clinical psychologist in Canberra. Nancy Pachana is Professor in the School of Psychology at the University of Queensland. A di.nical psychologist and clinical neuropsychologist, she received extensive postdoctoral training in the assessment and treatment of older populations at the UCLA-Neuropsychiatric Institute and the Palo Alto VA in California. She is a fellow of the Australian Psychological Society and the immediate past chair of the Society's national Psychology and Ageing Interest Group. She is ctiso on the Board of Directors of the International Psychogeriatric Association, and is a faculty affiliate of the Royal Australian and New Zealand College of Psychiatrists in the Faculty of Psychiatry of Old Age. She has published more than 170 peer-reviewed articles and book chapters in the field of ageing. Her main research interests include assessment and treatment of late-life anxiety disorders, driving and driving cessation in later life, and novel assessment and interventions for nursing home residents. Matthew Sanders is a Professor of Clinical Psychology and Director of the Parenting and Family Support Centre

Contributing authors

at the University of Queensland. He is also a consulting Professor at The University of Manchester, a, 'visiting Professor at the University of South Carolina and holds adjunct Professorships at Glasgow Caledonian University and The University of Auckland. As the founder of the Triple P-Positive Parenting Program, Professor Sanders is considered a world leader in the development, implementation, evaluation and disse~ination of population based approaches to parenting and family interventions. Triple P is currently in use in many countries worldwide. Professor Sanders' work has been widely recognised by his peers as reflected by a number of prestigious awards. In 2007, he received the Australian Psychological Society's President's Award for Distinguished Contribution to Psychology and in 2004 he received an International Collaborative Prevention Science award from the Society for Prevention Research · in the United States. In 2007 he received a Trailblazers Award from the Parenting and Families Special ·· Interest Group in the Association for Behavioural and Cognitive Therapy and in 2008 became a fellow of the New Zealand Psychological Society. Professor Sanders has also won a Distinguished Career Award from the Australian Association for Cognitive Behaviour Therapy, was named Honorary President of the Canadian Psychological Association (2009) and Queenslander of the Year (2007). In 2013, Professor Sanders was named one of the University of Queensland's top five innovators for his work with Triple P. Marianna Szabo is a Senior Lecturer in Psychology at the School of Psychology, University of Sydney. She coordinates the Abnormal Psychology course in the school and lectures on conceptual issues in classification and diagnosis, as well as on the nature and causation of anxiety and ~epression in adults and youth. She also contributes to teaching abnormal psychology at different levels of training, from the first year Introductory Psychology course to postgraduate training. Her research interests include examining basic diagnostic and conceptual issues in abnormal psychology, as well

as further understanding the nature of child and adult anxiety and mood disorders, particularly generalised anxiety disorder and depression. She is a registered clinical psychologist in private practice and member of the Australian Psychological Society College of Clinical Psychologists. Robert Tait is a senior research fellow at the National Drug Research Institute, Faculty of Health Sciences, Curtin University. His research interests are around alcohol, tobacco and other drug use and in particular how these relate to mental health disorders. He has used administrative health data to assess the long-term relationships between substance use, mental health and self-harm behaviours. He is also interested in the development of new interventions and continues to work with former colleagues at The Australian National University, Centre for Mental Health Research on internet delivered programs. His work has included those in the general population, high-risk groups and clinical samples. Stephen Touyz is Professor of Clinical Psychology and Clinical Professor in Psychiatry at The University of Sydney. He is also the executive Chair of the Centre for Eating and Dieting Disorders. He has written or edited six books and more than 270 research articles and book chapters on eating disorders and related topics. He is a Fellow of the Academy of Eating Disorders and the Australian Psychological Society and is a past President of the Eating Disorders Research Society. Stephen was the inaugural treasurer of the Australian and ' New Zealand Academy of Eating Disorders and a past executive member of the Eating Disorders Foundation. He is the Co-founding Editor of the Journal of Eating Disorders and a member of the Editorial Advisory Boards of the International Journal of Eating Disorders, European Eating Disorders Review and Advances in Eating Disorders: Theory, Research and Practice. In 2012 he was presented with a Leadership in Research award by the prestigious Academy of Eating Disorders (International).

xix

I I I I I I

EATING DISORDERS: AN AUSTRALASIAN FOCUS

DEVELOPED FOR LOCAL STUDENTS BY LOCAL AUTHORS

In

2012,

the

Butterfiy

Foundation

commissioned a report by Deloitte Access

Abnormal Psychology 3e has been developed by expert authors to help students studying in Australia and New Zealand engage with and apply the concepts and theories of abnormal psychology. Research by Australian and New Zealand academics and researchers, local statistics, case studies and examples are used throughout the book.

(2013)

Economics

on

the

economic and social costs of eating disorders in Australia. Entitled 'Paying the Price: the findings of the report are a deeply concerning portrayal of the significant burden imposed by eati ng disorders on affected individuals and their carers, and the inadequacy of current treatment services to address these problems. The report documents

TBC

that more than 913 000 people in Australia met the diagnostic criteria for an eating disorder in 2012 (estimated to rise to more than one million by 2022), the annual socioeconomic cost of which was $69.7 billion. Of the financial costs, productivity costs ranked highest, wh ich included an annual cost of $15.1 billion resulting from factors such as lower employment participation and greater absenteeism from work among those w ith an eating disorder and the loss of lifetime earnings from the significant number of young people w ho die as a result of their eating disorder. These productivity costs are comparable to those stemming from anxiety disorders and depression in Australia. Since this loss in productivity results in lost taxation revenue for the federal government, the report argues that increasing government financial support to enable people to access appropriate eating disorder treatment services (which would in turn assist these individuals to become more productive) would likely have little impact on the Commonwealth budget. At present, 60 per cent of

CRITICAL EXAMINATION This text has been written to help students develop their critical thinking skills by providing tools within the text. Case study features provide an in-depth focus on topics from the chapter. When related to a specific disorder, the case studies cover the history, assessment ,apd treatment of the subject involved. Review questions have been written to help students improve their critical thinking skills.

Paula's parents divorced when she was 8 years old. The events leading up to the divorce were extremely st not only for Paula but also for her mother, brother and sister. They had seemed to be the perfect family, livin beautiful home with a tennis court and pool, and Paula attending an elite private girls school. Paula's father highly successful lawyer who was a senior partner in one of Australia's leading law firms. When Paula's mother became aware of her husband's infidelity, she tried to protect her children, esp Paula who was the youngest. However, when negotiations broke down over the financial settlement and her admitted to having had a child with the woman he was having an affair with, Paula's mother became extr angry and openly blamed her husband for destroying their family. The children all sided with their mother, re to have regular contact with their father. They would only agree to see him under sufferance and,tti~nl (such as on their birthdays). The divorce was finally settled following a protracted, bitter legal battle. Shortly after this, Pa depressed and her brother failed some of his university examinations for the first time. Paula's mothei becoming frequently short-tempered and usually down in her mood. Paula alone seemed to be c shining light, taking the divor~ in her stride and becoming a wonderful support for her mother (of bed) and excelling at her schoolwork. This was very consistent with Paula's past behaviour, being

in the family, always eager to please and regarded by all as being 'the best little girl in the world'. pointed out, Paula had been the perfect child and had never given either parent a moment of serio problem had been that Paula wa s somewhat obsessional, preferring routine to the unknown and risks. This tendency had somewhat hampered her relationships with her peer group (e.g., she woul

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to go to new places or events where there were people she was unfamiliar with). But at age 14, the family noticed a change in Paula's personality. Her once bubbly disposi left her, she became much more serious and driven and showed less interest in her relationsh was in the context of her wanting to study more intensely and taking more frequent walks. Fo had started to argue about the size and way in which her mother cooked their meals, often comments. She would accuse her siblings of eating in an unhealthy manner and placed imm mother to cook only healthy meals using organic products. Whenever her mother prepared me stop her adding any butter/ oil to the food. If her mother refused to acquiesce to her demands, anger and try to forcefully stop her mother from doing so by grabbing her arms and trying to food she was trying to prepare. During this time, Paula retained her friendship with only one school friend-Emma-and w at Emma's home after school. She told her mother that they worked well together and that i conducive to study at Emma's home than her own. She would often get home around 8 p eaten with Emma and her family. However, when her mother bumped into Emma's mother thanked her for feeding her daughter so often, Emma's mother said that no thanks were nece a thing at their home (stating that her mother would insist she ate when she returned home

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SUPPORTING STUDENT LEARNING This book supports student reading and comprehension of material through a pedagogical framework that provides learning connections throughout the chapters. This framework uses each chapter's learning objectives (LO) to keep the core concepts in front of the student from the beginning to the end of the chapter and beyond. These learning objectives are tagged to sections in the chapter where students can find the information, as well as to the Review questions so students can check their understanding of key concepts. Key term definitions from the chapter are now provided as a margin definition on the page the term first appears and the end of chapter summary aids student revision and summarises core concepts befot e moving on to the next chapter.

I .. ns resembling anorexia nervosa . d to be recognised. Cond1t10 . d (Bell 1985). However, · d1sor er d. l peno ' Anorexia nervosa was the first :t;:!ing female saints during the -~::e;;70s, when the British physician£ can be found among accounts f the disorder did not appear u~tl t 1873) provided detailed accounts o definitive clinical description~ o ch neuropsychiatrist Henri Lasegu:. ( day Gull (1874) proposed the term\ William Gull (1874) and the ren s have remained unchanged to t is t ~fa nervous (nervosa) or menta a condition whose essential/ea;:: a loss of appetite (anorexia) as a re;u:h century, biological approaches to anorexia nervosa, which re er~ period in the first half of the twen 1e ult from dysfunction of the pitmtar\ rather than a biological cause .. or: when the disorder was thought to re~l948) demonstrated that the clinic~

ANOREX\

anorexia nervosa

Eating disorder ,.jnwhichthe individual is significantly below a body weight that ·is normal for his/her age and height and suffers from a fear of gaining weight and from body image disturbance

A NERVOSA

anorexia nervosa became domin~e~ review by Sheehan and Summer: Psychological understandings ~f ~e gland (Simmonds, 1914). Yet a c: pituitary disease were in fact d1sH~C~ork of Hilde Bruch beginning in e' features of anorexia nervos~ an inant, largely through the influent~a defined and the term 'anorexia nervosa disorder again became pre o; in this period were, however, loos_e io ical basis. 1960s. Diagnostic cntena use f weight loss without a b10 g tended to be used to embrace all forms o

CONNECTING WITH TODAY'S STUDENTS Today's students learn in multiple modalities. Not every student will sit down and read traditional printed chapters in linear fashion from beginning to end; students tend to prefer materials that are more visual and more interactive, and they often read and study in short bursts. This text responds to contemporary students' needs through Connect. Connect brings every learning resource that accompanies this text together in one place and can integrate and interact with your LMS. Connect includes: • Faces Interactive, a completely rebuilt and contemporary experiential learning tool that allows students to interact with real-world case studies • interactive activities and videos cater for students who prefer more visual and interactive content • an optional upgrade to an integrated, high-functioning eBook that allows lecturers to assign readings, and students to highlight, take notes, search and experience integrated media • Power Point® study aids for students • for instructors, a testbank that instructors can use to create quizzes and assignments as well as newly authored PowerPoint presentations, text artwork and videos to supplement lectures and course materials.

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Communication: Begin Right Here!

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2

Abnormal Psychology 3e

ABNORMAL PSYCHOLOGY: AN AUSTRALASIAN FOCUS In 1929, Henry Tasman Lovell, whose interest was in abnormal psychology, became the first Professor of Psycho logy in Australia at the University of Sydney. A more recent, yet also momentous, milestone for the fie ld of abnormal psychology occurred with the Australian Government's all ocation of $1.9 billion over five years in the 2006 Federa l Budget to improve mental health services. Part of this funding supported the creation of an extra 200 student places in university clinica l psychology training programs, and the availability of Medicare rebates for psychological treatment provided by trained mental health professionals through the Better Access to Menta l Health Care program. These reforms constituted a significant recognition of the effectiveness of psychological treatments, representing a major mi lestone for mental health and the profession of psychology. Since its inception in November 2006 to Apri l 2010, the Better Access to Mental Health Care program provided 12.8 million mental health services, including

Henry Tasman (Tassie) Lovell (pictured with his son) was the first Professor of Psychology in Australia, taking up his position in the Department of Psychology at the University of Sydney in 1929.

1.9 million mental health treatment plans provided by general practitioners to enab le patients to access Medicare rebates for psychological treatme~t; 2.6 million visits to clinical psychologists; and 4.9 million visits to psychologists, social workers or occupational therapists, attesting to the w idespread need for menta l health -services in the community. Nevertheless, important weaknesses in the mental he 91th system remained unresolved. For example, many experts believed that the Better Access to Mental Health Care program failed to provide services for people who need them most, iricluding young people, the poor and rura l Australians. As such, in 2011 when the Austra li an Government allocated a further $2.2 billion over five years, severa l reforms were introduced that sought to add/ess previous weaknesses by targeting support to areas and communities in the greatest need, through such programs as the Access to All ied Psychological Services (ATAPS) and E-mental Health. As a result, there was a redirection of funds away from the Better Access program so that the number of Medicare-supported psycholog ical consu ltations was reduced to 10 sessions from the previous ly available 18 sessions per ca lendar year. Unfortunately, this number of sessions is inadequate to treat many psycho logical disorders. In addition, while the Better Access to Menta l Health Care program has increased treatment rates, estimates from 2010 suggest that on ly 46 per cent of people with mental health disorders accessed treatment (Pirkis, Harris, Hall,

& Ftanou, 2011 ). According to the latest National Survey of Mental Health and Wellbeing, conducted by the Australian Bureau of Statistics (ABS) in 2007, almost half of Australians aged 16 to 85 years (45% or 7.3 million peop le) experienced an anxiety, affective or substance use disorder at some point in their lifetime. One in five

Chapter 1

Conceptual issues in abnormal psychology

3

(20% or 3.2 mi lli on) Australians experien'c:id one of these mental disorders during the 12-month period prior to the survey being conducted but only one-third of these individuals used mental health services over the 12 months. Women and older people are more likely to access services and people are more likely to see general practitioners than any other type of health professional (ABS, 2008; Slade et al, 2009). The ability to address the mental health needs of all groups in society remains a significant challenge. This chapter traces the development of abnorma l psycho logy and the mental health professions from their beginnings to the present and looks at possible future directions. Abnormal psychology is commonly defined as the field of psychology that aims to understand, explain and modify abnormal behaviours. Most of the field of abnormal psycho logy today, however, is concerned only with a specia l subset of abnormal behaviours, a subset labelled 'mental disorders'. Indeed, most of the following chapters focus upon a specific category of mental/psychological disorder. The present chapter serves as an introduction to some of the fundamental concepts of abnormal psychology. First, definitions of abnorma lity and mental disorder w ill be discussed. The bulk of the chapter wi ll focus on the main theoretical perspectives that have shaped current knowledge in abnorma l psycho logy. In this section, the biological perspective (the oldest and currently dom inant approach to understanding mental disorders) will be contrasted w ith various psychological perspectives to underline the d ifferences in their approaches to the conceptualisation, classification, aetiology and treatment of mental disorders. The chapter w ill end w ith a description of one of the major systems for diagnosing mental disorders and a consideration of directions for future developments in the fie ld of psychiatric classification.

The definitions of abnormal behaviour and mental disorder ABNORMALITY Although the distinction between 'normal' and 'abnormal' behaviours seems intuitively clear to most people, a more careful consideration reveals that this distinction is often difficult to make. Although no clear rules have yet been id~ntified to differentiate normality and abnormality, several elements have been proposed. The most common ones are statistical rarity, deviance or norm violation, distress and dysfunction.

STATISTICAL RARITY Statistical rarity is one criterion that has been used to define abnormality. Individuals who possess a characteristic that is rarely found in society can be said to be abnormal, in the sense that they deviate from the average to a large extent. This element of abnormality, of course, can include positive deviations as well. So, according to this definition, people who are known for their musical or scientific genius, for example, can be considered abnormal. Clearly, the field of abnormal psychology cannot be defined on the basis of statistical rarity alone, otherwise individuals such as Wolfgang Amadeus Mozart or Albert Einstein would be prime candidates for treatment!

DEVIANCE OR NORM VIOLATION The criterion of 'deviance' or norm violation includes a value component, according to which a behaviour is considered to be abnormal if it is deemed to be socially unacceptable. The 'abnormal' intelligence level of Albert Einstein is positively valued by society and thus would not be defined as abnormal according to the criterion of norm violation. On the other hand, being unable to socialise because of extreme anxiety, avoiding all forms

LO 1.1

4

Abnormal Psychology 3e

of public transport, hearing voices, physically assaulting one's spouse, engaging in reckless:or risky sexual behaviours, driving while drunk or making a living by armed robbery are generally seen as violating social expectations. While adding the element of norm violation to statistical rarity can give a more precise definition of abnormality, it still leaves a very broad class of behaviours for abnormal psychology to be concerned with. Norm-violating behaviours encompass a diverse range of behaviours that may include instances of harmless eccentricity, non-conformist behaviours and serious criminal acts, as well as instances of mental disorder. Moreover, using norm violation as a sole requirement to define abnormality can be dangerous as it can be used to oppress any non-conformist behaviours. For example, homosexuality and a range of other sexual behaviours such as masturbation were seen as both statistically rare and unacceptable by society only a few decades ago. Therefore, people engaging in these behaviours were viewed as in need of either punishment or treatment (Szasz, 1961).

DISTRESS

elieved, by depression and self-deprecation. The reaction is precipitated by a current situation, frequently by some loss sustained by the patient, and is often associated with a feeling of guilt for past failures or deeds. The degree of the reaction in such cases is dependent upon the intensity of the patient's ambivalent feeling toward his loss (love, possession) as well as upon the realistic circumstances of the loss' (APA, 1952, pp. 33-34).

LIMITATIONS OF THE DSM-/ AND DSM-I/ In general, the constructs involved in psychoanalysis were complex and difficult to measure with precision. The same problem applied to the diagnostic systems based on psychoanalytic thinking. Foremost among the problems was the limited reliability of the diagnostic categories. Reliability refers to the ability of a measurement system to yield the same results, no matter when, where and by whom it is used. So, a 30-centimetre ruler measures exactly the same length in Sydney or in Perth, whether it is used by one person or another, and whether it is used today or in six months' time. Similarly, diagnostic categories need to be defined clearly enough to enable different clinicians at different locations and times to arrive at the same diagnosis when assessing the same person. In order to apply modern scientific methods and empirically investigate the causes of a mental disorder or its treatment, researchers at different sites need to be able to apply diagnostic criteria with a high level of agreement between them. At a more fundamental level, the investigators need to be able to agree on whether a person meets the criteria for a disorder or not. That is, the line between mental health and disorder needs to be clearly identifiable. Psychoanalytic theory, and hence the first two editions of the DSM, were unable to meet these needs. Returning to the example of the description of depressive reaction in the DSM-I, a number of obstacles to reliable diagnosis become apparent. First, at the very basic level, the description does not give the diagnostician any indication as to when a depressive reaction becomes severe enough to warrant a diagnosis and treatment, that is, when it ceases to be a normal reaction and becomes 'abnormal'. How much of each of the listed symptoms is required to be considered abnormal? For example, how much self-deprecation is required? How long does the self-deprecation need to continue for? These considerations were not important for psychoanalysis, as the theory explicitly accepted that the dividing line between normality and disorder is blurred. In addition to not giving any indication regarding the difference between normal and abnormal lev'ets of the symptoms, it is also not known whether all of the symptoms are required or only some of them to establish a diagnosis. Should a person who feels depressed but does not express self-deprecation be diagnosed with a depressive reaction or not? Are some of the symptoms more important than others? Such questions were not explicitly stated in the diagnostic criteria in the first two editions of the DSM and it was left to individual therapists or researchers to make decisions regarding the answers. This subjective judgment introduced a great deal of unreliability to the diagnostic process since it allowed a high level of disagreement to occur between individual therapists making diagnoses. The other important limitation of the first two editions of the DSM was the lack of evidence for their assumptions regarding causation. The ultimate aim of medical diagnostic systems is to classify different disorders according to their underlying causation. The fact that psychoanalytic concepts were extremely difficult to research empirically meant that the presumed psychodynamic causation underlying the diagnostic categories in the DSM-I and DSM-II received no empirical support. The diagnostic system was ultimately based on unproven and untestable assumptions about the aetiology of the disorders. It was not possible to ascertain whether the disorders really existed as described-that is, whether the category descriptions were consistent with what occurs in nature. In other words, the diagnostic system had limited validity. By the 1970s this state of affairs was no longer acceptable to the medical profession. Psychiatry needed to introduce a new system for the classification of mental disorders that was more consistent with the prevailing

reliability Degree of consistency in a measure, that is, the extent to which it yields accurate measurements of a construct across different trials, samples, raters and forms of the measure.

34

Abnormal Psychology 3e

values of modern medical science. The next edition of the DSM, therefore, represented a significant departure from the psychoanalytic model.,'

·.;:;

·cen

-.. 0

Pre-gain session 4

V

0

C

::s 0 E

cc

2

CBT1

CBT2

FIGURE 3.3 In both forms of cognitive behaviour therapy (CBTl and CBT2), there was a significantly greater amount of improvement in negative thinking in the session (the 'pre-gain session') before a large improvement in depressive 1 symptoms compared with the control session (the sessio n just before the pre-gain session) Source: From Tang, T. Z., DeRubeis, R., Beberman, R., & Pham, T. (2005). Cognitive changes, critical sessions, and sudden gains in cognitive-behavioural therapy for depression. Journal of Consulting and Clinical Psychology, 73, 168-172, © 2005 The American Psychological Association. Used with permission.

Behavioural theories

Behavioural theories of depression focus on the environmental conditions and contingencies associated with depressed and non-depressed behaviours. These models suggest that depression is maintained because there are benefits for depressed behaviours (such as avoidance of unpleasant or stressful tasks, deferring responsibilities to others and receiving sympathy from others). In contrast, the depressed individual obtains fewer of the benefits typically associated with healthy, autonomous behaviours because s/he has withdrawn from many of the situations that previously provided the individual with a sense of pleasure or success (Jacobson, Martell, & Dimidjian, 2001 ). Other behavioural theories of depression highlight the role of poor coping skills. For some people, a lack of effective coping skills to deal with life stressors can contribute to the onset of a depressive episode (Arean et al., 1993). For example, individuals who lack effective problemsolving skills may experience increasing helplessness in the face of mounting stressors. There are two main behavioural theories regarding the aetiology and maintenance of depression. One theory is that some life events or stresses can reduce the opportunity to experience positive reinforcers (Lewinson and Gotlib, 1995). This lack of reinforcement over time can result in gradual withdrawal from previously enjoyable activities or behaviours and increase the risk of depression. For example, if a person gets retrenched from their job they may experience financial difficulties and miss the opportunity for regular social interaction with their work colleagues. Chronic financial constraints and lack of social supports over time could lead to the later development and maintenance of a depressive illness in this person. Another behavioural theory proposed by Seligman (1975) is that uncontrollable negative life events, especially those that are frequent and/or chronic, can lead to feelings of helplessness and the behavioural manifestations of depression. Seligman coined the expression 'learned helplessness' to refer to a constellation of behaviours characterised by low motivation, passivity and indecisiveness (Seligman 1975), which resembled those commonly seen in clinical depression.

