Clinical Psychology

Clinical Psychology: An Introduction is for students studying clinical

psychology as part of an undergraduate programme in psychology,
nursing, sociology or social and behavioural sciences. Undergraduate
students who wish to know if postgraduate study in clinical psychology
would be of interest to them will find this book particularly useful.
The book will inform students about
● the profession of clinical psychology
● how to get onto a clinical psychology postgraduate training pro-
gramme
● the way clinical psychologists work with children, adolescents and
adults with common psychological problems
● the main models of practice used by clinical psychologists, and
● the scientific evidence for the effectiveness of psychological
interventions.

There is a focus on both clinical case studies and relevant research,

and the book includes summaries, revision questions, advice on further
reading and a glossary of key terms, all of which make it an excellent,
student-friendly introduction to an exceptionally interesting subject.
Alan Carr is director of clinical psychology training at University College
Dublin and has a clinical practice at the Clanwilliam Institute, Dublin. He
has produced over 20 volumes and 200 papers and presentations in the
areas of clinical psychology, family therapy and positive psychology.
His books include the Handbook of Child and Adolescent Clinical
Psychology, the Handbook of Adult Clinical Psychology, the Handbook
of Intellectual Disability and Clinical Psychology Practice, and What
Works with Children, Adolescents and Adults? A Review of Research
on the Effectiveness of Psychotherapy and Positive Psychology. He
has worked in the fields of clinical psychology and family therapy in the
UK, Ireland and Canada.

Book 1.indb i 06/03/2012 13:47

Book 1.indb ii 06/03/2012 13:47
 Clinical Psychology
An Introduction
Alan Carr

Book 1.indb iii 06/03/2012 13:47

 First published 2012
by Routledge
27 Church Road, Hove, East Sussex BN3 2FA
Simultaneously published in the USA and Canada
by Routledge
711 Third Avenue, New York NY 10017
Routledge is an imprint of the Taylor & Francis Group, an Informa business
© 2012 Alan Carr
The right of Alan Carr to be identified as author of this work has been asserted
by him in accordance with sections 77 and 78 of the Copyright, Designs and
Patents Act 1988.
All rights reserved. No part of this book may be reprinted or reproduced or
utilised in any form or by any electronic, mechanical, or other means, now
known or hereafter invented, including photocopying and recording, or in
any information storage or retrieval system, without permission in writing
from the publishers.
Trademark notice: Product or corporate names may be trademarks or
registered trademarks, and are used only for identification and explanation
without intent to infringe.
British Library Cataloguing in Publication Data
A catalogue record for this book is available from the British Library
Library of Congress Cataloging in Publication Data
Carr, Alan, 1957–
Clinical psychology : an introduction / Alan Carr.
p. cm.
Includes bibliographical references.
ISBN 978-0-415-68396-8 (hardback)—ISBN 978-0-415-68397-5 (paperback)
1. Clinical psychology—Textbooks. I. Title.
RC467.C35 2012
616.89—dc23 2011038606

ISBN: 978-0-415-68396-8 (hbk)

ISBN: 978-0-415-68397-5 (pbk)
ISBN: 978-0-203-09763-2 (ebk)

Typeset in Arial MT and Frutiger by RefineCatch Limited, Bungay, Suffolk

Paperback cover design by Andrew Ward

Book 1.indb iv 06/03/2012 13:47

 Contents
List of figures ix
List of tables xi
Preface xiii
Acknowledgements xvii
1 What is clinical psychology? 1
● Learning objectives 1
● Introduction 1
● The profession and scientific discipline of clinical psychology 2
● Clinical psychologists’ roles 3
● Clinical psychology training 9
● Getting a place on a clinical psychology programme 12
● Training abroad 24
● Choosing courses 26
● Clinical psychology and related professions 27
● Controversies 29
● Pros and cons of selecting clinical psychology as a career 30
● Summary 31
● Questions 32
● Further reading 33
● Websites 33

2 Childhood behaviour disorders 35

● Learning objectives 35
● Introduction 35
● Attention deficit hyperactivity disorder 36
● Conduct disorder and oppositional defiant disorder 49
● Psychodynamic theories 60
● Cognitive-behavioural theories 61
● Systems theory 63
● Assessment 65
● Intervention 66
● Controversies 68
● Summary 70
● Questions 71
● Further reading 72
● Websites 72

3 Eating disorders 73
● Learning objectives 73
● Introduction 73
● Case study of anorexia nervosa 75
● Epidemiology, course and outcome 79
● Clinical features 80
● Aetiological theories 82

Book 1.indb v 06/03/2012 13:47

 vi C L I N I C A L P S Y C H O L O G Y : A N I N T R O D U C T I O N

● Biological theories 83
● Psychoanalytic theories 84
● Cognitive-behavioural theories 85
● Systemic theories 87
● Assessment 90
● Intervention 91
● Controversies 92
● Summary 92
● Questions 94
● Further reading 94
● Websites 94

4 Drug misuse 95
● Learning objectives 95
● Introduction 95
● A case of harmful polydrug use 96
● A case of early drug experimentation 98
● Comparison of cases 99
● Classification, epidemiology, risk factors and

protective factors 99
● Clinical features 101
● Theories 105
● Intrapsychic deficit theories 110
● Cognitive-behavioural theories 112
● Systemic theories 114
● Integrative theories 117
● Assessment 119
● Treatment 120
● Controversies 121
● Summary 122
● Questions 124
● Further reading 124
● Websites 124

5 Anxiety disorders 126

● Learning objectives 126
● Introduction 126
● Separation anxiety disorder 127
● Phobias 130
● Generalized anxiety disorder 131
● Panic disorder 133
● Posttraumatic stress disorder 136
● Obsessive compulsive disorder 137
● Clinical features of anxiety disorders 140
● Epidemiology, risk factors and course 145
● Aetiological theories 146
● Biological theories 147
● Temperament, traits, cognitive biases and coping strategies 149
● Psychoanalytic theories 151
● Cognitive-behavioural theories 153
● Family systems theory 157
● An integrative perspective 159
● Assessment 159
● Treatment 160

Book 1.indb vi 06/03/2012 13:47

 CONTENTS vii

● Controversies 162
● Summary 163
● Questions 165
● Further reading 165
● Websites 166

6 Depression 167
● Learning objectives 167
● Introduction 167
● Case example of major depression 169
● Clinical features 172
● Classification 176
● Epidemiology, course and risk factors 177
● Aetiological theories 179
● Temperament, traits, cognitive biases, coping

strategies and interpersonal styles 183

● Psychoanalytic theories 186
● Cognitive and behavioural theories 189
● Family systems theory 194
● An integrative approach 195
● Assessment 196
● Suicide risk 196
● Treatment 199
● Controversies 200
● Summary 203
● Questions 204
● Further reading 205
● Websites 205
7 Schizophrenia 207
● Learning objectives 207
● Introduction 207
● Case example of schizophrenia 208
● Clinical features 213
● Classification 217
● Epidemiology, course, outcome and risk factors 218
● Aetiological theories 221
● Biological theories 222
● Antipsychotic medication 227
● Stress-vulnerability theory 227
● Multimodal interventions 228
● Assessment 237
● Treatment 239
● Controversies 239
● Summary 244
● Questions 245
● Further reading 245
● Websites 246

8 Personality disorders 247

● Learning objectives 247
● Introduction 247
● Clinical features and case examples 248
● Cluster A: The odd, eccentric group 250

Book 1.indb vii 06/03/2012 13:47

 viii C L I N I C A L P S Y C H O L O G Y : A N I N T R O D U C T I O N

● Cluster B: The dramatic, emotional, erratic group 254

● Cluster C: The anxious, fearful group 259
● Epidemiology and course 263
● Theories 265
● The effectiveness of psychotherapy and medication 269
● Psychodynamic approaches 269
● Cognitive-behavioural approaches 276
● Marital and family therapy 278
● Risk of violence 278
● Assessment 279
● Treatment 280
● Controversies 281
● Summary 288
● Questions 289
● Further reading 290
● Websites 290

9 Models that influence the practice of clinical psychology 291

● Learning objectives 291
● Introduction 291
● Biological model 292
● Psychoanalytic model 298
● Cognitive-behavioural model 300
● Family systems model 303
● Other influential models 305
● Summary 306
● Questions 308
● Further reading 308
● Websites 308

10 Effectiveness of psychological therapies 310

● Learning objectives 310
● Introduction 310
● Evidence-based practice 311
● How effective is psychotherapy? 314
● Medical cost offset 321
● Common factors and specific psychotherapies 322
● Summary 328
● Questions 329
● Further reading 329
● Website 329

Glossary 330
References 342
Index 387

Book 1.indb viii 06/03/2012 13:47

 List of figures
2.1 Formulation of a case of ADHD 38
2.2 General formulation model for ADHD 48
2.3 Formulation of a case of conduct disorder 54
2.4 General formulation model for conduct disorder and
oppositional defiant disorder 66
3.1 Formulation of a case of anorexia nervosa 78
3.2 Fairburn’s cognitive-behavioural model of eating disorders 87
3.3 General formulation model for eating disorders 91
4.1 Formulation of a case of harmful drug use 97
4.2 The reward system in the human brain 109
4.3 General formulation model for adolescent drug misuse 120
5.1 Formulation of a case of separation anxiety disorder 129
5.2 Formulation of a case of generalized anxiety disorder 132
5.3 Formulation of a case of panic disorder with agoraphobia 135
5.4 Formulation of a case of obsessive compulsive disorder 139
5.5 Psychodynamic triangles of conflict and person 153
5.6 General formulation model for anxiety disorders 160
6.1 Formulation of a case of depression 172
6.2 Cognitive-behavioural model of depression 191
6.3 General formulation model for depression 197
7.1 Formulation of a case of schizophrenia 212
7.2 Beck’s integrated model of schizophrenia for use in CBT 230
7.3 General formulation model for schizophrenia 238
9.1 MRI image of grey matter loss in very early
onset schizophrenia 296
10.1 Hierarchy of evidence 312
10.2 Case studies 312
10.3 Improvement in mean symptom scores on the
Beck Depression Inventory 313
10.4 Graphic representation of an effect size of 1 315
10.5 Success rates of psychotherapy with adults and children 320
10.6 The effects of psychotherapy compared with
placebo control groups 323
10.7 Factors that affect the outcome of psychotherapy 324

Book 1.indb ix 06/03/2012 13:47

Book 1.indb x 06/03/2012 13:47
 List of tables
1.1 Main elements of clinical psychologists’ roles 3
1.2 Populations, problems and work settings 6
1.3 Components of professional clinical psychology training
programmes 10
1.4 Building your profile for admission to clinical
psychology training 13
2.1 Diagnostic criteria for attention and hyperactivity
syndromes in DSM-IV-TR and ICD-10 40
2.2 Diagnostic criteria for oppositional defiant disorder
and conduct disorder in DSM-IV-TR and ICD-10 50
3.1 DSM-IV-TR and ICD-10 diagnostic criteria for
anorexia and bulimia nervosa 74
3.2 Risk factors for eating disorders 80
4.1 DSM-IV-TR and ICD-10 diagnostic criteria for
drug abuse and dependence 100
4.2 Risk factors for adolescent drug use 102
4.3 Clinical features of drug use 103
4.4 The 12 steps of Narcotics Anonymous 106
5.1 Clinical features of anxiety disorders 141
6.1 Criteria for a major depressive episode 168
6.2 Clinical features of depression 174
6.3 Risk and protective factors for suicide 198
7.1 Diagnostic criteria for schizophrenia 209
7.2 Clinical features of schizophrenia 213
7.3 Risk factors for schizophrenia 219
7.4 Risk factors for a poor outcome in schizophrenia 220
8.1 Main clinical features of major personality disorders 251
8.2 Epidemiology of major personality disorders 263
8.3 Defence mechanisms at different levels of maturity 271
8.4 Factors and facets of the five-factor model of personality 282
8.5 Profiles of DSM-IV personality disorders from a
meta-analysis of 30 facets of the five-factor model
of personality 284
8.6 Comparison of personality disorders and Axis 1
disorders with similar features 286
9.1 Model of abnormal behaviour 293
9.2 Rates of diagnosis of schizophrenia in the US and the UK 294
10.1 Interpretation of effect size 316
10.2 Therapy, client and therapist ‘common factors’ that
affect positive psychotherapy outcome 325

Book 1.indb xi 06/03/2012 13:47

Book 1.indb xii 06/03/2012 13:47
 Preface
This book will help you find out about the profession of clinical
psychology, how to get a place on a training programme, what it’s like to
work as a clinical psychologist, and the theoretical and scientific basis
for clinical psychology. The first chapter answers the questions: ‘What
is it like working as a clinical psychologist?’ and ‘How do I get a place
on a training programme?’ It provides an overview of the profession
and academic discipline of clinical psychology. There is a discussion of
the many settings in which clinical psychologists work, the wide range
of topics researched in this field, and advice on how to obtain a place
on a postgraduate clinical psychology professional training programme
in the UK and Ireland. Reference will be made to training in the US and
Australia.
Chapters 2–8 cover common psychological problems of childhood,
adolescence and adulthood. In Chapter 2 on childhood problems,
conduct disorder, oppositional defiant disorder and ADHD are
discussed. Chapters 3 and 4 deal with eating disorders and drug abuse,
which are common difficulties in adolescence. Anxiety, depression,
schizophrenia and personality disorders are considered in Chapters
5–8. In these chapters on specific disorders, case examples are given
along with relevant theory and research on the diagnosis, classification,
epidemiology, course, assessment and treatment of these conditions.
Controversies relevant to each condition are addressed.
In all of these chapters a description of the principal clinical features
of a disorder or group of disorders is given, with illustrative clinical
examples. Formulations and treatment plans, based on best practice
principles, are included where appropriate. This shows how clinical
psychologists approach common psychological problems in routine
practice. Epidemiological information on the prevalence, patterns of
comorbidity and outcome for each disorder is given. This is followed
by theoretical explanations from neurobiological and psychological
perspectives. Where appropriate, psychological explanations from
psychodynamic, cognitive-behavioural and family systems perspectives
are given. Reference is made to empirical research relevant to each
theoretical perspective and to research on the effectiveness of various
treatments. However, this is not intended as a textbook for clinical
practice, so insufficient information is given for such purposes.
Virtually all of the assertions made about the psychological problems
in Chapters 2–8 require qualification as to the limits of their reliability
and validity. However, I have not peppered the text with statements of
qualification, since this would detract from the clarity of the prose. In

Book 1.indb xiii 06/03/2012 13:47

 xiv C L I N I C A L P S Y C H O L O G Y : A N I N T R O D U C T I O N

adopting this style, there is a risk that readers may get the impression
that there is considerable consensus within the field about most key
issues and that most empirical findings are unquestionably reliable
and valid. To guard against this risk, in Chapters 2–8, a section on
important controversies about the clinical problems considered in each
chapter are included. Each chapter opens with learning objectives and
concludes with a summary and recommendations for further reading.
An attempt has been made throughout the text to take account of
two widely used classification systems for psychological problems: the
fifth chapter of the World Health Organization’s (1992) International
Classification of Diseases – Tenth Edition (ICD-10) and the American
Psychiatric Association’s (2000) Diagnostic and Statistical Manual
of Mental Disorders – Fourth Edition Text revision (DSM-IV-TR). In
DSM-IV-TR and ICD-10 there are slight differences in terminology and
diagnostic criteria. There are, in addition, differences in the way disorders
are clustered and subclassified. Also, in routine clinical practice and in
the scientific literature, in some instances the terminology used differs
from that in ICD-10 and DSM-IV-TR. Care has been taken throughout
the text to employ those terms that have widest usage in the clinical
field and to clarify terminological ambiguity, where appropriate, without
inundating the reader with multiple terms and criteria for each condition.
Chapter 9 deals with models that inform clinical psychology research
and practice. The biological, psychodynamic, cognitive-behavioural and
family systems models are considered in detail with reference to their
assumptions, their contributions to our understanding and treatment of
psychological problems, and their limitations. Other perspectives are
also mentioned, including humanistic–client-centred tradition, personal
construct psychology and the positive psychology. This chapter provides
an opportunity to reconsider the material in the body of the text from a
critical standpoint and to question the limits of the knowledge claims
made throughout the text. I was tempted to place this chapter after
Chapter 2, but my undergraduate students at UCD have told me that
reviewing models of practice is a more productive learning experience
after topics contained in the main body of the text have been covered.
In the final chapter, evidence for the effectiveness of psychological
interventions is summarized. Evidence-based practice is now embraced
by clinical psychologists around the world. This chapter underlines the
importance of evidence-based practice within clinical psychology, and
the centrality of a scientific perspective to ethical practice.
Because this text was written with brevity as a central feature,
inevitably it is not comprehensive in its coverage. Many important topics
often covered in larger introductory clinical psychology texts have not
been addressed in this book and these deserve mention, if only to alert
you to their existence and importance. They include: intellectual disability;
language delay; specific learning disabilities; pervasive developmental
disorders; psychological problems of old age, particularly dementia;
psychological problems secondary to medical conditions such as
heart disease or epilepsy; neuropsychological problems; somatoform
disorders such as conversion hysteria; dissociative disorders such

Book 1.indb xiv 06/03/2012 13:47

 PREFACE xv

as dissociative amnesia; factitious disorders; sexual and gender

identity disorders; paraphilias such as pedophilia; sleep disorders
such as insomnia; impulse control disorders such as kleptomania; and
adjustment disorders which are transient responses to acute stresses.
In writing this text I have tried to show, as simply as possible,
that understanding psychological problems in a rigorous clinical and
scientific way is a complex matter.
If you read this book with a view to deciding on whether or not to
become a clinical psychologist, I hope that it helps you make up your
mind.

Alan Carr, July 2011

Book 1.indb xv 06/03/2012 13:47

Book 1.indb xvi 06/03/2012 13:47
 Acknowledgements
Throughout Clinical Psychology the following are widely taken into
account:

Diagnostic and Statistical Manual of Mental Disorders, fourth edition,

text revision (copyright © 2000) American Psychiatric Association,
reprinted with permission.

The ICD-10 Classification of Mental and Behavioural Disorders World

Health Organization (1992), copyright © World Health Organization
1992, reprinted with permission.

Book 1.indb xvii 06/03/2012 13:47

Book 1.indb xviii 06/03/2012 13:47
 What is clinical
psychology? 1
Learning objectives
After studying this chapter you will be able to:
● outline the basic aspects of the profession of clinical
psychology
● give an account of the main features of professional
clinical psychology training
● plan your career so as to maximize your chances of
getting a place on a clinical psychology programme
● explain the difference between clinical psychology,
other applied psychology specialties and related
mental health professions
● give a balanced view on the pros and cons of clinical
psychology as a prospective career.

Introduction
This chapter will give an overview of the profession and discipline of
clinical psychology. There will be a description of clinical psychology
training. The selection procedures used by clinical psychology training
programmes in the UK and Ireland will be discussed, and there will be
guidance on how to get a place on a clinical psychology programme. A
brief account will be given of clinical psychology training in the US and
elsewhere. The factors that distinguish clinical psychology from other
types of applied psychology and other mental health professions will be
discussed. The chapter will close with a consideration of the pros and
cons of clinical psychology as a career.

Book 1.indb 1 06/03/2012 13:47

 2 CLINICAL PSYCHOLOGY: AN INTRODUCTION

The profession and scientific discipline

of clinical psychology
Clinical psychology is both a health care profession (like medicine,
surgery or social work), and a health-related scientific discipline (like
physiology or sociology).

The profession
The profession of clinical psychology involves using clinical judgement
to apply knowledge from the scientific discipline of clinical psychology in
clinical practice with clients and patients. Clinical practice refers
to the assessment, treatment and prevention of psychological prob-
lems in a range of populations. For example, assessing a boy who is
failing in school and defiant with parents and teachers; helping a woman
with depression regulate her mood more effectively; or helping the
family of a person whose psychotic symptoms have been reduced
through using medication to develop a supportive style to prevent
relapse.
Clinical judgement is developed through supervised clinical practice
while undertaking professional training, and during post-qualification
clinical experience. Psychologists who have worked with a wide variety
of cases over an extended time period have a broader experiential base
on which to draw when making clinical decisions than their less experi-
enced colleagues. Scientific knowledge about clinical psychology is
developed through initial academic training, ongoing continuing profes-
sional development (CPD) and research. Throughout their careers clin-
ical psychologists keep up to date with recent developments through
CPD and must show evidence of this periodically to retain practising
certificates.

The scientific discipline

Within the scientific discipline of clinical psychology, research is
conducted to find out about how best to understand, assess, treat and
prevent psychological problems, and also to find out how widespread
psychological problems are. The results of clinical psychology research
provide information for planning services for whole populations, and
evaluating and treating individual cases in an evidence-based way. For
example, the results of epidemiological research indicate that depression
and anxiety are the most common problems that need to be addressed
by clinical psychologists in outpatient adult mental health services (Carr
& McNulty, 2006). The results of research on intelligence testing show
that people with IQs below 50 require considerable support in community
settings to be able to sustain a reasonable quality of life (Carr et al.,
2007). Psychotherapy research shows that family therapy is more
effective than individual therapy in the treatment of anorexia nervosa in
young adolescent girls (Carr, 2009a).