101

102

Abnormal Psychology 3e

Psychoanalytic theories

Psychoanalytic theories hold that depression is a form of pathological grief. These grief-like responses may occur within the context of the break-up of a close relationship, loss of a job with income and status, deterioration in health and even the shattering of one's ideals and beliefs. Disruptions in early childhood bonding experiences with caregivers are thought to sensitise people to losses in adulthood which, in turn, leads to vulnerability to depression. Such individuals are thought to be ambivalent in their relationships and excessively dependent on others for support, encouragement, guidance, admiration and confirmation of their self-worth. Ambivalent feelings in relationships are heightened with experiences ofloss, which results in anger directed toward the self. Such self-directed anger is thought to manifest as guilt and self-blame.

SOCIAL FACTORS expressed emotion (EE)

Family interaction style in which fami ly members are overly protective and self-sacrificing towards the person with a psychological disorder wh ile also expressing high levels of criticism and hostility; this may contribute to the person's relapse.

A range of interpersonal difficulties may be involved in the development and maintenance of depressive episodes. One type of interpersonal difficulty is the family communication style of expressed emotion (EE), which entails high levels of criticism, hostility and/or over-involvement. Researchers have found an association between high levels of expressed emotion in the families of depressed patients and the patient's risk of relapsing after a depressive episode (Hooley & Teasdale, 1989). Lack of an intimate relationship has also been found to be a risk factor for depression, especially for women (Brown & Harris, 1978). Interpersonal theories of depression highlight the cyclical nature of these episodes, where disturbances in social functioning (e.g., relationships characterised by high levels of criticism) trigger depressive symptoms (such as depressed mood, low energy and social withdrawal) that in turn lead to a further deterioration in social functioning, and hence a worsening of the depression in a vicious cycle. In addition, because depressive behaviours in a social context can be aversive to others, they can lead to others spending less time with the depressed person and in this way amplify both the self-criticism and withdrawal of the depressed individual, which further maintains his/her depression.

PROTECTIVE FACTORS While the focus thus far has been on factors that are believed to contribute to the development of depression, other factors are thought to be protective of developing a depressive episode (Australian Institute of Health and Welfare, 1999). Some of the factors that may reduce an individual's chances of developing depression are as follows: • • • • • • • protective factors

Conditions or variables associated with a reduced risk or chance of developing a disorder.

good interpersonal skills and positive relationships with others high levels of family cohesion (i.e., strong supportive ties with at least one parent or significant other) a sense of being connected with one's community a sense of achievement in a valued area of pursuit (e.g., academically or athletically) a temperament characterised by optimism and low anxiety an openness to the possibility of exploring new experiences effective coping skills such as constructive problem-solving and negotiation skills.

As with risk factors for depression, many of these protective factors tend to cluster together, making it difficult to tease out the relative importance of any one of them. For example, an individual who comes from a close, supportive family environment and who has developed a good relationship with one or both parents may also have developed good interpersonal skills and thus may be better equipped to participate in local sporting activities. Active participation in sporting activities may help to develop a sense of achievement and boost self-esteem, thus lessening the likelihood of developing a depressive episode.

Chapter 3

Mood disorders

THE TREATMENT OF UNIPOLAR DEPRESSION Some depressive disorders, especially those associated with acute stressors, may improve with time in the absence of treatment. However, effective treatment can speed up recovery and reduce the risk of relapse. Depressive episodes that are prolonged and untreated can often result in chronic psychosocial difficulties, including poor academic and work histories, damaged social relationships, and a lowered sense of self-worth and self-confidence. Unfortunately, most,reople with depression never seek care or wait, sometimes for years, before seeking help (Kohn, Saxena, Levav, & Saraceno, 2004). In addition, because the severity of depressive symptoms can fluctuate depending on outside factors and because it is an episodic condition, it is important to assess the severity and profile of the sufferer's symptoms using reliable and valid measures of depression. Besides the instruments used to screen for depression at a population or community level such as the Kl0 (Kessler et al., 2002) or the Centre for Epidemiologic Studies Depression Scale (Radloff, 1991 ), a number of psycho metrically sound patient-focused instruments are commonly used in treatment settings to assess depression severity and treatment response. There are a range of general measures as well as those that are designed for specific populations of patients such as the elderly, those presenting with depression in the context of medical illness or youth and children. In the Australian context, the frequently used measures include the Beck Depression Inventory (Beck, Steer & Garblin, 1988), Hopkins Symptom Checklist (Hesbacher, Rickels, Morris, Newman, & Rosenfeld, 1980), Symptom Check List 90 (Derogatis & Savutz, 2000), Geriatric Depression Inventory (Sheikh & Yesavage, 1986), Reynolds Adolescent Depression Scale (Osman, Gutierrez, Bagge, Fang & Emmerich, 2010) and the Children's Depression Inventory (Kovacs, 1985). Treatments for depressive disorders comprise both medical and psychological interventions, which may also be combined. Research suggests that a combined approach is especially beneficial for more severe, chronic or recurrent depression (Pampallona, Tibalbi, Kupelnick, & Munizza, 2004; Petersen, 2006; Thase et al., 1997). While the review of treatment will focus on depression generally, evidence is gradually accruing to suggest that different types of depressive disorders may require different treatment approaches (Parker, Roy, & Eyers, 2003). For example, a more biologically-driven depression may require antidepressant and other medical interventions as a primary focus of treatment. In contrast, a depressive disorder brought about by an acute stressful life event, such as a relationship break-up, may be more responsive to psychological approaches. However, further research is needed to examine whether more targeted treatments based on addressing ,the hypothesised cause of the depressive disorder will lead to greater improvements and reduced relapse rates.

MEDICAL APPROACHES Antidepressants are the most frequently used medications for both unipolar and bipolar depression. This class of medications_includes the tricyclic antidepressants (TCAs), the selective serotonin reuptake inhibitors (SSRis) , serotonin-noradrenaline reuptake inhibitors (SNRis), monoamine oxidase inhibitors (MAOis) and several other newer medications that do not easily fit into the previous four categories. Antidepressants are thought to work by increasing the availability of neurotransmitters or increasing the sensitivity of neuron receptors in the brain. Antipsychotic medications may also be used to control psychotic symptoms (e.g., delusions or hallucinations) in some types of severe depressive disorders. There is ongoing debate regarding which class of antidepressants is the most beneficial. The findings from a review of studies indicated that, among depressed patients being treated in general practice settings, the newer forms of antidepressants (such as the SSRis) were similar in efficacy to tricyclic antidepressants for the treatment of depression, both of which were more effective than placebo (Mulrow et al., 2000). However, newer antidepressants were associated with a decreased risk of treatment dropout due to the reduced negative side effects of these medications.

antidepressants

Drugs used to treat the symptoms of depression such as sad mood, negative thinking, and disturbances of sleep and appetite; three common types are monoamine oxidase inhibitors, tricyclics and selective serotonin reuptake inhibitors. tricyclic antidepressants

(TCAs) Class of antidepressant drugs such as imipramine and amitriptyline. selective serotonin reuptake inhibitors (SSRls)

Class of antidepressant drugs (such as fluoxetine) that inhibit the reuptake of serotonin. monoamine oxidase inhibitors

(MAOls) Class of antidepressant drugs. antipsychotic medications

Drugs used to treat psychotic symptoms such as delusions and hallucinations. p'sychotic symptoms

Accord ing to the narrow definition, delusions and hallucinations; according to the broader definition, also includes disorganised speech and disorganised or catatonic behaviour.

104 repetitive transcranial magnetic stimulation

(rTMS) Biological treatment that exposes patients to repeated, high-intensity magnetic pulses that are focused on particular brain structures in order to stimulate them. vagus nerve stimulation

Biological treatment in which the vagus nerve (the part of the autonomic nervous system that carries information from the head, neck, thorax and abdomen to several areas of the brain) is stimulated by a small electronic device similar to a cardiac pacemaker, which is surgically implanted under a patient's skin in the left chest wall. bright light therapy Treatment

that involves exposure to bright light; used particularly during the winter months for individuals with seasonal affective disorder. seasonal affective disorder

Depressive disorder characterised by a two-year period in which the individual experiences major depression during winter months and then recovers during the summer.

Abnormal Psychology 3e

In addition to medication, a number of non-pharmacological medical interventions are being investigated for the treatment of depressive disorders. Repetitive transcranial magnetic stimulation (rTMS) comprises the application of repeated, high-intensity magnetic pulses to the brain, which is thought to change the way in which neurotransmitters function. Preliminary evidence has supported its efficacy in the treatment of depression when compared to placebo treatment (Loo & Mitchell, 2005) and it has been approved for clinical use in the United States. However, further research is required to refine and develop rTMS as a general treatment for depressive disorders. Another approach, vagus nerve stimulation via a small implanted electrical device in the chest wall, is thought to increase activity in the hypothalamus and amygdala, which in turn alleviates depressive symptoms. Bright light therapy may be especially relevant to the treatment of seasonal affective disorder. This treatment involves regular exposure to light of a particular frequency and intensity that is thought to affect levels of melatonin, serotonin and noradrenaline (Wehr et al., 2001) . In one study, bright light therapy was compared to antidepressant medication in 102 depressed participants. Those who received bright light therapy demonstrated greater reductions in their depression symptoms at the end of the five-week trial period (Martiny, Lunde, Unden, Dam, & Bech, 2005). Non-pharmacological medical therapies of this kind tend to have minimal side effects and thus hold particular promise for managing depressive disorders in children, adolescents and adults who may be sensitive to the side effects of antidepressant medications. Severe depressive disorders are often treated successfully with electroconvulsive therapy (ECT) , which involves the application of an electrical current to the brain. The use of ECT has been controversial because it was allegedly used as a form of punishment in some facilities in the past. Furthermore, it can lead to permanent memory loss and difficulties in learning new information. However, the modern use of ECT typically involves the delivery of an electrical current to only one side of the brain (usually the right side), which minimises the likelihood of long-term memory and learning problems. Several studies have found that ECT is an effective and suitable treatment especially for severe depression (Carney et al., 2003; Pagnin, de Queiroz, Pini, & Cassano, 2004). Variations in the placement of the ECT electrodes and the width of the electrical pulse have been shown to enhance the efficacy of this treatment while minimising adverse cognitive effects (Sackeim et al., 2008). Although the treatment is considered to be safe, it is generally contraindicated among those with a history of myocardial or cerebrovascular accidents. A potential alternative to ECT is direct current stimulation, which is a mild form of brain stimulation Transcranial magnetic stimulation (TMS) being trialled for depression (Loo et al., 2012). This is a brain stimulation technique that uses approach is thought to increase brain activity in areas magnetic fields to stimulate focal brain of the brain that are underactive and to decrease brain areas. The rl)agnetic field is produced by a coil in either a figure 8/butterfly or a circular activity in those areas that are overactive. This novel shape depending on the type of stimulation treatment holds promise especially for young people or required. The coil is held against the scalp at the identified site. The stimulation is nonthose where ECT is contraindicated (e.g., those who have invasive and is given while the person is fully experienced a recent myocardial infarction or vascular awake and alert. aneurysm).

Chapter 3

Mood disorders

PSYCHOLOGICAL APPROACHES Each of the major psychological therapies for depression seeks to address specific vulnerabilities that are thought to contribute to the onset and/or maintenance of a depressive episode. Many psychological interventions are relatively short term (approximately 12-20 sessions) and may be administered in an individual or group format. They usually incorporate relapse-prevention strategies for long-term improvement. Most psychological therapies also share important components such as developing a strong therapeutic relationship between the cltent and therapist and increasing the client's coping skills, which are thought to play a crucial role in therapy outcome. Cognitive behaviour therapy (CBT) (Beck, Rush, Shaw, & Emery, 1979; Ellis & Harper, 1961) is one of the most widely used and well-supported psychological interventions for depression. CBT utilises a combination of cognitive and behavioural strategies. Treatment often begins with the behavioural strategy of pleasant activity scheduling, whereby the therapist and client work together to gradually increase the number of rewarding activities the client engages in each day as a way of improving his/her mood. Another behavioural technique involves teaching clients the skills of effective problem-solving so that they can overcome feelings of hopelessness and helplessness in the face of negative life events. A key cognitive technique is cognitive restructuring. Here, the client is introduced to the ABC Model in which activating events trigger dysfunctional beliefs that in turn result in negative consequences (i.e., negative mood and behaviours). The client is encouraged to keep a daily record of the thoughts associated with depressed mood, known as a 'thought monitoring form'. Once dysfunctional thinking patterns have been identified, the therapist assists the client to challenge these thoughts and replace them with more realistic ones. The client is asked to examine the evidence supporting or contrary to the dysfunctional thought and to consider alternative ways of viewing the situation that are more accurate. These more realistic thoughts in turn give rise to more positive feelings and behaviours. An example of a cognitive restructuring exercise is shown in Table 3.1.

105 electroconvulsive therapy (ECT) Treatment for mood disorders that involves the induction of a brain seizure by passing an electrical current through the patient's brain whiles/ he is anaesthetised. cognitive behaviour therapy (CBT) Type of psychological treatment that combines both cognitive and behavioural concepts and techniques.

TABLE 3.1 A common exercise in CBT is to ask clients to record the thoughts that trigger negative mood and behaviours and then to rep lace these thoughts with more realistic ones that are supported by evidence

ACTIVATING EVENT Trying to find a vacant car space in a busy car park

RATIONAL RESPONSE

BELIEFS I'm so stupid-I should have known I wou ldn't find a spot.

Depressed and angry at myself. Tempted to turn around and go home.

There's no way I could have known the car park wou ld be like this-the supermarket isn't usually busy this early in the

Still a bit frustrated by the situation but no longer down on myself. Kept looking until I eventua lly found a spot.

morning=-·- - - - - - · - ~ ~ - - - - - - - - - - -

The efficacy of CBT has been extensively evaluated since the first controlled study was carried out in the 1970s. Gloaguen, Cottraux, Cucherat, and Blackburn (1998) conducted a meta-analysis of 48 controlled trials that investigated the efficacy of CBT in the treatment of mild to moderately severe unipolar depression. Across studies, CBT was found to be significantly more effective than no-treatment control groups, antidepressant medication and some other forms of psychological treatment for depression. For non-hospitalised individuals with severe depression, CBT and medication appear to have comparable effects (DeRubeis, Gelfand, Tang, & Simons, 1999), although medication is recommended as a first-line treatment for severe melancholic depression or for depression with psychotic features (Royal Australian and New Zealand College of Psychiatrists Clinical Practice Guidelines Team for Depression, 2004). CBT is also well supported as a treatment for depression in adolescents (Clarke, Rohde, Lewinsohn, Hops, & Seeley, 1999) and may be more

pleasant activity scheduling Behavioural technique entai ling planning a gradual increase in the level of pleasant activities the client engages in as a way of improving his/ her mood.

106 meta-analysis

Statistica l technique for summarising resu lts across several stu dies. interpersonal psychotherapy (IPT) Short-term

psychologica l treatment originally developed by Gerald Klerman, Myrna Weissman and their colleagues for the treatment of depression; addresses the client's interpersonal problems as a way of improving his/ her psychological symptoms.

psychodynamic therapies

Therapies foc used on uncoveri ng and resolving unconscious confli cts that drive psychologica l symptoms.

Abnormal Psychology 3e

effective than medication in this age group (Melvin et al., 2006). In addition to its beneficial effects in the treatment of depression, CBT has also been found to be extremely cost-effective (Vos, Corry, Haby, Carter, & Andrews, 2005) . Interpersonal psychotherapy (IPT) focuses on interpersonal problems that may be related to the onset and/or maintenance of a depressive episode (Klerman, Weissman, Rounsaville, & Chevron, 1984). In the most recent form of IPT, the interpersonal problem areas that are believed to have triggered the depressive episode and are therefore t~rgeted during treatment are: (a) grief over an interpersonal loss; (b) interpersonal disputes (e.g., a wife may not feel adequately supported by her husband); and/or (c) life transitions (e.g., becoming a parent) (Stuart & Robertson, 2012) . IPT aims to help clients resolve dysfunctional interpersonal relationships and/or encourages them to develop new relationships as a means of improving their mood. IPT has received considerable support in the treatment of depressive di~orders and is now regarded as one of the standard treatments for mood disorders (Feijo de Mello, de Jesus Mari, Bacaltchuk, Verdeli, & Neugebauer, 2005). Current treatment guidelines state that IPT is as effective as CBT in the treatment of moderately severe depression (Royal Australian and New Zealand College of Psychiatrists Clinical Practice Guidelines Team for Depression, 2004). Based on a purely behavioural model of depression, Jacobson's behavioural activation approach for the treatment of depression focuses on helping clients re-engage in their lives through strategies (such as getting in touch with an old friend or participating in a team sport) that act to offset patterns of withdrawal and inactivity that contribute to depressive episodes (Dimidjian et al., 2006) . Strategies are designed to help individuals approach and access sources of positive reinforcement in their lives that can serve as a natural antidepressant. In psychodynamic therapy, the therapist attempts to reconstruct past experiences and interpret patterns of emotions and behaviours, in order to enhance the patient's insight about the repetitive conflicts maintaining his/her current problems (Leichsenring & Leibing, 2007) . In contrast to both CBT and IPT, there is only limited evidence to support psychodynamic therapy for depression (Connolly Gibbons, Crits-Christoph, & Hearon, 2008).

RELAPSE PREVENTION Since major depressive disorder is often a reoccurring condition, and the occurrence o( an episode can increase the risk of future episodes, one of the major challenges for the treatment of depression is how to reduce the likelihood of further episodes once the person is well. One method for doing this is the continued use of antidepressant medication over a number of years. Other approaches to preventing future depressive episodes involve psychological interventions. Relapsep.cevention training within CBT focuses on planning how to cope with potential future triggers to depressed mood by continued use of cognitive strategies and problem-solving skills, as well as identifying early signs of a deterioration in functioning (e.g., sleeping problems re-emerging) and developing a plan fo~ how to respond if depressive symptoms do re-emerge. The meta-analytic study by Gloaguen et al. (1998) mentioned previously investigated the effectiveness of CBT to prevent relapse. Although there were only eight studies that included a follow-up period of at least one year (thus rendering the conclusions tentative), five studies found a significantly greater effect of CBT compared to medication in preventing relapse, with no study supporting medication over CBT. The overall relapse rate was 29.5 per cent for clients who received CBT versus 60 per cent for those treated with medication. Subsequent research continues to support the benefits of CBT in reducing the rate of relapse (Fava et al., 2004). A type of psychological intervention combining elements of meditation and CBT, namely mindfulnessbased cognitive therapy, developed by Segal and his colleagues (2002), has shown promising results in preventing relapse in depressed people successfully treated with CBT or medication (Eisendrath et al., 2008;

I

Chapter 3

Mood disorders

Kenny & Williams, 2007; Ma & Teasdale, 2004; Teasdale et al., 2000). The key aim of this approach is to teach individuals to develop a different relationship to their negative thinking. For example, instead of repeatedly engaging with and focusing on negative thoughts (which produces a downward spiral in mood), individuals are taught to simply notice their thoughts (as mental phenomena that come and go, just as clouds move across the sky). Further research is needed to evaluate the effectiveness of mindfulness-based cognitive therapy compared to other psychological interventions for unipolar depression.

PREVENTION As stated, unipolar depression is highly prevalent, often beginning in adolescence or early adulthood and becoming a major and lifelong burden for sufferers, their families and the community. In addition, the occurrence of a first depressive episode may itself cause enduring psychological and neurological changes that in turn increase the risk of further depressive episodes. For these reasons, over the past decade there has been a growing focus on preventing depression. Most interventions to prevent depression have had a CBT and/or an interpersonal focus and teach cognitive, interpersonal and coping skills for dealing with life stress. Outcomes in controlled trials have been mixed, with the largest positive effects for preventing depression observed when the targeted group has some risk of developing depression, either because they already have some symptoms of depression or have a family history of depression, or because of adverse environmental factors (Horowitz & Garber, 2006). In contrast, programs that are directed to all members of a population (e.g., high-school students), regardless of their level of risk for developing depression, have shown inconsistent effects (Merry, McDowell, Hetrick, Bir, & Muller, 2004). These universal programs have also been criticised because they typically require substantial resources, which makes it difficult for them to be sustained over time and to reach large numbers of the population (O'Kearney, Kanwal, Christensen, & Griffiths, 2009). The use of internet delivery of both treatment and prevention programs for depression may help overcome some of these issues (Calear, Christensen, Griffiths, McKinnon, & O'Kearney, 2009; Clarke et al., 2005).

CA S E

S T UDY

THE SYMPTOMS OF MAJOR DEPRESSIVE DISORDER .

Judy is a 32-year-old lawyer who reported a gradual change in her satisfaction with work and her relationship over the previous 12 to 18 months. She initially attributed this to working longer hours and the fact that her husband was increasingly required to spend more time away from home for work. But she became concerned when she noticed that she was being uncharacteristically irritable with her work colleagues and that she was frequently avoiding meetings and social activities because she found them 'too much of a hassle'. Judy felt particularly low on the weekends when her husband was working. She started staying at home more and had to push herself to get out. Even when she did manage to go out, she no longer enjoyed her usual activities and was anxious that she would see someone she knew. She described feeling anxious when her phone rang and would often ignore it. She also had begun to feel very anxious at night and was preoccupied with the thought that she was a burden on her husband and that he was going to leave her and that her work supervisor was unhappy with her performance. She frequently awoke during the night and most nights she was awake at 4 am when she would be unable to get back to sleep. She had lost considerable weight because 'she wasn't cooking with her husband away' and really she didn't feeling like eating anyway.

continued

108

Abnorm al Psycholog y 3e

continued Judy had seen her mother go th rough a period of depression after her parents' marriage broke up when she was a teenager. The break-up had affected her too and she had dieted to excess and then started binge eating. But these eating problems only lasted for a few months and it was only recently that she began to experience problems with eating again, thi s time in the form of not feeling like eating rather than deliberately restricting her food intake in order to lose weight. Judy was reluctant to see~ help for her current problems and was very critical of herself-she believed that the fact that she was not able to 'pull herself together ' showed that she was a failure. She started to feel that there wa s no solution to how she wa s feeling. Her husband became concerned enough after a weekend of frequent, distressed phone calls from Judy when he was at a conference to insist that th ey both go to the family GP. After seeing the GP, Judy accepted the need for treatment of her depression and she began to see a clinical psychologi st for psychotherapy and to take antidepressant medication. As her sleep and eating improved and she began to engage more again with her friends, family and work colleagues, her mood returned to its usual ups and downs. The psychotherapy she undertook helped her to better understand her feelings of anger and loss during her husband's absences and also her avoidance of these feelings because of a strong need not to be dependent. She also took the risk of talking about these feelings with her husband. Over a peri od of time, Judy developed more confidence in recognising and accepting these feelings but also in trying solutions to solve what was triggering them.

L03.2

Bipolar disorder THE HISTORY OF BIPOLAR DISORDER

bipolar disorder Mood disorder marked by man ic/hypomanic episodes and depressive episodes (previously ca lled man ic-depression). lithium carbonate Drug class ified as a mood stabiliser th at is used in the treatment of bipolar disorder.

Bipolar disorder has a long history. The earliest descriptions of mania and melancholia can be traced back to classical Greek times. Throughout most of history, mania and depression were viewed as separate illnesses. However, a turning point for the contemporary view of bipolar disorder took place in the nineteenth century in France when Jean-Pierre Falret (1851) referred to the condition as 'la Jolie circulaire' (the cycle of madness), thus describing a single entity involving the sequential change between mania and melanch0lia. It was also during the late nineteenth century that Kraepelin formally made the landmark distinction between 'manic depressive insanity' and other forms of severe mental illness, particularly 'dementia praecox' (an early term for schizophrenia). Kraepelin (1896) observed that patients with dementia praecox generally experienced ongoing symptoms of cognitive impairment and social withdrawal whereas manic-depressive p~tients tended to experience better functioning between episodes of mood disturbance. The next landmark occurrence in the classification of mood disorders was made by Leonhard ( 1957), who argued that,the term 'manic depressive insanity' was too inclusive. He coined the term bipolar disorder to refer to those individuals who experience both depressive and manic episodes, and distinguished such individuals from those who experience depressive episodes alone. The treatments for bipolar disorder have changed dramatically, as illustrated by historical records of the lives of some great artists. For example, the composer Robert Schumann was struck down by manic-depressive psychosis and admitted to an asylum in the mid-1800s. He succumbed to madness, experiencing auditory hallucinations that consisted alternately of glorious music and being tormented with terrible threats. Later descriptions suggest that when he was not arguing with the demons inside his head or shouting at the doctors, he would sit for days feverishly composing fugues . However, none of these compositions satisfied him and he burnt them all. Schumann had lost everything: his inspiration, his job, his home, his children and his wife. These tragic effects on the lives of so many people made the discovery of lithium carbonate in the treatment of mania so significant. It was a quiet and unassuming Australian psychiatrist, John Cade, who made the

Chapter 3

Mood disorders

serendipitous yet remarkable discovery of lithium in an old wooden building on the grounds of the Repatriation Mental Hospital, Bundoora, Victoria (Mitchell & HadziPavlovic, 1999). He believed that urea (a protein breakdown product in urine) was a causal factor in what he referred to as 'manic depressive insanity'. While trying to overcome a technical difficulty in experiments on guinea pigs, he began using lithium urate (being the most soluble of the urates) to alter the toxicity of urea. Cade witnessed, unexpectedly, that the lithium itself was acting as a protective agent against the toxicity of urea. He deduced that lithium alone may have a therapeutic effect in mania, and further experiments found this to be true. Therein lies one of the most profound discoveries in modern medicine. After conducting the trials on guinea pigs and then on himself and finding no adverse effects, Cade administered the lithium (in an uncontrolled trial) to 10 patients with mania, six with schizophrenia and three with depression. In contrast to the minimal benefits John Cade, the Australian psychiatrist who discovered the beneficial effects of lithium, experienced by the patients with the other conditions, the which was to transform the treatment of effect on the patients with mania was dramatic. A number individuals with bipolar disorder. of other Australian researchers extended Cade's research, leading to some pivotal clinical studies on bipolar disorder in the 1950s (Cade, 1979). In honouring the significant contribution made by Cade in the treatment of mania, some researchers have proposed that bipolar I disorder (defined below) be known as 'Cade's Disease' (Ghaemi, Ko, & Goodwin, 2002). The following four decades were marked by a growth in genetic studies that revealed the high heritability of bipolar disorder. In addition, new classes of mood stabiliser and antidepressant medications began to emerge. More recently, there has been exponential interest in studies exploring diagnostic models and the neurobiological and psychological factors underpinning the condition.

THE DIAGNOSIS OF BIPOLAR DISORDERS The DSM-5 (APA, 2013) includes a chapter entitled 'Bipolar and Related Disorders' in recognition of the fact that the term 'hipolar disorder' actually embraces a spectrum of disorders, primarily consisting of bipolar I disorder, bipolar II disorder and cyclothymic disorder. What unites these conditions is the fact that affected individuals experience symptoms of pathologically elevated mood termed 'mania' or 'hypomania'.

MANIC, HYPOMANIC AND MIXED EPISODES A manic episode as defined by the DSM-5 requires that a person show an elevated, expansive or irritable mood and abnormally and persistently increased goal-directed activity or energy (this latter criterion being an addition to the criteria listed in the DSM-IV-TR) (APA, 2000; 2013). The individual must experience these abnormalities in mood and goal-directed activity for at least one week, plus at least three of the following symptoms: • inflated self-esteem • grandiosity-that is, a sense that anything is possible e.g. a belief that one can fly or that one can read the thoughts of other people • sleep disturbance-that is, a decreased need for sleep accompanied by a belief that there is too much to achieve to spend time sleeping

manic episode State of persistently elevated or irritable mood and abnorma lly increased goaldirected activity accompanied by symptoms such as inflated selfesteem, decreased need for sleep, racing thoughts, pressured speech and impulsive, self-destructive behaviours. grandiosity Inflated belief about one's worth, power, knowledge, abil ity or identity; when extreme, may constitute a grandiose delusion.

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• pressure of speech, in which the individual is more talkative than usual or experiences a sense of pressure to keep talking • flight of ideas, in which the individual's thoughts race from one idea to another • distractibility-that is, difficulty focusing on one thing and ignoring irrelevant stimuli • heightened activity, in which the individual is restless and overly zealous in pursuing goals • risk taking, whereby the individual becomes excessively involved in potentially dangerous activities (such as embarking on ,unsound business ventures, driving dangerously or engaging in risky sexual practices). These behaviours, thoughts and emotions are only regarded as symptoms of mania if they are out of character for the individual. Hypomania basically has the same symptom profile as mania with the key distinction being that in hypomania the symptoms are not severe enough to markedly interfere with daily functioning, do not necessitate hospitalisation, and do not involve hallucinations or delusions. Also, the disturbance is of shorter duration, with the DSM-5 criteria for hypomania specifying a period of persistently elevated, expansive or irritable mood that is clearly different from the individual's usual non-depressed mood, lasting for at least four days.

THE BIPOLAR DISORDERS

bipolar I disorder Form of bipolar disorder characterised by manic episodes; maj or depressive episodes often occur but are not necessa ry for the diagnosis.

bipolar II disorder Form of bipolar disorder characterised by hypomanic and major depressive episodes.

As shown in Table 3.2, the various bipolar disorders are characterised in terms of the distinct patterning of manic, hypomanic and major depressive episodes that the individual experiences. According to the DSM-5, bipolar I disorder is defined by the presence of one or more manic episodes. The individual has also usually experienced major depressive episodes but they are not necessary for the diagnosis. In contrast, the individual must have experienced at least one episode of major depression to be diagnosed with bipolar II disorder as well as at least one period of hypomania. Also in contrast to bipolar I disorder, manic episodes are not a feature of bipolar II disorder. Dunner and Fieve (1974) were the first to distinguish between bipolar I and II disorders, although there is ongoing debate as to whether these represent distinctive forms of the condition or simply differences in severity.

TABLE 3.2 The OSM-5 (APA, 2013) diagnoses of bipolar I and bipolar II disorders according to the constellation of major depressi ve, mani c and hypoman ic episodes

MOOD EPISODE Major depressive episode

.

I Manic episode Hypomanic episode

rapid cycling bipolar disorder Diagnosis given when an individual has four or more bipolar ep isodes (ma nia or depression) withi n a si ngle year.

•

•

1

BIPOLAR II

•

an be present but not necessary for a iagnosis

Present

Present

Not present

Can be present but not necessary for a diagnosis

Present

.,

About 90 per cent of individuals with bipolar disorder experience multiple episodes of mood disturbance during their lifetime (Mitchell, Hadzi-Pavlovic, & Loo, 2011). The period of mood disturbance is variable for the individual but generally occurs over weeks or months rather than a matter of days. Over time, the episodes may become more frequent and closer together. The subtype of rapid cycling bipolar disorder is diagnosed in those individuals who experience four or more bipolar episodes (mania or depression) within a year. This definition includes those who recover between episodes and those who switch continually from one polarity to the other.

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A less severe but more chronic disorder is referred to as cyclothymic disorder, in which the symptoms lack the severity to meet criteria for bipolar I or II disorders. In the case of cyclothymic disorder, the individual experiences numerous periods of hypomanic and depressive symptoms, none of which is severe enough to meet criteria for manic or major depressive episodes. There are increased rates of cyclothymic disorder in the family members of individuals with bipolar I or II disorders, and those with this condition may respond well to treatment with lithium (a major treatment for bipolar disorder). These findings suggest a connection between cyclothymic disorder and bipolar I and II disorders, although the nature of the relationship is still not fully understood. The DSM-5 also includes a condition referred to as 'other specified bipolar disorder'. This is designed to take into account people who may, for example, have a history of depression and meet all the criteria of hypomania except the duration. This diagnosis may also be appropriate for someone who has too few symptoms to meet the criteria for bipolar II disorder but has been symptomatic for more than four days. In addition to the diagnosis of a bipolar disorder, further information can be denoted with a specifier. In the DSM-5, one such specifier is 'with mixed features'. This means, for example, that a person might have a manic episode with mixed features (if some depressive features are present). Another specifier is 'with anxious distress', which is added if the person with a bipolar disorder is also experiencing elevated anxiety.

cyclothymic disorder Milder

PROBLEMS WITH THE UNDERDIAGNOSIS AND OVERDIAGNOSIS OF BIPOLAR DISORDER Bipolar disorder can be prone to both underdiagnosis and overdiagnosis. The most common forms of underdiagnosis are for patients with bipolar disorder to be misdiagnosed as having schizophrenia (particularly in men) or unipolar depression (particularly in women). The misdiagnosis of schizophrenia probably reflects similarities between the psychotic features (especially the delusions and hallucinations) of acute mania and schizophrenia. A major population study from Scandinavia convincingly demonstrated that there are shared genetic factors between schizophrenia and bipolar disorder, as well as distinct genetic contributions (Lichtenstein et al., 2009). The existence of shared and distinct features between these two major psychotic disorders can make their differential diagnosis challenging. In addition to schizophrenia, individuals with bipolar disorder can be misdiagnosed with unipolar depression. This is more lilcely to occur when past episodes of hypomania or mania are not actively explored by the clinician when assessing individuals presenting with depression. The diagnosis of bipolar disorder may also be missed in patients with anxiety disorders and substance use disorders, perhaps reflecting a lack of appreciation that these disorders frequently coexist with bipolar disorder. Sometimes patients with bipolar disorder are misdiagnosed with personality disorders, particularly borderline and antisocial types. The overdiagnosis of bipolar disorder can also be a problem (Mitchell, 2012). Specifically, there is concern that bipolar disorder (especially bipolar II disorder) may be overdiagnosed, particularly in those individuals with unipolar depression or borderline personality disorder. Some authorities recommend diagnosing hypomania even for brief periods of elevated mood (i.e., of only a few hours in duration), rather than the DSM-5 criterion of hypomania lasting for at least four days. Such a diagnostic shift risks either labelling normal exuberance and enthusiasm as a pathological mood disturbance, or misconstruing the mood instability common in those with borderline personality traits as hypomania. This is not a mere esoteric academic debate. Overdiagnosis could mean inappropriate and excessive use of mood stabilising treatments, as well as insufficient attention paid to the psychological aspects of unipolar depression or the personality disorder.

but more chronic form of bipolar disorder.

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THE EPIDEMIOLOGY OF BIPOLAR DISORDER PREVALENCE Australian data from the 2007 National Survey of Mental Health and Wellbeing indicate that 0.9 per cent of Australians have major symptoms of bipolar disorder in any 12-month period and 1.3 per cent over the lifetime (Mitchell et al., 2013). The United States National Comorbidity Survey Replication study, based on the DSM-IV-TR criteria, originally estimated a lifetime prevalence of 3.9 per cent for bipolar disorders I and II (Kessler, Chiu, et al., 2005), although the interview instrument used in this study has been criticised for its tendency to overdiagnose bipolar disorder. By comparison, unipolar depression was estimated to have a lifetime prevalence of 16.6 per cent. In addition to the fact that unipolar depression is more common than bipolar disorder, the two conditions differ in their gender ratio. While unipolar depression is more common in females, women and men are equally likely to develop bipolar I disorder. Since women report more episodes of depression than do men, however, they are more likely to meet criteria for bipolar II disorder.

AGE OF ONSET The median age of onset for bipolar disorder has been found to be 25 years, with approximately 25 per cent of individuals experiencing onset of the illness by age 17. There appears to be a poorer outcome if the onset occurs in childhood or adolescence (National Institute of Mental Health, 2012).

COURSE OF THE DISORDER

hypomanic episode Less severe form of a manic episode that is an essential feature of bipolar II disorder.

In terms of the course of the illness, it is becoming increasingly apparent that the depressed phase of bipolar disorder (bipolar depression) is the predominant mood disturbance (Mitchell et al., 2009). A longitudinal study following patients over an average of 13 years reported that those with bipolar I or II disorder spent much more of their lives depressed than manic or hypomanic (Judd, Akiskal, & Schettler, 2002; 2003). Those with bipolar I disorder experienced 32 per cent of their time in depression compared with 9 per cent in mania or hypomania. For those with bipolar II disorder, the disparity was even greater, with 50 per cent of the time spent depressed compared with 1 per cent spent in hypomania. The median duration is 15 weeks for bipolar depressive episodes, seven weeks for manic episodes and three weeks for hypomanic episodes (Solomon et al., 201Q). The recurrent nature of bipolar disorder makes it particularly difficult on the lives of sufferers. Despite considerable advances in medications, about 40 per cent of bipolar disorder patients relapse within one year, 60 per cent in two years and 73 per cent over five years. Lithium fully protects only 25-50 per cent of patients against further episodes and there are often problems with gaining compliance from patients in taking their mooication. A high correlation has been found between poor medication adherence and low levels of acceptance of the diagnosis of bipolar disorder, highlighting the importance of psychological treatments that t:?cus on helping patients gain acceptance of their illness and understand the necessity of medication adherence.

PROBLEMS ASSOCIATED WITH BIPOLAR DISORDER Comorbidity of bipolar disorder with other psychiatric illnesses is common, particularly with anxiety disorders and substance abuse. Other associated problems include social and economic costs and the increased risk of suicide.

ANXIETY DISORDERS Recognition of the relationship between anxiety disorders and mood disorders has traditionally been limited to unipolar depression. However, epidemiological and clinical studies have also highlighted a significant comorbidity between anxiety disorders and bipolar disorder (Mitchell et al., 2013; Perugi, Akiskal, Toni,

Chapter 3

Mood disorders

Simonini, & Gemignani, 2001). In fact, it has become evident that the comorbidity between anxiety disorders and bipolar disorder may be even higher than for unipolar depression (Chen & Dilsaver, 1995). According to Goodwin and Sachs (2004), as many as 93 per cent of bipolar I disorder patients have an anxiety disorder at some time in their life. In the Australian National Survey (Mitchell et al., 2013), about 50 per cent of people with bipolar disorder had a concurrent anxiety disorder (most commonly panic disorder, generalised anxiety disorder and social phobia). Another study revealed that the lifetime prevalence of panic disorder was 20.8 per cent in patients with bipolar disorder, compared with 10 per cent in those with unipolar depression and 0.8 per cent in the general population (Chen & Dilsaver, 1995). The same study found that the lifetime prevalence rate of obsessive-compulsive disorder among bipolar patients was 21 per cent as compared to 12.2 per cent in unipolar depression and 2.5 per cent in the general population. In the National Comorbidity Survey, 47.2 per cent of patients with bipolar I disorder were found to have comorbid social phobia compared to 13.3 per cent of the general population (Kessler, Rubinow, Holmes, Abelson, & Zhao, 1997). The same survey revealed a lifetime diagnosis of posttraumatic stress disorder in 38.8 per cent of patients with bipolar I disorder. This high level of comorbidity between bipolar and anxiety disorders raises the question of their temporal sequence. Perugi and colleagues (2001) studied the temporal relationship between bipolar disorder and a range of comorbid disorders, specifically anxiety disorders (i.e., panic disorder and social anxiety disorder) and obsessive-compulsive disorder. The study included 63 patients with panic disorder, social phobia (social anxiety disorder) or obsessive-compulsive disorder who also had comorbid bipolar I or II disorder. As seen in Figure 3.4, the results revealed that the comorbid disorder preceded (hypo)mania in 33.3 per cent of individuals with panic disorder, 94.7 per cent of individuals with social phobia and 52.2 per cent of individuals with obsessive-compulsive disorder. The comorbid disorder had its onset during the (hypo)manic episode in 28.6 per cent of those with panic disorder, yet in none of those with social phobia and only one of the participants with obsessive-compulsive disorder. Finally, the comorbid disorder followed the onset of (hypo )mania in 38.1

100

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~ 40 CII

Panic disorder OCD Social phobia

~

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Before

During

After

FIGURE 3.4 The percentage of patients who developed panic disorder, obsessive-compulsive disorder (OCD) or social phobia before, during or after their first manic or hypomanic episode. Source: From Perugi, G., Akiskal, H. 5., Toni, C., Simonini, E., & Gemignani, A. (2001 ). The temporal relationship between anxiety disorders and (hypo)mania: A retrospective examination of 63 panic, social phobic and obsessive-compulsive patients with comorbid bipolar disorder. Journal ofAffective Disorders, 67, 199-206, Elsevier.

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per cent of those with panic disorder, 5.3 per cent of those with social phobia and 43.5 per cent of those with obsessive-compulsive disorder. In other words, anxiety symptoms preceded, occurred during and followed (hypo )manic symptoms at different rates depending on the type of comorbid disorder. For instance, in the case of social phobia, the anxiety symptoms almost always preceded (hypo )mania. These findings have several implications. First, they conflict with the common perception that the relationship between anxiety and mood disorders is limited to unipolar depression. Second, they suggest that anxiety may at times be an initial sign of an evolving bipolar disorder.,Third, anxiety disorders are often treated with antidepressants, which, given these findings, suggests that antidepressants may at times be triggering manic or hypomanic symptoms. Finally, there is a clear pattern of social phobia preceding (hypo )mania, which warrants further study since it may suggest a causal role of social fears (e.g., thoughts about the self as inadequate) in triggering mania or hypomania.

SUBSTANCE MISUSE Substance misuse has been reported in 39 per cent of people with bipolar disorder. In fact, bipolar disorder has frequently been found to be the psychological disorder most strongly associated with substance misuse (Todd & Sellman, 2004). There are various possible interactions between substance misuse and mood disorders. Drug amphetam ines Stimu lant drugs that can produce symptoms of euphoria, self-confidence, alertness, agitation, paranoia, perceptual illusions and depression.

use (particularly marijuana, amphetamines and alcohol) is thought to be commonly used to self-medicate against emotional disturbances. Unfortunately, many of these drugs, particularly marijuana, inadvertently lead to mood destabilisation. Furthermore, manic symptoms such as elevated mood, increased activity and decreased need for sleep may be part of substance intoxication and withdrawal. It is therefore considered important to delay diagnosis until drugs or alcohol are no longer affecting the patient's presentation. Since these coexisting disorders may interact and influence the course of each other, appropriate assessment and effective treatment of substance misuse is an essential part of the treatment of bipolar disorder (Goodwin & Sachs, 2004).

SOCIAL AND ECONOMIC COSTS Given the severely disabling symptoms of manic and depressive episodes, together with high rates of comorbidity with other psychological disorders, it is not surprising that the social and economic costs to individuals with bipolar disorder and society are substantial. Following manic episodes, almost one-third of patients cannot work for six months and only one-fifth return to work at their former skill level. In an Australian survey, people with bipolar disorder were found to be almost five times more likely ,than the general population to have disrupted relationships, and more than twice as likely as those with unipolar depression to have such difficulties (Mitchell et al., 2013).

SUICIDE The suicide rate in people with bipolar disorder is about 15 times that of the general population, with 80 per cent of suicides occurring during episodes of depression (Harris & Barraclough, 1997). At least 25 per cent of patients will attempt suicide and 10-20 per cent will complete suicide. It would appear that rates of su'icide are higher among individuals with bipolar II disorder compared to those with bipolar I disorder, most probably due to the more frequent episodes of depression in the former compared to the latter.

LIVING WITH BIPOLAR DISORDER Meg Smith, an Australian Associate Professor in Psychology and a highly respected writer and community researcher, gives a poignant personal account of life with bipolar disorder, with its broad range of associated problems and perhaps even some gains:

C

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ii

There is a current debate going on in my support group about whether one has bipolar disorder or

b

is bipolar. My first inclination was to say that I have bipolar disorder-in the sense that I experience episodes of manic illness and depression and that this constitutes the syndrome of bipolar disorder.