Book 1.indb 2 06/03/2012 13:47

 1 • WHAT IS CLINICAL PSYCHOLOGY? 3

TABLE 1.1
Main elements of clinical psychologists’ roles
• Direct work with clients, patients, service users
• Indirect work
• Administration and management
• Research
• Continuing professional development

Clinical psychologists’ roles

The main elements of clinical psychologists roles are listed in Table 1.1.
Clinical psychologists’ jobs typically involve both direct and indirect
work with clients, patients or service users. (Throughout this book the
terms client, patient and service user will be employed interchangeably,
as there is not currently a consensus on the most appropriate term to
use.) Clinical psychologists’ jobs also involve administration or manage-
ment, research, and continuing professional development (CPD) (Carr,
2000; Hall & Llewelyn, 2006). Beinart et al.’s (2009) Clinical Psychology
in Practice gives many detailed example of clinical psychologists’ roles
from a UK perspective.

Direct work
With direct work, clinical psychologists meet with clients, patients or
service users, and in some instances with their families. In these meet-
ings they assess psychological problems and provide psychological
interventions. Assessments may include interviews, psychological test-
ing and observation. For most cases, psychologists interview clients
(and in some instances members of their families) to find out about the
history of the presenting problem, previous attempts to resolve the
problem, the person’s personal and family history and any other rele-
vant details. In some cases psychologists administer tests to assess
patient’s intelligence, memory, personality, psychopathology, family
relationships and other aspects of their functioning. The main benefit of
psychological tests is that they measure constructs in a reliable and
valid way, and yield scores that can be interpreted within the context of
population norms. For example if a person returns an IQ score of 100,
the norms indicate that this person is more intelligent than 50% of
people of the same age within the normal population. With regard to
intervention, the media typically associate individual psychotherapy
with the practice of clinical psychology. However, clinical psychologists
use many other interventions such as parent training to equip parents
with skills to manage their children’s problems, training in meditation to
help people regulate depressed mood or impulsivity, and family psycho-
education to help families provide a supportive environment for family
members with psychosis. Psychological interventions may be offered
to individuals, groups with similar sorts of problems, couples and
families. Increasingly clinical psychologists are supplementing direct

Book 1.indb 3 06/03/2012 13:47

 4 CLINICAL PSYCHOLOGY: AN INTRODUCTION

face-to-face work with clients with bibliotherapy and computer-based

interventions (Carr, 2009a). With bibliotherapy patients are invited to
read specific self-help books that address their main presenting prob-
lems. For example, a person with panic disorder could be given a book
that outlines how to manage panic attacks using evidence-based proce-
dures. There are a growing number of computer-based interventions,
but the best validated are structured cognitive behavioural programmes
for managing depression. With these programmes clients work though
a series of web-based mood management exercises over period of
weeks.

Indirect work
With regard to indirect work, psychologists provide training, clinical
supervision and consultation to colleagues in psychology, psychother-
apy, social work, child care, medicine, nursing and other disciplines to
empower them to provide services to patients. This is referred to as
indirect work because psychologists influence patients indirectly through
the actions of their colleagues. In the area of training, clinical psycholo-
gists may offer lectures or skills building programmes on particular top-
ics relevant to specific groups, for example teaching foster parents
about the psychology of attachment. In the area of clinical supervision,
most senior psychologists in public health services provide placements
of supervised clinical practice to clinical psychologists in training to help
them develop the technical and self-reflective skills to practise profes-
sionally. Technical skills refer to those procedures used to evaluate and
treat clients. Self-reflective skills refer to the capacity to monitor accu-
rately the interactions between oneself, clients and colleagues, and the
impact of these interactions on oneself. With regard to consultation,
clinical psychologists may advise others how best to manage clients
with specific problems. For example, in an intellectual disability service
where a client engages in repeated challenging behaviour (such as
aggression or self-harm), a clinical psychologist may advise staff in the
service how to manage this on the basis of a thorough functional analy-
sis. This type of assessment is used to establish the function of the
challenging behaviour (for example, communicating to staff that they
are stressed or bored) by carefully observing, recording and analysing
the antecedents and consequences of the challenging behaviour.

Administration and management

Most clinical psychologists manage waiting lists, set appointment
schedules, document clinical sessions by writing reports, and commu-
nicate with colleagues through correspondence, phone calls and meet-
ings. As psychologists gain increasing managerial responsibility, they
not only fulfil these functions for their own clinical work, but also support
their more junior staff in doing so. Psychologists with managerial
responsibilities also contribute to policy development and service
planning for clinical psychology services, and in some instances for

Book 1.indb 4 06/03/2012 13:47

 1 • WHAT IS CLINICAL PSYCHOLOGY? 5

wider multidisciplinary teams in which clinical psychologists are

involved.

Research
Clinical psychologists conduct a range of different types of research.
They conduct literature searches to find out about recent developments
in assessment and treatment, so that their practice with clients is
informed by up-to-date research findings. Periodically they conduct
service-based research projects to answer specific questions such as
‘What are the profiles and outcomes of referrals over a one-year period?’
or ‘What are the main reasons clients give for dropping out of therapy?’
Large specialist psychology services within university-affiliated agen-
cies may have broad ongoing research programmes on specific themes
such as eating disorders, drug abuse or attention deficit hyperactivity
disorder (ADHD). Postgraduates on clinical psychology training pro-
grammes may conduct their doctoral research theses within these
research programmes. In services without such research programmes,
but which provide placements of supervised clinical practice, psycholo-
gists in clinical training may initiate smaller research projects to address
questions of concern to the service, themselves and their university-
based academic supervisors.

Continuing professional development

Clinical psychologists devote a proportion of their time each year to
CPD. This is a requirement for remaining a registered practitioner. CPD
includes regular participation in clinical supervision and journal clubs;
attendance at professional short courses and conferences; and en-
rolment in advanced specialist training programmes, for example in
psychotherapy or neuropsychology.

Populations and work settings

Clinical psychologists provide services to a wide range of people with
diverse difficulties in an array of different work settings, as outlined in
Table 1.2 (Carr, 2000; Hall & Llewelyn, 2006; Beinart et al., 2009).

Populations and problems

Clinical psychologists work with people across the life-span including
children, adolescents, adults and older adults. They provide services to
people with psychological disorders, intellectual and physical disabili-
ties and psychological difficulties secondary to physical illnesses such
as HIV/AIDS, heart disease or cancer. They also work with people
experiencing significant stress associated with major life transitions and
challenges such as infertility, child bearing, adoption, fostering, marital
discord and bereavement.

Work settings
Clinical psychologists work in a wide variety of settings including pri-
mary care, community mental health teams, general and specialist adult
and paediatric hospitals, disability services, services for older adults,

Book 1.indb 5 06/03/2012 13:47

 6 CLINICAL PSYCHOLOGY: AN INTRODUCTION

TABLE 1.2
Populations, problems and work settings
Populations Children
Adolescents
Adults
Older adults
Problems Mental health problems
Adjustment of physical health problems
Intellectual disability
Physical disability
Adjustment to major life transitions
Work settings Primary care
Community mental health teams
Hospitals
Disability services
Older adult services
Family services (e.g. fostering, adoption)
Specialist services (e.g. addiction, chronic pain)

prisons, fostering and adoption services and hospices. They also work
in a wide variety of specialist services for people with specific difficulties
such as addiction, eating disorders, aggression, sexual offending,
chronic pain and head injury. Most clinical psychologists in the UK and
Ireland work mainly within the public health service, although some
work in private practice. The following statements are first-hand
accounts of a typical day’s work of psychologists working in a number
of different settings.

Child and adolescent mental health

Martin, a clinical psychologist working on a child and adolescent mental
health team, offered the following brief description of a typical day.

Today I saw two families in the morning; went to a case conference

after lunch; made some calls to clients and colleagues after 4pm;
and (finally) finished a report that I’d been working on for 2 weeks.
The first family I saw this morning was a case of school refusal or
separation anxiety. The little fellow was 8 and very anxious. So were
his parents. We’ve met for three sessions, and worked today on the
final elements of a return to school plan. The second case was a
review of long-term client. This is a 16-year-old girl who came to our
service first because she was cutting herself. I’ve seen her for nearly
2 years and she is doing much better now. This afternoon the case
conference was about a chaotic family, where there are major child
protection concerns. The report I finished was an assessment of
need report on a 7-year-old boy with ADHD.

The child and adolescent mental health curriculum for the UCD clinical
psychology programme is contained in the Handbook of Child and
Adolescent Clinical Psychology (Carr, 2006a).

Book 1.indb 6 06/03/2012 13:47

 1 • WHAT IS CLINICAL PSYCHOLOGY? 7

Adult mental health

Rose is a clinical psychologist working on a community adult mental
health team. She gave this account of one day in her working life.

On Wednesday myself and Paul, my clinical psychology trainee, had

our anxiety management group for people with panic disorder. This
was fairly demanding. There are 10 patients in the group and we were
on session 6 of a 12 week CBT programme. A lot of unexpected
issues came up, around abuse one of the group members had expe-
rienced, that we had to deal with. Afterwards at lunch I debriefed Paul,
who found the group heavy going. After lunch, we ran our ‘hearing
voices’ group for people with psychosis. This was a lower key affair. A
few issues came up around medication and compliance, so after the
group I phoned Seamus, the psychiatrist to discuss the meds issue.
I picked up my son, Ruan, from the childminder’s at 5. What a day!

The adult mental health curriculum for the UCD clinical psychology
programme is contained in Handbook of Adult Clinical Psychology (Carr
& McNulty, 2006).

Older adults
Fintan works for a specialist older adult service attached to a large
general hospital. Here is how he described a day at this service.

On Thursday morning we had a team meeting at 9. The psychiatrist,

social worker, physiotherapist and occupational therapist were there
and the secretary for the unit. A lot of the meeting was about
discharge planning for patients who were about to leave hospital. We
also reviewed follow-up support plans for some cases where there
were snags in the support plans that needed to be ironed out.
Between 11 and 1 the social worker, Sue, and I ran our reminiscence
group for older adults recovering form depression. We had a journal
club at lunch time where our team discussed two really interesting
papers on cognitive rehabilitation for older adults with dementia. In
the afternoon I did an assessment with a 75-year-old woman. The
main issue was whether she had dementia or depression. I scored
the tests and drafted the report. Just as I was leaving at 6, one of the
nurses on the ward called to ask about a patient whose relatives
were visiting and wanted some information, so I didn’t leave work till
nearly 7. It was a long day.

The older adult mental health curriculum for the UCD clinical psychology
programme is contained in Handbook of the Clinical Psychology of
Ageing (Woods & Clare, 2008).

Intellectual disability service

Karen is a clinical psychologist working in a community based early
intervention intellectual disability service. Here is what she had to say
about her day.

Book 1.indb 7 06/03/2012 13:47

 8 CLINICAL PSYCHOLOGY: AN INTRODUCTION

Monday is always a strange sort of day. I don’t start till 12 but go

through till 8pm because we run our parent training programme on
Monday evenings from 6 to 8. This went very well yesterday. We
have six mums and four dads in the group. We have been doing
behavioural parent training with them. They are beginning to ‘get it’.
I like when it clicks and they ‘get it’. They also find the support they
get from each other very useful too. I think the younger parents in the
group felt very isolated, and like they were the only ones with
parenting issues. But now they have other people to talk to about the
same stuff they are facing. Before the group session, I did a home
visit at 12 with a single mother who was having a crisis with managing
her son’s challenging behaviour. She was very distressed, so I
stayed quite a while and didn’t make it to the centre till 3. Most of the
afternoon was spent preparing for the evening group session with
the social worker who runs the group with me and doing routine
phone calls and reports.

The intellectual disability curriculum for the UCD clinical psychology

programme is contained in Handbook of Intellectual Disability and
Clinical Psychology Practice (Carr et al., 2007).

Hospital clinical neuropsychology service

Morgan, a clinical psychologist working with a neuropsychology service
in a busy university hospital, gave this account.

First thing on Friday our team met to review referrals which had
come in on Thursday afternoon (mainly from the neurological wards).
I got two cases. One was a 63-year-old woman who had had a
stroke. I had to do a preliminary assessment of her neuropsychological
functioning to get a baseline. The second case was a man in his late
20s who had been in a road traffic accident and had a closed head
injury. I plan to do periodic follow-up assessments of both of these
cases to monitor their recovery. It took all day to do these two
assessments, score tests, phone relatives and get their views, write
up reports and discuss them with the relevant neurologists. I’ll be
following up both of them next week and meeting with the families
and patients to talk about how to manage things after discharge.

Lezak et al.’s (2004) Neuropsychological Assessment is a widely used

neuropsychology text on many clinical psychology programmes.

Specialist family therapy service

I run a family therapy clinic on Thursday evenings at the Clanwilliam
Institute in Dublin. Here is what happened last Thursday.

There was a request from a couple for an emergency appointment,

so I saw them first at 5pm. The husband has bipolar disorder, which
is moderately well controlled with medication. I’ve been seeing the
couple for a long time for relapse prevention therapy. When this
couple came to me first the husband was being hospitalized five

Book 1.indb 8 06/03/2012 13:47

 1 • WHAT IS CLINICAL PSYCHOLOGY? 9

times a year. This has reduced significantly in the past few years.
The main issue on Thursday was helping the couple handle the
husband’s sudden dip in mood without hospitalization. The next
clients were a couple who are working on addressing trauma-related
issues. The woman is a courageous survivor of long-term child
sexual abuse, who is using couples therapy to find ways to expand
her constricted lifestyle and deal with trauma-related flashbacks. The
last family I saw on Thursday night included a 9-year-old girl who has
difficulty controlling her temper. This leads to major problems at
home and in school. This little girl was a neglected and abused
Vietnamese orphan when her parents adopted her 7 years ago. She
has always had significant behaviour problems, and I have been
working long-term with this family to help them address these.

The family therapy curriculum for the UCD clinical psychology pro-
gramme is contained in Family Therapy: Concepts, Process and Prac-
tice (Carr, 2006b).

Clinical psychology training

The central objective of clinical psychology programmes is to train can-
didates to a level that will enable them to work safely, competently and
ethically as basic grade clinical psychologists and to provide a founda-
tion for later specialization through CPD. Clinical psychology graduates
are able to provide clinical services to a wide range of client groups, use
their academic knowledge to solve clinical problems, provide consul-
tancy and teaching services to colleagues and clients and use their
research skills to address relevant questions in a scientific way.
Currently in the UK and Ireland professional clinical psychology train-
ing programmes are 3 year doctorates and are variously called D Clin
Psych, Clin Psy D, and D Psych Sc (Clin Psych). In 2011 there were 30
such programmes in Britain (including England, Scotland and Wales)
and five in Ireland (including Northern Ireland). The UK programmes
are listed on the website for Clearing House for Postgraduate Courses
in Clinical Psychology. The Irish programmes are in UCD, Trinity
College Dublin (TCD), the National University of Ireland Galway (NUIG),
the University of Limerick (UL) and Queen’s University Belfast (QUB).
Web addresses for the clearing house and the Irish universities are
included at the end of the chapter. All of these programmes are accred-
ited by professional associations: the British Psychological Society
(BPsS) or the Psychological Society of Ireland (PsSI). Since the end of
the first decade of the 21st century they have been approved by statu-
tory registration bodies. These are the Health Professions Council
(HPC) in the UK and the Health and Social Care Professional Council
(HSCPC) in Ireland. Effectively the BPsS and PsSI regulate the content
of courses, and the HPC and HSCPC approve such courses and pro-
vide statutory registration for their graduates.
The roles for which clinical psychologists are trained are conceptual-
ized by different programmes in different ways. The most common

Book 1.indb 9 06/03/2012 13:47

 10 C L I N I C A L P S Y C H O L O G Y : A N I N T R O D U C T I O N

orientations are the scientist-practitioner and the practitioner-scholar

(McFall, 2006). With the scientist-practitioner model, there is a strong
emphasis on training psychologists in research skills so that they can
both generate scientific knowledge and apply scientific knowledge in
clinical practice. With the practitioner-scholar model, the emphasis
is predominantly on clinical practice, and on training psychologists
to inform their clinical work with scholarly knowledge of the relevant
scientific literature. Most UK and Irish courses tend more towards the
scientist-practitioner than the practitioner-scholar model.
The role of the clinical psychologist has also been conceptualized as
that of a reflective practitioner (Scaife, 2010); that is, as a professional
who enhances their practice by sensitively reflecting on the way in
which personal psychological strengths and vulnerabilities impinge on
skilled clinical practice. Reflective practice is enhanced through
engaging in experiential personal and professional processes such as
personal psychotherapy and process-oriented supervision. Reflective
practice is increasingly receiving greater emphasis on UK and Irish
clinical psychology training programmes (Hughes & Youngson, 2009).
For example, at UCD it is mandatory for postgraduates to engage in
personal psychotherapy during their training.
In the UK and Ireland each clinical psychology programme is run by
a partnership involving a university and a public health service unit. The
university provides the academic and research foundation for the
course; the health service unit provides the clinical practice foundation
for the course and placements of supervised clinical practice. These
doctoral programmes in clinical psychology have three main elements:
(1) academic course work, (2) placements of supervised clinical prac-
tice, and (3) research requirements. A summary of these components is
given in Table 1.3.

Academic coursework
Academic coursework covers theory, research and practice-related
material essential for developing competencies required to practise as a

TABLE 1.3
Components of professional clinical psychology training programmes
Research Doctoral thesis on major research project
Small-scale service-based research project
Coursework or research design, methods and statistics
Academic course Children and adolescents
work Adults and older adults
Intellectual disability
Assessment and intervention competencies
Clinical Range of populations (child, adult, older adult, disability,
placements specialties)
Range of competencies (assessment, intervention, training)
Quality control (placement contract and monitoring)
Regular supervision (observe and be observed)

Book 1.indb 10 06/03/2012 13:47

 1 • WHAT IS CLINICAL PSYCHOLOGY? 11

clinical psychologist. These competencies include the ability to assess

and formulate psychological problems using relevant psychological meth-
ods and theories; treat psychological problems using evidence-based
interventions and evaluate the effectiveness of treatment; and work within
psychology services, multidisciplinary teams, and wider health service
and multiagency contexts using appropriate communication and organ-
izational skills. Within academic courses on clinical psychology pro-
grammes, these issues are covered with reference to psychological
disorders and problems typical in the fields of child and adolescent men-
tal health, adult and older adult mental health, intellectual and physical
disability, and neuropsychological problems. A range of teaching formats
are used including lectures, video-modelling, role-playing, video feed-
back, discussion groups, and problem-based learning.

Placements of supervised clinical practice

On doctoral programmes in clinical psychology, most of the time is
spent on placements of supervised clinical practice. For example, on
the UCD clinical psychology training programme, each year there are
two 4.5 month placements of supervised clinical practice. This is sig-
nificantly longer that the two 6 week periods devoted to academic
coursework. Placements occur in a range of services including primary
care, secondary and tertiary services; adult mental health services;
child and adolescent mental health services; intellectual disability ser-
vices; services for older adults; neuropsychology services; paediatric
services; and various specialist adult health services such as cardiology
and oncology. In the UK and Ireland, clinical psychology training pro-
grammes provide supervisors with ongoing training and CPD to ensure
that they develop strong supervision skills (Fleming & Steen, 2004;
Milne, 2009).

Placement contracts
At the outset of each clinical placement, contracts are formed between
postgraduates and clinical supervisors specifying the overall placement
goals. These goals refer to competencies to be developed, the kinds of
assessment and treatment procedures to be learned, the types of cases
to be seen and other types of professional skills to be developed. These
placement contracts are based on the minimum experience requirements
listed in the course logbook, the learning opportunities available on the
placement, the unique skills of clinical supervisors, and the unique
clinical interests of postgraduates. Over the course of placements,
postgraduates and supervisors work together to ensure that these goals
are reached.

Supervision and quality control

On most clinical psychology programmes the supervision and quality
control procedures described below are used to facilitate the develop-
ment of clinical competence. Postgraduates on clinical placements
receive a minimum of an hour’s supervision per week, and the ratio of

Book 1.indb 11 06/03/2012 13:47

 12 C L I N I C A L P S Y C H O L O G Y : A N I N T R O D U C T I O N

postgraduates to supervisors is never greater than 2:1. ‘Observe and

be observed’ is a central training process on clinical psychology place-
ments. That is, postgraduates develop clinical competencies by observ-
ing their supervisors’ clinical practices, and also by having their
supervisors observe their clinical practice and give feedback on this.
Video or audio recording of clinical sessions may be used to facilitate
this ‘observe and be observed’ training process. In an Irish study,
Hughes and Byrne (2011) identified the ‘observe and be observed’
aspect of supervision as that most valued by clinical psychology post-
graduates. Progress on clinical placements is monitored through place-
ment visits made by members of the course team. These visits are
made towards the middle and end of clinical placements. Mid-placement
visits offer an opportunity to monitor progress and resolve any teething
difficulties that have arisen. End-of-placement visits provide a context
for evaluating whether postgraduates pass or fail placements and for
identifying areas for competency development in future placements.