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Chapter 3

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But somehow this does not really encompass the effect that bipolar disorder has had on my life. There was the long period of undiagnosed and untreated episodes of mood disorder. My mother described me as a miserable child-and so I was with a number of early episodes of depression that turned me from a happy and interesting child to a whiny, miserable one prone to constipation, headaches, social withdrawal and attacks of anxiety where I would cry hopelessly. By the time I reached adolescence, I conceptualised myself as a shy, withdrawn and uninteresting person. Then the hypomanic episodes started. I discovered an extroverted, somewhat grandiose, confident, outgoing and attractive person. I remember thinking that life would be all right if it weren't for the ups and downs-with no idea about why I should think such a thing. I am still searching for a conceptualisation of what I have and who I am. Bipolar disorder has affected my life profoundly. It has ended relationships, changed my career and carried me to places I would probably never have gone without the mood swings and the changes in perception that the moods bring to the world. I can't say that I regret having experienced a mood disorder but I do regret not knowing more about it a long time ago. Maybe I would have ended up as an English teacher in some country high school without it. It has been said that people with bipolar disorder have\ nter~sting lives and I have certainly had that. I don't know if I would have been happier not having bipolar. I do know that I value my stability now. I

Personal communication, 7 November 2Q06

BIPOLAR DISORDER AND CREATIVITY While the focus thus far has been on the problems associated with bipolar disorder, researchers have proposed that there may be at least one positive aspect of bipolar disorder, namely its potential association with creativity. Since the late twentieth century researchers have been intrigued by an apparent relationship between creativity and psychopathology, particularly bipolar disorder, with theorists noting the similarities in the cognitive and affective processes of those with the disorder and creativity. For example, according to Winnicott (1971), creativity is an expression of vitality, while Murray and Johnson (2010) have described the main features of the creative process as fluency of associations, positive affect, divergent thinking and cognitive over-inclusion-features evident in those with bipolar disorder. There is certainly much anecdotal evidence of a connection between bipolar disorder and creativity as evident in the lives of eminent people such as Stephen Fry who, in the BBC2 documentary, The Secret Life of Manic Depression (Gallagher, 2013), stated that, 'I rely on it to give my life a sense of adventure and I think that most of the good about me has developed as a result of my mood swings. It has tormented me all my life with the deepest of depressions, but also given me the energy and creativity which has perhaps made my career'. The postulated association between bipolar disorder and creativity is controversial and the research findings are inconsistent. In support of an association between bipolar disorder and creativity a study of 36 British and Irish poets born between 1705 and 1805 found symptoms of mood disorders among half of the poets and about one-quarter were thought to have bipolar disorder (Jamison, 1989). More recently, Tremblay, Grosskopf, and Yang (2010) examined occupational creativity among patients with bipolar disorder. Based on the Epidemiological Catchment Area Study, people with bipolar disorder were found to have more creative occupations (e.g., musicians, writers and poets) than the general population. Additional support for the notion of a link between bipolar disorder and creativity stems from research highlighting elevated aspects of creativity in individuals with bipolar disorder. For instance, Santosa and colleagues (2007) found that individuals with bipolar disorder (but not those with major depressive disorder) demonstrated similar levels of creativity to a creative control group (comprising individuals with no psychological disorder who were enrolled in a creative writing, fine arts or product design postgraduate program) but significantly higher creativity than a healthy

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Abnormal Psychology 3e control group. In another study, Strong and colleagues (2007) found that a combination of cyclothymia, dysthymia and neuroticism predicted higher creativity scores. Further support for a link between creativity and bipolar disorder is found in research indicating a genetic connection between the two, with one study showing that children with bipolar disorder who had parents with bipolar disorder were more creative than healthy controls (Simenova, Chang, Strong, & Ketter, 2005). Carson (2011) developed the Shared Vulnerability Model in an attempt to understand the link between creativity and psychopathology. This model proposes that a vulnerability to psychopathology shares features that also predispose individuals to creativity. Among these shared factors are cognitive disinhibition (so that more stimuli enter into awareness), an attentional bias toward novel stimuli and neural hyperconnectivity (which is proposed to increase associations between different stimuli). Carson suggests that these factors, which are common to both types of psychopathology and creativity, result in an increased range of stimuli available in conscious awareness that can then be combined in novel ways. Actor and comedia n Stephen Fry has spoken publicly about his life with bipolar disorder, Yet there are also research findings that challenge the including hi s belief that the disorder has postulated association between bipolar disorder and co ntributed to his creative achievements. creativity. For instance, Weisberg (1994) analysed the musical compositions of Robert Schumann (known to have had bipolar disorder) and found that periods of positive mood were associated with an increase in the quantity but not the quality of his compositions. Such findings are contrary to the notion that mania alters an individual's cognitive processes in such a way as to encourage greater creativity. While the research findings are inconsistent in terms of a connection between bipolar disorder and creativity, accepting such a link can pose challenges to treatment. Patients with bipolar disorder may cease treatment (e.g., stop taking their medication) if they think that their creative potential will be reduced. The issue of creativity .may therefore need to be addressed during treatment. Any negative consequences of treatment compliance on the patient's creativity need to be considered within the context of the profoundly atlverse consequences of non-compliance on the individual's social, emotional and occupational functioning.

THE AETIOLOGY OF BIPOLAR DISORDER Traditionally, theories of bipolar disorder have focused almost exclusively on biological factors, with the recognition of psychosocial factors a more recent phenomenon. Thus current understandings of bipolar disorder are consistent with a biopsychosocial approach.

BIOLOGICAL FACTORS Genetic factors are among the biological vulnerabilities to bipolar disorder. The lifetime risk of bipolar disorder in the family members of bipolar disorder patients is about 6-9 per cent compared with a rate of about 0.5- 1.0 per cent in the general population. The strong genetic component of bipolar disorder has been supported by both a large study of twins, which estimated a heritability rate of about 85 per cent, and a Danish population study sample of several million participants, which reported a 13-fold increased risk of bipolar

FIG SoU1

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117

disorder in the first-degree relatives of affected individuals (Mortensen, Pedersen, & Melbye, 2003). Bipolar disorder therefore runs in families. The specific risk genes for bipolar disorder are now being gradually identified, with genome-wide association studies (GWAS) of large international samples now confirming involvement of a number of genes (Psychiatric GWAS Consortium Bipolar Disorder Working Group, 2011).

STRESSFUL LIFE EVENTS As described in the section on unipolar depression, the role of stressful life events in precipitating depression has been well researched. Extending this research, it would appear that stressful life events can also lead to bipolar episodes. Individuals with bipolar disorder who experience high levels of stress are four and a half times more likely to have a mood relapse than individuals with low levels of life stress (Ellicott, Hammen, Gitlin, Brown, & Jamison, 1983). The Diathesis-Stress Model holds that psychological disorders result from an interaction between an underlying vulnerability and a stressful life event. This model is well established in relation to schizophrenia, and has subsequently been applied to bipolar disorder (Jones, 2004). As shown in Figure 3.5, the model emphasises the role of stressful life events that result in disrupted routines and sleep deprivation in triggering episodes of mania (Frank, Swartz, & Kupfer, 2000). Examples of such events include long flights, childrearing, jobs involving shift work and certain patterns of social stimulation (e.g., rave parties, rock concerts and huge crowds at sporting events). These events interact with an underlying biological vulnerability that, in the case of bipolar disorder, is thought to be a circadian system (the 24-hour rhythmic cycle of physiological processes) that is highly sensitive to disruption. This disruption of the circadian rhythm results in the early signs of mood disturbance (such as restlessness, sleeplessness and feeling wired). The individual may use poor coping strategies (such as substance abuse) to deal with these symptoms, which in turn results in a full-blown manic or depressive episode. These episodes in turn constitute a considerable source of stress (e.g., straining the individual's relationships), thereby exacerbating the cycle.

Stressfu l life events causing disrupted routines or sleep deprivation

Biological vulnerability (i.e., circadian rhythm instability)

Manic, hypomanic, or depressive episode

Early symptoms of mood disturbance

Poor coping strategies

FIGURE 3.5 The Diathesis-Stress Model of bipolar disorder Source: Adapted from Jones, S. (2004). Psychotherapy of bipolar disorder: A review. Journal of Affective Disorders, 80, 101 - 114.

Diathesis-Stress Model Originally developed in the context of schizophrenia, the view that abnormality is caused by the combination of a vulnerability or predisposition (the diathesis) and life events (the stressor).

118

Goal Dysregulation Model Theory that man ic episodes may be triggered by dysregulated goal pursuit which entails the person being excessively involved in the purs uit of goals.

Abnormal Psychology 3e

One type of life event that may have particular relevance in terms of disrupting routines and hence triggering manic or hypomanic episodes is the excessive pursuit of goals. The Goal Dysregulation Model suggests that mania is the result of excessive goal engagement (Johnson et al., 2000). Even when not in an episode, individuals with a history of bipolar I disorder have been found to place a higher emphasis on rewards and to be excessively engaged in the pursuit of achieving goals compared to those without the disorder. The model proposes that excessive reward sensitivity may heighten the experience of positive states following success and therefore increase the probability of mania. Supporting the Goal Dysregulation Model, it has been found that increases in goal-setting and time spent pursuing goals accelerate the development of hypomanic or manic symptoms such as inflated self-esteem, decreased need for sleep, flight of ideas and increased talkativeness. Johnson et al. (2000) examined whether goal-directed behaviour would predict increases in mania among individuals with bipolar disorder. They found that specifically goal-directed life events, and not general positive life events, were associated with elevations in subsequent manic symptoms. In contrast, goal attainment was not associated with changes in depression.

PSYCHOLOGICAL FACTORS Similar to the research on unipolar depression, cognitive disturbance (relating to thoughts, beliefs and attitudes) is believed to be a causal factor for bipolar disorder. Individuals with bipolar disorder endorse a greater number of dysfunctional attitudes compared to healthy controls even when euthymic (i.e., normal in mood) (Alloy, Reilly-Harrington, Fresco, Whitehouse, & Zechmeister, 1999). For instance, in contrast to controls, it has been reported that those with bipolar disorder have greater negative beliefs regarding their worth, leading to lower self-esteem. It is proposed that individuals prone to mania may be characterised by certain response styles. Specifically,

when negative events activate low self-esteem, the individual may respond defensively with grandiose ideas, which inhibit negative thoughts about the self (Winters & Neale, 1985). Thomas and Bentall (2002) have similarly proposed that hypomania and mania represent a deliberate, defensive attempt to avoid the negative cognitions and emotions associated with depression and low self-esteem. Supporting their theory, they found that a combination of rumination (i.e., thinking the same thought over and over again), distraction and risktaking coping styles predicted higher scores on a measure of hypo mania in a sample of university students. As a final comment on cognitive approaches to mania, it is likely that at least some aspe'cts of the cognitive disturbance evident in individuals with bipolar disorder are a consequence of the disorder rather than a causal factor. For example, many individuals with bipolar disorder experience a change in their self-concept after episodes of hypomania, mania or depression (Lam, Jones, Haywood, & Bright, 1999). In particular,

temperament Personality traits believed to be genetically based.

negative self-evaluation accompanied by feelings of guilt, shame and anger are common responses as a result of experiencing an episode of illness. This is particularly relevant in mania as individuals often behave in an uncharacteristically disinhibited manner (such as inappropriate social and sexual interactions and overspending) which has potentially adverse, humiliating and debilitating consequences. In addition to cognitive factors, temperament may be another psychological factor relevant to the development of bipolar disorder. Temperament refers to enduring personality traits and characteristics (such as introversion and interpersonal sensitivity) . It has been found to be a significant factor in the tendency to develop manic and/or depressive episodes and may affect the course and outcome of bipolar disorder once it has developed. Several studies have found significant temperamental differences between those with bipolar I disorder, bipolar II disorder, unipolar depression and controls (Akiskal et al. , 2006). For example, traits such as perfectionism and sociotropy (a high need for social acceptance) have been found to be more prevalent in individuals with bipolar disorder than unipolar depression. In addition, studies have foun d that symptom severity in bipolar disorder is significantly associated with sociotropy, negative interpersonal events (e.g., ongoing conflicts with others) and the interaction of the two (Hammen, Elliott, & Gitlin, 1992;

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Reilly-Harrington, Alloy, Fresco, & Whitehouse, 1999). In other words, bipolar symptoms may be triggered if an individual with an extreme need for social approval perceives that s/he has been rejected. Temperamental tendencies can adversely affect a person's ability to accept and adapt to their illness, which can lead to poor compliance with treatment and a high risk of relapse. It is therefore extremely important to examine and address temperament factors when managing patients with bipolar disorder (Ball, Mitchell, Malhi, Skillecorn, & Smith, 2003).

PSYCHOLOGICAL MEASURES OF SYMPTOMS Psychological measures of symptoms commonly used in Australia include: I. Depression Anxiety Stress Scale (DASS-21) (Lovibond & Lovibond, 1995). The DASS-21 is a 42-item

measure with three subscales: depression, anxiety and stress. 2. Dysfunctional Attitudes Scale 24 (DAS-24) (Weissman, 1979; Power et al., 1994). The DAS-24 assesses attitudes toward achievement, dependency and self-control. 3. BIS/BAS Scales (Carver & White, 1994). These combined scales assess behavioural inhibition and behavioural activation and comprise four subscales: behavioural inhibition, drive, fun seeking and reward responsiveness. 4. Response Style Questionnaire (RSQ) (Thomas & Bentall, 2002). This is a 48-item measure comprising

three subscales: rumination, adaptive coping and risk taking. 5. Internal State Scale (ISS) (Bauer et al., 1991). The ISS is a 16-item measure assessing current mood state in bipolar disorder. It has four subscales: activation, wellbeing, depression and perceived conflict.

THE TREATMENT OF BIPOLAR DISORDER PHARMACOLOGICAL APPROACHES Drug treatments for bipolar disorder vary according to the acute or maintenance phases of the condition. Acute drug treatments target the existing episode of mood disturbance while maintenance treatments focus on minimising the chances of relapse. The task of mood stabilisers is to effectively treat or prevent bipolar episodes (manic, depressive or mixed episodes) without triggering a mood shift to the opposite pole. Today, there are six mood stabilisers commonly administered: lithium, carbamazepine, valproate, olanzapine, quetiapine and lamotrigine. A number of other 'atypical antipsychotics' are also effective in treating (and, in some cases, preventing relapse of) mania: these include aripiprazole, risperidone and ziprasidone. There have been some excellent recent reviews and meta-analyses of the current evidence for the role of medications in the treatment of bipolar disorder (Cipriani et al., 2011; Geddes & Miklowitz, 2013).

PSYCHOLOGICAL APPROACHES There is now convincing evidence that psychological therapies, used in conjunction with drug treatments, are likely to contribute to a significant improvement in the symptoms and quality of life for people with bipolar disorder as well as being cost effective ( e.g., reducing the costs of further use of health services due to relapse). Psychological interventions aim to reduce symptoms, prevent relapse and recurrence, restore healthy psychological functioning, and provide support to the patient and family. Specific goals include establishing medication adherence, promoting regular cycles of activity and sleep, improving coping strategies and emotional regulation techniques, addressing the psychosocial effects of the illness and identifying early signs of relapse. Psychological treatments differ in the mechanisms through which they produce recovery, the time at which they are delivered in relation to the episode, and whether they are individual or group-based treatments. Although the psychological treatments are presented separately, in clinical practice a number of interventions are often included in a treatment program.

mood stabilisers

Group of drugs including lithium and anticonvulsants that are used to treat psychological disorders characterised by unstable mood (such as bipolar ·disorder).

120

psychoeducation Treatment technique that entai ls providing the client with information regarding the nature, causes, effects and treatment of his/ her psychological problem.

Abnormal Psychology 3e

Psychoeducation Psychoeducation is a component of all psychological interventions for bipolar disorder and entails providing the patient and family with information regarding the illness and its treatment. The main strategies include providing education regarding the importance of identifying early signs of relapse so that preventative action can be taken, medication adherence, minimising risk factors (e.g., substance abuse) and maximising protective factors (e.g., maintaining a regular sleep/wake cycle) . One study found that the addition of 7-12 sessions of psychoeducation, to medication resulted in a 30 per cent reduction in the rate of manic relapse compared to medication alone (Perry, Tarrier, Morriss, McCarthy, & Limb, 1999). Mood monitoring is an important intervention in the early stages of therapy. Encouraging clients to keep structured mood diaries helps in identifying th e triggers to mood shifts and the associated changes in thoughts and feelings . Patterns may become apparent in the role of particular stressors such as a series of late nights, pressure at work or interpersonal difficulties. Early warning signs may also be identified through monitoring (e.g., irritability or anxiety preceding hypomania). The Black Dog Institute has a number of Mood Diaries available that clients can access.

Cognitive behaviour therapy Cognitive behaviour therapy (CBT) is a well-established psychological treatment of choice for m any disorders, including anxiety disorders and unipolar depression, and has been adapted for the needs of patients with bipolar disorder. The aims of CBT are to alleviate acute symptoms and prevent relapse and recurrence through identifying and challenging unhelpful thoughts and assumptions; improving adherence to medication; and implementing adaptive coping and problem-solving strategies. A key technique of CBT is cognitive restructuring, which involves identifying and challenging hyper-positive cognitions (e.g.,

'No

one else can see it, but I will be highly successful if I race ahead with this business plan') as well as negative underlying beliefs (e.g., 'I need to be highly successful to prove that I am worthwhile') . Cognitive adaptation to the experience of mental illness refers to the meaning a patient assigns to the illness, including his/her beliefs regarding its causes and how best to m anage it. These are key beliefs that are addressed in CBT as they play an important role in determining a patient's acceptance of appropriate treatment and hence the ultimate level of social and psychological functioning that s/he is able to attain. self-efficacy Person's belief that s/ he has the ability to succeed in a specific situation.

The advantages of CBT are its brevity, its coherent theoretical framework, and the fosterin~ of self-efficacy as patients learn the skills of managing their symptoms. The first randomised controlled trial of CBT for bipolar disorder was conducted by Cochrane in 1984. Since then, there has been a substantial increase in studies testifying to the efficacy of CBT for bipolar disorder (Ball, Mitchell, Corry, Skillecorn, & Malhi, 2006; Lam et al., 2003; Lam, Hayward, Watkins, Wright, & Sham, 2005; Patelis-Siotis et al., 2001; Scott, Garland, & Mqorhead, 2001; Scott et al., 2006; Zaretsky, Segal, & Gemar, 1999). Lam et al. (2003; 2005) conducted one of the largest randomised controlled trials of patients with bipolar disorder using a relapse-prevention approach. Patients with bipolar I disorder were randomly assigne'ci to the control group (minimal psychiatric care that primarily consisted of medication) or the CBT group (an average of 14 CBT sessions combined with minimal psychiatric care) for a six-month period. The CBT sessions focused on the monitoring of symptoms, modification of behaviours (e.g., ensuring regular sleeping times), and addressing extreme goal-pursuit attitudes and behaviours. Both groups were followed up for a total of two years after treatment ended. As shown in Figure 3.6, patients who received CBT experienced significantly fewer manic/hypomanic and depressive episodes compared to those in the control group. Thus CBT in addition to pharmacological treatment was found to be beneficial in reducing relapse rates compared to medication alone. However, the beneficial effect

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Chapter 3

Mood disorders

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FIGURE 3.6 The percentage of bipolar disorder patients in the CBT and control groups who experienced a manic/ hypomanic episode or a depressive episode over a two and a half year period. Source: From Lam, D. H., Hayward, P., Watkins, E. R., Wright, K., & Sham, P. (2005). Relapse prevention in patients with bipolar disorder: Cognitive therapy outcome after 2 years. American Journal of Psychiatry, 162, 324-329, American Psychiatric Association .

Interpersonal and Social Rhythm Therapy (IPSRT)

Interpersonal and social rhythm therapy (IPSRT) was developed by Frank, Swartz, and Kupfer (2000) based on their earlier work on interpersonal psychotherapy for depression. IPSRT is targeted towards reducing disruptions in daily routines and sleep/wake cycles that trigger bipolar episodes. Patients are taught to regulate their social rhythms (e.g., establish good routines for eating, socialising and sleeping), particularly during times of stress, and to address interpersonal difficulties that may be triggering or maintaining emoti?nal instability. In the Pittsburgh Maintenance Therapies study (Frank et al., 2005), patients with bipolar disorder were randomly assigned to receive one of two psychosocial treatments in addition to medication: IPSRT or standard management. IPSRT delivered in the acute phase was found to be more effective than standard management in preventing relapses. Family interventions

Family interventions have been used effectively for patients with bipolar disorder since the 1970s. Miklowitz and Goldstein (1990) designed a family-focused therapy program for patients with bipolar disorder who had recently experienced an episode of mood disturbance. This approach aims to reduce relapse through improving the family's knowledge about bipolar disorder, communication and problem-solving skills. Compared to the brief psychoeducation control group, patients who received the family-focused therapy program were three times more likely to complete treatment without relapsing and demonstrated lower relapse rates after treatment (Miklowitz, George, Richards, Simoneau, & Suddath, 2003). Relapse prevention

Relapse prevention is an essential component of interventions for bipolar disorder since it is a highly recurrent condition with 70- 75 per cent of patients having at least one relapse within 4- 5 years after recovering from an episode of mania (Gitlin, Swendsen, Heller, & Hammen, 1995). Not only are there immense psychological,

121

Abnormal Psychology 3e

financial and social costs for sufferers and their families, but the economic costs to society are also substantial. In addition, the comorbidity rates and mortality rates (due to suicide) are worryingly high. Consequently, increasing emphasis is being placed on implementing relapse prevention strategies after recovery from an acute episode. Until recently, traditional relapse prevention treatment has entailed medication. However, the medical approach in isolation has been shown to have limitations, including poor adherence due to factors such as unpleasant side effects of medication (Sorenson, Done, & Rhodes, 2007). Furthermore, medication has been found to have limited long-term effectiveness, with one longitudinal study reporting relapse rates of 37 per cent after one year and 73 per cent after five years or more among patients on mood stabilisers alone (Gitlin et al., 1995). This has led to a move towards a biopsychosocial approach to managing bipolar disorder and the inclusion of psychological interventions in relapse prevention in addition to medication (Royal Australian and New Zealand College of Psychiatrists Clinical Practice Guidelines Team for Bipolar Disorder, 2004). Psychological approaches to relapse prevention have highlighted the role of risk factors predisposing individuals to manic and depressive episodes. CBT strategies for relapse prevention include psychoeducation for patients and their families regarding the risk factors for relapse (e.g., drug and alcohol misuse), the importance of medication compliance and the importance of establishing a daily routine. Patients are taught to self-monitor early symptoms of relapse and to have a plan of action available should early warning signs arise. Family, friends and other sources of support are also educated about the early warning signs of relapse. This is especially important in bipolar disorder, as a lack of insight into symptoms or a reluctance to receive help (e.g., if symptoms are valued by the patient) is often present in mania. Given the role of the patient's belief system in his/her acceptance of and adjustment to the illness, emphasis is placed on identifying and challenging any unhelpful cognitions that may predispose him/her to a relapse (e.g., 'I don't feel unwell so I must not need treatment'). Comorbid problems, particularly anxiety disorders and substance abuse, need to be addressed as they interact with bipolar disorder and can negatively affect outcome. While CBT has been shown to achieve some reduction in relapse rates for unipolar depression, there are few studies currently available on bipolar disorder. Sorenson and colleagues (2007) developed a brief psychological intervention based on what they termed 'the instability model of bipolar disorder relapse'. This model assumes that there are four· key mechanisms that trigger relapse in bipolar disorder. The four mechanisms, as illustrated in Figure 3.7, are a biological vulnerability (e.g., neurotransmitter disturbance) in combination with medication non-adherence, disrupted routines (e.g., working longer hours) and dysfunctional interpretations oflife events (including past episodes of mood disturbance that the individual might misinterpret as a sign of personal failure). The model proposes that any of these mechanisms can lead to relapse via a common pathway of sleep disruption. According to the authors, it follows that each of these four mechanisms should be addressed with..specific interventions that all have the aim of reducing the risk of relapse. Key components include identifying the early warning signs of relapse, ensuring medication adherence, interpersonal social rhythms therapy and cognitive therapy. In a recent study, patients with bipolar disorder received four treatment sessions and were followed up for five weeks after they completed treatment (Sorenson et al., 2007). The results revealed that patients achieved significant reductions in hopelessness (and thus suicide risk) and greater perceived control over internal states, both of which are known to be key aspects in recovery from bipolar disorder. This provided initial evidence for the efficacy of a brief psychological intervention in preventing relapse in bipolar disorder, although clearly a longer follow-up period is necessary to determine the longer-term benefits.