Research requirements
On UK and Irish programmes, clinical psychologists are trained to be
competent in research as well as clinical practice. All clinical psychology
programmes provide training in research design, methods and statistics,
and require postgraduates to complete small-scale service-based
research and a major doctoral research thesis. On the UCD clinical psy-
chology programme, postgraduates have regular research seminars
over the 3 years of the programme and complete small quantitative and
qualitative service-based research projects, in addition to a major doc-
toral research project. A day a week over the 3 years of the programme
is set aside for research, as well as 2 weeks’ study leave per year.

Assessment
A range of procedures is used for assessment on doctoral programmes
in clinical psychology. Academic coursework may be assessed by
exams or continuing assessment assignments such as essays or
clinical case studies. Placements are assessed by end-of-placement
competency ratings. Research competence is usually assessed by the
submission and oral defence of a doctoral thesis with an internal and
external examiner at the end of the programme.

Getting a place on a clinical

psychology programme
Admission information for UK clinical psychology training programmes
is available on the website of the Clearing House for Postgraduate
Courses in Clinical Psychology. For Irish programmes, details are given
at the websites for UCD, TCD, NUIG, UL and QUB. Web addresses for
these universities and the clearing house are given at the end of the

Book 1.indb 12 06/03/2012 13:47

 1 • WHAT IS CLINICAL PSYCHOLOGY? 13

chapter. The intake for most doctoral programmes in clinical psychology

in the UK and Ireland varies from about eight to 42 candidates, with
most courses having annual intakes. In 2010 there were just over 600
places on UK courses and just under 50 on Irish courses. Between
2005 and 2010 about 20–30% of applicants were offered places on
doctoral programmes in clinical psychology in the UK and Ireland. Entry
requirements for all of these courses are a 2.1 honours degree or higher
diploma in psychology recognized by the BPsS or PsSI as conferring
graduate basis for registration, and about a year’s relevant clinical
experience.

Planning to get onto a clinical psychology programme

Because entry to doctoral programmes in clinical psychology in the UK
and Ireland is highly competitive, it is useful to develop a strategy to
maximize your chances of getting a place. Guidance on applying for UK
and Irish clinical psychology programmes is given in Knight (2002),
O’Shea and Byrne (2010), Papworth (2004, 2007) and Roth (1998).
Most course selection teams judge suitability on the basis of academic
and clinical criteria. Your strategy should take account of this, and
balance your efforts so that you do well academically but also make
time to get relevant clinical experience. A summary of items to consider
when building your profile for admission to clinical psychology training
is given in Table 1.4.
Studies of successful entrants to UK and Irish clinical psychology
programmes have reached a number of important conclusions (Clare,
1995; O’Shea & Byrne, 2011a; Phillips et al., 2004; Scior et al., 2007).
With regard to the academic domain, candidates with better secondary
school results, higher undergraduate grades, master’s and PhD
degrees, more favourable academic references and greater research
achievements and publications are more likely to be admitted to clinical
psychology programmes. Those with first class undergraduate degrees
and master’s degrees are admitted to clinical programmes at a younger
age. In the clinical domain, candidates who have acquired basic clinical
skills by working in a variety of assistant psychologist or research
assistant posts, and have more favourable clinical references, are more
likely to obtain a clinical psychology programme training place.

TABLE 1.4
Building your profile for admission to clinical psychology training
Academic and Honours undergraduate degree in psychology
research Postgraduate degree in area relevant to clinical psychology
competence Short courses relevant to clinical psychology
Other qualifications relevant to clinical psychology
Experience doing clinical research
Theses, publications and presentations
Clinical Relevant clinical experience
competence Basic clinical skills

Book 1.indb 13 06/03/2012 13:47

 14 C L I N I C A L P S Y C H O L O G Y : A N I N T R O D U C T I O N

Academic qualifications
Academic suitability for doctoral programmes in clinical psychology is
assessed by taking account of performance in high school and on
undergraduate degree programmes; completion of postgraduate
degrees in psychology, short courses relevant to clinical psychology,
and other non-psychological qualifications; and research achievements
and publications.

Undergraduate degree
While a 2.1 honours degree is the minimum academic requirement for
entry to a clinical psychology programme, many successful candidates
exceed this minimum standard. Some have first class honours under-
graduate degrees. Many have master’s degrees. Some have PhDs. In
planning your strategy, provided it does not tax your personal resources
too much and leave little time and energy for relevant clinical experi-
ence, it’s a reasonable strategy to aim for a first class honours under-
graduate degree. However, if things do not go well for you in your
undergraduate programme and you get a 2.2, this does not prevent you
from entering the profession. Some clinical psychology programmes will
accept applications from candidates with a 2.2 honours degree or higher
diploma in psychology provided they also have a master’s or PhD
degree.

Master’s programmes
There are a number of types of master’s degree in psychology that
enhance chances of gaining a place on a clinical psychology pro-
gramme. These include master’s by research on a clinical topic, mas-
ter’s in applied psychology (with a clinical emphasis), master’s in
neuropsychology or neuroscience, master’s in developmental psychol-
ogy, master’s in health psychology, master’s in counselling psychology,
master’s in psychotherapy or counselling and master’s in applied
behaviour analysis. All master’s programmes that include advanced
research and statistics coursework and a minor or major thesis con-
ducted on a clinical topic enhance your profile because they give you
advanced research skills and may give you clinical interviewing skills if
you collect interview data from people with psychological problems for
your thesis.
Master’s programmes in applied psychology (that include course-
work on psychopathology and related topics), neuropsychology or
neuroscience, health psychology, disability, and developmental psy-
chology are a useful preparation for clinical psychology because they
provide a grounding in academic areas relevant to the practice of clini-
cal psychology. Insofar as neuropsychology programmes include skills
training in administering and interpreting psychological tests, they are
an academic route to acquiring relevant clinical experience. Master’s
programmes in psychotherapy, counselling and applied behaviour
analysis may also help you acquire relevant clinical experience and basic
clinical skills if they include placements of supervised clinical practice.

Book 1.indb 14 06/03/2012 13:47

 1 • WHAT IS CLINICAL PSYCHOLOGY? 15

From this, it is clear that there is no single best master’s programme

to opt for as a stepping stone to obtaining a place on a clinical psychology
programme. You will maximize your chances of gaining a place if you
take account of your overall profile (including academic and clinical
suitability) when choosing a master’s programme. For example, if you
have acquired a lot of relevant clinical experience, but limited research
experience, then it might improve your profile to opt for a master’s
programme with a strong academic and research orientation rather
than a clinical practice orientation.

PhDs
PhDs in psychology can enhance chances of admission to a clinical
psychology programme, especially if the research is conducted on a
clinical topic, involves interviewing or assessing people with psycho-
logical problems, and if the work is conducted within a health service
setting. All of these factors make the process of conducting a PhD a
relevant clinical experience. At UCD my colleagues and I have super-
vised PhD candidates who did their theses in psycho-oncology, the psy-
chology of sex-offenders, neuropsychology and the psychology of
eating disorders. All obtained places on clinical psychology programmes
on the grounds that their PhD research provided them with both rele-
vant clinical experience and research skills. If you want to undertake a
PhD as a stepping stone to getting onto a clinical psychology training
programme, make sure at the outset that your research project will
involve significant contact with people with psychological problems, and
be conducted within a public health service context, or a context that
has much in common with the public health service. PhDs conducted in
university laboratories with non-clinical participants or animals are not a
useful preparation for clinical psychology training.

Short courses
Diploma and certificate courses, CPD short courses and workshops
and attendance at psychology conferences that facilitate the develop-
ment of clinical skills for understanding, assessing and treating psycho-
logical problems are taken into account by many selection panels in
judging academic suitability for clinical psychology programmes. If you
want to enhance your chances of getting a place on a clinical psychol-
ogy programme, consider taking a diploma or certificate course in basic
assessment or counselling skills and regularly attend CPD short courses
and conferences to develop your clinical skills. Such courses are adver-
tised in the BPsS magazine, The Psychologist, and the PsSI magazine,
The Irish Psychologist.

Non-psychology qualifications
For mature students who have come to psychology (possibly through
the higher diploma in psychology route) after a career in nursing,
counselling, social work, occupational therapy, speech and language
therapy or teaching, some selection panels will take account of your
prior qualifications in assessing your suitability for clinical psychology

Book 1.indb 15 06/03/2012 13:47

 16 C L I N I C A L P S Y C H O L O G Y : A N I N T R O D U C T I O N

training. In filling out your application form, be sure to include these prior
relevant qualifications and to state the academic and clinical skills you
acquired from them relevant to engaging in clinical psychology training.

Research competence
One aspect of academic suitability for a clinical psychology programme
is research competence. In rating research competence, selection
panels take account of research and statistics skills; participation in
clinical research projects; publication of research presentations, reports
and articles; and relevant qualifications such as diplomas or certificates
in specific research methods, statistics or data analysis. Research
competence may be assessed by taking account of the highest research
thesis completed (e.g. undergraduate thesis, master’s thesis or PhD),
involvement in other research projects (e.g. conducting clinical audits or
working as a research assistant on a big project), and the number of
conference presentations, research reports and academic publications.
To enhance your chances of being rated well for research competence,
present the results of your undergraduate and postgraduate theses,
and any other research projects in which you have been involved at
academic conferences, and publish them as reports or academic journal
articles. List these presentations and publications in your application
form chronologically in the style used in BPsS, PsSI or American
Psychological Association (APA) journals.

Relevant clinical experience

Relevant experience includes part-time or full-time, voluntary or paid
clinical or research work, involving interaction with patients, clients or
service users in health service settings. The sorts of work experience
that count as relevant experience are discussed in Knight (2002) and
Williams (2001). Working as an assistant psychologist in a clinical psy-
chology service, a psychology research assistant on a major clinical
project, or conducting a master’s or PhD postgraduate research degree
that involves extensive interaction with people with psychological prob-
lems are all types of relevant experience frequently reported by suc-
cessful applicants to clinical psychology programmes (O’Shea & Byrne,
2011a, 2011b; Phillips et al., 2004; Scior et al., 2007). Work as a thera-
pist within the IAPT (Improving Access to Psychological Therapies) pro-
gramme in the UK, a clinical associate in applied psychology (or
associate psychologist) in the UK, or a psychometrist in the US is a very
good way to acquire relevant clinical experience. The weblink for IAPT
is given at the end of the chapter.
Other ways to acquire relevant clinical experience are to work as a
care worker (with children, older adults or people with disabilities), a
nursing assistant, a psychiatric day centre assistant, a support worker
for people with mental health problems or disabilities, an applied behav-
ioural analysis (ABA) tutor with children with autism spectrum disorders,
a special educational needs assistant for children with psychological
problems, a volunteer with a development agency that offers health or

Book 1.indb 16 06/03/2012 13:47

 1 • WHAT IS CLINICAL PSYCHOLOGY? 17

educational services in underdeveloped countries, a children’s summer

camp counsellor, or a mental health helpline worker. Work that is super-
vised by a clinical psychologist and is conducted within a psychology
service or within a public health service multidisciplinary team is often
judged by selection panels to prepare people better for clinical psychol-
ogy training than work conducted in other settings.
Some UK programmes require applicants to have gained their
relevant experience within the NHS. Check if this is a requirement for
your preferred courses, and plan your relevant experience to take
account of this requirement. If relevant experience is not supervised by
a clinical psychologist, then it will enhance your chances of getting a
place on a clinical programme if you arrange regular supervision from
a clinical psychologist who will give you a reference when you apply for
a place on a clinical psychology programme and comment on the clinical
skills you have acquired during your relevant experience.
Relevant experience is an entry requirement for clinical psychology
training programmes because it familiarizes candidates with the sorts of
setting in which clinical psychologists work, their roles, the types of
people with whom they work and also because it equips candidates with
basic clinical skills. These include skills for interacting with clients with
psychological problems, and skills for working in a psychology service
or on a multidisciplinary team in a health service organization. During
relevant clinical experience you may gain interviewing skills; skills for
administering and interpreting psychological tests; skills for engaging
clients in therapy; specific therapeutic procedures for treating clients
with particular psychological problems such as anxiety, depression,
autism, or ADHD; teamwork skills; report writing skills and so forth.
Clinical suitability is assessed by clinical psychology course selection
panels with reference to the way in which candidates have made use of
the opportunities available to them to engage in relevant clinical
experiences. This means that candidates with more experience are not
always rated as more suitable. The key issue is how candidates have
used the opportunities available to them. For example, young candidates
who have had less time to acquire relevant experience than older
candidates, but who have used the time available to them during their
undergraduate and postgraduate years to maximize their clinical skills,
may be rated as more suitable than older candidates who have used
the time available to them to acquire relevant clinical experience less
efficiently.
From the foregoing, it is clear that it is never too early to start acquiring
relevant experience. If you have not already done so, now is a good
time to start. When filling out an application form for clinical psychology
training it is vital to list both the relevant clinical experience jobs you
have done and the skills you have acquired while doing those jobs.
Finding relevant clinical experience is challenging. Some jobs are
advertised in the Psychologist and Irish Psychologist. Others are
advertised in national newspapers such as the Guardian or the Irish
Times. The Psyclick website (listed at the end of the chapter) contains
links to many websites where ‘relevant experience jobs’ may be

Book 1.indb 17 06/03/2012 13:47

 18 C L I N I C A L P S Y C H O L O G Y : A N I N T R O D U C T I O N

advertised. A good source of information on relevant experience for

Irish candidates is the assistant psychologist Ireland Google group
(listed at the end of the chapter). Many people get relevant clinical
experience by sending their CVs to clinical psychologists or managers
of relevant agencies. If you do this, make it clear that you wish to acquire
relevant experience to increase your suitability for clinical psychology
training and are available for voluntary or paid work, and are prepared
to be flexible and fit in with the overall needs of the service. The key
thing is to convey that you are prepared to make a contribution to the
service in return for the opportunity to acquire relevant experience.
The process of acquiring psychology assistant or research assistant
posts, or other good relevant experience positions, is highly competitive.
Your chances of being successful in job competitions for relevant
experience will be enhanced if you have a master’s degree, so it may
speed up your acquisition of relevant experience if you obtain a master’s
degree as soon as possible after your primary degree.
There is a danger of viewing the process of obtaining a portfolio of
academic, research and clinical requirements to get onto a clinical
psychology programme as having value only insofar as it makes you
eligible for selection onto a clinical course. This may not be the most
useful way to think about it. A postgraduate on the UCD clinical
psychology programme who gave feedback on this chapter remarked,
‘I wonder also if it is worth discouraging people who want to get onto
clinical programmes from thinking of clinical experience like a means to
an end, and encourage them to conceptualize it as part of the process
of getting on training, yes, but also as a valuable journey!’

The application process

To get a place on a clinical psychology programme it is essential to
manage the application process well. This includes completing the
application form and submitting it prior to application deadlines; arrang-
ing references; attending interviews; engaging in assessment exer-
cises; accepting negative feedback; and reapplying if you do not get a
place first time round.

Application forms
Begin the application process well in advance of application deadlines.
This will give you time to refine your application, obtain supporting
documents and invite referees to write your references. The clearing
house deadline, which is posted on the clearing house website, is
usually at the end of November or in early December. For Irish courses,
deadlines are posted on college websites, but they are usually in the
winter months (December–February). Relevant web addresses are
given at the end of this chapter. Download application forms and write
answers to questions in the application form in a Word document. Read
and edit your answers until you have produced your best draft. Ask a
recent successful applicant to a clinical psychology course for feedback

Book 1.indb 18 06/03/2012 13:47

 1 • WHAT IS CLINICAL PSYCHOLOGY? 19

on this draft, and use their comments to refine your application. Then
submit your final ‘polished version’ through the electronic application
process or in hardcopy, as directed in the application guidelines.
When completing application forms give concise accurate informa-
tion about your secondary school exam results, university degree
results, other relevant qualifications, publications and details of relevant
clinical and research experience jobs. For master’s degrees give the
type of master’s degree (by thesis only, applied psychology, health
psychology, etc.) and your mark (e.g. 70%). This is important to include
if the degree was awarded on a pass/fail basis, since some selection
panels will take high marks on a master’s degree into account in judging
suitability. If the master’s degree included a placement of supervised
clinical practice, note this on the form (e.g. MSc, Counselling Psychology,
65%, containing a 100 hour placement of supervised clinical practice).
When listing theses, reports, presentations and publications, use the
format in BPsS, PsSI or APA academic journals. For relevant clinical or
research experiences, give the name of the job, the employer, and the
main duties, the dates of employment, the number of hours per week,
and whether the job was voluntary or paid. Keep these descriptions
concise.
Most application forms include a section where there is an opportunity
to indicate other relevant life experiences such as world travel or past
career (for mature applicants); to reflect on the clinical and personal
skills you have acquired from graduate degrees, relevant clinical and
research experiences and other life experiences; and to make a
personal statement about your own evaluation of your suitability for
clinical psychology training. There are usually word limits for these
sections, so it is useful to draft, edit and redraft these statements a few
times until you get them right. One way to go about this is to list the skills
you have developed, and for each skill state how your qualifications and
experiences have helped you develop it. Another approach to state the
skills that each of your main qualifications or experiences helped you
develop. In writing a personal statement it is important to show why you
consider that your skills and personal qualities make you ready to train
as a clinical psychologist in the public health services. To write a credible
statement of this type, it is important to convey that you know about the
roles clinical psychologists fulfil within the UK National Health Service
(NHS) or the Irish Health Service Executive (HSE).

Supporting documents
When planning your application strategy, leave lots of time to obtain
supporting documents that must accompany your application. If your
primary degree is from a non-UK university and you apply to UK courses
through the clearing house, you will be required to submit a letter from
the BPS indicating that your degree confers graduate basis for
membership. If you are applying to Irish universities you may be asked
to submit university transcripts for your primary degree, so you will need
to request these from your alma mater.

Book 1.indb 19 06/03/2012 13:47

 20 C L I N I C A L P S Y C H O L O G Y : A N I N T R O D U C T I O N

Arranging references
The clearing house and most clinical psychology courses require one
academic reference and one reference from a clinical psychologist or
clinical manager who supervised your relevant clinical experience. Invite
referees who know you fairly well; are familiar with your work and so can
accurately comment on your skills, personal qualities and suitability for
clinical psychology training; and are willing to write a reference by the
deadline date. As a courtesy, when inviting referees to write you a refer-
ence, send them an up-to-date copy of your CV. Unless there are no
other options, do not invite colleagues to be referees if they have close
personal connections to you (e.g. family members or business partners).

Short listing
Clinical psychology courses establish selection panels to shortlist
applicants for interview. These panels typically include a group of staff
with a range of academic and clinical expertise. Panels read and rate
large numbers of application forms during the short-listing process;
make collective judgements about the suitability of candidates for
clinical psychology training; and select the most suitable for interview.
While applying for clinical psychology training is stressful for applicants,
short listing is very demanding for selection panel members, and this is
worth keeping in mind when writing your application. The easier you
make it for selection panel members to read and rate your application,
the better. Our experience at UCD last year gives an idea of how
demanding short listing is. Each member of our panel read and rated
over 160 applications. This took a number of days. They rated responses
to all questions on application forms using objective criteria, and then
summarized these into an overall score reflecting academic and clinical
suitability. In an all-day panel meeting, ratings of panel members were
aggregated, rank ordered, and approximately 40 applicants were
selected and invited to interviews.
Some courses are experimenting with using writing assignments to
assist with the short-listing process. For example, the UK Lancaster
course has published a report on its use of written assignments in short
listing and shown that these assignments predict academic performance
on clinical psychology programmes (Hemmings & Simpson, 2008).
Lancaster’s written task was adapted from one designed by the
University of Surrey, and applicants were invited to complete the task
on a computer. The task involved reading five abstracts, synthesising
them into a 250-word summary that answered a specific question,
answering a number of short statistical and methodological questions
about the studies described in the abstracts, and completing the
assignment within an hour. Applicants’ answers were rated for writing
skills, critical thinking skills and methodology skills. If you apply for
courses with these types of short-listing tasks, it may be useful to speak
to successful applicants about them and practise similar sorts of task
before completing the actual short-listing task.