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Chapter 3

Mood disorders

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FIGURE 3.7

The Instability Model of relapse in bipolar disorder

Source: Adapted from Sorenson, J., Done, D. J., & Rhodes, J. (2007). A case series eva luation of a brief, psychoeducation approach intended for the prevention of relapse in bipolar disorder. Behavioural and Cognitive Psychotherapy, 35, 93-107.

In summary, the existing evidence demonstrates the efficacy of using psychological relapse prevention strategies in addition to medication in the management of bipolar disorder. However, more studies are needed to identify the most effective type and length of treatment. Hospitalistion Bipolar disorder is a serious condition and the person can be at risk to themselves or others if their behaviour is suicidal or psychotic. During a manic episode, the acutely unwell person may well lose insight and bt;come non-compliant to treatment. Manic episodes are often associated with high risk-taking behaviour · and aggression when attempts are made to contain him or her. In such instances, hospitalisation in an acute psychiatric unit is necessary so acute pharmacological treatment can take place. If resistant, the unwell person may need to be certified under the Mental Health Act 2007. New developments There have been several new developments in the psychological treatment of bipolar disorder. Mindfulness-based cognitive therapy has been shown by recent studies to offer significant benefits for people with bipolar disorder. The focus is on assisting the patient to manage both anxiety and depressive symptoms primarily between episodes (Williams et al., 2008). Australian research suggests that the main benefit of mindfulness-based CBT in bipolar disorder may be for the anxiety symptoms that are frequently comorbid with this condition (Perich, Manicavasgar, Mitchell, Ball, & Hadzi-Pavlovic, 2013). In addition, internet-based treatments are being developed and evaluated, such as the beyondblue funded self-help program for people with bipolar disorder available at www.moodswings.net.au (Lauder, Berk, Castle, Dodd, & Chester 2007) .

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Abnormal Psychology 3e

CA S E

S T UDY

Michael is a 28-year-old law student who has experienced numerous admissions to hospital for mania and depression. During his first manic episode'. at the age of 21, he thought that his doctor was involved with a secret intelligence organisation and that his hospitalisation was a conspiracy to imprison and subdue him, a delusional belief that was exacerbated by being given injections against his wishes. Michael was traumatised by these frightening experiences long after the manic episode subsided. As such, ever since this original episode he has experienced severe anxiety at the first sign of depression or elevated mood. Fear of losing control and having his current life destroyed are never far from his mind. His illness has also affected his relationships, with several of these ending under the strain of Michael's bipolar disorder. His current girlfriend is fearful he will have another episode and, if he does, whether they will be able to cope. Michael's treatment has entailed a combination of medication (mood stabilisers) and psychological therapy. Adjustment issues, including the traumatic and frightening nature of his episodes and the chronic issues associated with managing his mental illness even when not experiencing acute symptoms, have featured in Michael's therapy. Treatment has also entailed teaching Michael to notice the early warning signs of relapse so that he can take immediate action to minimise the likelihood of a full-blown episode from developing. During the course of therapy he has been able to identify his signature signs of a developing mania, including a rise of blood pressure, feeling wired, not being able to focus on his studies, being flooded with ideas and feeling irritable. He has learned to be mindful of his circadian rhythms by structuring his day so as to keep his eating and sleeping routines stable. Cognitive techniques have been used to help him regulate his emotions more effectively by bringing his thoughts back into perspective. Therapy has also helped him to address his deeper attitudes regarding his fear of failure and unlovability. The frequency of his episodes of mania and depression have significantly reduced and his confidence in being able to manage his bipolar disorder has increased.

USEFUL RESOURCES Several self-help books and websites have been developed in Australia and New Zealand in order to provide greater understanding of mood disorders. Examples of these resources are as follows .

.SELF-HELP BOOKS Berk, L., Berk, M., Castle, D., & Lauder, S. (2008). Living with bipolar: A guide to understanding and managi'!_g the disorder. Sydney: Allen & Unwin.

Eyers, K., & Parker, G. (2008) . Mastering bipolar disorder: An insider's guide to managing mood swings and finding balance. Sydney: Allen & Unwin.

Macneil, C., Hasty, M., Conus, P., Berk, M., & Scott, J. (2010). Bipolar disorder in young people: A psychological intervention manual. Cambridge: Cambridge University Press.

Tanner, S., & Ball, J. (1991 ). Beating the blues: A self-help approach to overcoming depression. Sydney: Tower Books.

WEBSITES beyondblue: The National Depression Initiative, www.beyondblue.org.au Black Dog Institute, www.blackdoginstitute.org.au New Zealand Ministry of Health, www.health .govt.nz/your-health/ conditions-and-treatments/mentalhealth/depression

Chapter 3

Mood disorders

SUMMARY Unipolar depression is characterised by periods of depressed mood and/or a loss of interest in activities, together with a range of other symptoms. These symptoms often include a sense of hopelessness that may result in attempted or completed suicid.e. The main depressive disorders included in the DSM-5 are major depressive disorder and persistent depressive disorder (dysthymia) . An alternative subtyping model for the depressive disorders has been proposed by an Australian research group that identifies three broad classes of depressive disorders: psychotic, melancholic and non-melancholic depression. This model combines information about symptoms with aetiological factors and, through its attention to causal factors, aims to guide the selection of the most effective types of treatment. Depressive disorders are among the most prevalent psychological problems in Australia and it is estimated that 1 in 10 Australians are affected by someone close to them suffering from a mood disorder. International data indicate that women are twice as likely to experience depressive episodes compared to men. These prevalence figures are of concern given the range of serious psychological and medical problems associated with depression, including suicide, anxiety disorders and a number of health-risk behaviours such as drug and alcohol abuse. The aetiology of depressive disorders is thought to be related to biological, social, environmental and psychological factors, and this multiplicity of factors is reflected in the diverse treatments for depression, which include a range of both medical and psychosocial approaches. One focus of current research is to identify strategies that may be useful in preventing the development and recurrence of depressive episodes. The bipolar disorders are mainly defined by the occurrence of manic or hypomanic episodes. These episodes are characterised by a period of abnormally elevated or irritable mood with a range of accompanying symptoms such as inflated self-esteem, a decreased need for sleep, and increased talkativeness, goal-pursuit and risk-taking behaviours. While bipolar disorders are less prevalent than unipolar depression, they entail considerable suffering for the individual, with high rates of comorbid psychological disorders (especially anxiety disorders and substance abuse), social and economic problems, and suicide. Over the past decade, substantial progress has been made in developing a better understanding of the biological, psychological and social factors associated with bipolar disorder. The disorder appears to entail a genetically determined pathology in brain structure and function related to emotional regulation. In terms of psychosocial factors, increasing evidence suggests that excessive goal pursuit, behavioural disturbances such as irregufar sleeping patterns, and defensiveness to negative thoughts about the self are pathways to mania. The efficacy of psychological treatments in conjunction with pharmacotherapy has now been established in the treatment of bipolar disorder. Further psychological research is needed to develop interventions that will result in greater long-term maintenance of the benefits from these psychosocial treatments.

125

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Abnormal Psychology 3e

KEY TERMS amphetamines . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 114 amygdala . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 98 anhedonia . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 91 anorexia . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 92 antidepressants . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 103 antipsychotic medications . . . . . . . . . . . . . . . . . . . . . . . . 103 bipolar disorder . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 108 bipolar I disorder . . . . . . . .. . . . . . . .. . . . . . . . . . .. . . . . . ll0 bipolar II disorder . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 110 bright light therapy. . ... ..... .......... ...... ... .... 104 conduct ......... .... . .. ..... .. ......... .. . ................ 95 cortisol . . . . . .. . . . . .. . . . . .. . . . . ... . . .. . . . . . .. . . . . . . . .. . . . . . 98 cyclothymic disorder . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 111 Diathesis-Stress Model . . . . . . . . . . . . . . . . . . . . . . . . . . . 117 dysthymia (dysthymic disorder) .................. 93 disruptive mood dysregulation disorder . . . . . . . . . 93 electroconvulsive therapy (ECT) . . . . . . . . . . . . . . . 104 expressed emotion (EE) . . . . . . . . . . . . . . . . . . . . . . . . . . . 102 generalised anxiety disorder (GAD) ... . ... .. ...... 93 Goal Dysregulation Model........... ...... ... .... 118 grandiosity . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 109 hormone .... .... ............. . ......... . ...... ... ... ....... 98 hypomanic episode ...... . ....................... .... . . 112 hypothalamic-pituitary-adrenal (HPA) axis .. . .. . 98 interpersonal difficulties . . . . . . . . . . . . . . . . . . . . . . . . 102 interpersonal psychotherapy (IPT) . . . . . . . . . . . . 106 limbic system . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 98 lithium carbonate . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 108 longitudinal design. ....... . ........... .......... .. .... 95

major depressive disorder .... ......... . .. ........... 91 major depressive episode .. .. ... ........... . ... .... . 92 manic episode.. ........ .. ............ . . . . . . . . . . . . . . . 109 meta-analysis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 105 monoarnine oxidase inhibitors (MAOis) . . . . . . 103 monoamines . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 98 mood stabilisers . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 119 negative cognitive triad . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 99 neuron ............... ........... . ..... . .. .. ... . ... . ... 98 neurotransmitters ... ..... ... .... ... .... . .. ...... .. ...... 98 oppositional defiant disorder ....... ..... . .. ..... .... 95 pleasant activity scheduling . . . . . . . . . . .. . . . . . . . . . 105 prefrontal cortex .... . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 98 protective factors . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 102 psycho dynamic therapies . . . . . . . . . . . . . . . . . . . . . . . . 106 psychoeducation . .. .... ........ . .. . . . .. . . . . . . . . . . . . . 120 psychotic symptoms . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 103 rapid cycling bipolar disorder . . . . . . . . . . . . . . . . . . 110 receptors . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .. . . . . . . . . . . . . 98 repetitive transcranial magnetic stimulation (rTMS) . . . . . . . . . . . . . . . . . . ... . . . . . . . . . 104 seasonal affective disorder . .... .. ... ........... ... 104 selective serotonin reuptake inhibitors (SSRis) 103 self-efficacy.............. .. ... ..... .......... ........ 120 specifier ... . .... . ... .... ... ......... .... . .. , . : . . . . . . . . . . 92 synapse ............... .. .. ....... .. ..... . .. .... ..... .. . 98 temperament . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 118 tricyclic antidepressants (TCAs) . . . . . . . . . . . . . . . 103 vagus nerve stimulation . . . . . . . . . . . . . . . . . . . . . . . . . . . 104

REVIEW QUESTIONS L03.1 3.1

What are the defining features of the main depressive disorders included in the OSM-5 and what aspects of the OSM-5 categories of depressive disorders have proven to be controversial?

3.2

While depressive disorders are among the most common psychological disorders for both females and males, females are especially vulnerable to these disorders. What factors might account for this gender difference?

3.3

List the factors that feature within a biospychosocial model of the aetiology of depression.

3.4

Describe the key components of CBT for depression. What are some of the advantages of this approach?

3.5

Why have prevention approaches been developed for depression and what prevention strategies are best supported by the research?

Chapter 3

Mood disorders

L03.2 3.6

Distinguish between bipolar I and bipolar II disorders.

3.7

With which conditions are the overdiagnosis and underdiagnosis of bipolar disorder most likely to occur? What are the consequences for treatment?

3.8

Describe the Diathesis-Stress Model as it relates to the aetiology of bipolar disorder.

3.9

Describe how cognitive factors and temperament are associated with bipolar disorder.

3.10 What are the main psychological approaches used in the treatment of bipolar disorder? Which of these is unique to bipolar disorder? '

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Chapter 3 Patelis-Siotis, I., Young, L. T., Robb,]. C., Marriott, M., Bieling, P. J., Cox, L. C., & Joffe, R. T. (2001). Group cognitive behavioural therapy for bipolar disorder: A feasibility and effectiveness study.journal ofAffective Disorders, 65, 145-153. Perich, T., Manicavasgar, V., Mitchell, P. B., Ball, J. R., & Hadzi-Pavlovic, D. (2013). A randomized controlled trial of mindfulness-based cognitive therapy for bipolar disorder. Acta Psychiatrica Scandinavica, 127, 333-343. Perry, A., Tarrier, N., Morriss, R., McCarthy, E., & Limb, K. (1999). Randomised controlled trial of efficacy of teaching patients with bipolar disorder to identify early symptoms of relapse and obtain treatment. B ritish Medical journal, 16, 149-153. Perugi, G., Akiskal, H. S., Toni, C., Simonini, E., & Gemignani, A. (2001). The temporal relationship between anxiety disorders and (hypo)mania: A retrospective examination of 63 panic, social phobic and obsessive-compulsive patients with comorbid bipolar disorder. j ournal of Affective Disorders, 67, 199-206. Petersen, T. (2006) . Enhancing the efficacy of antidepressants with psychotherapy.journal ofPsychopharmacology, 20, 19-28. Peterson, C., & Seligman, M . E. (1984). Causal explanations as a risk factor for depression: Theory and evidence. Psychological R eview, 91, 347-374. Power,M . J., Katz, R., McGuffin, P., Duggan, C . F., Lam, D., Beck, A. T. (1994). The Dysfunctional Attitude Scale (DAS). journal ofResearch in Personality, 28, 263-276. Psychiatric GWAS Consortium Bipolar Disorder Working Group (2011). Large-scale genome-wide association analysis of bipolar disorder identifies a new susceptibility locus near OD24. Nature Genetics, 43, 977-983. ~inn, C. R., Dobson-Stone, C., Outhred, T., Harris, A. & Kemp, A.H. (2012). The contribution ofBDNF and 5-HTT polymorphisms and early life stress to the heterogeneity of major depressive disorder: A preliminary study.Australian and New Zealand journal ofPsychiatry, 46, 55-63. Radloff, L. S. (1991). The CES-D Scale: A self-report depression scale for research in the general population.Applied Psychological Measurement, 1, 385-401. Reilly-Harrington, N. A., Alloy, N . B., Fresco, D. M., & Whitehouse, W G. (1999). Cognitive styles and life events interact to predict bipolar disorder and unipolar symptomatology.journal ofAbnormal Psychology, 108, 567- 578. Royal Australian and New Zealand College of Psychiatrists Clinical Practice Guidelines Team for Bipolar Disorder. (2004). Australian and New Zealand clinical practice guidelines for the treatment of bipolar disorders. Australian and N ew Zealand]ournal ofPsychiatry, 38, 280-305. Royal Australian and New Zealand College of Psychiatrists Clinical Practice Guidelines Team for Depression. (2004). Australian and New Zealand clinical practice guidelines for the treatment of depression. Australian and New Zealand journal ofPsychiatry, 38, 389-407. Rutter, M. (1986). The developmental psychopathology of depression: Issues and perspectives. In M. Rutter, C. E. Izard & P. B. Read (Eds.), Depression in young people: D evelopmental and clinical perspectives (pp. 3-30). New York: Guilford Press. Sackeim, H., Prudic, J., Nobler, M., Fitzsimons, L., Lisanby, S., Payne, N., ... Devanand, D. (2008). Effects of pulse width and electrode placement on the efficacy and cognitive effects of electroconvulsive therapy. Brain Stimulation, 1, 71-83. Santosa, C. M., Strong, C. M., Nowakowska, C., Wang, P. W., Rennicke, C. M., & Ketter, T. A. (2007) . Enhanced creativity in bipolar disorder patients: A controlled study. journal of Affective Disorders, 100, 31-39.

Mood disorders

Sawyer, M. G., Kosky; R. J., Graetz, B. W., Arney, F., Zubrick, S. R., & Baghurst, P. (2000). The National Survey of Mental Health and Wellbeing: The child and adolescent component. Australian and New Zealandjournal ofPsychiatry, 32, 214-220. Scott, J., Garland, A., & Moorhead, S. (2001). A pilot study of cognitive therapy in bipolar disorders. Psychological Medicine, 31, 459-467. Scott, J., Paydel, E., Morriss, R., Bentall, R., Kinderman, P., Johnson, T., ... Hayhurst, H. (2006). Cognitive behavior therapy for severe and recurrent bipolar disorders: A randomised controlled trial. British Journal of Psychiatry, 188, 313-320. Segal, Z. V., Williams, M., & Teasdale,]. D. (2002) . Mincifulnessbased cognitive therapy for depression: A new approach to preventing relapse. New York: Guilford Press. Seligman, M . E . P. (1975). H elplessness: On depression, development and death. San Francisco: Freeman, Cooper.

Sheikh,]. I., & Yesavage,J. A. (1986). Geriatric Depression Scale (GDS). Recent evidence and development of a shorter version. In T.L. Brink (Ed.), Clinical Gerontology:A Guide to Assessment and Intervention (pp. 165-173). New York: The Haworth Press, Inc. Simenova, D. I., Chang, K., Strong, C., & Ketter, T. A. (2005). Creativity in familial bipolar disorder. journal of Psychiatric R esearch, 39, 623-631. Slade, T., Johnson, A ., Oakley Browne, M., Andrews, G., & Whiteford, H . (2009). 2007 National Survey of Mental Health and Wellbeing: Methods and key findings. Australian and New ZealandJournal ofPsychiatry, 43, 594-605. Solomon, D. A., Leon, A. C., Coryell, W. H., Endicott, J., Li, C., Fiedorowicz,]. G., ... Keller, M. B. (2010). Longitudinal course of bipolar disorder: Duration of mood episodes. Archives of General Psychiatry, 67, 339-347. Sorenson, J., Done, D. ]., & Rhodes, J. (2007). A case series evaluation of a brief, psycho-education approach intended for the prevention of relapse in bipolar disorder. Behavioural and Cognitive Psychotherapy, JS, 93- 107. Southwick, S. M., Vythilingam, M ., & Charney, D. S. (2005). The psychobiology of depression and resilience to stress: Implications for prevention and treatment. Annual R eview of Clinical Psychology, 1, 255-292. Strong, C. M., Nowakowowska, C. M ., & Santosa, P. (.:~007). Temperament-creativity relationships in moods disorder patients, healthy controls and highly creative individuals. journal ofAffective Disorders, 100, 41-48. Stuart, S., & Robertson, M. (2012). Interpersonal psychotherapy:A clinician's guide (2nd ed.). London: Hodder Arnold. Tang, T. Z., DeRubeis, R., Beberman, R., & Pham, T. (2005). Cognitive changes, critical sessions, and sudden gains in cognitive-behavioural therapy for depression. journal of Consulting and Clinical Psychology, 73, 168-172. Teasdale, J. D ., Segal, Z. V., Williams, J. M. G., Ridgeway, V. A., Soulsby, J. M., & Lau, M. A. (2000). Prevention of relapse/recurrence in major depression by mindfulness-based cognitive therapy.journal of Consulting and Clinical Psychology, 68, 615-623. Thase, M. E., Greenhouse, J. B., Frank, E., Reynolds, C. F., Pilkonis, P.A., Hurley, K., ... Kupfer, D.J. (1997). Treatment of major depression with psychotherapy or psychotherapypharmacotherapy combinations.Archives of General Psychiatry, 54, 1009-1015. Thomas, J., & Bentall, R. P. (2002). Hypomanic traits and response styles to depression. British journal of Clinical Psychology, 41, 309-313. Thorpe, I. (2012). This is me: The autobiography. London: Simon &Schuster.

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Abnormal Psychology 3e Todd, F. C., & Sellman, J. D. (2004). Alcohol and drug misuse and mood disorders. In P. R. Joyce & P. B. Mitchell (Eds.), Mood disorders: Recognition and treatment (pp. 298-311). Sydney: University of New South Wales Press. Tremblay, C. H., Grosskopf, S., & Yang, K. (2010). Brainstorm: Occupational choice, bipolar disorder and creativity. Economics and Human Biology, 8, 233-241. Vos, T., Corry, J., Haby, M., Carter, R., & Andrews, G. (2005). Cost-effectiveness of cognitive-behavioural therapy and drug interventions for major depression. Australian and New Zealand journal ofPsychiatry, 39, 683-692. Vos, T., Flaxman, A. D., Naghavi, M., Lozano, R., Michaud C., Ezzati, M., ... Memish, Z. A. (2012). Years lived with disability (YLDs) for 1160 sequelae of 289 diseases and injuries 19402010: A systematic analysis for the Global Burden of Diseases Study 2010. Lancet, 380, 2163- 2196. Wehr, T. A., Duncan, W . C., Sher, L., Aeschbach, D., Schwartz, P. J., Turner, E. H., .. . Rosenthal, N. E. (2001). A circadian signal of change of season in patients with seasonal affective disorder. Archives of General Psychiatry, 58, 1108-1114.

Weisberg, R. W. (1994). Genius and madness?: A quasiexperimental test of the hypothesis that manic-depression increases creativity. Psychological Science, 5, 361-367. Weissman, A. N. (1979). The Dysfunctional Attitude Scale: A validation study. Dissertation Abstracts International, 40, 1389-1390B. Weissman, M. M., Wickramaratne, P., Nomura, Y., Warner, V., Verdeli, H., Pilowsky, D. J., ... Bruder G. (2005). Families at high and low risk for depression: A 3-generation study. Archives of General Psychiatry, 62, 29- 36. Williams,]. M. G., Alatiq, Y., Crane, C., Barnhofer, T., Fennel, M. J. V., Duggan, D. S., . .. Goodwin G. M. (2008). Mindfulnessbased cognitive therapy (MBCT) in bipolar disorder: Preliminary evaluation ofimmediate effects on between-episodes functioning.journal ofAffective Disorders, 107, 275-279. Winnocott, D.W. (1971). Playing and reality. London: Tavistock. Winters, K. C., & Neale, J. M. (1985). Mania and low selfesteem.journal ofAbnormal Psychology, 94, 282-290. Zaretsky, A. E., Segal, Z. V., & Gemar, M. (1999). Cognitive therapy for bipolar depression: A pilot study. Canadian journal ofPsychiatry, 44, 491-494.