Book 1.indb 20 06/03/2012 13:47

 1 • WHAT IS CLINICAL PSYCHOLOGY? 21

Interviews
There is considerable variability in the types of interview and assessment
exercise used on the 35+ clinical psychology programmes in the UK
and Ireland (Hemmings & Simpson, 2008; O’Shea & Byrne, 2011b;
Phillips et al., 2001; Roth & Leiper, 1995). Find out the format and
duration of the interview and assessment exercises that will be used on
the courses for which you are shortlisted from their websites, and also
from previous successful applicants. All courses have selection
interviews in which candidates are asked about material relevant to
their academic and clinical suitability. In some courses there are
separate academic and clinical interviews, while in others both areas
are covered in one interview.
In preparing for these interviews, it is useful to list the main points
you want to make, and then illustrate each of these points with examples
from your academic career and relevant clinical experience. The kinds
of point that it is useful to make are that you know how to do research
(and can illustrate this by describing one of your research projects), that
you have basic clinical skills (and can illustrate these by describing
some clinical work you have done), and that you can work on a team
(and can illustrate this by describing some of your team work). It is also
useful to be able to show that you know about the roles of clinical
psychologists within the public health service and about recent relevant
policy documents. You can find these on the NHS or HSE websites,
which are listed at the end of the chapter.
It may also be worth mentioning that you have interests and hobbies
that allow you to maintain a degree of work–leisure balance in your life,
and that if you are offered a place on a course you intend to continue
these interests and hobbies to help you manage stress.
Most candidates find it helpful to rehearse their interviews with
previously successful applicants. When rehearsing for interviews, aim
to make your points and illustrate them with relevant examples in a
succinct way. It is also useful to prepare an opening statement that
gives your interviewers an overview of your career to date, and a closing
statement that summarizes the key points you made in your interview.
In doing this preparation and rehearsal, do not assume that your
interviewers will remember all of the detail in your application form. Most
interviewers on selection panels are on ‘information overload’ having
read 150+ applications during short listing and then interviewed a
number of candidates. It becomes difficult for panel members to
remember ‘who did what’. Your task is to make your points and illustrate
them with examples from your experience in a clear, engaging and
memorable way.
Selection interviews are stressful. Stress reduces our capacity to
focus on the concerns of others. It narrows our attention so that we tend
to focus on our own well-being, our own survival in the face of threat,
and our primary ‘emotional concerns’. In selection interviews common
emotional concerns are ‘I hope I’m doing OK here’, ‘I really want a place
on the programme’, ‘I’ll be disappointed if I don’t get on’, ‘I hope I’m not

Book 1.indb 21 06/03/2012 13:47

 22 C L I N I C A L P S Y C H O L O G Y : A N I N T R O D U C T I O N

making a mess of this’, and so forth. This stress-induced focus on the

self is compounded by exposure to ‘pop-psychology’ advice to use self-
focused stress management techniques during interviews. For example,
some pop-psychologists advise that you periodically ask yourself ‘How
am I doing?’, tell yourself mentally that you are doing OK, tell yourself to
stay calm, take deep breaths, relax your muscles, etc. There are two
problems with this. First, it is a waste of your cognitive capacity. In
selection interviews you should be using all your cognitive capacity to
listen to questions, give clear answers and make your points. It is a
waste of cognitive capacity to engage in an inner dialogue. When people
‘go blank’ in an interview it is usually because they have overloaded
their cognitive capacity by trying simultaneously to engage in the
interview and engage in an inner dialogue. Second, when candidates
engage in inner dialogues during interviews and tell themselves to calm
down etc., to interviewers they appear to be disengaged from the
interview process. For these reasons, it is best not to use any of these
strategies.
The most efficient interview stress management strategy is to focus
on addressing the interviewing panel’s agenda. In selection interviews
there are two parallel agendas. Your ‘emotional agenda’ is that you
want to get a place on a training programme because it’s what you’ve
always wanted, because it’s what you deserve after all your hard work,
and because you would be very disappointed if you didn’t get a place.
The panel’s agenda is different. They are not overly concerned about
what you always wanted, what you deserve or how disappointed you
will be if you don’t get a place. They want to know if you have the
qualifications, skills and potential to be a really good clinical psychology
trainee, compared to other applicants, or whether you will be the sort of
trainee who ‘doesn’t have what it takes to get the job done and go the
distance’.
If this is their agenda, then a very useful approach is to put your own
agenda to one side, and prioritize the panel’s agenda during your
interview preparation and during the interview itself. That is, in preparing
all the points you want to make, and in making your points in the
interview, frame what you say in terms of the panel’s agenda, not your
own ‘emotional agenda’. This is very difficult to do when the possibility
of failure is so high. Under stress we all tend to prioritize our own
agendas rather than those of others. However, if you prepare with the
panel’s agenda in mind, then in the interview you will be better able to
show the panel how your qualifications and relevant experiences have
given you the skills and personal qualities necessary for training as a
clinical psychologist.
You should try to show the panel, through the way you talk about
your past achievements, that in the future, if you get a place on the
course you will be the sort of trainee who will work hard, be reliable, do
good academic work, do rigorous research in a clinically sensitive way,
work with clients in a respectful way that is informed by psychological
science, and fit in with course staff and clinical teams. If you prepare for
your interview with the panel’s agenda in mind, then in the interview

Book 1.indb 22 06/03/2012 13:47

 1 • WHAT IS CLINICAL PSYCHOLOGY? 23

itself you will be more likely to show the panel that you have the profile
and potential to be a good clinical psychology trainee.
When you attend a selection interview, listen carefully to the
questions you are asked. Answer these specific questions, and then
expand your answers to include relevant points that you have prepared
prior to the interview. You will probably be asked about the clinical and
research experiences and skills you have developed, and you will have
prepared points you want to make in these areas, so building them into
your answers will not be too challenging. You may also be asked
hypothetical ‘problem solving’ or ‘competency testing’ questions during
the interview, for which you are unlikely to have a prepared answer. In
these questions the panel may ask you how you would manage a
specific clinical or research problem. Listen to these questions very
carefully. Reflect for a moment or two, and then give your answer in a
step-by-step manner, so the panel can hear how you reason, make
decisions and solve problems. Panels ask these sorts of question
because they are interested in how you think and make judgements, not
because they want to see if you can come up with the right answer.
Towards the end of the interview, you may be asked if there is
anything you would like to add or ask. The most useful thing to do at this
point is to mentally go down your checklist of prepared points you
wanted to make in the interview, make any points you have not already
made, and briefly summarize how you think your qualifications and
relevant experiences have given you the basic academic, research and
clinical skills required to undertake professional training in clinical
psychology.
Some courses include various individual and group assessment
exercises and psychological tests (Hemmings & Simpson, 2008;
O’Shea & Byrne, 2011b; Phillips et al., 2001; Roth & Leiper, 1995). For
example, to assess capacity for teamwork, some course selection
panels invite groups of applicants to work as teams and solve specific
problems. To assess basic clinical skills, some courses observe
candidates conducting role-play interviews. To assess academic writing
skills, some panels ask applicants to read an article and write an
abstract, or to write an essay. To assess critical thinking skills, some
courses ask applicants to read academic material and then answer a
series of questions. To assess clinical judgement, some courses invite
candidates to read case vignettes and answer questions about them.
For the assessment of oral presentation skills, candidates may be
invited to make a preliminary presentation of their career to date and
indicate how this has prepared them for clinical psychology training.
Personality and aptitude tests are used by some courses, usually to
identify candidates with positive traits and rule out candidates with traits
that would make them unsuitable for clinical psychology training. It’s
useful to get formal information on selection procedures from the
courses for which you are applying and also to talk to previously
successful applicants about their experiences of engaging in these
procedures so that you will have a clear idea about what to expect.
Practising writing abstracts, essays, giving presentations, interviewing

Book 1.indb 23 06/03/2012 13:47

 24 C L I N I C A L P S Y C H O L O G Y : A N I N T R O D U C T I O N

and answering questions on academic material or case vignettes may

improve your performance during the assessment tasks mentioned
above.

Reapplying
Only 20–30% of candidates get places on clinical psychology courses,
and a proportion of these are people who have been unsuccessful in
previous years. O’Shea and Byrne (2011) in an Irish study of the 10
year period 2000–2009 found that the average successful applicant had
previously made about three unsuccessful applications, and the range
was 0–22! If you are not offered a place in a course, this does not
necessarily mean that you will be judged to be unsuitable if you reapply.
Rather, failure to be selected one year means that you were not as
suitable as the candidates selected in that particular year. Enhance
your portfolio of qualifications and relevant clinical and research
experiences over the next year, and reapply. As your portfolio expands
it becomes more likely that your application will be ranked highly
enough, in comparison with other applicants, to be selected.

Professional society membership

If your career plan is to become a clinical psychologist and practise in
the UK or Ireland, then join the BPsS and/or the PsSI sooner rather than
later. Website addresses are given at the end of the chapter. The
appointments sections of their monthly publications (the Psychologist
and the Irish Psychologist) contain advertisements for psychology
assistant and research assistant posts that may count as relevant clini-
cal experience in your application for clinical psychology programmes.
These publications will also contain articles on topics relevant to clinical
psychology and help you develop an understanding of current profes-
sional issues. Some selection panels for clinical psychology training
programmes rate candidates favourably if they have BPsS or PsSI
membership, so you should mention your membership status on clinical
psychology programme application forms.
Both the BPsS and the PsSI have Divisions of Clinical Psychology. It
is useful to become an affiliate member of the clinical division of the
BPsS because it publishes a monthly journal – Clinical Psychology
Forum – that contains articles and information on the profession of
clinical psychology and current issues of concern to the profession
within the UK.

Training abroad
Apart from the UK and Ireland, there are well-developed doctoral clinical
psychology training programmes in other English speaking countries
including the US, Canada, South Africa and Australia. These may be of
interest to you if decide to train abroad. If you return to the UK or Ireland
to work as a psychologist you will be required to submit your clinical

Book 1.indb 24 06/03/2012 13:47

 1 • WHAT IS CLINICAL PSYCHOLOGY? 25

psychology qualification to the BPsS or PsSI for evaluation. If it is judged

to be similar to a UK or Irish qualification you will receive a statement of
equivalence. In some instances you may be required to complete an
extra placement or some extra coursework or research to bring your
qualification into line with UK and Irish standards. For example, when I
moved to the UK from Canada (where I did a PhD in clinical psychology),
to bring my qualification into line with its standards the BPsS required
me to complete an intellectual disability placement in the NHS.
In 2010 in the US there were 232 clinical psychology training pro-
grammes accredited by the APA. Norcross et al. (2010) surveyed these
programmes and what follows is based on this survey. In the US there
are two main types of clinical psychology doctoral training programmes:
the scientist-practitioner PhD, which places a strong emphasis on
research, and the practitioner-scholar PsyD, which places greater
emphasis on clinical practice. Both types of programme are of about
4 years’ duration and include academic coursework and clinical practi-
cums. However, on PhD programmes candidates are required to con-
duct a major research project and present it as a doctoral thesis,
whereas on PsyD programmes postgraduates conduct a less extensive
research project or a systematic literature review. Candidates must
complete a one-year clinical internship and both national and state reg-
istration exams to become a registered practitioner in the US after grad-
uating from a doctoral programme in clinical psychology. Most US
clinical psychology training programmes focus on a much narrower
range of problems and populations than UK or Irish training pro-
grammes. The broadest programmes focus on both child and adult
mental health, but rarely on intellectual disability and older adulthood in
the way that UK and Irish programmes do. Plante’s (2009) Contemporary
Clinical Psychology is a good undergraduate introduction to clinical psy-
chology from a US perspective.
In Norcross et al.’s study, the mean undergraduate psychology
degree grade point average for admission to US programmes was 3.6
and only 21% of entrants had master’s degrees. Along with undergrad-
uate psychology degree grades, the Graduate Record Examination
(GRE) results are used to select people onto US clinical psychology
programmes. There is a general GRE aptitude test and a specific GRE
test in psychology. GREs can be taken anywhere in the world. The web
address for the GRE is given at the end of the chapter and it contains
information on the tests and test centres. Most people practise for the
GRE general and psychology tests by taking preparation courses and
using practice test books. Some of the most widely used preparation
and practice test books are produced by Kaplan (2010a, 2010b), Barron
(2009a, 2009b) and Princeton Review (2010a, 2010b). These are re-
issued every year, so the editions I have cited may be out of date when
you read this. Web addresses for these three GRE preparation book
publishers are given at the end of the chapter.
In Norcross et al.’s study, 17% of applicants to US doctoral pro-
grammes obtained places, and 57% of these were given full financial
support by the courses that accepted them. They had their fees paid and

Book 1.indb 25 06/03/2012 13:47

 26 C L I N I C A L P S Y C H O L O G Y : A N I N T R O D U C T I O N

were given a fellowship or teaching/research assistantship. Norcross et

al. found that admission to university-based PhD clinical psychology pro-
grammes was far more competitive than admission to PsyD clinical psy-
chology programmes based in non-university professional schools. Also,
more university-based PhD programmes provided financial support than
non-university PsyD programmes. Detailed guidance on gaining admis-
sion to doctoral clinical psychology programmes in the US is given in
Insider’s Guide to Graduate Programs in Clinical and Counseling
Psychology (Sayette et al., 2010) and Getting In: A Step-by-Step Plan
for Gaining Admission to Graduate School in Psychology (American
Psychological Association, 2007). Canada’s approach to training clinical
psychologists is similar to that of the US, although its courses are accred-
ited by the Canadian Psychological Association. Hunsley and Lee’s
(2009) Introduction to Clinical Psychology is a useful undergraduate
overview of clinical psychology from a Canadian perspective.
In an Australian national survey Pachana et al. (2006) identified 34
universities or colleges that provided clinical psychology training. There
were 30 master’s programmes, 24 professional doctoral programmes
similar to the US PsyD practitioner-scholar programmes and 16 PhD
programmes similar to the US scientist-practitioner programmes. The
admission requirement for these programmes was a 2.1 honours
degree in psychology. One of the main differences between Australia
and other jurisdictions is the relative lack of funding to support post-
graduates during training. Page and Stritzke’s (2006) Clinical Psychology
for Trainees gives a good account of clinical psychology practice from
an Australian perspective. In Australia, New Zealand and much of
Europe, clinical psychologists can practise with master’s or diploma
level qualifications rather than a doctorate, so their doctoral programmes
are not required to meet doctoral training standards set by accrediting
bodies. Having said that, there are many exceptional doctoral clinical
psychology training programmes in these jurisdictions.

Choosing courses
When deciding which courses to apply to, or which offers to accept if
you are lucky enough to be offered places on more than one course, it’s
useful to base your decisions on your own clinical, academic and
research criteria.
Select courses that provide training with a research or clinical empha-
sis that suits you. Some courses are strongly clinically oriented. Others
are strongly research-oriented. Still others take a balanced approach,
with equal emphasis on clinical and research competence.
Choose a course that trains postgraduates in a clinical approach that
fits with your preferences. Some courses train postgraduates mainly in
cognitive behaviour therapy. Others adopt psychodynamic, systemic or
humanistic approaches (which are described in Chapter 9), while others
encourage the use of multiple models. For example, at UCD we train
postgraduates to adopt a systemic approach when working with
children, adolescents and people with intellectual disabilities. In the field

Book 1.indb 26 06/03/2012 13:47

 1 • WHAT IS CLINICAL PSYCHOLOGY? 27

of adult mental health we teach basic cognitive behaviour therapy skills

and basic psychodynamic therapy skills.
Choose courses where staff have research programmes that are of
interest to you, so that you can conduct your doctoral thesis under their
supervision. In applying for courses with a strong research orientation,
particularly in the US, it is useful to correspond with potential research
supervisors before you apply, indicating your interest in their work and
your wish to work under their supervision. If, while planning and
conducting your undergraduate research thesis, you correspond with
an academic who is an expert on your topic to ask them for recent
articles they have written or materials they have developed, they may
look favourably on your application if you apply to their department for
postgraduate clinical psychology training.

Clinical psychology and related professions

Clinical psychology can be distinguished from other types of applied
psychology, notably counselling psychology, educational psychology,
health psychology and forensic psychology. There is a significant over-
lap between the clinical practices and scientific foundations of these
other applied psychology specialties. Practitioners in all of these spe-
cialties assess and treat clients; engage in research and evaluation;
and conduct consultancy, supervision, administration and manage-
ment. To train in any of these specialties, an honours undergraduate
degree in psychology is a prerequisite. What distinguishes these spe-
cialties is (1) the extent to which they are embedded within national
public service organizations, (2) the establishment of professional doc-
toral level training as the norm, (3) the practices they emphasize, (4) the
populations they work with, and (5) the organizational contexts within
which they are grounded.
Clinical psychology differs from other applied psychology specialties
insofar as it is strongly embedded within the public health service in
both the UK and Ireland. There are well-established partnerships
between universities and public health services, supported by funding
systems. Just as ‘registrar’ is an established grade within medicine,
‘trainee clinical psychologist’ is an established paid professional career
grade within clinical psychology. In contrast, national funding systems
for other applied psychology specialties have not been developed.
In both Ireland and the UK, the 3 year professional doctorate has
been established as the required professional qualification in clinical
psychology for far longer than in other applied psychology specialties.
In other specialties, some universities still offer terminal master’s level
programmes and some professionals practise with master’s level quali-
fications.
Clinical psychologists work with a very wide range of populations
with diverse problems (described earlier in the chapter) and in the UK
and Ireland are employed predominantly within the public health
services. Other types of applied psychologist work with a narrower
range of populations, and some work outside the public health service.

Book 1.indb 27 06/03/2012 13:47

 28 C L I N I C A L P S Y C H O L O G Y : A N I N T R O D U C T I O N

What follows is a thumbnail sketch of the other applied psychology

specialties.
Educational psychology addresses learning problems, and social
and emotional problems encountered by young people in educational
settings. There is a strong emphasis within the profession on assess-
ment of children’s problems, recommending the provision of additional
resources and developing programmes that teachers and parents can
implement to deal with these difficulties. In the UK educational psy-
chologists are employed by local education authorities, and in Ireland
they are employed by the National Educational Psychology Service
(NEPS). Educational psychologists work in schools, colleges, nurseries
and special units. In North America educational psychology is referred
to as school psychology.
Counselling psychology places a strong emphasis on psychother-
apeutic processes in effecting change in people facing a range of nor-
mal life challenges as well as psychological disorders. The profession
places a premium on the use of process-oriented supervision and self-
reflective practices in training. Some counselling psychologists are
employed in public health services. Others work in private companies
and private practice.
Health psychology focuses on the application of psychology to help
people change their lifestyles and prevent physical health problems. It
is also concerned with treating psychological adjustment difficulties
associated with health problems, medical conditions, chronic pain and
disabilities. Health psychologists work in hospitals, universities and
health research settings. In North America, health psychology is some-
times referred to as behavioural medicine, and health psychology
applied to children is referred to as paediatric psychology.
Forensic psychology is concerned with applying psychology to
criminal investigation, understanding psychological risk and protective
factors associated with criminal behaviour, and the assessment and
treatment of offending behaviour from a psychological perspective. In
the UK forensic psychologists are mainly employed within the prison
service. In Ireland a process for registering forensic psychologists has
not been established, and the majority of psychologists working within
Irish prisons are clinical or counselling psychologists.
Clinical psychologists may also be distinguished from the grades
‘clinical associate in applied psychology’ (or ‘associate psychologist’) in
the UK and ‘psychometrist’ in the US and Canada. These grades are
below the level of a qualified clinical psychologist and above that of
psychology assistant. Duties of practitioners in these grades are similar
though more circumscribed than those of a qualified clinical psychologist.
Typically a master’s degree in applied psychology is required for posts
at these grades. Employment in these grades counts as relevant
experience when making an application for a clinical psychology degree.
Clinical psychology may also be distinguished from other mental
health professions including psychiatry, psychotherapy and counselling.
Psychiatry is a medical specialty concerned with the assessment
and treatment of psychological disorders using a range of methods

Book 1.indb 28 06/03/2012 13:47

 1 • WHAT IS CLINICAL PSYCHOLOGY? 29

including physical or pharmacological treatments on one hand and

psychological treatments on the other. To practise as a consultant
psychiatrist, a medical degree and specialist postgraduate training in
psychiatry are required. Psychiatry and psychiatry training are strongly
embedded within public health services around the world.
Psychotherapy is a contractual process in which trained profession-
als with expert knowledge of their discipline interact with clients to help
them resolve psychological problems. There are many different schools
of psychotherapy (e.g. psychoanalytic, cognitive-behavioural, humanis-
tic and systemic). There are also many training routes for becoming a
registered psychotherapist. Most involve acquiring a primary degree in
a health profession (e.g. psychology, social work, nursing or medicine)
and then completing a postgraduate professional psychotherapy train-
ing programme. In the UK and Ireland the many diverse psychotherapy
associations are united under the umbrellas of the UK Council for
Psychotherapy and the Irish Council for Psychotherapy. Psychotherapy
as an independent profession is not as well embedded within the public
health service as clinical psychology, and there are far fewer jobs with
the title ‘psychotherapist’. However, many clinical psychologists spend
a significant portion of their time in public health service jobs engaging
clients in psychotherapy.
Counselling is similar to psychotherapy but training programmes
usually focus on specific problems or client groups, for example drug
and alcohol abuse, or career guidance. Psychotherapy training
programmes cover a broader range of problems and client groups, but
usually focus on a specific therapeutic approach, for example systemic,
psychodynamic, humanistic, or cognitive behaviour therapy. In many
instances, training for counselling is not as long or as extensive as that
for psychotherapy.

Controversies
The history of clinical psychology in the UK, Ireland, the US, continental
Europe, Australia and New Zealand is marked by controversy over the
appropriate model for training clinical psychologists, the level to which
they should be trained, and the roles they should adopt when qualified
(Benjamin, 2005; Cheshire & Pilgrim, 2004; Hall & Llewelyn, 2006; Lunt,
2008; Pachana et al., 2008; Sammons et al., 2003). There has been
controversy over whether the research-oriented scientist-practitioner,
the practice-oriented practitioner-scholar, or the experientially oriented
reflective-practitioner should be the core model for training. Currently
the weight of opinion in the UK, Ireland and the US leans towards the
scientist-practitioner model as the dominant approach. There has been
controversy over whether registered clinical psychologists should be
trained to the diploma or master’s level, or to the doctorate level.
Currently in the UK, Ireland and the US, doctoral level training has
become the norm. However, in the UK and Ireland this is a relatively
recent development, and in continental Europe and the antipodes
master’s and diploma level training models are prevalent.

Book 1.indb 29 06/03/2012 13:47

 30 C L I N I C A L P S Y C H O L O G Y : A N I N T R O D U C T I O N

There has been controversy over whether clinical psychologists

should engage in assessment only, or assessment and treatment.
Historically clinical psychologists’ roles mainly involved psychometric
assessment. In the latter half of the last century this changed, and
psychological therapy became a central part of psychologists’ roles.
More recently, there has been controversy over whether clinical psy-
chologists should have the right to prescribe psychotropic medication,
with strong arguments on both sides. Currently in some US jurisdictions
clinical psychologists have acquired prescribing rights, but this trend
has not had a major impact in the UK or Ireland.
There is agreement among clinical psychologists that service-users
should contribute to clinical psychology training and service develop-
ment, but divergent opinions about how best to facilitate their involve-
ment. Clinical psychology has traditionally focused on psychological
disorders and disability. The positive psychology movement has chal-
lenged this and proposed that the focus of our work shift from deficits to
strengths and resilience (Carr, 2011).

Pros and cons of selecting clinical

psychology as a career
The down side
On the down side, it can take 8–10 years to become a qualified clinical
psychologist after graduating from secondary school. This time includes
3–4 years completing an honours undergraduate programme; 1–3
years obtaining relevant clinical experience (including a relevant mas-
ter’s degree in some cases); and 3 years completing a professional
doctorate in clinical psychology. Another major problem is the competi-
tion for places on clinical psychology doctoral programmes. In the UK
and Ireland during the period 2005–2010, only 20–30% of applicants
secured places. So the chances of getting a place on a programme are
approximately between 1 in 3 and 1 in 5. A third drawback to choosing
clinical psychology as a career is that doctoral programmes are excep-
tionally demanding. When you are training as a clinical psychologist,
there is limited room for much else in your life. A final problem with
clinical psychology as a career is that for qualified practitioners, issues
to do with staffing, resources, waiting lists, administrative procedures,
interprofessional rivalry and so forth can be stressful. Dealing with these
organizational and administrative issues within the public health service
over an extended time period in both the UK and Ireland can be very
challenging, and can wear you down.

Positive features
There are many pluses to clinical psychology as a career. In the UK and
Ireland, the public health service sponsors candidates with primary
degrees in psychology on doctoral programmes to train as clinical
psychologists, paying them a salary at the trainee clinical psychologist

Book 1.indb 30 06/03/2012 13:47

 1 • WHAT IS CLINICAL PSYCHOLOGY? 31

grade. (There is a loose parallel here with medicine, where candidates

with primary degrees in medicine are employed as non-consultant
hospital doctors during their specialist training in psychiatry, paediatrics
and other fields of medicine.) In the UK and Ireland there are many job
opportunities for clinical psychologists, and good career development
prospects.
Clinical psychologists have the opportunity to make a real difference
to a lot of people’s lives. Over a career of 35–40 years a clinical
psychologist may directly help (at a minimum) 1000 clients, and may
indirectly help a lot more.
Clinical psychology is an exceptionally interesting job. The role of the
clinical psychologist is complex, involving direct and indirect clinical
work, consultation, training and supervision, research, administration
and management. Over the course of a career there are opportunities
to work in many different services with different client groups, and to
progress from junior to senior career grades. For example, in my own
career I have worked in addiction services, child and adolescent mental
health, paediatric psychology, child protection, disability services, adult
mental health and specialist family therapy services. I have worked in
the public health service in Canada, the UK and Ireland; in private
practice; and in universities. Finally, it is worth mentioning that clinical
psychologists are reasonably well paid, although I have met very few
clinical psychologists who were ‘in it for the money’.

Summary
Clinical psychology is both a health care profession and a
health-related scientific discipline.
The clinical psychologist’s role has been conceptualized as
that of a scientist-practitioner and a practitioner-scholar.
Clinical psychologists’ jobs typically involve direct work with cli-
ents, indirect work, administration or management, research,
and continuing professional development. Clinical psycholo-
gists provide services to a wide range of people with diverse
difficulties in an array of different work settings.
In the UK and Ireland professional clinical psychology train-
ing programmes are 3 year doctorates run by partnerships
involving universities and public health service units. These
programmes include course work, clinical placements and
research. In the UK and Ireland there are about 35 clinical psy-
chology programmes. Between 2005 and 2010 about 20–30%
of applicants got places on these courses. Minimum entry
requirements for clinical psychology training in the UK and
Ireland are a 2.1 honours degree in psychology and about
a year’s relevant clinical experience. Because entry to pro-
grammes is very competitive, successful applicants typically
exceed these minimum requirements.

Book 1.indb 31 06/03/2012 13:47

 32 C L I N I C A L P S Y C H O L O G Y : A N I N T R O D U C T I O N

Academic suitability for doctoral programmes in clinical psy-

chology is assessed by taking account of performance in high
school and on undergraduate degree programmes; completing
postgraduate degrees in psychology, short courses relevant to
clinical psychology, and other non-psychological qualifications;
and research achievements. Clinical suitability is assessed with
reference to the way in which candidates have made use of the
opportunities available to them to engage in relevant clinical
experiences and to acquire basic clinical skills. Finding relevant
clinical experience is challenging and requires creativity and
persistence in opportunity searching and professional network-
ing. Getting a place on a clinical psychology programme
involves completing the application form and submitting it prior
to application deadlines; arranging references; attending inter-
views; completing assessment exercises; accepting negative
feedback if unsuccessful and reapplying. If your career plan is
to become a clinical psychologist and practise in the UK or
Ireland, join the BPsS and/or the PsSI sooner rather than later,
since their publications will keep you abreast of professional
developments and relevant experience opportunities. Apart
from the UK and Ireland, there are well-developed doctoral clin-
ical psychology training programmes in other English speaking
countries including the US, Canada and Australia.
Clinical psychology may be distinguished from other types
of applied psychology, notably counselling psychology, educa-
tional psychology, health psychology, and forensic psychology.
Clinical psychology may also be distinguished from other men-
tal health professions including psychiatry, psychotherapy and
counselling. There are pros and cons to choosing clinical psy-
chology as a career. Training can take up to 10 years, pro-
gramme entry is highly competitive, and working in the public
health service can be stressful. However, for qualified psychol-
ogists there are many job opportunities, good career develop-
ment prospects and the job is intrinsically very satisfying.

Questions
● What is clinical psychology?
● How are clinical psychologists trained?
● If you wished to train as a clinical psychologist, what steps would
you like to take to increase your chances of getting a place on a
professional training programme in clinical psychology?
● How does clinical psychology differ from other applied specialties,
such as educational, counseling, health and forensic psychology,
and from other professions such as psychiatry or psychotherapy?
● What are the advantages and disadvantages of choosing clinical
psychology as a career?

Book 1.indb 32 06/03/2012 13:47

 1 • WHAT IS CLINICAL PSYCHOLOGY? 33

● What is the most important thing you have learned from studying
this chapter?

FURTHER READING
● Beinart, H., Kennedy, P. & Llewelyn, S. (2009). Clinical psychology in
practice. London: British Psychological Society–Blackwell.
● Bennett, P. (2011). Abnormal and clinical psychology: An introductory
textbook (third edition). Maidenhead: Open University Press.
● Davey, G. (2008). Clinical psychology. London: Hodder Education
● Knight, A. (2002). How to become a clinical psychologist: Getting a foot
in the door. London: Routledge.

Major clinical psychology journals

● Annual Review of Clinical Psychology
● British Journal of Clinical Psychology
● Clinical Psychology Review
● Clinical Psychology: Science and Practice
● Journal of Consulting and Clinical Psychology

WEBSITES
Sites for relevant experience and general information
● Assistant Psychologists Ireland Google group:
ap_ireland@googlegroups.com
● Psyclick website:
www.psyclick.org.uk/

Sites for applying for clinical psychology courses

● Clearing House for Postgraduate Courses in Clinical Psychology:
www.leeds.ac.uk/chpccp
● Hull University (which is not a member of the UK clearing house because
the undergraduate psychology degree and postgraduate clinical degree
programmes are integrated):
www2.hull.ac.uk
● National University of Ireland Galway:
www.nuigalway.ie
● Queen’s University Belfast:
www.qub.ac.uk
● Trinity College Dublin:
www.tcd.ie
● University College Dublin:
www.ucd.ie
● University of Limerick:
www.ul.ie

Book 1.indb 33 06/03/2012 13:47

 34 C L I N I C A L P S Y C H O L O G Y : A N I N T R O D U C T I O N

Public health services

● Health Service Executive (Ireland):
www.hse.ie
● Improving Access to Psychological Therapies:
www.iapt.nhs.uk
● National Health Service (UK):
www.nhs.uk

Psychological societies and professional associations

● American Psychological Association:
www.apa.org
● American Psychological Association, Division 12, Society of Clinical
Psychology:
www.div12.org
● Australian Clinical Psychology Association:
www.acpa.org.au
● Australian Psychological Society:
www.psychology.org.au
● British Psychological Society:
www.bps.org.uk
● British Psychological Society Division of Clinical Psychology:
www.bps.org.uk/dcp
● Canadian Psychological Association:
www.cpa.ca
● European Federation of Psychologists’ Associations (EFPA):
www.efpa.eu
● International Union of Psychological Science (IUPsyS):
www.iupsys.org
● Irish Council for Psychotherapy:
www.psychotherapy-ireland.com
● New Zealand Psychological Society:
www.psychology.org.nz
● Psychological Society of Ireland:
www.psihq.ie
● UK Council for Psychotherapy:
www.psychotherapy.org.uk

Graduate Record Exam (GRE)

● Barron’s GRE preparation:
http://barronstestprep.com/gre
● Graduate record exam:
www.ets.org/gre
● Kaplan GRE preparation:
www.kaptest.com
● Princeton Review GRE preparation:
www.princetonreview.com/grad/gre-test-preparation.aspx

Book 1.indb 34 06/03/2012 13:47

 Childhood behaviour
disorders 2
Learning objectives
After studying this chapter you will be able to:
● list some of the main psychological disorders that
occur in childhood
● give an account of the main clinical features of
ADHD, oppositional defiant disorder and conduct
disorder
● summarize the epidemiology of disruptive behaviour
disorders
● outline the main biological and psychological
theories of disruptive behaviour disorders
● name the main evidence-based approaches to
assessment and treatment of disruptive behaviour
disorders
● give a considered view on some of the main
controversies surrounding the clinical psychology of
childhood disorders.

Introduction
A wide variety of psychological problems may occur in childhood. These
include problems that compromise children’s capacities to learn and
communicate such as intellectual disability, language delay, specific

Book 1.indb 35 06/03/2012 13:47

 36 C L I N I C A L P S Y C H O L O G Y : A N I N T R O D U C T I O N

learning disabilities, and pervasive developmental disorders including

autism spectrum disorders. Problems developing bowel and bladder
control, and difficulties with feeding, sleeping and waking routines may
also occur in childhood. Children and adolescents may develop neuro-
psychological problems and adjustment difficulties secondary to condi-
tions such as epilepsy or head injury. All of these difficulties are of
concern to clinical psychologists (Carr, 2006a). However, in addition to
these difficulties, two broad classes of conditions have been a focus for
clinical psychologists who work with children and adolescents. These
are disruptive behaviour disorders (such as attention deficit hyperactiv-
ity disorder (ADHD), oppositional defiant disorder and conduct disorder)
and emotional disorders (such as anxiety and depression). Disruptive
behaviour disorders are characterized principally by externalizing
behaviour problems such as rule-breaking, defiance and aggression. In
contrast, internalizing behaviour problems such as social withdrawal,
tearfulness and avoidance are the main features of emotional disor-
ders. Factor analyses of common childhood behaviour problems con-
sistently identify internalizing and externalizing behaviour problems as
the two main dimensions of childhood behavioural difficulties
(Achenbach, 2009).
In Chapters 5 and 6 the emotional disorders – anxiety and depression
– in children, adolescents and adults will be addressed. The central
focus of the present chapter will be disruptive behaviour disorders. The
diagnostic criteria for ADHD, oppositional defiant disorder and conduct
disorder are given in Tables 2.1 and 2.2. It is noteworthy that all three of
these conditions entail behaviour that is troublesome for others as well
as for the child. In this chapter case examples of ADHD and conduct
disorder will be given, along with an outline of the clinical features,
epidemiology and theoretical explanations for these problems. Some
comments will also be made on their assessment and treatment.

Attention deficit hyperactivity disorder

Attention deficit hyperactivity disorder, attention deficit disorder, hyper-
kinetic disorder, hyperkinesis, minimal brain damage and minimal brain
dysfunction are some of the terms used for a syndrome characterized
by persistent overactivity, impulsivity and difficulties in sustaining atten-
tion (Barkley, 2005). Children with this profile were first described in
modern medical literature by George Still in 1902. In this chapter prefer-
ence will be given to the widely used term – attention deficit hyperactiv-
ity disorder or ADHD.

Case example of ADHD

Timmy, aged 6, was referred for assessment because his teachers
found him unmanageable. He was unable to sit still in school and con-
centrate on his schoolwork. He left his chair frequently and ran around
the classroom shouting. This was distracting for his teachers and class-
mates. Even with individual tuition he could not apply himself to his

Book 1.indb 36 06/03/2012 13:47

 2 • CHILDHOOD BEHAVIOUR DISORDERS 37

school work. He also had difficulties getting along with other children.
They disliked him because he disrupted their games. He rarely waited
for his turn and did not obey the rules. At home he was consistently
disobedient and, according to his father, ran ‘like a motorboat’ from the
time he got up until bedtime. He often climbed on furniture and routinely
shouted rather than talked.

Family history
Timmy came from a well functioning family. His parents had a very
stable and satisfying marriage and ran a successful business together.
Their daughter, Amanda, was a well-adjusted and academically able
8-year-old. The parents were careful not to favour the daughter over her
brother or to unduly punish Timmy for his constant disruption of his
sister’s activities. However, there was a growing tension between each
of the parents and Timmy. While they were undoubtedly committed to
him, they were also continually suppressing their growing irritation with
his frenetic activity, disobedience, shouting and school problems. Within
the wider family there were few resources that the parents could draw
on to help them cope with Timmy. The grandparents, aunts and uncles
lived abroad and so could not provide regular support for the parents.
Furthermore, they were bewildered by Timmy’s condition, found it very
unpleasant and had gradually reduced their contact with Timmy’s
nuclear family since his birth.

Psychometric assessment and child interview

Psychometric evaluation showed that Timmy’s overall IQ was within the
normal range but he was highly distractible and had literacy and
numeracy skills that were significantly below his overall ability level.
Timmy perceived himself to be a failure. He believed that he could not
do anything right at home or at school and he was sad that the other
children did not want to play with him. He believed that his teacher
disliked him and doubted his parents’ love for him.

Developmental history
There were a number of noteworthy features in Timmy’s developmental
history. He had suffered anoxia at birth and febrile convulsions in
infancy. He had also had episodes of projectile vomiting. His high
activity level and demandingness had been present from birth. He
displayed a difficult temperament, showing little regularity in feeding or
sleeping; intense negative emotions to new stimuli; and was slow to
soothe following intense display of negative emotion.

Formulation
Timmy was a 6-year-old boy with home- and school-based problems of
hyperactivity, impulsivity and distractibility of sufficient severity to
warrant a diagnosis of attention deficit hyperactivity disorder. The
problems were longstanding, and there was no discrete factor that
precipitated his condition. However, his entry into the school system
precipitated the referral. Possible predisposing factors included anoxia

Book 1.indb 37 06/03/2012 13:47

 38 C L I N I C A L P S Y C H O L O G Y : A N I N T R O D U C T I O N

Figure 2.1 Formulation of a case of ADHD

at birth, subtle neurological damage due to febrile convulsions in

infancy, and a difficult temperament.
In Timmy’s case, ADHD had led to academic attainment difficulties,
low self-esteem, conflict with his school teacher, peer relationship prob-
lems and tension within the family. This wider constellation of difficulties
maintained and exacerbated his hyperactivity, impulsivity and distracti-
bility. The absence of an extended family support system for the parents
to help them deal with his difficulties was a possible maintaining factor.
Important protective factors in this case were the commitment of Timmy’s
parents and teachers to resolving the problem and the stability of
Timmy’s nuclear family. This formulation is diagrammed in Figure 2.1.

Treatment
Treatment in this case involved both psychosocial and pharmacological
intervention. The psychosocial intervention included parent and teacher
education about ADHD, behavioural parent training, self-instructional
training for the child, a classroom-based behavioural programme and
provision of periodic relief care/holidays with specially trained foster
parents. Timmy was also given stimulant therapy, specifically a twice-
daily dose of methylphenidate (Ritalin). These interventions led to a
significant improvement in his disruptive behaviour at home and school,
his academic performance in school, and the quality of his relationships
with his parents, teachers and friends.

Book 1.indb 38 06/03/2012 13:47

 2 • CHILDHOOD BEHAVIOUR DISORDERS 39

Clinical features
ADHD has distinct clinical features in the domains of cognition, affect,
behaviour, physical health and interpersonal adjustment. Timmy, in the
case example, showed all of these. With respect to cognition, short
attention span, distractibility and an inability to foresee the consequences
of action are the main features. There is usually a poor internalization of
the rules of social conduct, and in some instances low self-esteem may
be present. With respect to affect, excitability associated with lack of
impulse control is the dominant emotional state. This may be coupled
with depressed mood associated with low self-esteem in some cases.
With ADHD, the cardinal behavioural features are the high rate of
activity, common comorbid aggressive antisocial behaviour, excessive
risk-taking and poor school performance associated with inattention.
With respect to physical health in ADHD, in some instances food
allergies may be present. Injuries or medical complications associated
with antisocial behaviour such as fighting and drug abuse may also
occur. Relationship difficulties with parents, teachers and peers are the
principal interpersonal adjustment problems.
Difficulties with turn-taking in games due to impulsivity make children
with ADHD poor playmates. The failure of children with ADHD to inter-
nalize rules of social conduct at home and to meet parental expectations
for appropriate social and academic behaviour leads to conflictual
parent–child relationships. In school, youngsters with ADHD pose class-
room management problems for teachers and these children invariably
have problems in benefiting from routine teaching and instructional
methods. For these reasons, their relationships with teachers tend to be
conflictual.
Currently the World Health Organization’s (1992) International
Classification of Diseases (ICD-10) criteria for hyperkinetic disorder,
which are widely used in Europe, are stricter than those for ADHD in the
American Psychiatric Association’s (2000) Diagnostic and Statistical
Manual (DSM-IV-TR), which are widely used in North America. Both
sets of criteria are given in Table 2.1. The ICD criteria stipulate that the
actual symptoms of inattention, hyperactivity and impulsivity must be
present in two or more settings such as home and school for a positive
diagnosis to be made. In contrast, the more lenient DSM criteria specify
that only impairment in functioning arising from the symptoms, rather
than the actual symptoms or inattention, hyperactivity and impulsivity,
must be present in two or more settings for a positive diagnosis.