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PSYCHOTIC DISORDERS: AN AUSTRALASIAN FOCUS Psychotic disorders, for many sufferers and their families, are severe and often highly distressing conditions. Part of the tiagedy of psychot ic disorders is that they most often have their onset in late adolescence and early adulthood, just when young people are fac in g so much change and possib ility. As a result, a normally challenging and dynamic phase of life becomes a period of heightened distress and significant problems with everyday living. In 2011, SANE Austra lia published a report on living with psychotic illness in Australia that provides an overview of the challenges of livin g with these disorders in contemporary Austra li a. The report highlighted that around one in 200 Au;;tra li ans are affected by psychosis every year and around 64 000 Australians with a psychotic disorder are in contact with pub lic menta l health services. Compared with 61 per cent of the general popu lation, only 17 per cent of Austral ian s w ith a psyc hotic disorder had a life pa rtner (married or de facto) . Perhaps most striking was the fact that 90 per cent of people w it h a psychot ic disorder

Psychotic disorders are severe conditions that include distressing symptoms such as hallucinations.

experienced a severe impact on their ability to function in daily life. The physical health of Australians w ith a psychotic d isorder is also of major concern. For example, SANE (2011) reported that two-thirds of people with a psychotic disorder smoked tobacco compared with 25 per cent of the genera l populatio n, and although the rate was fall ing in the general popu lation it was unchanged over 10 years in those w ith psychosis. Socia l exc lu sion and deprivation is anothe r important outcome for many w ith severe psychosis. SANE (2011) reported that 21.5 per cent of peop le w ith psychosis we re in work compared with 72.4 per cent of the general population and that one-third of people with psychosis had left schd'ol with no qual ifi cations. One in eight had periods of being homeless in the previous year. In summary, th is report highlights that, in contemporary Austral ia, psychosis has critica l effects on the menta l, physical and soc ial wellbeing of affected individuals. This chapter on psychotic disorders wi ll begin by providing a definition of psychosis in terms of various positive and negative symptoms, and the types of psychotic conditions including schizophrenia. Problems associated w ith these disorders wil l be outl ined and information provided regarding thei r prevalence, age of onset and course over time. Some key findings regarding the aetiology of psychotic conditions, as well as the treatment approaches corresponding to the various stages of psychosis, will be outlined. Throughout, particular attention wi ll be given to Australasian developments in the understanding and treatment of psychotic disorders.

Chapter 4

The definition and symptoms of psychosis

Psychotic disorders

·

In spite of more than 100 years of empirical research into schizophrenia and the psychoses, there is still no universally agreed upon definition of psychosis. In the current version of the Diagnostic and Statistical Manual of Mental Disorders (DSM-5) (American Psychiatric Association [APA], 2013), psychotic disorders are conceptualised in terms of a spectr~m of severity and are characterised by the presence of five diverse symptom dimensions, namely, delusions, hallucinations, disorganised thinking (or thought disorder), grossly disorganised or abnormal motor behaviour and so-called negative symptoms. In clinical practice and in research, symptoms of psychosis are often collapsed into two categories of positive and negative. Positive symptoms include hallucinations (and more subtle perceptual disturbances), delusions, thought disorder and motor disturbances. They are referred to as 'positive' since they entail the addition of disturbance. In contrast, negative symptoms refer to deficits in psychological processes including avolition (the loss of drive or motivation), affective flattening (a dampening down in the expression of emotion) and alogia (a lack of unprompted speech, also referred to as 'poverty of speech'). Although positive and negative symptoms constitute the defining symptoms for a diagnosis of a psychotic disorder, researchers have increasingly recognised that other features associated with psychotic disorders, especially problems with cognition, may be the most disabling aspects of these conditions. These associated problems are therefore likely to become an important area of increased attention for treatment, including early intervention and prevention (Insel, 2010).

HALLUCINATIONS

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L04.1 positive symptoms In schizophrenia: hallucinations, delusions, and disorganisation in thought and behaviour. thought disorder State of highly disorganised thinking (also known as formal thought disorder or a loosening of associations) characteristic of individuals with schizophrenia. motor disturbance Disturbance of bodily movement.

Hallucinations are arguably the most distressing of psychotic symptoms. The DSM-5 defines a hallucination

as 'a perception-like experience with the clarity and impact of a true perception but without the external stimulation of the relevant sensory organ' (APA, 2013, p. 822). Approximately 75 per cent of patients diagnosed with schizophrenia report hallucinations (Bentall, 2006). These are generally auditory hallucinations, with between 60-70 per cent of patients diagnosed with schizophrenia reporting auditory hallucinations consisting of a voice speaking to them (Sartorius et al., 1986). Such voices are typically critical and hostile, but comforting voices are also reported. Command hallucinations, which entail specific instructions to the patient (e.g., to harm him/herself) are also described by between 33 per cent and 74 per cent of voice hearers (Braham, Trower, & Birchwood, 2004). Hallucinations can occur in sensory modalities other than the aural, including visual (e.g., seeing the face of a tormentor), olfactory (sensations of smell, such as the experience of a rotting odour), gustatory (sensations of taste, such as a metallic taste), tactile (sensations of touch, such as a hand on one's shoulder) and somatic (perception of physical experience located within the body) (Assad & Shapiro, 1986). Multimodal hallucinations (e.g., a voice accompanied by the image of a figure) are also reported by patients. Hallucinations can be associated with neurological conditions including temporal lobe lesions, complex partial seizures, migraine and brain injury. Intoxication with illicit substances, such as hallucinogens, is associated with alterations in visual perception of the colour, size and shape of objects and the perception of more abstract images (Assad & Shapiro, 1986). Interestingly, hallucinations are also known to be experienced by a sizeable minority of people in the general population, most of whom do not seek or require assistance, suggesting that the mere presence of hallucinations does not mark the presence of a mental disorder (Ohayon, 2000). This finding is consistent with a meta-analysis of psychotic symptoms in the general community that found that in about 70-95 per cent of cases, psychotic experiences disappear over time (van Os, Linscott, Myin-Germeys, Delespaul, & Krabbendam, 2009). However, in a small proportion of cases, especially when there are environmental risk factors, more serious psychosis that warrants treatment can develop.

negative symptoms In schizophrenia, deficits in functioning such as affective flattening, alogia and avolition. avolition Inability to initiate or persist with important activities; negative symptom of schizophrenia. affective flattening Severe reduction or the comp lete absence of affective (emotional) responses to the environment; negative symptom of schizophrenia. alogia Deficiency in the quantity of speech; negative symptom of schizophrenia.

136 hallucination

Psychotic symptom entailing perceptual experiences that are not rea l, which can occur in any sensory modality (e.g., the fa lse perception of sound or sight). auditory hallucination

Perception of a sound that it not real (such as hearing a voice when alone). hallucinogens

Substances including LSD and MDMA (i.e., 'ecstasy') that ca n produce perceptual illusions and distortions. delusion

Psychotic symptom entailing a strongly held belief that is not consistent with what almost everyon e else believes and despite obvious proof to the contrary. paranoid delusion False

belief of delusional intensity that someone is seeking to harm the individual or his/her interests. delusion of reference False

belief strongly held by an individ ual that envi ronmental stimu li have a particular significance for him/ her. somatic delusion False

belief of delusional intensity regarding the appearance or functioning of one's body.

Abnormal Psychology 3e

Certain features of the hallucinatory experience have been shown to be associated with the degree of impact of the hallucination upon the sufferer. For example, Birchwood, Iqbal, Chadwick, and Trower (2000) found that the beliefs and expectations sufferers hold in relation to their hallucinations, and the strategies they employ to cope with them, may influence the extent of distress associated with symptoms. For example, if the voice hearer assumes that the voice is malevolent or intends harm to the individual, then distress is more likely than if the voice is assumed to be benevolent (e.g., the belief that the voice aims to take the individual to a higher spiritual plane) (Birchwood & Chad.wick, 1997). A variety of assumptions may also be held regarding the identity or source of the voice, which may influence the extent of distress. For example, a belief that the voice is from the devil is likely to be associated with greater distress than if the voice is believed to be that of God.

DELUSIONS The DSM-5 defines delusion as 'a false belief based on incorrect inference about external reality that is firmly held despite what almost everyone else believes and despite what usually constitutes incontrovertible and obvious proof or evidence to the contrary. The belief is not one ordinarily accepted by other members of the person's culture or subculture (i.e., it is not an article of religious faith). When a false belief involves a value judgment, it is regarded as a delusion only when the judgment is so extreme as to defy credibility' (APA, 2013, p. 819). Researchers have described various features of delusions including their content, bizarreness, degree of complexity and consequences. Content is commonly used as a basis for categorising delusions, although in clinical practice delusions often defy being placed into a single category. Paranoid delusions (or 'persecutory delusions') are those most commonly reported by patients in clinical settings. These delusions entail a belief that someone, or a force or agency, is seeking to harm the patient or his/her interests (e.g., believing that the Australian Security Intelligence Organisation [ASIO] is tracking the individual's emails and phone calls). As a consequence, the patient may attempt to avoid the threat, such as minimising contact with strangers or remaining vigilant for possible threats. This state of vigilance is also associated with delusions of reference, which comprise a belief that messages of a highly personal nature are being conveyed via neutral sources, commonly the radio or television (e.g., that a newsreader is communicating coded warnings to the individual within a news bulletin). Somatic delusions, which entail a false belief regarding the appearance or functioning ,o f one's body (e.g., a belief that one has cancer), are also commonly described by patients in clinical settings. These beliefs are sometimes accompanied by somatic hallucinations such as the 'feeling of electricity through the body' or heightened vigilance for internal bodily sensations. They are often highly distressing and can lead to the pursuit of multiple medical interventions. . Grandiose delusions are primarily associated with, but not restricted to, the manic episodes of bipolar disorder, illustrating that psychotic symptoms are not solely experienced in the context of psychotic disorders. They include ideas that one has acquired special powers, worth, knowledge, abilities, influence, ass'ociations, achievements or even an alternative identity, often entailing power, wealth or fame. Related to this, religious delusions entail religious themes, such as a belief that one has acquired the identity of a religious figure - a belief which would not be shared by other members of the religious group. Between 25 and 39 per cent of patients diagnosed with schizophrenia have been found to show signs of religious delusions (Koenig, 2009) . Nihilistic delusions and delusions of guilt are typically associated with episodes of severe major depression, again highlighting that psychotic symptoms are not restricted to psychotic disorders. Nihilistic delusions include a conviction that one is dead or that parts of one's body or the environment have ceased to exist (Debruyne & Audenaert, 2012). On the other hand, delusions of guilt include beliefs of personal responsibility and that punishment is deserved for specific events or outcomes, often of catastrophic proportions, such as the Black

Chapter 4

Psychotic disorders

Saturday bushfires on 7 February 2009 in Victoria, or the spread of AIDS in the world, or sometimes specific negative events in the patient's personal experience such as the death of someone close to them. Delusions of jealousy and erotomanic delusions share a focus upon a specific person in the patient's life. Jealousy delusions-sometimes referred to as 'morbid jealousy' or the 'Othello syndrome' after Shakespeare's character who murdered his wife on the false premise that she had been unfaithful-are usually centred on the patient's partner and include beliefs of infidelity. Jealousy delusions may coincidentally be true but the process through which the patient has a,rrived at the conviction of his/her partner's infidelity is based on an illogical and arbitrary selection of supposed evidence, or actual evidence is not available to the patient. For example, a patient may be convinced that his partner is having an affair based on coded messages received via the television (a delusion of reference). Delusions of jealousy are known to cause significant relationship distress between sufferers and their partners and have been known to increase the risk of domestic violence (Smith & Buckley, 2006) . Although these beliefs are associated with dangerousness, they are also relatively rare in patients diagnosed with schizophrenia (Soyka & Schmidt, 2011). Erotomanic delusions entail a false belief that the patient's romantic feelings for another, often a person perceived by the patient to be of significant status or influence, are reciprocated by the other person. Apparent confirmation of the reciprocal feelings is often received through coded messages or signals. Beliefs of this kind are known to be highly enduring, even when the other person adamantly disavows having feelings for the patient. This disavowal might be justified in the patient's mind by alternative interpretations, including the conclusion that the person is prevented from directly expressing his/her love for the patient by other parties. A small proportion of stalkers are known to be motivated by erotomanic beliefs, but notably there is evidence suggesting that stalkers with a psychotic disorder are less likely to be violent than other stalkers (McEwan, Mullen, & Purcell, 2007). One hypothesis that has been put forward to account for this finding is that, compared with other stalkers, individuals diagnosed with a psychotic disorder may be less likely to have an actual history of intimacy with their victim. Recent evidence has suggested that violence by stalkers is more reliably predicted by the stalker's previous history of violence than by the presence of delusions (McEwan, Mullen, MacKenzie, & Ogloff, 2009). Delusions that entail a belief that the patient is under the control of some person, force or agency are known as passivity phenomena. Examples include a belief that one's thoughts are being interfered with in the form of thoughts being implanted ('thought insertion') or removed ('thought withdrawal') from the patient's mind, or a belief that one's actions, impulses or emotions are being directly influenced by some external force. Aside from their content, delusions are also categorised into bizarre and non-bizarre on the basis of whether they are considered physically possible within a person's culture. For example, delusions of thought broadcasting (the belief that one's thoughts can be heard by others) are bizarre, whereas a belief that one's neighbour has .5pread malicious gossip is categorised as non-bizarre. Another distinction is that between so-called primary and secondary delusions, although this dichotomy is debated because in practice it may be difficult to make an accurate demarcation (Sims, 1995). Primary delusions are those that have formed without a prior psychopathological event or process having led to the false conclusion. That is, the belief seems to have appeared de nova or 'out of the blue'. By contrast, secondary delusions are theoretically secondary to abnormal changes in mood, memory or perception (especially hallucinations). For example, auditory hallucinations might form the source of evidence for the patient's belief that ASIO is keeping him/her under surveillance. This distinction may have implications for the role of psychological treatments for delusions, which in some instances include the patient being encouraged to reflect with the therapist upon alternative, non-delusional interpretations of the patient's unusual experience (e.g., examining any evidence that the hallucinations may be the patient's own thoughts rather than the voices of spies) (McGowan, Lavender, & Garety, 2005). This process, at least in theory, is more difficult in the case of primary delusions where there is no unusual experience upon which the delusion is based.

137 grandiose delusion False belief of delusional intensity about the self including ideas of inflated worth, power, knowledge, ability, identity or relationships with well-known figures.

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Delusions range considerably in their complexity, from simple beliefs regarding specific people or situations to highly complex belief systems. An example of the former includes a delusion that one's boss is conspiring to make life difficult; the latter is illustrated by the belief that one's peers, family and government are collaborating in the conspiracy and that information is shared among them for malicious purposes via email and through thought transmission. Complex delusional belief systems are highly adaptive to the changing environment. For example, the patient's treating clinicians might become incorporated into , the belief system, which in turn makes it very difficult for the patient to obtain help. Clinical psychologists are interested in understanding the effects of hallucinations and delusions in order to lessen the impact of these symptoms on the day-to-day life of the sufferer. Haddock, McCarron, Tarrier, and Faragher (1999) have developed specific inventories for measuring these effects. The Psychotic Symptom Rating Scales (PSYRATS), for instance, measure the degree of preoccupation and distress associated with the delusional belief, the level of conviction in the belief and the disruption to the person's life caused by the belief. For example, one item rates the patient's level of preoccupation with the delusional belief, rated from a score of O ('no delusions, or delusions which the subject thinks about less than once a week') to 4 ('subject thinks about delusions continuously or almost continuously'). Clinicians are also mindful of the need to carefully assess the patient's tendency to act in response to hallucinations and delusions because this could be associated with potential risks to the patient or to those around him/her. For example, one patient may be inclined to cope with perceived threats by withdrawing and avoiding social interaction, whereas another may respond with assertion and counterthreats that could escalate to conflict.

DISORGANISED THINKING In addition to hallucinations and delusions, disorganised thinking (also known as 'formal thought disorder') is frequently categorised as a psychotic symptom. Formal thought disorder refers to disturbances in the logical sequencing and coherence of thought. In clinical practice and research on psychosis, the severity of formal thought disorder is inferred through assessments of the person's speech, which enables the dimensions of thought sequencing (flow) and form (structure or coherence) to be identified, as oppose~ to the content of thought (i.e., delusions) . The clinician listens for disturbances in the coherence of speech, which can range from subtle increases in the use of vague language to highly incoherent speech in which the individual's phrases are disjointed and nonsensical. Disturbances in thought form are common in psychotic disorders, but once again are not restricted to this group of diagnoses . •Disturbances in thought form can be divided into positive (the addition of disturbed thought processes) and negative (deficits in thoughts processes) manifestations. Examples of positive thought disorqer include circumstantiality, which describes speech that is very indirect and long-wi~ded in conveying meaning, although the goal may be eventually reached. Tangentiality describes oblique or irrelevant responses to questions. This is closely associated with the phenomenon of derailment, in which the person's comments slip off one idea onto another, only partially-related topic. In more extreme manifestations of thought disorder, phrases may become linked through sounds rather than meaning, a phenomenon known as clang associations (e.g., 'pass me the spoon, moon, I am cocoon'). During acute phases of psychosis, echolalia may be observed in which the utterances of others around the patient are repeated. Patients may also use words idiosyncratically (e.g., one patient referred to his 'human' when meaning his physical complaints) or produce false words, known as neologisms (e.g., 'it has been creatised by my doctor') . Negative thought disorder refers to a reduced stream of thought as evident in a poverty of speech.

I b p d S
www.betterhealth.vic.gov.au -> www.sane.org.au .....:, www.healthinsite.gov.au

A person experiencing a psychotic illness will require specialist assistance. Treatment for psychosis involves the use of antipsychotic medication, individual coun-

Locked Bag 10 Parkville Victoria 3052

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L04.3

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Historical and current conceptualisations of psychotic disorders HISTORICAL DEVELOPMENTS

paranoia State characterised by false beliefs that one is being harassed, persecuted or unfairly treated, which may reach delusional intensity. schizophrenia

Psychotic disorder characterised by two or more of the following: delusions, hallucinations, disorganised speech, grossly disorganised or catatonic behaviour, and negative symptoms.

The schizophrenia construct has a history of over 100 years and thus constitutes the most widely researched of the psychotic disorders and, indeed, of most mental disorders. However, there is current debate within the scientific community regarding the validity of the diagnosis. This section will trace the development of the schizophrenia construct from its initial identification in the era of modern medicine to the present debate regarding its validity, and proposed changes regarding its diagnosis. Richard Bentall (2003), in his award-winning book Madness Explained, provides a compelling history of the schizophrenia concept and its diagnosis. Bentall rightly gives particular prominence to the roles of Kraepelin, Bleuler and Schneider. Emil Kraepelin, a professor of psychiatry in Munich, Germany in the late 1800s, identified the disorder 'dementia praecox', the early term for schizophrenia, literally meaning 'senility of the young'. The term derived from Kraepelin's characterisation of the disorder as one entailing a gradual deterioration of mental functioning with an early onset. He differentiated dementia praecox from manic depression and from a separate illness of paranoia. The term schizophrenia was subsequently coined by the Swiss psychiatrist Eugen Bleuler, derived from the words schizein (meaning 'to split') and phren (meaning 'mind'). This term was intended to capture what he believed to be the hallmark feature of the disorder: that is, the loosening of the connections between thought structures, which he described metaphorically as a 'breaking of associative threads'. In contrast to Kraepelin, Bleuler conceptualised manic depression and schizophrenia as occurring on a continuum rather than arguing for a categorical distinction between these two diagnoses. The legacy of both of these pioneers of empirical research in psychosis can be seen in the modern diagnostic criteria for schizophrenia in the DSM-5, which include thought disorder (disorganised speech) and a deterioration in functioning. Kurt Schneider, another German professor of psychiatry based in Munich from the 1930s to 1950s, argued that symptoms specific to schizophrenia-the so-called 'first rank symptoms' -could be identified and these symptoms maintained a privileged place up until the DSM-IV-TR. They included hearing. voices arguing, hearing voices commenting on the individual's actions and bizarre delusions including passivity phenomena.

ONGOING CONTROVERSIES Dsspite attempts to improve the reliability of the diagnostic criteria for psychotic disorders in successive editions of diagnostic systems such as the DSM, considerable scientific debate continues regarding the validity;_of these constructs. Those who are sceptical regarding these disorders argue that psychotic diagnoses represent arbitrarily defined categories (Bentall, 2003 ). Large-scale surveys suggest that psychotic experiences are normally distributed across the general population, with a small proportion experiencing very severe and enduring symptoms that impact on their functioning in various important domains of daily living. As such, there is a degree of arbitrariness in determining the cut-off between those who supposedly have the disorder of schizophrenia (or other psychotic disorders) and those who do not. Van Os, Linscott, Myin-Germeys, Delespaul, and Krabbendam (2009) reviewed 42 studies published between 1950 and 2007 that investigated the prevalence of psychotic experiences, psychotic symptoms and psychotic disorders. The authors concluded that the same demographic, genetic and other risk factors predicted the occurrence of psychotic features of differing severity. In other words, there was an aetiological continuity between people with subclinical and clinical manifestations of psychotic symptoms. This dimensional approach to psychosis challenges the categorical view, which maintains that a

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Psychotic disorders

psychotic disorder is an 'entity' that 'people get' due to specific causes. The validity of the schizophrenia construct has also been challenged on the basis of the large overlap between schizophrenia and other mental disorders, particularly depressive and bipolar disorders. This suggests that to split depressive, bipolar and psychotic disorders into distinct domains does not fit with clinical reality. As a result of these concerns, researchers such as Richard Bentall favour abandoning the diagnosis of schizophrenia and instead adopting a dimensional approach to psychosis, including a general dimension of psychosis in addition to specific dimensions including positive symptoms, negative symptoms, disorganisation, mania and depression (Reininghaus, Priebe, & Bentall, 2013). Finally, some clinical psychologists and psychiatrists have argued that the stigma associated with the diagnosis of schizophrenia is associated with considerable emotional harm to the patient and thus should be abandoned (Read, Haslam, Sayce, & Davies, 2006). However, others have defended the schizophrenia concept, arguing, for instance, that the real issue related to stigma is ignorance and fear in the general community rather than the concept of schizophrenia itself (Lieberman & First, 2007). In Japan, an attempt to solve the stigma problem has been adopted by replacing the term 'schizophrenia' translated as Seishin Bunretso Byo ('disease of split and disorganised mind') with Togo-Shicchou-Sho ('a transient state of loosened association') (Sato et al., 2002). Whether this approach will permanently reduce stigma (or whether the new term will itself attract stigma over time) remains a point of ongoing debate (Bentall, 2013).

The epidemiology of psychotic disorders PREVALENCE AND AGE OF ONSET In comparison with disorders such as major depressive disorder and generalised anxiety disorder, psychotic conditions have a relatively low prevalence. For example, the lifetime prevalence of schizophrenia is approximately 1-2 per cent. Traditionally it was believed that, over the lifetime, the prevalence of psychotic disorders was equal across genders. However, more recent evidence suggests that for every three men who develop schizophrenia, two women will develop the disorder (McGrath, 2007). Epidemiologists have argued for many years, based on a series of studies conducted around the world by the World Health Organization, that the prevalence of psychotic disorders is consistent across Western industrialised and developing nations. This finding would suggest that the primary causal factors are underlying genetic and biological processes, and that variations in environment play a much smaller role in the pathway to the disorder. However, there has since been a reconsideration of the view that psychotic disorders have an equal prevalence rate internationally with the finding that there is considerable variation across countri~s and across specific settings within countries. Specifically, there is now evidence of an increased prevalence rate of psychotic conditions among migrants and in developed nations compared with developing nations, and a two-fold risk for those born in urban compared to rural settings (McGrath, 2006). The peak period of onset for psychotic disorders is during late adolescence and early adulthood. Unfortunately this is a period of life which corresponds with a range of developmental and social challenges (e.g., leaving school and the transition to adulthood) that are substantially complicated by the onset of symptoms and their associated effects.

THE COURSE OF PSYCHOTIC DISORDERS Psychotic disorders can be described in terms of specific phases, which include the premorbid phase, prodromal phase, the acute phase and the recovery phase, with the latter sometimes divided into early and late recovery. Enduring, treatment-resistant forms of psychotic disorders also occur.

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THE PREMORBID PHASE It is well known that the presence of risk factors prior to the onset of any mental health symptoms are markers of subsequent prognosis after the onset of psychosis. For example, viral infections in utero, behavioural problems evident to school teachers and poor peer relationships in adolescence may be subtle markers of risk for psychosis or may indicate a poorer prognosis (Larsen et al., 2004) .

THE PRODROMAL PHASE

prodromal symptoms In

schizophrenia, milder symptoms prior to an acute phase of the disorder during which behaviours are unusual but not yet psychotic.

Researchers have recognised for many decades that the active symptoms of psychosis typically develop in late adolescence and early adulthood, often following a period of gradual deterioration in the individual's mental state and functioning. This preliminary period of change, which precedes the onset of delusions, hallucinations and other symptoms of psychosis, is often referred to as the 'prodromal phase'. Researchers at the Personal Assessment and Crisis Evaluation (PACE) Clinic in Melbourne have pioneered a strategy for identifying a group of young people who are known to be at very high risk of developing psychosis based on their having a close relative who has experienced psychosis and their own experience of subtle, potentially indicative signs and symptoms (Yung et al., 2003), known as prodromal symptoms. The duration of the prodromal phase is known to be highly variable across individual cases, ranging from absent to many years (Yung & McGorry, 1996). During this phase, non-specific changes (i.e., changes that occur across a range of disorders and are not specific to psychotic conditions) in the individual's mental state often emerge, such as depressed mood and symptoms of anxiety, which may lead to a deterioration in performance at school and with social relationships. Brief or attenuated psychotic symptoms are also common, such as very occasional and fleeting auditory hallucinations, or suspicious and paranoid thoughts that might fluctuate in intensity. However, even when these features are evident, the progression to the acute phase of psychosis is not inevitable. While previous editions of the DSM included the diagnosis of 'prodromal schizophrenia: the high prevalence of these features among adolescents led to questions regarding the validity of this diagnosis and it was excluded from the DSM-IV (APA, 1994; Jackson, McGorry, & McKenzie, 1994). More recently, researchers prefer terms such as 'at-risk mental state' to reflect this lack of certainty that the symptoms will necessarily result in schizophrenia.

THE ACUTE PHASE For those individuals whose symptoms do intensify, the next stage is the 'acute phase'. Acute psychotic episodes are characterised by the emergence of persistent positive and negative symptoms that clearly identify the condition as a psychotic disorder. Unfortunately, young people often suffer very prolonged periods of acute psychosis without the disorder being accurately diagnosed or treated. Studies in the 1990s highlighted that, on

EPPIC in Melbourne, part of the Orygen Youth Health Clinical Program, pioneered early intervention in Australia for young people with psychosis.

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average, there was a one-year delay between the onset of the acute phase and effective treatment in Western industrialised countries (Loeb el et al., 1992 ). This delay in seeking treatment seemed to result partly from the individual withdrawing from others and partly from health professionals failing to accurately diagnose the disorder, despite families often attempting to seek help for their relative. This delay, known as the 'duration of untreated psychosis' (DUP) appears to be related to the time taken to respond to treatment once it commences (Marshall et al., 2005). That is, the longer the DUP, the longer the patient's symptoms take to improve with treatment. This finding has encouraged clinicians and researchers around the world to improve the early detection and intervention for both acute psychosis and those with an 'at-risk mental state; an approach that has been pioneered at the EPPIC in Melbourne under the leadership of Patrick McGorry (McGorry, Edwards, Mihalopoulos, Harrigan, & Jackson, 1996).

THE EARLY RECOVERY PHASE Once the acute phase develops, the individual may experience marked fear, confusion and agitation. In clinical settings it is important to differentiate acute psychosis from other conditions, such as intoxication. Thus routine medical investigations should be carried out in order to rule out medical conditions associated with psychotic symptoms. Fortunately, in the majority of cases, symptoms will slowly begin to improve over several months once treatment commences. During this early recovery phase, problems with depression and social anxiety may emerge for the first time as the person begins to reflect on their diagnosis and its significance for their future (Birchwood, Mason, Macmillan, & Healy, 1993). In addition, some patients will be traumatised by their experience of psychosis (Morrison et al., 2003; Mueser, Lu, Rosenberg, & Wolfe, 2010). Psychologists and psychiatrists have observed that as the symptoms improve, patients have a variety of recovery styles in reaction to the experience of the disorder (Drayton, Birchwood, & Trower, 1998). For example, some patients appear to respond defensively to their experience of psychosis and strive to seal over the details, while others appear to engage in an active effort to make sense of their experiences and understand their vulnerability. Improved recovery seems to be associated with the latter style (Thompson, McGorry, & Harrigan, 2003). The acute phase and the commencement of treatment are often highly distressing for family members who may have endured many months of emerging mental health problems in their unwell relative. Distress and loss are common themes for family members once a diagnosis is received and treatment commences. They may often remain distressed and worried even when treatment seems effective, suggesting that family members cal?- also benefit from support and education about the disorder (Addington, Coldham, Jones, Ko, & Addington, 2003).

THE LATE RECOVERY PHASE Even when recovery from the acute symptoms progresses well, further challenges arise in the late recovery phase. These challenges include re-integrating into social, recreational and vocational pursuits. Unfortunately, high unemployment rates exist for individuals with psychotic disorders (Killackey et al., 2006). In addition, the risk of recurrence in the form of further episodes of psychosis remains high during the first 2-5 years after treatment is commenced. In approximately 80-90 per cent of cases, relapse will occur during this period (Robinson et al., 1999). Recurrence is associated with discontinuation of antipsychotic medication, the use of cannabis and amphetamines, poorer premorbid adjustment and by conflictual interpersonal relationships, referred to by researchers as high expressed emotion (EE) (Alvarez-Jimenez et al., 2012). EE is typically measured using standardised methods of observing and rating patterns of family interactions, and comprises three components-namely, high levels of criticism, hostility and emotional over-involvement (i.e., the tendency to be over-concerned, over-protective, or overly self-sacrificing in caring for the individual). EE is now a well-established predictor of psychotic relapse. Studies have repeatedly demonstrated that patients with schizophrenia who return home to high-EE families after hospitalisation for a psychotic episode are two to three times more likely to relapse during the following year compared to patients who

!i!Xpressed emotion (EE) Family interaction style in which fami ly members are overly protective and selfsacrificing towards the person with a psychological disorder while also expressing high levels of criticism and hostility; this may contribute to the person's relapse.

Abnormal Psychology 3e

return to low-EE families. Some studies have also found that the adverse impact of high-EE families can be lowered through medication and a reduction in face-to-face contact between family members. For instance, in a famous study by Vaughn and Leff ( 1976), which instigated much of the interest in EE in schizophrenia, 128 patients with schizophrenia were followed up for a nine-month period after discharge from hospital. It was found that 51 per cent of patients who returned to high-EE homes relapsed within nine months after discharge compared to 13 per cent of patients who returned to low-EE families. However, the relapse rates of patients in high-EE families were reduced if they had less than 35 hours per week of face-to-face contact with family members (28% of whom relapsed compared to 69% of those with more than 35 hours of contact) and if they were on medication. For example, 92 per cent of patients in high-EE families with high amounts of face-to-face contact and no medication relapsed compared with 53 per cent of patients in high-EE families with high amounts of face-to-face contact who were on medication. The findings of this study (which are displayed in Figure 4.1) highlight the importance of providing timely and appropriate support to families.

High EE families

Low EE families 13%

51%

Low contact 28%

Drugs 12%

No drugs 15%

Drugs 15%

No drugs 42%

High contact 69%

Drugs 53%

No drugs 92% •

FIGURE 4.1 The percentage of patients with schizophrenia who relapsed in the nine-month period following their discharge from hospital depending on whether they returned home to high or low expressed emotion (EE) families, had high or low amounts of contact with family members, and were taking medication or not. Source: From Vaughn, C., & Leff, J.P. (1976). The influence of family and social factors on the course of psychiatric illness. British Journal of Psychiatry, 129, 125-137, The Royal College of Psychiatrists.

ENDURING PSYCHOSIS Unfortunately, a sizeable minority of patients will suffer from more severe and enduring psychosis. The pattern of symptoms varies in this group but can include periods of very acute symptoms which might require periods of hospitalisation, interspersed by continuing symptoms that do not fully disappear. Other individuals may gain relief from the positive symptoms of psychosis but suffer from enduring negative symptoms that can also profoundly inhibit the extent of recovery. More severe and persisting forms of psychosis are known to be associated with an earlier and more gradual onset of symptoms. Co-occurring problems such as substance abuse and longstanding personality traits, which might compromise the individual's capacity to cope with stress, are also recognised risk factors for a more complicated course of the disorder. Long-term enduring forms of psychosis have also been associated

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151

with increased problems in cognitive processes, especially attention, memory and executive functioning (i.e., planning and problem-solving abilities). This chronic pattern of psychosis can lead to other major problems in living. For example, the children of individuals with severe enduring or recurring psychosis may be at risk of suffering from periods of inadvertent neglect as a result of their parents' inability to effectively care for their material or emotional wellbeing during periods of active psychosis. Unfortunately, the needs of children in this predicament have only relatively recently begun to receive adequate attenfam, with programs developed in Australia and elsewhere to address this issue (Pitman & Matthey, 2004). Other problems of patients with a chronic psychosis can include problems with maintaining adequate housing, poverty, physical health complications and the long-term side effects of antipsychotic medications. However, many contemporary researchers have challenged Kraepelin's assumption that patients with enduring psychosis follow a dementia-like progressive deterioration (Menezes, Arenovich, & Zipursky, 2006). For example, Harding, Zubin, and Strauss (1992) conducted a long-term follow-up study in Vermont, USA, which found that approximately half of the patients significantly improved and/or recovered from schizophrenia or a first episode of psychosis when followed up over several decades.

The aetiology of psychosis Despite more than 100 years of research, there is much that remains unknown about the causes of psychosis. There is interest among researchers in a wide variety of possible causal factors for psychotic disorders, ranging from genetic factors to specific environmental problems. This wide array of factors has been often subsumed under the broad aetiological model known as the Diathesis-Stress Model, which was first espoused by Zubin and Spring (1977) . The model assumes that a psychotic episode occurs when a triggering event interacts with an underlying vulnerability and overwhelms the coping resources of the individual. Zubin and Spring further maintained that vulnerability to psychosis can include biological and psychosocial factors. Triggering events can also theoretically be biological or psychosocial. Many of the possible causal factors associated with psychotic disorders identified by research are not specific to psychosis but are instead associated with a br?ad range of mental health problems. This highlights that there remains much that is not understood about tli.e specific pathways to psychosis.

VULNERABILITY FACTORS: BIOLOGICAL Research aimed at characterising the biological vulnerabilities that place an individual at heightened risk for psychosis extends across a vast range of risk factors including genetics, prenatal and birth complications, a wide variety of biochemical factors and structural brain problems (Lieberman et al., 2001).

GENETIC BASIS A large body of research- including family, twin and adoption studies-supports the existence of a genetic basis for schizophrenia (Read, Potter, & Gurling, 1992). Family studies indicate that the risk of developing schizophrenia increases as the degree of genetic relatedness with an affected individual (referred to as the 'proband') increases. Thus the percentage of individuals with schizophrenia at differing degrees of relationship with the pro band are as follows: 1 per cent for spouses (no genetic relationship), 2.8 per cent for grandchildren, 7.3 per cent for siblings, 9.4 per cent for children with one affected parent and 46.3 per cent for children with both parents affected. In twin studies, the concordance rate for schizophrenia between monozygotic twins (who have the same genes) has been found to be higher than that for dizygotic twins (who, on average, have

L04.5 adoption study Study of the heritability of a disorder by finding adopted people with a disorder and then determining the prevalence of the disorder among their biological and adoptive relatives in order to separate contributing genetic factors from environmental factors.

family study Study of the heritability of a disorder involving identifying people with a pa rticu la r disorder and people without the disorder and then determining the disorder's frequency within each person's family.

concordance rate Probability that both members of a twin pair will develop the same disorder.

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monozygotic twins Identical

twins who share 100 per cent of their genes because they developed from a single fertilised egg. dizygotic twins

Non-identical twins who share with each other, on average, SO per cent of their genes because they developed from two separate ferti lised eggs (comparable to non-twin siblings).

only 50 per cent of their genes in common), again supporting a genetic contribution. However, family and twin studies cannot provide definitive evidence of a genetic role since the higher rates of schizophrenia among family members of patients with the disorder and the higher number of both twins having the condition among monozygotic compared with dizygotic twins may be due to their shared environment. In the case of family studies, for example, an individual who has two parents with schizophrenia may be at heightened risk of developing the disorder compared with an individual who has only one affected parent, since s/he is likely to have experienced a mori! disturbed upbringing. In twin studies, monozygotic twins may be treated by others more similarly than dizygotic twins due to their greater similarity. Adoption studies offer the strongest support for familial genetic factors because with this approach genes and the environment are more clearly separated than in family and twin studies. In these studies, children whose parents had schizophrenia but who were reared by parents without schizophrenia from infancy are compared with adopted children who have no biological parents with schizophrenia. It has been found that adopted children who had a biological parent (mother or father) with schizophrenia have a higher rate of the disorder than adopted children whose biological parents did not have the disorder (Read et al., 1992). Geneticists have also investigated the possibility that rare and genetic structural variations that arise in individual cases de nova, or have arisen recently in individual families, may increase the risk for schizophrenia (Levinson et al., 2011). Rare microdeletions (i.e., the loss of a very small piece of a chromosome), or replications of genes that are known to play a role in neurodevelopment, have been shown to occur at significantly higher rates in individuals diagnosed with psychosis compared to a control group matched in terms of racial ancestry (Levinson et al., 2011; Walsh et al., 2008).

GENE-ENVIRONMENT INTERACTIONS Critics of traditional genetics research in psychosis have argued that the interaction between genetic and environmental factors has been given insufficient prominence in the research (Bentall, 2003) . Indeed, in recent years increased attention has been given by researchers to hypotheses relating specific environmental exposure during specific phases of development- including during foetal development (e.g., maternal infection), early childhood (e.g., trauma), middle childhood and adolescence (e.g., exposure to illicit substances)- and wider social and environment factors (e.g., living in an urban environment) to a wide range of candidate genes to increase the risk for vulnerability or expression of psychosis (van Os, Rutten & Poulton, 2008).

NEUROTRANSMITTERS neurotransmitters

Biochemicals released from a sending neuron to a receiving neuron so as to tra nsmit messages in the brain and nervous system.

Much research has focused on abnormalities in certain neurotransmitters, such as dopamine, noradrenaline and serotonin, as contributing to psychosis. The dopamine hypothesis of schizophrenia states that the disorder is -associated with excessive dopaminergic function in the central nervous system. This hypothesis evolved from two main sources of evidence: (a) drugs which reduce dopamine activity were found to be eff.\!ctive in treating the symptoms of schizophrenia, and (b) amphetamines, which cause the release of dopamine, can produce symptoms of schizophrenia (Leuner & Muller, 2006). While researchers initially postulated that individuals with schizophrenia have excessively high levels of dopamine, several findings failed to support this contention. For instance, homovanillic acid, the major metabolite (breakdown product) of dopamine, is not found in greater amounts in individuals with schizophrenia compared to healthy individuals (Sumiyoshi et al., 1999). Thus the dopamine hypothesis was revised such that schizophrenia was proposed to be associated with excessive numbers of or oversensitive dopamine receptors, rather than high levels of dopamine. Subsequent work suggests that excessive dopaminergic activity is more related to the positive symptoms of schizophrenia (e.g., antipsychotics that reduce dopamine activity lessen positive symptoms but have little or no effect on negative symptoms). Thus, while dopamine has been the most widely investigated neurotransmitter in schizophrenia research, it is likely that multiple neurotransmitters are involved given the

Chapter 4

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complex array of disturbances associated with schizophrenia. As such, the role of other neurotransmitters (such as glutamate), either alone or in conjunction with dopamine, have also been investigated (Stone, Morrison, & Pilowsky, 2007).

BRAIN STRUCTURE Numerous abnormalities in brain structure have also been investigated as possibly contributing to psychotic symptoms, whether these abnormalities are a result of genetic factors or prenatal factors (e.g., viruses) affecting foetal development. The most consistent finding has been that of enlarged ventricles (the spaces containing cerebrospinal fluid), which indicates a loss of brain tissue (Pantelis et al., 2005). Researchers have turned their attention to investigating possible tissue loss in specific brain regions. For example, researchers have found evidence that negative symptoms (e.g., a lack of speech, affect and behaviour) are closely associated with a loss of grey and white matter in the brain, including a loss of tissue within regions of the prefrontal cortex (Stahl & Buckley, 2007). The finding that regions of the prefrontal cortex are relevant for negative symptoms is perhaps not surprising given that this part of the brain is associated with executive functioning-that is, cognitive abilities related to the planning, initiation and monitoring of goal-directed behaviour. Christos Pantelis at the Melbourne Neuropsychiatry Centre and his team have led research examining structural brain abnormalities in psychosis using magnetic resonance imaging (MRI) (Pantelis et al., 2005). These studies typically include patients at ultra-high risk of developing psychosis, patients experiencing first acute episodes, patients with longer term forms of psychosis and healthy control groups matched on variables such as age and gender. By including a group of ultra-high risk individuals, this research enables the identification of factors that characterise those who go on to develop psychosis versus those who do not and thus highlights factors that may be specific to the development of schizophrenia rather than general psychological disturbance. The comparison between patients experiencing first acute episodes and those with longer term psychosis helps in the identification of factors that may be associated with vulnerability to the disorder versus those that may be associated with the disorder's progression and/or its treatment with medication. Among this research group's findings is evidence of certain non-genetic structural brain abnormalities. Specifically, compared with the ultra-high risk group who have a family history of schizophrenia, those without a family history were found to have significantly smaller volumes of the 'left hippocampus. Thus early neurodevelopmental damage (occurring during pregnancy, for example) may be a key vulnerability factor for these individuals rather than a genetic predisposition. Patients experiencing a first episode of schizophrenia have also been found to have significantly smaller left hippocampal volume while patients with chronic schizophrenia have significantly smaller bilateral hippocampal size. In summary, abnormalities in the hippocampus appear to predate the onset of psychosis (at least among those without a family history of psychosis) and to worsen over the course of the illness. One hypothesis put forward by the researchers is that the progressive changes in the hippocampus throughout the early stages of psychosis reflect the impact of stress hormones on the brain, which may result from the stress of the pre- and earlyphase of the disorder (Phillips et al., 2006). The existence of these abnormalities in high-risk and early onset patients suggests that they may be of causal significance.

VULNERABILITY FACTORS: PSYCHOSOCIAL Researchers have become increasingly interested in the role ofpsychosocial factors in increasing the vulnerability for psychosis. Social factors include residing in an urban environment, migration, being socially excluded and experiences of childhood abuse (McGrath, 2007; Read, van Os, Morrison, & Ross, 2005; van Os, Hanssen, Bak, Bijl, & Vollebergh, 2003). Further evidence supporting the view that environmental factors can influence the

enlarged ventricles Fluid-filled spaces in the brain that are larger than normal and suggest a deterioration in brain tissue. prefrontal cortex Region at the front of the brain important in language, emotional expression, the planning and producing of new ideas, and the mediation of social interactions. magnetic resonance imaging (MRI) Method of measuring both brain structure and function through the construction of a magnetic field that affects hydrogen atoms in the brain, emitting signals that a computer then records and uses to produce a threedimensional image of the brain.

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development of psychosis can be gleaned from data on the rates of psychosis in the Maori population and in Indigenous Australians. In New Zealand, Kake, Arnold, and Ellis (2008) reported that the annual prevalence rates of schizophrenia for Maori individuals were approximately three times the non-Maori rate (with the latter similar to rates found in the general Australian population). This finding is consistent with the role of accumulated adverse social and environmental circumstances, such as racial discrimination, in substantially increasing the risk ofpsychosis. In the Indigenous Australian population very high levels ofpsychological distress related to marginalisation, dispossession, exposure to violence, racism and other forms of chronic stress pose a major risk to health and wellbeing (Cunningham & Paradies, 2012). In line with the New Zealand data, the rates ofhospitalisation for schizophrenia spectrum disorders among Indigenous Australians in 2005-2006 were 2.7 times higher for males and 2.5 times for females than expected, based on data from the rest of the Australian population (Australian Bureau of Statistics & Australian Institute of Health and Welfare, 2008). Researchers are attempting to discover how exposure to the adverse social factors early in life may increase the risk of psychosis later in life. Cognitive models propose that these early experiences (such as exposure to stress and trauma) result in the formation of dysfunctional cognitions that in turn trigger psychotic symptoms (Bentall, 2006; Morrison, 2001). These approaches highlight the role of cognitive factors in increasing vulnerability to psychosis. Morrison (2001) has proposed a cognitive model in understanding the development of positive psychotic symptoms such as delusions and hallucinations. At the core of this model is the notion that psychosis entails culturally unacceptable interpretations of'intrusions into awareness: which are defined as thoughts, images or impulses that intrude upon the individual's consciousness and are uncontrollable. Intrusions into awareness are potentially experienced by anyone and are themselves not an indication of psychosis. For instance, one study found that 82 per cent of bereaved older adults experienced hallucinations (e.g., hearing the deceased's voice) in the month following bereavement. According to Morrison (2001), it is the manner in which such intrusions into awareness are interpreted that is central in the development of psychosis. Examples of culturally unacceptable interpretations of intrusions into awareness include a woman interpreting intrusive thoughts (e.g., 'I hate my child') as evidence that thoughts are being inserted into her mind by an evil force; interpreting intrusive impulses (e.g., the impulse to hit one's child) as evidence of external control over her body; and interpreting auditory hallucinations (e.g., a voice saying 'hit her') as evidence that the devil is trying to make her hurt her child. In contrast, a non-psychotic interpretation of such intrusions into aw,areness would be 'That was a strange thought/impulse/image. I must be over-tired'. While other psychological disorders entail distorted interpretations, it is the culturally unacceptable nature of these distortions that is characteristic of psychosis. For example, an individual with obsessive-compulsive disorder might experience the obsessional thought 'I hate my child' and interpret this as a need to engage in some kind of ritual to prevent harm coming to his/her child but would not interpret the thought as a sign of thought insertion by an evil force. Morrison (2001) proposes that these culturally unacceptable interpretations are a result,, of faulty knowledge about the self (e.g., 'I am a bad person if I have thoughts of hating my child', which makes the person prone to mis attributing the thought to an external force rather than seeing it as a product of her own mind), and faulty knowledge about others (e.g., 'Adults cannot be trusted around children'). Such faulty knowledge is in turn theorised to be the product oflife experiences (e.g., having been sexually, physically or emotionally abused as a child). The final aspect of Morrison's (2001) model asserts that interpreting intrusions into awareness in a culturally unacceptable and typically distressing manner triggers responses that serve to increase the likelihood of further intrusions into awareness. These counterproductive responses include disturbances in mood (e.g., anxiety) and physiological arousal (e.g., a lack of sleep), which research suggests can intensify intrusive thoughts, images and impulses. These responses also include behaviours such as those designed to keep the individual or others safe (e.g., a mother avoiding being alone with her child so that she fails

Chapter 4

Psychotic disorders

to disconfirm the false belief that she might hurt her child). Other unhelpful responses include a range of cognitive changes such as selective attention (e.g., the mother might constantly be on the lookout for any negative thoughts regarding her child, thereby increasing the likelihood of noticing such thoughts) and attempting to suppress intrusive thoughts, images and impulses by pushing them out of one's mind. Thought suppression, however, is known to actually increase the frequency of intrusive thoughts (as demonstrated in the exercise developed by Salkovskis and Kirk (1989) in which the individual is asked to not think about a pink rabbit, which results in the individual immediately thinking about a pink rabbit). The full model proposed by Morrison (2001) is shown in Figure 4.2.