Epidemiology
In a review of 15 international epidemiological studies, Costello et al.
(2004) found that the prevalence of ADHD ranged from 0.3% to 11.3%,
with a median prevalence rate of 2.7%. The variability in rates may be
due to the stringency of the diagnostic criteria applied and the demo-
graphic characteristics of the populations studied. Using stringent ICD-
10 hyperkinetic disorder criteria demanding cross-situational stability of

Book 1.indb 39 06/03/2012 13:47

 40 C L I N I C A L P S Y C H O L O G Y : A N I N T R O D U C T I O N

TABLE 2.1
Diagnostic criteria for attention and hyperactivity syndromes in DSM-IV-TR and ICD-10
DSM-IV-TR: Attention deficit hyperactivity disorder ICD-10: Hyperkinetic disorder
A. Either 1 or 2 The cardinal features are impaired
1. Six or more of the following symptoms of inattention have attention and overactivity. Both are
persisted for at least 6 months to a degree that is maladaptive necessary for the diagnosis and
and inconsistent with developmental level. should be evident in more than one
situation (e.g. home or school).
Inattention
a. Often fails to give close attention to details or makes careless Impaired attention is manifested by
mistakes in schoolwork, work or other activities prematurely breaking off from tasks
b. Often has difficulty sustaining attention in tasks or play activities and leaving activities unfinished. The
c. Often does not seem to listen when spoken to directly children change frequently from one
d. Often does not follow through on instructions and fails to finish activity to another, seemingly losing
schoolwork, chores or work duties interest in one task because they
e. Often has difficulty organizing tasks and activities become diverted to another. These
f. Often avoids or dislikes tasks that require sustained mental effort deficits in persistence and attention
g. Often loses things necessary for tasks or activities should be diagnosed only if they are
h. Is often easily distracted by extraneous stimuli excessive for the child’s age and IQ.
i. Is often forgetful in daily activities Overactivity implies excessive
restlessness, especially in situations
2. Six or more of the following symptoms of hyperactivity– requiring relative calm. It may,
impulsivity have persisted for at least 6 months to a degree that depending on the situation, involve
is maladaptive and inconsistent with developmental level. the child running and jumping
Hyperactivity around, getting up from a seat when
a. Often fidgets with hands or feet or squirms in seat he or she was supposed to remain
b. Often leaves seat in classroom or in other situations in which seated, excessive talkativeness and
remaining seated is expected noisiness, or fidgeting and wriggling.
c. Often runs about or climbs excessively in situations in which it is The standard for judgement should
inappropriate be that the activity is excessive in the
d. Often has difficulty playing or engaging in leisure activities context of what is expected in the
quietly situation and by comparison with
e. Is often on the go or acts as if driven by a motor other children of the same age and
f. Often talks excessively IQ. This behavioural feature is most
evident in structured, organized
Impulsivity
situations that require a high degree
g. Often blurts out answer before questions have been completed
of behavioural self-control.
h. Often has difficulty awaiting turn
i. Often interrupts or intrudes on others The characteristic behaviour
problems should be of early onset
B. Some of these symptoms were present before the age of (before the age of 6 years) and long
7 years duration.
Associated features include
C. Some impairment from the symptoms is present in two or more disinhibition in social relationships,
settings (e.g. home and school) recklessness in situations involving
some danger, impulsive flouting of
D. Clinically significant impairment in social, academic or social rules, learning disorders, and
occupational functioning motor clumsiness.

E. Not due to another disorder Specify:

Hyperkinetic disorder with
Specify: disturbance of activity and attention
Combined type if inattention and overactivity–impulsivity are when antisocial features of conduct
present; disorder are absent.
Inattentive type if overactivity is absent; Hyperkinetic conduct disorder when
Hyperactive–impulsive type if inattentiveness is absent criteria for both conduct disorder and
hyperkinetic disorder are met.

Note: Adapted from DSM-IV-TR (APA, 2000) and ICD-10 (WHO, 1992).

Book 1.indb 40 06/03/2012 13:47

 2 • CHILDHOOD BEHAVIOUR DISORDERS 41

symptoms, a prevalence rate of 1% was obtained in a UK national epi-

demiological study (Meltzer et al., 2000).
The prevalence of ADHD varies with gender and age, and the occur-
rence of comorbid conditions is common (Brown, 2009; Carr, 2006a).
ADHD is more prevalent in boys than in girls, and in preadolescents
than in late adolescents. Comorbidity for conduct disorder and ADHD is
about 20% in community populations and possibly double this figure in
clinic populations. Comorbidity for emotional disorders, such as anxiety
or depression, and ADHD is about 10% in community populations. In
clinical populations the comorbidity rate may be twice this figure.
Virtually all children with ADHD have attainment problems. However,
comorbid severe specific learning difficulties have been estimated to
occur in 10–25% of cases. A proportion of children with ADHD have
comorbid developmental language delays, elimination problems and
multiple tics or Tourette’s disorder, although reliable epidemiological
data are not available.
About a third of children with ADHD have a good prognosis, about a
third have a moderate prognosis and a third have a poor prognosis
(Faraone et al., 2006; Hinshaw, 1994). For two thirds of cases, the
primary problems of inattention, impulsivity and hyperactivity persist
into late adolescence and for some of these the primary symptoms
persist into adulthood. Roughly a third develop significant antisocial
behaviour problems in adolescence, including conduct disorder and
substance abuse, and for most of this subgroup these problems persist
into adulthood, leading to criminality. Occupational adjustment problems
and suicide attempts occur in a small but significant minority of cases.

Etiological theories
Biological, cognitive-behavioural and family systems theories have
been developed to explain the aetiology of ADHD.

Biological theories
Biological theories that focus on the role of genetic factors, structural
brain abnormalities, neurotransmitter dysregulation, dietary factors and
hypo-arousal have guided much research on the aetiology of ADHD.

Genetics
The genetic hypothesis proposes that ADHD symptomatology or a pre-
disposition to hyperactivity is inherited by children who develop the con-
dition. In support of this hypothesis, twin, adoption and family studies all
show that rates of ADHD are higher in the biological relatives of children
with ADHD than of those without the disorder (Taylor, 2008; Thapar &
Scourfield, 2002; Thapar & Stergiakouli, 2008). Twin studies show that
ADHD is 80% heritable, making it one of the most heritable psychologi-
cal disorders. Twenty percent of the variance in ADHD symptomatology
may be accounted for by environmental factors. The nature and extent
of the contribution made by genetic and environmental factors varies

Book 1.indb 41 06/03/2012 13:47

 42 C L I N I C A L P S Y C H O L O G Y : A N I N T R O D U C T I O N

from case to case. Extreme levels of the temperamental characteristic

of overactivity, which is normally distributed within the population and
polygenetically determined, probably interacts with environmental fac-
tors (either intrauterine or psychosocial) to give rise to the clinical syn-
drome of ADHD. It may be that in some cases, temperamentally
overactive children sustain a prenatal or early childhood neurological
insult and go on to develop ADHD, whereas others with an overactive
temperament develop the syndrome following participation in ongoing
non-optimal parent–child interactions.
Molecular genetic studies have found an association between ADHD
and the dopamine transporter gene (DAT1) and the dopamine D4
receptor gene (DRD4). The search for these genes was informed by
evidence for dysregulation of the dopamine system in the prefrontal
region of the brain, associated with executive function in children with
ADHD. For a small subgroup of children with ADHD, the syndrome
appears to be caused by a genetic condition resulting in a generalized
resistance to thyroid hormone (Hauser et al., 1993).

Organic deficits
Early work on ADHD was premised on the hypothesis that the syndrome
reflected an organic deficit: probably some form of minimal brain
damage (Strauss & Lehtinen, 1947). In support of this hypothesis, a
number of factors that might be associated with brain damage or
dysfunction during the prenatal or perinatal periods and in early
childhood have been found to be more prevalent among youngsters
with ADHD than normal controls. These include prenatal difficulties;
maternal stress during pregnancy; maternal nicotine, alcohol, cocaine
and anticonvulsant use during pregnancy; low foetal heart rate during
delivery; small head circumference at birth; low birth weight; minor
physical abnormalities; a high rate of diseases of infancy; lead poisoning
and early neurological insult or severe head injury (Barkley, 2005;
Taylor, 2008; Taylor & Rogers, 2005). It is important to point out that
these factors which may be associated with, or contribute to, the
development of an organic deficit are not unique to ADHD and also
occur in youngsters with other disorders. Therefore they probably
interact with other factors in contributing to the development of ADHD.
Neuroimaging studies have shown that ADHD is associated with a
range of structural and functional neuroanatomical abnormalities (Shaw,
2010). The best established of these is lobar volume loss of around
3–4%, and abnormalities of the frontostriatal circuitry which underpins
executive function (Makris et al., 2009). The frontostriatal circuitry of
children with ADHD is less efficient than that of normal children and this
may account for their executive function deficits, such as difficulties with
planning and following through on tasks (mentioned below under
psychological theories).
Neuroimaging studies have also found abnormalities in the cerebel-
lum, which may underpin deficits in temporal information processing
such as learning ‘what to expect when’, and in the parietal lobes, which
may affect the capacity to attend to one stimulus without being dis-

Book 1.indb 42 06/03/2012 13:47

 2 • CHILDHOOD BEHAVIOUR DISORDERS 43

tracted by another (Cherkasova & Hechtman, 2009). Ongoing research

continues to identify other neural mechanisms associated with ADHD.
Not all cases of ADHD show all abnormalities. It is likely that the symp-
tom patterns of different subgroups of cases are associated with differ-
ent neurophysiological abnormalities.

Neurotransmitter dysregulation
In 1937 Charles Bradley reported that Benzedrine – a stimulant – had a
calming effect on the behaviour of hyperactive children. Subsequent
research showed that methylphenidate, which is also a stimulant, and
atomoxetine, a non-stimulant selective noradrenalin reuptake inhibitor,
had similar affects (Taylor, 2008). Neurotransmitter dysregulation
hypotheses have been proposed to explain the effects of these drugs
on ADHD. These hypotheses attribute the symptoms of ADHD to abnor-
malities in neurotransmitter functioning at the synapses affected by
medications that ameliorate the symptomatology of ADHD. Results of
research in this field have converged on the view that a dysregulation of
the dopaminergic system in the ventral tegmental areas of the brain and
noradrenergic and adrenergic systems in the locus coeruleus may be
present in ADHD (Solanto, 1998). Dexamphetamine and methylpheni-
date appear to improve functioning in people with ADHD by increasing
extracellular dopamine, while atomoxetine has beneficial effects by
increasing extracellular noradrenaline levels (Pliszka, 2007).
Controlled trials show that approximately 70% of children with ADHD
respond to these medications (Hinshaw et al., 2007). Medicated children
with ADHD show a reduction in symptomatology and an improvement in
both academic and social functioning, although positive effects dissipate
when medication ceases, if psychological interventions to improve
symptom control have not been provided concurrently with medication.
One of the most remarkable findings of the Multimodal Treatment study
of ADHD (MTA) – the largest ever long-term controlled trial of stimulant
medication for ADHD, involving over 500 cases – is that stimulant
medication ceased to have a therapeutic effect after 3 years (Swanson
& Volkow, 2009). It also led to a reduction in height gain of about 2 cm,
and a reduction in weight gain of about 2 kg. Furthermore, it did not
prevent adolescent substance misuse as expected. The MTA trial
showed that tolerance to medication used to treat ADHD occurs and
this medication has negative side-effects. These findings underline the
importance of using medication to reduce ADHD symptoms to
manageable levels for a time-limited period, while children and their
parents engage in psychological interventions to develop skills to
manage symptoms through psychological means.

Diet
The dietary hypothesis attributes the symptoms of ADHD to children’s
reaction to certain features of their daily diet. Originally Feingold (1975)
argued that artificial food additives such as colourants accounted for a
substantial proportion of ADHD symptomatology. However, controlled
trials of additive-free diets did not support his position. Egger et al.

Book 1.indb 43 06/03/2012 13:47

 44 C L I N I C A L P S Y C H O L O G Y : A N I N T R O D U C T I O N

(1985) refined Feingold’s original allergy theory and argued that particu-
lar children with ADHD may have unique allergy profiles and if their diet
is modified so as to exclude the precise substances to which they are
allergic, then their activity and attention problems may improve.
Carefully controlled dietary studies have supported Egger’s theory,
showing that children with ADHD and food allergies can benefit from
placement on a ‘few foods’ diet (Jacobson & Schardt, 1999; Stevenson,
2010). Results of controlled trials show that removal of food colours
from the diet can have beneficial effects on the behaviour of children
with and without ADHD, but evidence for the value of omega-3 supple-
mentation in reducing hyperactivity is inconsistent (Stevenson, 2010).

Hypo-arousal
The hypo-arousal hypothesis explains hyperactivity and inattention as a
failure to be sufficiently aroused by signal stimuli to attend to them and
regulate activity levels. Psychophysiological studies in which arousal is
assessed by electroencephalograph (EEG), skin conductance and heart
rate recordings indicate that ADHD children show reduced psycho-
physiological responsiveness to novel stimuli with signal value (Rowe
et al., 2005). The use of vivid stimuli in academic settings and highly
salient and immediate reinforcers is implicated by the hypo-arousal
hypothesis. Reward systems and operant programmes conforming to
these specifications have been found to have significant short-term
effects (Hinshaw et al., 2007). EEG neurofeedback to increase cortical
arousal has been shown in preliminary trials to improve ADHD symp-
toms (Sherlin et al., 2010).

Cognitive-behavioural approaches
A number of theories that highlight the importance of deficits in specific
cognitive or behavioural processes as the central factor underlying
ADHD symptomatology have been proposed. Four of these will be
mentioned below. All attempt to show how the overall syndrome of
inattention, overactivity and impulsivity may be accounted for by a
single underlying core deficit, be it one of the three core symptoms of
ADHD or some other cognitive or behavioural process.

Inattention
The attentional deficit hypothesis proposes that problems with sustain-
ing attention on a single task and screening out other distracting stimuli
is the core difficulty that underpins the other symptoms of impulsivity
and overactivity in ADHD (e.g. Douglas, 1983). That is, youngsters with
ADHD at the outset of a task requiring attention will perform at a level
equivalent to normal children but, over time, will show more errors that
are directly attributable to the inability to sustain attention. This problem
with sustaining attention leads them to change the focus of their atten-
tion frequently and is manifested at a behavioural level as excessive
impulsivity and overactivity. On certain laboratory tasks children with
ADHD show a gradual deterioration in sustained attention, as predicted

Book 1.indb 44 06/03/2012 13:47

 2 • CHILDHOOD BEHAVIOUR DISORDERS 45

by the inattention hypothesis. However, contrary to the inattention

hypothesis, on other tasks they show immediate selective attention, like
children without ADHD, and they also display overactivity while asleep
(Barkley, 2003). These findings suggest that a deficit in the capacity for
sustained attention alone cannot fully account for the ADHD syndrome.

Hyperactivity
The hyperactivity hypothesis argues that a problem with inhibiting motor
activity is the core deficit that underpins the ADHD syndrome and can
account for inattention and impulsivity (e.g. Schachar, 1991). There is a
large body of evidence which shows that hyperactivity is unique as a
symptom to children with ADHD compared to children with other
psychological problems, and that hyperactivity as a construct correlates
with many academic indices of attentional problems (Barkley, 2003).

Impulsivity
The impulsivity hypothesis proposes that a core problem in inhibiting
cognitive and behavioural responses to specific stimuli leads to poor
performance on tasks apparently requiring good attentional abilities and
also to tasks requiring careful regulation of behaviour. Thus the central
problem in ADHD, according to this hypothesis, is with cognitive and
behavioural impulsivity (e.g., Nigg, 2001). According to this theory, with
academic tasks requiring high levels of sustained attention, children
with ADHD have problems using systematic cognitive problem-solving
strategies because they are cognitively impulsive. Also, in both aca-
demic and social situations, children with ADHD engage in careless
work practices in school and engage in socially inappropriate behaviour
with peers, parents and teachers because they are behaviourally impul-
sive. There is some evidence to show that while children with ADHD
may know and understand problem-solving skills and social skills, they
fail to use them appropriately in academic and social situations (Barkley,
2003).

Executive function
Russell Barkley (2003, 2005) argues that the symptoms of ADHD
(impulsivity, overactivity and inattention) reflect a central deficit in the
core executive function of behavioural inhibition that is neurodevelop-
mental (rather than social) in origin. Children with deficits in behavioural
inhibition cannot delay gratification, so as to reap better rewards later.
This core deficit in behavioural inhibition is associated with, and rein-
forced by, secondary deficits in four other executive functions: (1) non-
verbal working memory, (2) verbal working memory (or internalization of
speech), (3) self-regulation of affect, arousal and motivation, and (4)
verbal and behavioural creativity and fluency (or internalization of play).
With poor verbal and non-verbal working memory, ADHD children can-
not hold a picture of events in the mind, or obey a set of self-directed
instructions so as to delay gratification or sustain planned sequences of
goal-directed behaviour. With poor self-regulation of affect, arousal and
motivation, ADHD children have difficulty in preventing strong emotional

Book 1.indb 45 06/03/2012 13:47

 46 C L I N I C A L P S Y C H O L O G Y : A N I N T R O D U C T I O N

experiences and motives from interfering with planned goal-directed

behaviour. With poor verbal and behavioural creativity and fluency,
ADHD children have difficulty in developing, rehearsing and implement-
ing creative plans to achieve novel goals.
The four secondary executive function deficits, according to Barkley,
reflect failures to internalize and privatize functions that in early devel-
opment were external features of the child’s interactions with care-
givers. In normal development the emergence of these four executive
functions reflects a shift in the source of control of behaviour from exter-
nal events to mental representations of events; from control by others to
control by the self; and from immediate to delayed gratification. This
complex and elaborate executive function hypothesis has to some
degree supplanted earlier simpler psychological theories and is partially
supported by a growing body of empirical evidence (Barkley, 2003,
2005; Nigg, 2005).
To compensate for deficits in attention, regulation of motor activity,
impulsivity and executive function, various skills training programmes
have been developed, largely within the cognitive-behavioural tradition.
Self-instructional training for managing academic tasks and social skills
training to manage relationship problems (particularly those involving
peers) are the main types of training provided within these programmes.
Because of the negligible impact that such programmes had when con-
ducted in isolation, they are now offered as one element of a multimodal
package involving stimulant medication, family intervention and school
intervention (Hinshaw et al., 2007). Compensatory problem-solving and
social skills training programmes can have optimum effect when offered
after a consistent home- and school-based contingency management
programme has been established and stimulant treatment is in progress.

Systemic theory
Family systems theories have focused largely on the role of the family
system or the wider social context in the aetiology and maintenance of
ADHD. Parental psychological problems such as depression, aggression
or alcohol and substance misuse; exposure to severe marital discord or
domestic violence; extreme abuse and neglect in infancy; and coercive
parent–child interactions in childhood and adolescence have all been
found to have associations with ADHD (Deault, 2010; Johnston & Mash,
2001; Taylor, 2008). With respect to the wider social system, the follow-
ing factors have been found to be associated with ADHD: institutional
upbringing, low socio-economic status, peer relationship problems, and
relationship problems with school staff (Barclay, 2005; Taylor, 2008).
A problem with much of the research on psychosocial factors in the
aetiology and maintenance of ADHD is the fact that in many cases
comorbid conduct disorders are present and the risk factors that are
identified, which bear a close resemblance to those identified for
conduct disorders, may primarily be associated with the aetiology of
conduct problems rather than ADHD. A second difficulty is untangling
the causal chain, establishing which family and relationship difficulties

Book 1.indb 46 06/03/2012 13:47

 2 • CHILDHOOD BEHAVIOUR DISORDERS 47

precede the development of ADHD and are predisposing factors, and

distinguishing these from relationship difficulties that evolve in response
to ADHD and possibly maintain or exacerbate the condition. Results of
longitudinal studies and family intervention studies suggest that chronic
exposure to extremely adverse institutional or family environments early
in life may heighten the risk of developing ADHD, and for children with
predominantly biologically determined ADHD, improved parenting
practices can affect the course of the disorder (Taylor, 2008).
Family-based interventions and multisystemic intervention pro-
grammes involving the child’s wider social network have evolved from
family systems theories of ADHD. These programmes focus on improv-
ing parenting skills and enhancing the child’s relationships with mem-
bers of the family and the wider network. Such programmes have been
shown to have positive short-term effects on both symptomatology and
social adjustment (Anastopoulos et al., 2005; Barkley et al., 1992;
Young & Amarasinghe, 2010).

Assessment
Assessment and treatment of ADHD is usually carried out by multidisci-
plinary teams which include clinical psychologists, and colleagues from
other disciplines such as psychiatry or paediatrics. Children with ADHD
require assessment of their behaviour, abilities, and family and school
situations. The revised Conners’ Rating Scales (CRS-R, Conners,
1997) are widely used to assess ADHD behaviour. Conners’ parent,
teacher and self-report rating scales each contain almost 100 items and
yield a range of scores on scales that assess aspects of ADHD and
related difficulties. Computer scoring systems are available and norma-
tive data are used to interpret scores. To establish a DSM-IV-TR or
ICD-10 diagnosis, a structured interview for parents and children may
be administered, such as the attention and activity module of the
Development and Well-Being Assessment (DAWBA, Goodman et al.,
2000). Abilities may be assessed with intelligence tests such as the
Wechsler Intelligence Scale for Children (WISC-IV, Wechsler, 2004a)
for school-aged children and the Wechsler Preschool and Primary
Scale of Intelligence (WPPSI-III, 2004b) for preschoolers. These tests
yield full-scale IQs as well as scores for specific abilities that throw light
on cognitive strengths and weaknesses.
Attainments may be assessed with tests such as the Wechsler
Individual Achievement Test (WIAT-II, Wechsler, 2005), which assess
reading, numerical and language attainments. Family and school
situations may be assessed by conducting interviews with parents and
school teachers about the young person’s behaviour in these contexts.
Assessment information is integrated into a formulation that is used for
treatment planning as illustrated in the case study that opened the
chapter. This should link predisposing, precipitating and maintaining
factors to the child’s presenting problems and specify protective factors
that may be drawn on during treatment. A general clinical formulation
model for ADHD is given in Figure 2.2.