Intrusions into awareness (intrusive thoughts, images or impulses) the intrusive thought'! hate my child' intrusive auditory imagery of a voice saying 'hit her' the intrusive impulse to hit one's child

.. . • .

. ...

i Culturally unacceptable interpretations of intrusions into awareness • 'The devil is putting thoughts into my mind' • 'The devil is tel li ng me to hurt my child' • 'The devil is trying to take control of my body'

'-

...

...

-

Mood and physiological disturbance anxiety, guilt, arousal, poor sleep

'

Cognitive and behavioural responses safety behaviours such as not being alone with child, selective attention to unwanted thoughts, thought suppression

Faulty knowledge regarding the self and others the self:'I am a bad person if I have thoughts of hating my child' • the world: 'Adults cannot be trusted around children'

•

t .

Life experiences childhood sexual abuse • strict relig ious upbringing

FIGURE 4.2 The cognitive model of psychosis developed by Morrison (2001) using as an example the case of a mother distressed by fears of hurting her child. Source: From Morrison, A. P. (2001 ). The interpretation of intrusions in psychosis: An integrative approach to hallucinations and delusions. Behavioural and Cognitive Psychotherapy, 29, 257-276, Cambridge University Press.

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TRIGGERING FACTORS

pituitary Major endocrine gland that produces the largest number of different hormones and controls the secretions of other endocrine glands.

Among vulnerable individuals, the occurrence of certain events will trigger psychosis. Triggering events can entail biological processes (e.g., using illicit substances such as cannabis), psychosocial processes (e.g., stressful life events), or an interaction between the two (e.g., disturbances in hormonal functioning induced by stress) (Nuechterlein et al., 1992; Tarrier & Turpin, 1992). In support of the latter, Pantelis and colleagues (2005) found that patients ~ssessed as being at high risk of developing psychosis who later in fact did go on to develop psychosis had significantly larger volumes of the pituitary (indicating higher levels of stress hormones) compared with high-risk patients who did not go on to develop psychosis. In terms of psychosocial factors, both retrospective and prospective studies have found that stressful life events (such as exposure to negative interpersonal dynamics as characterised by the expressed emotion construct, financial strain or health problems) occur significantly more often in the weeks preceding the onset of psychotic episodes. In one such prospective study, Ventura, Nuechterlein, Lukoff, and Hardesty (1989) asked patients with schizophrenia to record any life events at monthly intervals for one year. It was found that the number of life events in the month preceding the onset of a psychotic episode was significantly higher than in the other months, as well as being significantly higher than the number of life events experienced by patients who did not relapse.

SYMPTOM-SPECIFIC AETIOLOGICAL FACTORS: HALLUCINATIONS Doubts concerning the validity of diagnoses such as schizophrenia have provided impetus for researchers to focus their investigations at the level of individual symptoms (rather than disorders) with the aim of understanding biological and psychological processes that might account for their aetiology and persistence (Bentall, 2006). Hallucinations research is one example, in which patients with hallucinations are compared with non-hallucinating patients with psychosis, and other comparison groups such as depressed patients and healthy controls who are usually matched on demographic variables (e.g., age and gender) with the target group. This extensive field of psychological research has produced several theories concerning the aetiology of hallucinations, which were reviewed by Seal, Aleman, and McGuire (2004) with reference to auditory hallucinations (the most common among patients with schizophrenia). These theories attempt to account 'for the process by which self-generated mental events are transformed into the experience of perceived sound, usually speech. The first and oldest theory-the dysfunction in auditory imagery theory-states that individuals prone to auditory hallucinations are able to imagine particularly vivid sounds. This auditory imagery is so lifelike that the individual mistakes it for an actual sound. Yet research testing this theory has been generally urlsupportive, with one study finding that hallucinating patients with schizophrenia actually experienced less vivid imagery than non-hallucinating patients. This led to the refined auditory imagery theoi:,y, which suggests that hallucinating individuals typically experience deficits in the vividness of their auditory imagery so that when they do experience unusually vivid auditory imagery, this is more likely to be confused for the actual perception of sound. Again, however, this theory has received minimal support. In contrast, Seal et al. (2004) report evidence to support a second theory, which proposes that auditory hallucinations involve a dysfunction in verbal self-monitoring. According to this theory, auditory hallucinations stem from a breakdown in the individual's ability to notice his/her intentions to act (e.g., the intention to make internal speech). As a result, the individual confuses internally generated actions (e.g., making internal speech) with externally generated actions (e.g., someone else speaking). In support of this theory, research has found that hallucinating patients are more likely than non-hallucinating patients to misattribute their own speech to an external source when their speech is distorted in some way (e.g., the pitch is altered), suggesting that they are failing to notice their intention to speak.

Chapter 4

Psychotic disorders

Bentall and Fernyhough (2008) developed a model of hallucinations that integrates cognitive deficits (such as poor verbal self-monitoring) with dysfunctional beliefs (of the type identified in Morrison's [200 l] model described in Figure 4.2) and environmental adversity (specifically, childhood trauma). More specifically, this model proposes that trauma, such as early childhood adversity, may lead to increased susceptibility to intrusive and unwanted cognitive activity and that poor self-monitoring ability may result in these traumarelated cognitions being misattributed to an external source, giving rise to the subjective experience of a voice. The individual may use unhelpful strategies, such as thought suppression, in an attempt to reduce the hallucinatory experience which, however, inadvertently maintains the experience.

SYMPTOM-SPECIFIC AETIOLOGICAL FACTORS: DELUSIONS Psychological processes in delusions have also been extensively investigated. Garety and colleagues (2005), for example, have studied the tendency of patients with delusions to make cognitive errors (such as a tendency to rapidly jump to a conclusion based on relatively small amounts of information) in tasks of general reasoning. In one of these tasks, participants were shown the images of two jars on a computer screen containing yellow and black beads. In one jar the number of black beads outweighed the number of yellow beads, while in the second jar this ratio was reversed. The jars were then hidden from view and participants were asked to request as many beads as they required before deciding from which of the two jars the beads were drawn. Patients with delusions, and those recently recovered from delusions, were found to jump to a conclusion based on relatively few beads compared with healthy controls. Emotional states can also contribute to the tendency to make cognitive errors, with anxiety found to be associated with a higher degree of certainty regarding the validity of delusional beliefs (Garety et al., 2005). In another line of investigation, Bentall, Corcoran, Howard, Blackwood, and Kinderman (2001) have led research focusing on the explanations or attributions formed by people prone to delusions when they are faced with negative life events. Results from this research demonstrate that individuals prone to delusions tend to blame other people, rather than themselves or random misfortune, in explaining the causes of negative events (e.g., attributing failure on an exam to someone trying to prevent the individual from succeeding rather than a lack of preparation). While this style of attribution assists people to protect their self-esteem by avoiding self-blame, it may contribute to delusional thinking because it creates a bias towards suspiciousness of otliers.

SYMPTOM-SPECIFIC AETIOLOGICAL FACTORS: THOUGHT DISORDER For many years, psychologists have been developing theoretical models and researching factors associated with thought disorder. Researchers have found associations between the severity of thought disorder (as reflected in disordered speech) and deficits in certain cognitive processes. More specifically, there is evidence of problems in the storage of information among patients with schizophrenia, which ·may in turn give rise to disordered speech (Leeson, Laws, & McKenna, 2006). Rossell and David (2006) conducted a study that provided evidence of a deficit in the information storage system of patients with schizophrenia. They recruited 32 patients who had been diagnosed with schizophrenia and 32 healthy controls who were matched with the patient group by age and years of education. The participants were given a word association task that consisted of a key word (e.g., 'fog') presented with four other words: a word related in meaning to the key word (e.g., 'mist'), a word similar but unrelated in meaning to the key word (e.g., 'steam') and two words related to each other but unrelated to the key word (e.g., 'bolt' and 'lock'). The participant's task was to identify the word related in meaning to the key word. Thirty key words were presented in total, consisting of 15 words that are in frequent use in the English language and

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IS low-frequency words. It was found that the control group made a significantly higher number of accurate responses compared to the patients with schizophrenia. In addition, both groups provided significantly more accurate responses to the high-frequency words compared with the low-frequency words. However, the main finding was that the poorer performance on low-frequency versus high-frequency words was more evident in the patient group compared to the control group. Rossell and David (2006) interpreted this finding as evidence of dysfunction in the information storage system among patients with schizophrenia. In other words, the normal connections between related terms that are stored closely together in memory was somehow impaired in the patient group, leading to retrieval problems. This is based on the idea that damage to the information storage system will affect those terms with weaker connections first (i.e., the low-frequency items). Other investigators have suggested that thought disorder is more apparent in patients with schizophrenia during speech regarding topics of heightened emotional salience compared with discussions on more neutral topics. This finding suggests that emotional distress may contribute to disrupted thought processes, similar to the research on delusional thinking (Haddock, Wolfenden, Lowens, Tarrier, & Bentall, 1995).

L04.6

The treatment of psychotic disorders The emergence of the Diathesis-Stress Model of psychosis in the late 1970s has shaped treatment frameworks towards a biopsychosocial or integrated approach, involving assessment and intervention across biological, psychological and social domains (Zubin & Spring, 1977). The influence of this model is reflected in expert guidelines for the treatment of psychotic disorders such as the 'Royal Australian and New Zealand College of Psychiatrists (RANZCP) clinical practice guidelines for the treatment of schizophrenia and related disorders' (McGorry, 2005). Treatment guidelines are developed by panels of experts in the field who review the evidence for the effectiveness of specific treatments and then reach a consensus on recommended best practice. The guidelines are organised with reference to the specific phases of psychosis and outline the optimal combination of biological, psychological and social interventions corresponding to each stage of the disorder.

PRODROMAL PHASE INTERVENTIONS Within Australia and internationally there is a growing emphasis upon early detection of individuals at risk of developing psychosis and offering them intensive interventions in order to prevent progression to more severe and enduring psychological disturbance. Researchers at the Personal Assessipent and Crisis Evaluation (PACE) clinic in Melbourne have pioneered the development of criteria for identifying individuals at high risk for psychosis. These criteria include less severe features of psychosis (e.g., an increase in suspicious thinking), transient psychotic symptoms (e.g., auditory hallucinations that might appear intermittently for very brief periods of time), a substantial deterioration in general psychological functioning, and a family history of psychosis in a firstdegree relative. Research has found that 40 per cent of individuals defined as Australian of the Year (201 O) Professor Patrick McGorry is a leading researcher in the area of psychosis.

being at risk for psychosis using these criteria go on to develop psychosis over a nine-month period (Yung et al., 1998). Researchers led by Patrick McGorry and Alison Yung at the PACE clinic have also conducted interventions targeting high-risk individuals. This team

Chapter 4

Psychotic disorders

has reported promising results for the early use of antipsychotic medication combined with cognitive behaviour therapy (CBT) with a group of young people at high risk of developing psychosis (McGorry et al., 2002). Specifically, the researchers found that this combined treatment seemed to delay the proportion of young people who developed an acute episode of psychosis. In other words, in the short term there were fewer young people developing full-threshold psychosis but this difference was unfortunately not sustained over the longer term. This finding indicates the need for more research to identify strategies for maintaining wellbeing. Subsequent research has found that CBT alone is successful in reducing transition to psychosis for individuals at high risk of developing a first episode of psychosis (Morrison et al., 2004). In this study, 58 highrisk patients were randomly allocated to receive either six months of CBT or regular monitoring of symptoms. The CBT intervention was based on Morrison's (2001) cognitive model of psychosis (see Figure 4.2) and aimed to challenge patients' culturally unacceptable interpretations of their intrusions into awareness, to correct faulty knowledge regarding the self and others, and to alter responses (disturbances in mood, arousal, behaviours and cognition) that intensify intrusive thoughts, images and impulses. For example, one patient had the thought that people were looking at him while he was driving (intrusion into awareness), which he interpreted as evidence that his family was arranging for him to be followed (culturally unacceptable interpretation) (French, Morrison, Walford, Knight, & Bentall, 2003) . The therapist helped the patient to challenge this interpretation by questioning the patient regarding how many people would be required for this surveillance operation to succeed and the cost involved, which would be beyond his family's means. The results of the study are displayed in Figure 4.3. One year after treatment commenced it was found that significantly fewer patients in the CBT group had developed psychosis (6%) compared to those in the monitoring group (22%). In addition, significantly fewer CBT patients had been prescribed antipsychotic medication (6%) compared to the monitoring group (30% ). Importantly, the significant advantage of the CBT group over the monitoring group was sustained at a three-year follow-up (Morrison et al., 2007). One notable advantage of

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FIGURE 4.3 The percentage of high-risk patients developing psychosis and being prescribed antipsychotic

medication one year after commencing CBT or regular symptom monitoring. Source: From Morrison et al. (2004). Cognitive therapy for the prevention of psychosis in people at ultra-high risk-Randomised controlled trial. British Journal of Psychiatry, 785, 291-297, The Royal College of Psychiatrists.

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CBT as an intervention for high-risk individuals is that it avoids prescribing antipsychotic medication (with its potentially serious side effects) to individuals who may not even have a developing psychosis. The scientific community is in agreement that further research is needed before these interventions can be recommended in routine clinical practice. For instance, it is not clear whether the beneficial effects reported by Morrison and colleagues (2004) were specifically due to the CBT techniques that were used or stemmed from the support patients obtained by meeting regularly with a therapist. However, it does appear that CBT offers a specific benefit to ,patients at risk for psychosis, especially in relation to their positive symptoms (French, Shryane, Bentall, Lewis & Morrison, 2007). These preliminary results are promising and highlight the importance of ongoing efforts to improve the early identification of individuals who will develop psychosis and to provide preventative interventions for this high-risk group.

ACUTE PHASE INTERVENTIONS Compared to the relatively recent focus on interventions at the prodromal stage, interventions for acute psychosis have been more thoroughly researched and are more firmly established in routine clinical practice. Given the finding that a greater delay in obtaining treatment after the development of psychosis is associated with a longer time before the patient responds to treatment, there is a growing international trend towards encouraging timely access to expert assessment and acute treatment facilities (Marshall et al., 2005). Specialist early psychosis intervention programs within mental health services have become increasingly common in Australia over the previous ten years, strongly influenced by the development of the EPPIC program. The dissemination of the early intervention model across Australia is currently being supported via the establishment of the Headspace Foundation, a federal government initiative to support innovations in the delivery of youth mental health initiatives, including early intervention (McGorry et al., 2007). In the case of first-episode psychosis, the initial priority once contact is made with specialist mental health services is the comprehensive assessment of the person's mental state along with an assessment of his/her physical health and an understanding of his/her individual and family history, including any previous mental health problems. If an episode of psychosis is diagnosed, then treatment should preferably be commenced in the person's home and the patient and family members should have 24-hour access to mobile treatment teams who can come to the patient's home. However, often the severity of symptoms and associated risks to the person, combined with the stress upon the family attempting to care for the individual at home, necessitates a period of hospitalisation. If this is required, it should ideally be provided within units specifically designed for young people in the early stages of the disorder, because adult inpatient units with patients whose psychosis is chronic may inadvertently provide a pessimistic message to the young person regarding his/her own likely mental health outcome. Psychological support and the provision of basic psychoeducation about the disorder and its treatment are critical in order to engage the young person and his/her family at the commencement of treatment. Social needs also often require immediate attention, including accommodation and financial problems, and communicating appropriately with the patient's employer or educational institution. Pharmacological approaches are at the centre of care for the treatment of acute psychosis. These include antipsychotic medication (also known as neuroleptics) for the active symptoms, often in combination with the brief use of benzodiazapines to assist the person to regulate their sleep and to reduce the severe anxiety associated with the acute phase. Commonly prescribed antipsychotics in Australia include the newer so-called 'atypical antipsychotics' such as risperidone, olanzapine, quetiapine and clozapine, and the older 'typical neuroleptics' including haloperidol (Mond, Morice, Owen, & Korten, 2003). Pharmacologists agree

Chapter 4

Psychotic disorders

that antipsychotics should be used at the lowest effective dose for the treatment of first-episode psychosis in order to minimise the adverse side effects of medication, such as weight gain, and in order to reduce the long-term health risks associated with antipsychotic medications (McGorry, 2005). Although the extent and timing of the response to antipsychotic medication varies between patients, it is known that the majority of first episode patients will experience significant reductions in acute symptoms over the early months of treatment in response to these medications (Emsley, Rabinowitz, & Medori, 2007). Trials have shown that a shorter duration of untreated psychosis and an early response to medication in the first six weeks of treatment predict a greater chance of reaching a remission from the acute symptoms. One side effect that is of greatest concern is tardive dyskinesia, which occurs in approximately 10 per cent of patients treated with neuroleptics for more than a year and is perhaps the most serious limitation associated with the long-term use of neuroleptics. This condition consists of a range of abnormal body movements such as lip smacking, facial grimacing, piano player-like movements of the fingers and toes, and writhing movements of the trunk. Some researchers, such as Loren Mosher and colleagues, have evaluated the effectiveness of alternative approaches, including the Soteria Model, first developed in California in the early 1970s, which includes highly supportive 24-hour support in a home-like setting, usually without medication (Bola & Mosher, 2003). The outcomes from the program have been found to be comparable with standard care within a state hospital in terms of symptom recovery and return to the community (Mosher, 1999). Once the most severe psychotic symptoms begin to improve, the priorities shift towards addressing other psychological problems such as anxiety and depression through both psychological interventions and appropriate medication. Comorbid substance abuse is highly prevalent in people with psychosis. So-called 'dual-diagnosis' services have been established in an attempt to treat both the psychosis and substance abuse problems simultaneously, in recognition that the two disorders influence one another. For example, Jane Edwards at EPPIC has led a team of researchers evaluating the effectiveness of careful education and psychological treatments for young people experiencing both psychosis and cannabis abuse problems (Edwards et al., 2006). Psychosocial approaches also target social and occupational functioning once the most severe psychotic symptoms begin to improve, especially since these aspects of functioning may be less responsive to medication. That is, while positive symptoms are often eliminated by drug treatment, the negative symptoms may be only moderately improved and thus continue to impair the individual's social and occupational functioning. Group-based interventions are often available in early psychosis programs to foster social support and social confidence, and encourage reintegration into recreational, vocational and educational activities. Symptomatic recovery is not always necessary or sufficient for reintegration into vocational and educational activities. Indi~idual support programs that encourage people back to work and continue to support them once employment is obtained have been shown to be effective for people diagnosed with schizophrenia. Associate Professor Eoin Killackey from Orygen Youth Health, together with Professor Henry Jackson from the University of Melbourne, have been leading a team of researchers in evaluating ways to support young people in gaining employment or returning to study after a first episode of psychosis (Killackey et al., 2006). Their trial involved the provision of one-on-one employment or educational support as a component of a comprehensive program of mental health care to assist young people to either enter or return to employment or education. This research, which built upon work undertaken with older people with a longer term form of psychosis (Cook et al., 2005), showed that those who received the additional support had significantly better outcomes in their level of employment, hours worked per week, jobs acquired and longevity of employment compared with those receiving treatment-as-usual within a specialist first-episode psychosis program (Killackey, Jackson, & McGorry, 2008).

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tardive dyskinesia

Neurological disorder characterised by involuntary movements of the tongue, face, mouth or jaw, which may result from taking neuroleptic drugs.

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Abnormal Psychology 3e

INTERVENTIONS TO PREVENT RELAPSE Relapse is a major risk once symptoms have remitted. As with interventions for the acute psychotic episode, medication is essential in reducing the risk of relapse, with an estimated relapse rate of 65 per cent one year after hospitalisation among those who have discontinued their medication (Hogarty & Ulrich, 1998). However, even with ongoing medication, relapse rates are still high, with approximately 40 per cent of patients on medication relapsing wi!hin one year. These findings highlight the importance of adding psychosocial interventions to medication, with a combined treatment approach found to halve the relapse rates associated with medication alone. Effective preventive treatments have included both individual and family approaches. Examining an individual approach, Gumley and colleagues (2003) randomly allocated 144 patients with schizophrenia to receive either standard treatment alone (medication and regular symptom review) or CBT plus standard treatment. In the CBT intervention, patients were introduced to a cognitive model of relapse, which states that early signs of relapse (e.g., racing thoughts) trigger negative beliefs (e.g., 'I have no control over what is happening to me and am going to end up in hospital'), which in turn trigger negative emotions (e.g., anxiety) and behaviours (e.g., substance use, withdrawal and avoidance of mental health services) that can intensify psychotic symptoms. Given this model, treatment aimed to help patients develop more optimistic beliefs regarding symptoms (e.g., 'I can learn skills to manage my thoughts'). The results revealed that, one year after commencing treatment, fewer patients in the CBT group had relapsed (18.1 %) compared to those receiving standard treatment (34.7%). The percentage of patients who relapsed across the 12 months of the study is shown in Figure 4.4. In addition, significantly fewer patients in the CBT group were admitted to hospital (15.3%) compared to the standard group (26.4%) . CBT was also significantly more effective than standard treatment in reducing positive and negative psychotic symptoms and increasing social functioning.

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