Book 1.indb 47 06/03/2012 13:47

 48 C L I N I C A L P S Y C H O L O G Y : A N I N T R O D U C T I O N

Figure 2.2 General formulation model for ADHD

Treatment
There is a growing consensus within the field that single factor theories
are unlikely to be able to explain the complex and heterogeneous
population of youngsters who qualify for a diagnosis of ADHD (Barkley,
2005). It is probable that a variety of biological and psychosocial factors
interact in complex ways to give rise to the syndrome and that problems
with a number of psychological processes particularly those involved in
regulating both cognitive and motor responses underpin symptomatology.
The symptomatology is probably partially maintained and exacerbated by
problematic relationships within the family, the peer group and the school.
In view of this integrative formulation, it is not surprising that multi-
modal treatment packages that include behavioural parent training, self-
instructional and social skills training and school-based contingency
management combined with stimulant therapy have been found to be
most effective. International best practice guidelines recommend that
multimodal programmes involving stimulant medication and behaviour-
ally oriented family, school and individual psychological interventions
should be offered to children with ADHD (American Academy of Child
and Adolescent Psychiatry, 2007a; American Academy of Paediatrics,
2001; Consensus Development Panel, 2000; Kutcher et al., 2004,
NICE, 2008a).

Book 1.indb 48 06/03/2012 13:47

 2 • CHILDHOOD BEHAVIOUR DISORDERS 49

With behavioural parent training, parents are coached in how to

consistently reinforce socially appropriate behaviour and extinguish
inappropriate behaviour. School-based contingency management pro-
grammes extend this type of approach into the child’s classroom envi-
ronment. In self-instructional training, children with ADHD are coached
in the use of self-instructions to regulate the way in which they deploy
their attention and control their impulses. With stimulant therapy, chil-
dren receive regular doses of methylphenidate which is available in a
form that is taken twice or three times a day, or as a slow-release prep-
aration taken only once a day. Psychological interventions collectively
contribute to normalizing ADHD behaviour, largely by improving parent-
ing practices and enhancing the way children with ADHD interact with
their families and social networks, and pharmacological interventions
reduce symptom intensity and so make it easier for parents and chil-
dren to make these changes. However, as mentioned earlier, stimulant
treatment loses its effectiveness after 3 years, so it is important that
this 3 year window of opportunity be used to help children and parents
develop ways to manage ADHD symptoms. Two promising innova-
tions in child-focused psychological treatments of ADHD are the use of
computer-based programmes to train children to enhance the function-
ing of working memory, and neurofeedback in which children modify the
frequency, amplitude or other characteristics of their electroencephalo-
gram (EEG) brain-wave patterns (Toplak et al., 2008).

Conduct disorder and oppositional

defiant disorder
Conduct disorder refers to a pattern of persistent, serious, aggressive
and destructive rule-breaking behaviour at home and within the wider
community, while oppositional defiant disorder refers to a persistent
pattern of oppositional and hostile behaviour confined to the home con-
text (American Psychiatric Association, 2000a; World Health Organ-
ization, 1992). Diagnostic criteria for these two conditions are given in
Table 2.2. Conduct problems constitute a third to a half of all clinic refer-
rals, and chronic conduct problems are the single most costly disorder
of adolescence for three reasons (Kazdin, 1995; Moffitt & Scott, 2008;
Scott, 2009).
First, they are remarkably unresponsive to traditional individual
approaches to treatment. Positive outcome rates for routine treatments
range from 20% to 40%. Second, about 60% of adolescents with con-
duct problems have a poor prognosis. Adolescents with chronic con-
duct disorder turn to adult criminality and develop antisocial personality
disorders, alcohol-related problems and a variety of psychological diffi-
culties. They also have more problems with health, educational attain-
ment, occupational adjustment, marital stability and social integration.
The third reason for the high cost of conduct problems is the fact that
they are intergenerationally transmitted. Adults with a history of conduct
disorder rear children with a high prevalence of conduct difficulties.

Book 1.indb 49 06/03/2012 13:47

 50 C L I N I C A L P S Y C H O L O G Y : A N I N T R O D U C T I O N

TABLE 2.2
Diagnostic criteria for oppositional defiant disorder and conduct disorder in DSM-IV-TR and ICD-10
DSM-IV-TR ICD-10
Oppositional defiant disorder
A. A pattern of negativistic, hostile and defiant behaviour The essential feature of this disorder is a
lasting at least 6 months, during which four or more of pattern of persistently negativistic, hostile,
the following are present: defiant, provocative and disruptive behaviour
1. Often loses temper which is clearly outside the normal range of
2. Often argues with adults behaviour for a child of the same age in the
3. Often actively defies or refuses to comply with adults’ same sociocultural context and which does
requests or rules not include the more serious violations of the
4. Often deliberately annoys people rights of others associated with conduct
5. Often blames others for his or her mistakes or disorder.
misbehaviour
6. Is often touchy or easily annoyed by others Children with this disorder tend frequently and
7. Is often angry or resentful actively to defy adult requests or rules and
8. Is often spiteful or vindictive deliberately to annoy other people. Usually
they tend to be angry, resentful, and easily
B. The disturbance in behaviour causes clinically annoyed by other people whom they blame
significant impairment in social, academic or for their own mistakes and difficulties. They
occupational functioning generally have a low frustration tolerance and
readily lose their temper. Typically their
C. The behaviours do not occur exclusively during the defiance has a provocative quality, so that
course of a psychotic or a mood disorder they initiate confrontations and generally
exhibit excessive levels of rudeness,
D. Criteria are not met for conduct disorder or antisocial uncooperativeness and resistance to
personality disorder. authority.

Frequently this behaviour is most evident in

interactions with adults or peers whom the
child knows well, and signs of the disorder
may not be present during clinical interview.

The key distinction from other types of

conduct disorder is the absence of behaviour
that violates the law and the basic rights of
others such as theft, cruelty, bullying, assault
and destructiveness.
Conduct disorder
A. A repetitive and persistent pattern of behaviour in which Conduct disorders are characterized by a
the basic rights of others or major age-appropriate repetitive and persistent pattern of dissocial,
societal norms or rules are violated, as manifested by aggressive, or defiant conduct. Such
the presence of three or more of the following criteria behaviour, when at its most extreme for the
in the past 12 months with at least one criterion present individual should amount to major violations of
in the past 6 months. age-appropriate social expectations, and is
Aggression to people and animals therefore more severe than ordinary childish
1. Often bullies, threatens or intimidates others mischief or adolescent rebelliousness.
2. Often initiates physical fights
3. Has used a weapon that can cause serious physical
harm to others
4. Has been physically cruel to people
5. Has been physically cruel to animals
6. Has stolen while confronting a victim
7. Has forced someone into sexual activity

Book 1.indb 50 06/03/2012 13:47

 2 • CHILDHOOD BEHAVIOUR DISORDERS 51

DSM-IV-TR ICD-10
Destruction of property
8. Has deliberately engaged in firesetting Examples of the behaviours on which the
9. Has deliberately destroyed others’ property diagnosis is based include the following:
excessive levels of fighting or bullying; cruelty
Deceitfulness or theft
to animals or other people; severe
10. Has broken into someone’s house, building or car
destructiveness to property; firesetting;
11. Often lies to obtain goods or favours or avoid
stealing; repeated lying; truancy from school
obligations
and running away from home; unusually
12. Has stolen items without confronting the victim
frequent and severe temper tantrums; defiant
Serious violation of rules provocative behaviour; and persistent and
13. Often stays out late at night despite parental severe disobedience. Any one of these
prohibitions (before 13 years of age) categories, if marked, is sufficient for the
14. Has run away from home overnight at least twice while diagnosis, but isolated dissocial acts are not.
living in parental home or once without returning for a
lengthy period Exclusion criteria include serious underlying
15. Is often truant from school before the age of 13 conditions such as schizophrenia,
hyperkinetic disorder or depression.
B. The disturbance in behaviour causes clinically
significant impairment in social, academic or The diagnosis is not made unless the duration
occupational functioning. of the behaviour is 6 months or longer.

C. In those over 18 years, the criteria for antisocial Specify:

personality disorder are not met. CD confined to family context where the
symptoms are confined to the home.
Specify childhood-onset (prior to 10 years) or adolescent Unsocialized CD where there is a pervasive
onset. abnormality in peer relationships.
Specify severity (mild, moderate or severe) Socialized CD where the individual is well
integrated into a peer group.

Note: Adapted from DSM-IV-TR (APA, 2000) and ICD-10 (WHO, 1992).

Case example of conduct disorder

Bill, aged 11, was referred by his social worker for treatment following
an incident in which he had assaulted neighbours by climbing up onto
the roof of his house and throwing rocks and stones at them. He also
had a number of other problems according to the school headmaster,
including academic underachievement, difficulty in maintaining friend-
ships at school and repeated school absence. He smoked, occasionally
drank alcohol, and stole money and goods from neighbours. His prob-
lems were longstanding but had intensified in the 6 months preceding
the referral. At that time his father, Paul, was imprisoned for raping a
young girl in the small rural village where the family lived.

Family history
Bill was one of five boys who lived with his mother, Rita, at the time of
the referral. The family lived in relatively chaotic circumstances. Prior to
Paul’s imprisonment, the children’s defiance and rule-breaking, particu-
larly Bill’s, was kept in check by their fear of physical punishment from
their father. Since his imprisonment, there were few house rules and
these were implemented inconsistently by Rita, so all of the children
had conduct problems but Bill’s were by far the worst.

Book 1.indb 51 06/03/2012 13:47

 52 C L I N I C A L P S Y C H O L O G Y : A N I N T R O D U C T I O N

Rita had developed intense coercive patterns of interaction with Bill

and John (the second eldest). That is, she and the children engaged in
escalating arguments, from which she typically withdrew when her sons
became overly verbally or physically aggressive towards her. This
coercive process of escalation and withdrawal led to Rita and her sons
experiencing relief. The outcome of this was that the next time they
engaged in conflict, they were likely to be even more abusive and
aggressive to each other, since their expectations were that escalation
would lead to withdrawal and relief.
In addition to the parent–child interaction difficulties, there were no
routines to ensure that bills were paid, food was bought, washing was
done, homework completed or regular meal and sleeping times
observed. Rita supported the family with welfare payments and money
earned illegally from farm-work. Despite the family chaos, she was very
attached to her children and would sometimes take them to work with
her rather than send them to school because she liked their company,
and because they helped her to earn more money.
At the preliminary interview, Rita said that ‘her nerves were in tatters’.
She was attending a psychiatrist intermittently for treatment of
depression with medication. She had a longstanding history of conduct
and mood regulation problems, beginning early in adolescence. In
particular she had had conflictual relationships with her mother and
father, which were characterized by coercive cycles of interaction,
similar to those in which she engaged with her sons. In school she had
academic difficulties and peer relationship problems.
Rita had been ostracized by her own family when she married Paul,
whom her parents saw as an unsuitable partner for her, since he had a
number of convictions for theft and assault. Paul’s family never accepted
Rita, because they thought she had ‘ideas above her station’. Rita’s and
Paul’s parents were in regular conflict, and each family blamed the other
for the chaotic situation in which Paul and Rita had found themselves.
Rita was also ostracized by the village community in which she lived.
The community blamed her for driving her husband to commit rape.
Paul, the father, also had longstanding difficulties. His conduct
problems began in middle childhood. He was the eldest of four brothers,
all of whom developed conduct problems, but his were by far the most
severe. He had a history of becoming involved in aggressive exchanges
that often escalated to violence. He and his mother had become involved
in coercive patterns of interaction from his earliest years. He developed
similar coercive patterns of interaction at school with his teachers, at
work with various foremen and also in his relationship with Rita. He had
a distant and detached relationship with his father.

Developmental history
From Bill’s developmental history, it was clear that he was a child with a
difficult temperament who did not develop sleeping and feeding routines
easily and responded intensely and negatively to new situations. His
language development had been delayed and he showed academic
difficulties since his first years in school. On the positive side, Bill had a

Book 1.indb 52 06/03/2012 13:47

 2 • CHILDHOOD BEHAVIOUR DISORDERS 53

strong sense of family loyalty to his brothers and parents and did not
want to see the family split up.

Psychometric assessment
From the Child Behaviour Checklists (CBCLs) completed by Rita, it was
clear that Bill and his three brothers had clinically significant conduct
problems and Bill’s were by far the most extreme. A similar pattern
emerged from behaviour checklists completed by the boys’ teachers. A
psychometric evaluation of Bill’s abilities and attainments showed that
he was of normal intelligence, but his attainments in reading, spelling
and arithmetic fell below the 10th percentile. From his subtest profile on
the psychometric instruments, it was concluded that the discrepancy
between his attainment and abilities was accounted for by a specific
learning disability – dyslexia.

School report
The headmaster at the school that Bill and his brothers attended
confirmed that Bill had academic, conduct and attainment problems, but
was committed to educating the boys and managing their conduct and
attendance problems in a constructive way. The headmaster had a
reputation (of which he was very proud) for being particularly skilled in
managing children with behaviour problems.

Formulation
Bill was an 11-year-old boy with a persistent and broad pattern of con-
duct problems both within and outside the home, consistent with a diag-
nosis of conduct disorder. Bill’s conduct problems had an insidious
onset, beginning with wilfulness in early childhood and escalating as he
developed. Thus there was no discrete precipitating factor to account
for the onset of Bill’s conduct disorder. However, the father’s imprison-
ment 6 months prior the referral led to an intensification of Bill’s conduct
problems and precipitated the referral. Factors that predisposed Bill to
develop conduct problems included a difficult temperament, a develop-
mental language delay, dyslexia, exposure to paternal criminality,
maternal depression and a disorganized family environment. The con-
duct problems were maintained at the time of the referral by engage-
ment in coercive patterns of interaction with his mother and teachers;
regular absences from school; rejection of Bill by peers at school; and
isolation of his family by the extended family and the community.
Protective factors in the case included the mother’s wish to retain cus-
tody of the children rather than have them taken into foster care; Bill and
his siblings’ sense of family loyalty; and the school’s commitment to
retaining and dealing with Bill and his brothers rather than expelling
them for truancy and misconduct. This formulation is diagrammed in
Figure 2.3.

Treatment
The treatment plan in this case involved a multisystemic intervention
programme. The mother was trained in behavioural parenting skills. A

Book 1.indb 53 06/03/2012 13:47

 54 C L I N I C A L P S Y C H O L O G Y : A N I N T R O D U C T I O N

Figure 2.3 Formulation of a case of conduct disorder

series of meetings between the teacher, the mother and the social
worker were convened to develop and implement a plan for regular
school attendance. Occasional relief foster care was arranged for Bill
and John (the second eldest) to reduce the stress on Rita. Social skills
training was provided for Bill to help him deal with peer relationship
problems.
There was some improvement in Bill’s conduct problems, school
attendance and academic performance. However, Bill continued to
have residual conduct and academic problems throughout his adoles-
cence. Coercive cycles of interaction between Bill and Rita, and family
isolation and lack of support continued to be major factors maintaining
Bill’s difficulties. Rita required periodic crisis intervention and social
work support throughout Bill’s teenage years. Periodically, with social
work assistance, Bill was placed for brief periods in voluntary care at
Rita’s request.

Clinical features
From Table 2.2 it may be seen that a distinction is made between oppo-
sitional defiant disorder and conduct disorder, with the former reflecting
a less pervasive disturbance than the latter. In a proportion of cases
oppositional defiant disorder is a developmental precursor of conduct
disorder (Moffitt & Scott, 2008; Scott, 2009). The main behavioural fea-

Book 1.indb 54 06/03/2012 13:47

 2 • CHILDHOOD BEHAVIOUR DISORDERS 55

ture of conduct disorder is a pervasive and persistent pattern of anti-

social behaviour that extends beyond the family to the school and
community; involves serious violations of rules; and is characterized by
defiance of authority, aggression, destructiveness, deceitfulness and
cruelty. Youngsters with conduct disorder show a limited internalization
of social rules and norms and a hostile attributional bias. That is, the
youngster interprets ambiguous social situations as threatening and
responds with aggressive retaliative behaviour. Anger and irritability are
the predominant mood states.
Problematic relationships with significant members of the child’s net-
work typify children with conduct disorder. Negative relationships with
parents and teachers typically revolve around the youngster’s defiant
behaviour. Negative relationships with peers typically centre on aggres-
sion and bullying, which is guided by the hostile attributional bias with
which conduct disordered youngsters construe many of their peer rela-
tionships. There may also be problematic relationships with members of
the wider community if theft or vandalism has occurred. Multiagency
involvement with juvenile justice or social work agencies is common.
Also, because conduct disorder is associated with family disorganiza-
tion, child abuse and neglect, parental criminality and parental psycho-
logical adjustment difficulties, professionals from child protection, adult
mental health and justice systems may be involved.
Disruptive behaviour disorders follow three main developmental
trajectories: life-course-persistent, adolescent limited, and childhood
limited (Moffitt & Scott, 2008; Pardini et al., 2010). For about half of all
children with childhood behavioural problems, their difficulties are
limited to childhood or adolescence. The other half follow a life-course-
persistent pathway and grow up to have antisocial personality disorders.
The adolescent limited pathway is associated with deviant peer group
membership. The life-course-persistent pathway is associated with a
greater number of risk factors. Three classes of risk factors increase the
probability that conduct problems in childhood or adolescence will
escalate into later life difficulties. These are personal characteristics,
parenting practices and family organization problems (McMahon et al.,
2010; Moffitt & Scott, 2008; Scott, 2009).
Early onset, callous unemotional traits (absence of guilt, lack of
empathy, shallow affect, and lack of concern about performance), diffi-
cult temperament, aggressiveness, impulsivity, inattention and educa-
tional difficulties are the main personal characteristics of children and
adolescents that place them at risk for long-term conduct problems.
Ineffective monitoring and supervision of youngsters, providing incon-
sistent consequences for rule violations, and failing to provide reinforce-
ment for prosocial behaviour are the main problematic parenting
practices that place children and adolescents at risk for the develop-
ment of long-term antisocial behaviour patterns. The family organiza-
tion problems associated with persistence of conduct problems into
adulthood are parental conflict and violence, a high level of life stres-
sors, a low level of social support, and parental psychological adjust-
ment problems such as depression or substance abuse.

Book 1.indb 55 06/03/2012 13:47

 56 C L I N I C A L P S Y C H O L O G Y : A N I N T R O D U C T I O N

Epidemiology
In a review of 12 international epidemiological studies, Costello et al.
(2004) found that the prevalence of conduct disorder ranged from 1.1%
to 10.6%, with a median prevalence rate of 3.7%. The range for opposi-
tional defiant disorder was 1.3–7.4% and the median prevalence rate
also 3.7%. The variability in rates may be due to the diagnostic criteria
applied (DSM or ICD) and the demographic characteristics of the popu-
lations studied. Using ICD criteria, a prevalence rate of 5.3% was
obtained in a UK national epidemiological study (Meltzer et al., 2000).
The prevalence of conduct disorder varies with gender and age, and the
occurrence of comorbid conditions is common (Carr, 2006a). Conduct
disorder is more prevalent in boys than in girls, with male/female ratios
varying from 2:1 to 4:1. It is also more prevalent in adolescents than in
children. The comorbidity rate for conduct disorder and ADHD in com-
munity populations is 23%. The comorbidity rates for conduct disorder
and emotional disorders in community populations are 17% for major
depression and 15% for anxiety disorders.

Etiological theories
Biological, psychodynamic, cognitive-behavioural and social systems
theories have been proposed to explain the development of conduct
problems and to inform their treatment. Since the distinction between
oppositional defiant disorder and conduct disorder is a relatively recent
development, most theories in this area have been developed with
specific reference to conduct disorder but have obvious implications for
oppositional defiant disorder, which is a developmental precursor of
conduct disorder in many cases.

Biological theories
Biological theories have focused on the roles of genetic factors,
neurobiological deficits, neurotransmitter dysregulation, neuroendocrine
factors, arousal levels, temperament and neuropsychological deficits in
the aetiology of conduct problems.

Genetics
There are many lines of research that focus on genetic and constitutional
aspects of children with conduct disorder, and these are guided by the
hypothesis that biological factors underpin antisocial behaviour. The
predominance of males among youngsters with conduct disorders and
the finding from a review of over 100 twin and adoption studies that
antisocial behaviour is about 50% heritable point to a role for genetically
transmitted constitutional factors in the aetiology of conduct disorders
(Moffitt, 2005).
Current neuroscientific studies of conduct disorder aim to link specific
genes with specific structural and functional brain abnormalities. At
present a number of genes are being investigated. One of the most

Book 1.indb 56 06/03/2012 13:47

 2 • CHILDHOOD BEHAVIOUR DISORDERS 57

promising lines of research in this area has established a link between

the monoamine oxidase A (MAOA) gene and conduct disorder in boys
at risk of antisocial behaviour as a result of exposure to physical child
abuse. In a meta-analysis of a series of studies, Kim-Cohen et al. (2006)
found that physically abused children with the MAOA genotype
conferring low levels of the MAOA enzyme, developed conduct disorder
more often than abused children with a high-activity MAOA genotype.
MAOA plays a key role regulating aggressive behaviour by selectively
breaking down a number of neurotransmitters including serotonin,
which has been found to be abnormally low in antisocial individuals.
The MAOA gene has earned the nickname ‘warrior gene’ because of its
link with aggression (McDermott et al., 2009). While specific genes,
such as the MAOA gene, may contribute to the risk of antisocial
behaviour, their contributions are probably quite small compared with
the larger polygenetic effects of collections of genes on personal
attributes such as temperament, executive function and verbal ability,
all of which have strong associations with conduct disorder.

Neurobiological deficits
Neurobiological theories propose that antisocial, immoral and aggres-
sive behaviour, typical of people with life-course-persistent disruptive
behaviour disorders, is subserved by structural and functional brain
abnormalities. In a wide-ranging review of evidence drawn mainly from
studies of antisocial adults with histories of childhood conduct disorder,
Raine and Yang (2006) concluded that antisocial behaviour is associ-
ated with structural and functional abnormalities of a number of brain
regions including the prefrontal cortex, which subserves executive func-
tion and judgement, and the limbic system (including the amygdala,
hippocampus and cingulate), which subserves learned emotional
responses, particularly fear conditioning. People with antisocial person-
ality disorder and psychopathy (who as children had disruptive behav-
iour disorders) have significantly reduced prefrontal lobe grey matter,
reduced amygdala and hippocampus volume, and reduced activity in
these areas compared with normal people. These abnormalities may be
due to genetic factors or prenatal, perinatal or early childhood adversity
(Moffitt, 2005; Taylor & Rogers, 2005).

Neurotransmitter dysregulation
Neurotransmitter dysregulation hypotheses propose that low levels of
serotonin lead to aggression against others in the case of disruptive
behaviour disorders (or the self in the case of depression) by enhancing
sensitivity to stimuli that elicit aggression and reducing sensitivity to
cues that signal punishment (Spoont, 1992). Studies of adults show that
antisocial behaviour is associated with low levels of serotonin, but in
studies of children the results are more mixed (van Goozen et al., 2007).
However, medications that target serotonin, such as the selective
serotonin reuptake inhibitors, do not modify aggression or antisocial
behaviour in children or adults.

Book 1.indb 57 06/03/2012 13:47

 58 C L I N I C A L P S Y C H O L O G Y : A N I N T R O D U C T I O N

Neuroendocrine hypothesis
The hypothesis that antisocial behaviour is caused by androgens such
as testosterone and dehydroepiandrosterone (DHEA) is premised on
the fact that higher rates of both occur in males, and in animal studies a
strong correlation has been found between aggression and testosterone
levels. Research on adults has established a link between testosterone
and violent crime, but studies of children and adolescents have yielded
mixed results. In contrast, there is some evidence for higher levels of
DHEA in children and adolescents with conduct disorder (van Goozen
et al., 2007).
Hypo-arousal
In the most sophisticated version of the hypo-arousal hypothesis, Van
Goozen et al. (2007, 2008) proposed that people who show marked
aggression and antisocial behaviour do so because their stress res-
ponse systems are underreactive, a neurobiological vulnerability that
may arise from genetic factors or early adversity. This underreactivity
accounts for fearless rule-breaking behaviour and risky sensation-
seeking behaviour typical of young people with conduct disorder. In a
previous version of this hypothesis, Raine (1996) proposed that because
of their fearlessness, children with conduct disorder are insensitive to
the negative consequences of antisocial behaviour, and so have diffi-
culty learning and internalizing societal rules. Zuckerman (2007) argued
that their low arousal levels lead them to become easily bored and they
address this by engaging in risky, sensation-seeking behaviour. The
hypo-arousal hypothesis is supported by a large body of evidence which
shows that antisocial children and adults show low resting heart rate,
skin conductance and cortisol levels, which are indices of hypoactivity
within the autonomic nervous system and the hypothalamic–pituitary–
adrenal (HPA) axis (Van Goozen et al., 2007, 2008).
There is also growing evidence that both genetic factors and adverse
prenatal and early life environments may contribute to the development
of underreactive stress response systems. The heritability of antisocial
behaviour is well established (as noted above), and future research
may indicate a mechanism that links specific genes to the stress
response system. With regard to the prenatal environment, maternal
smoking, drug and alcohol use, psychopathology and poor diet during
pregnancy all compromise normal development of the central nervous
system and may possibly compromise the development of the stress
response system (Huizink et al., 2004). Stressful parenting environments
in the early years associated with parental psychopathology, harsh,
critical parenting, child abuse and neglect and domestic violence may
adversely affect brain development and lead to an adaptive down-
regulating of the stress response system to avoid the negative effects of
chronic hyper-arousal (Dawson et al., 2000; Susman, 2006).
Treatment of conduct disorder based on the hypo-arousal hypoth-
esis involves the use of highly structured and intensive learning situ-
ations to facilitate the internalization of social rules. The positive and
negative reinforcers used must be highly valued and delivered immedi-
ately following responses. All rule infractions must lead to immediate

Book 1.indb 58 06/03/2012 13:47

 2 • CHILDHOOD BEHAVIOUR DISORDERS 59

withdrawal of desired stimuli. Rule-following should be immediately and

intensely rewarded on a variable interval schedule, since this leads to
learning that is maximally resistant to extinction. These treatment impli-
cations of arousal theory have been incorporated into the design of
residential token economies for delinquent adolescents, behavioural
parent training programmes, school-based behavioural programmes
and treatment foster care (Carr, 2009a).

Temperament
The temperament hypothesis proposes that difficult temperament is a
risk factor for disruptive behaviour disorders. Children with difficult
temperaments, which are predominantly inherited, have difficulty
establishing regular routines for eating, toileting and sleeping; tend to
avoid new situations; and responded to change with intense negative
emotions. Their temperamental style tends to elicit negative reactions
from their parents, teachers and peers, to which they respond with
defiance, aggression and other antisocial behaviour. The temperament
hypothesis has been supported by many studies including Chess and
Thomas’s (1995) original New York longitudinal study (De Pauw &
Mervielde, 2010).
There may appear to be an inconsistency between the hypo-arousal
hypothesis and the temperament hypothesis, with the former proposing
that antisocial behaviour is associated with low arousal and the latter
with difficult temperament, possibly associated with high arousal in new
situations. It may be that low arousal and difficult temperament are
separate routes to antisocial behaviour or to different types of antisocial
behaviour, with low arousal being associated with callous unemotional
psychopathy and difficult temperament associated with aggressive
behaviour. Lorber (2004) found support for this position in a meta-
analysis of studies of heart rate and skin conductance resting levels and
reactivity to various stimuli. All forms of antisocial behaviour were
associated with low resting arousal levels, but individuals with aggressive
conduct problems showed high reactivity, whereas those with callous
unemotional psychopathic traits did not.

Neuropsychological deficits
The neuropsychological deficits hypothesis proposes that deficits in
executive function and verbal reasoning underpin self-regulation diffi-
culties that contribute to conduct problems. Executive function deficits
limit the capacity to plan and follow through on prosocial courses of
action, and so give rise to disruptive behaviour disorders. Children with
verbal reasoning deficits may have difficulty remembering instructions,
developing private speech to facilitate self-control, and using verbal
strategies rather than aggression to resolve conflicts.
Executive function and verbal reasoning deficits may also account for
academic underachievement typical of young people with conduct disor-
ders, and this underachievement may lead to frustration and consequent
aggressive behaviour. This position is supported by a substantial body of
evidence that documents verbal reasoning and executive function defi-
cits in children and teenagers with conduct problems, by studies that

Book 1.indb 59 06/03/2012 13:47

 60 C L I N I C A L P S Y C H O L O G Y : A N I N T R O D U C T I O N

confirm a strong association between reading difficulties and conduct

problems, and by studies which show that unsocialized conduct prob-
lems are associated with self-regulation problems (Moffitt & Scott, 2008;
Nigg & Huang-Pollock, 2003; Teichner & Golden, 2000). Remedial inter-
ventions that facilitate the development of language and academic skills
are the principal types of treatment deriving from this theory.

Psychodynamic theories
Classical psychoanalytic theory points to superego deficits and
attachment theory to the role of insecure attachment in the development
of conduct problems.

Psychoanalytic perspectives
Within psychoanalysis it is assumed that societal rules and expecta-
tions are internalized through identification with the parent of the same
gender. This internalization is referred to as the superego. Aichorn
(1935) argued that antisocial behaviour occurs because of impover-
ished superego functioning. The problems with superego functioning
were thought to arise from either overindulgent parenting on one hand
or punitive and neglectful parenting on the other. With overindulgent
parenting, the child internalizes lax standards and so feels no guilt when
breaking rules or behaving immorally. In such cases any apparently
moral behaviour is a manipulative attempt to gratify some desire. With
punitive or neglectful parenting, the child splits the experience of the
parent into the good caring parent and the bad punitive/neglectful par-
ent and internalizes both of these aspects of the parent quite separately
with little integration. In dealing with parents, peers and authority fig-
ures, the child may be guided by either the internalization of the good
parent or the internalization of the bad parent. Typically at any point in
time such youngsters can clearly identify those members of their net-
work who fall into the good and bad categories. They behave morally
towards those for whom they experience a positive transference and
view as good, and immorally to those towards whom they have a nega-
tive transference and view as bad.
Individual psychoanalytic psychotherapy has been used in the
treatment of children and adolescents with conduct problems (e.g.,
Kernberg & Chazan, 1991). However, there are limits to the effectiveness
of psychoanalytically based treatment for those with disruptive behaviour
disorders (Fonagy & Target, 1994; Winkelmann et al., 2005). For
example, in a naturalistic study, Fonagy and Target (1994) found that
children with oppositional defiant disorder responded better than
children with conduct disorder or ADHD.

Attachment
Bowlby (1944) pointed out that children who were separated from their
primary caregivers for extended periods of time during their first months

Book 1.indb 60 06/03/2012 13:47

 2 • CHILDHOOD BEHAVIOUR DISORDERS 61

of life failed to develop secure attachments and so, in later life, did not
have internal working models for secure trusting relationships. He
referred to such children as displaying affectionless psychopathy. Since
moral behaviour is premised on functional internal working models of
how to conduct oneself in trusting relationships, such children behave
immorally.
Later studies of children reared in intact families have established a
link between attachment insecurity and behaviour problems (e.g., Moss
et al., 2006). Treatment according to this position should aim to provide
the child with a secure-attachment relationship or corrective emotional
experience which will lead to the development of appropriate internal
working models. These in turn will provide a basis for moral action.
More secure attachment relationships may be facilitated within families
of young people with disruptive behaviour disorders through parent
training (Forgatch & Patterson, 2010; Webster-Stratton & Reid, 2010),
family therapy (Carr, 2006b), multisystemic therapy (Henggeler &
Schaeffer, 2010) and treatment foster care (Smith & Chamberlain,
2010), all of which are described later in this chapter.

Cognitive-behavioural theories
A range of theories of conduct problems have been developed within
the broad cognitive behavioural tradition. Problems with social
information processing and social skills deficits are the principal factors
highlighted in cognitive theories. Social learning theories highlight the
importance of modelling, and behavioural theories focus on the role of
reinforcement contingencies in the maintenance of conduct problems.

Social information processing

Dodge and colleagues proposed that children with conduct disorders
process social information in a different way to other children (Crick &
Dodge, 1994). In ambiguous social situations their cognition is charac-
terized by a hostile attributional bias. That is, children with conduct dis-
orders attribute hostile intentions to others in social situations where the
intentions of others are ambiguous. The aggressive behaviour of chil-
dren with conduct disorders in such situations is, therefore, intended to
be retaliatory. The aggression is viewed as unjustified by those against
whom it is directed, and this leads to impaired relationships with peers
and others in their social networks. The reactions of others to such
apparently unjustified aggression provide confirmation for the aggres-
sive child that others have hostile intentions, which justifies further retal-
iatory aggression. This social information procession theory of conduct
disorder has been supported by extensive research (Dodge et al.,
2006).
Dodge has embedded his social information processing theory within
a more general model of the development of aggressive behaviour, in
which he proposes that social information processing patterns are the
proximal mechanism through which aggressive behaviour occurs

Book 1.indb 61 06/03/2012 13:47

 62 C L I N I C A L P S Y C H O L O G Y : A N I N T R O D U C T I O N

(Dodge, 2011; Dodge & Pettit, 2003). However, these patterns are sub-
served by neural and psychophysiological processes and are acquired
through genetic and environmental processes, especially in negative
interaction with parents, teachers and peers.

Social skills deficits

The social skills deficit hypothesis is that conduct disorders involve
inappropriate social behaviours, such as aggression or defiance, which
have developed to compensate for social skills deficits. Research
conducted to test this hypothesis has highlighted the social skills deficits
of children with conduct disorders, and the value of training in social
problem-solving in reducing antisocial behaviour (Losel & Beelmann,
2005). This position proposes that antisocial children lack the skills to
generate alternative solutions to social problems such as dealing with
an apparently hostile peer. They also lack the skills to implement
solutions to social problems such as these, for example using humour
or shared interests to reduce hostility.
Within the cognitive-behavioural tradition, group-based social skills
programmes have been developed that aim to train youngsters in the
social problem-solving skills they lack. A growing body of evidence
shows that social problem-solving skills can reduce antisocial behaviour
when offered alone (Lochman et al., 2010) or combined with parent
training and other systemic interventions (Kazdin, 2010).

Modelling
Bandura and Walters (1959) proposed that aggression, characteristic of
children and adolescents with conduct disorders, is learned through a
process of imitation or modelling. Children subjected to harsh, critical
parenting, neglect or physical abuse, or who witness domestic violence,
become aggressive through a process of imitation. This position is sup-
ported by a large body of evidence, particularly that which points to the
intrafamilial transmission of aggressive behaviour associated with
harsh, inconsistent parenting, child abuse and neglect, and exposure to
domestic violence (Moffitt & Scott, 2008; Taylor & Rogers, 2005).
According to modelling theory, treatment should aim to help parents,
through parent training or family therapy, to model appropriate behav-
iour for their children (Carr, 2006a; Forgatch & Patterson, 2010;
Webster-Stratton & Reid, 2010) or provide alternative models of appro-
priate behaviour in a residential or treatment foster care setting (Smith
& Chamberlain, 2010).

Coercive family process

Patterson and his group proposed that children with conduct disorders
learn their antisocial behaviours from involvement in coercive patterns
of interaction with their parents, and these behaviours are then exhib-
ited in school and community contexts (Forgatch & Patterson, 2010;
Patterson, 1982). Marital discord, parental psychopathology, a variety

Book 1.indb 62 06/03/2012 13:47

 2 • CHILDHOOD BEHAVIOUR DISORDERS 63

of social and economic stressors and social isolation all contribute to

the parents’ use of a coercive parenting style. This style has three main
features.
First, parents have few positive interactions with their children.
Second, they punish children frequently, inconsistently and ineffectively.
Third, the parents of children with conduct problems negatively reinforce
antisocial behaviour by confronting or punishing the child briefly and
then withdrawing the confrontation or punishment when the child
escalates the antisocial behaviour, so that the child learns that escalation
leads to parental withdrawal. By middle childhood children exposed to
this parenting style have developed an aggressive relational style which
leads to rejection by non-deviant peers. Such children, who often have
comorbid specific learning difficulties, typically develop conflictual rela-
tionships with teachers and consequent attainment problems.
In adolescence, rejection by non-deviant peers and academic failure
make socializing with a deviant, delinquent peer group an attractive
option. Patterson’s group have shown that this developmental trajectory
is common among youngsters who first present with oppositional defiant
disorder. The delinquency of adolescence is a staging post on the route
to adult antisocial personality disorder, criminality, drug abuse and
conflictual, violent and unstable marital and parental roles for more than
half of all youngsters with conduct disorder (Farrington, 1995). Therapy
for families with preadolescent children based on this model aims to
help parents and children break coercive patterns of interaction and
build positive relationships, but most importantly it helps parents develop
skills for effectively disciplining their children. There is considerable
evidence for the effectiveness of this type of behavioural parent training
(Forgatch & Patterson, 2010).

Systems theory
Systems theories highlight the role of family systems and broader social
systems in the aetiology and maintenance of conduct problems.

Family systems approaches

Within the family therapy tradition, a number of assumptions have been
influential in offering a framework for understanding how conduct
disorders are maintained by patterns of family interaction and how they
may be resolved by intervening in these patterns (Carr, 2006b).
According to family systems theory, families with youngsters who have
conduct problems are more disorganized than other families. Rules,
roles and routines are unclear, and parental supervision of children is
deficient. Communication is problematic, unclear and confusing. There
is also an absence of systematic family problem-solving skills.
The members of these families are more emotionally disengaged
from each other in comparison with other families, and parent–child
relationships may be lacking in warmth and empathy. In addition,
families with youngsters who display conduct problems have difficulties
maintaining clear, unambiguous intergenerational hierarchies and

Book 1.indb 63 06/03/2012 13:47

 64 C L I N I C A L P S Y C H O L O G Y : A N I N T R O D U C T I O N

negotiating life-cycle transitions. With respect to ambiguous hierarchies,

conduct problems are maintained if parents do not both agree on a
basic set of rules of conduct for their children which they consistently
enforce, with clear consequences for rule violations. With respect to
lifecycle transitions, conduct problems are more likely to occur at
transitional points in the life cycle, when there are changes in routines
and a build-up of stress, such as starting primary school, moving to
secondary school and entering adolescence, or leaving secondary
school and entering adulthood.
Available evidence supports many of these assumptions of family
system theory. Families of young people with disruptive behaviour dis-
orders are more likely to be characterized by disorganization; harsh,
critical and inconsistent parenting; lack of parental warmth; physical
child abuse and neglect; parental criminality and psychopathology;
marital discord; domestic violence; and many life stresses, notably pov-
erty (Crosnoe & Cavanagh, 2010; Moffitt & Scott, 2008). Family therapy
addresses disruptive behaviour disorders by helping families become
more coherently organized, with better relationships, communication,
problem solving, and fair, consistent parenting. There is good evidence
for the effectiveness of family therapy in reducing adolescent antisocial
behaviour (Carr, 2009b).

Sociological perspectives
A variety of sociological theories have posited a causal link between
deviant antisocial behaviour and aspects of the wider socio-cultural
context within which such behaviour occurs. Anomie theory is a
commonly cited exemplar of this body of theories (Cloward & Ohlin,
1960). According to anomie theory, theft and related antisocial
behaviours such as mugging and lying are illegitimate means used by
members of a socially disadvantaged delinquent subculture to achieve
material goals valued by mainstream culture. Anomie is the state of
lawlessness and normlessness that characterizes such subcultures. In
support of this position, there is good evidence for a link between
antisocial behaviour and poverty (Moffitt & Scott, 2008), and that
membership of deviant peer groups can facilitate antisocial behaviour
(Dishion & Dodge, 2005). Treatment premised on this theory must
provide delinquents and their peer groups with legitimate means to
achieve societal goals. Remedial academic programmes, vocational
training programmes, and treatment foster care are the main treatment
approaches implicated by this theory. There is good evidence for the
efficacy of treatment foster care (Smith & Chamberlain, 2010), and
some evidence for the value of academic and vocational programmes
in the rehabilitation of juvenile delinquents (Lipsey, 2009).

Multisystemic ecological theory

This position, proposed by Henggeler, entails the view that multiple sys-
tems (including the individual, the family, the school and the community)

Book 1.indb 64 06/03/2012 13:47

 2 • CHILDHOOD BEHAVIOUR DISORDERS 65

are involved in the genesis and maintenance of conduct problems, and

consequently effective treatment must target multiple systems rather
than any single system (Henggeler & Schaeffer, 2010). Bronfenbrenner’s
model of ecologically nested systems is the foundation for this theory
(Bronfenbrenner & Morris, 2006). Conduct disorders, it is argued, are
maintained by multiple factors in these multiple ecologically nested sys-
tems. Important individual factors include difficult temperament, early
separation experiences, hostile attributional bias, poor social skills, diffi-
culties learning prosocial behaviour from experience, and academic
learning difficulties. Family factors include family disorganization, ambig-
uous family hierarchies, parent–child attachment difficulties, parenting
and discipline problems, marital discord and difficulty negotiating family
life-cycle transitions. School factors include patterns of interaction that
maintain school-based discipline problems, attainment difficulties and
lack of educational resources. Community factors include involvement
with deviant peers, drug abuse and involvement in poorly co-ordinated
multiagency networks.
Henggeler developed multisystemic therapy (MST) based on this
ecological conceptualization of disruptive behaviour disorders. MST is a
comprehensive empirically supported programme for antisocial young
people and their families. For each case, treatment is individually tai-
lored and based on a multisystem ecological assessment. Treatment
packages include family therapy to reduce family disorganization,
school-based interventions to deal with interactional patterns that main-
tain school-based conduct problems and underachievement, individual
and group cognitive and social skills training, and peer-group-based
interventions to enhance prosocial peer relationships and reduce
involvement in deviant peer groups. Evidence from a series of trials
supports the effectiveness of this approach (Henggeler & Schaeffer,
2010).

Assessment
Assessment and treatment of children with conduct disorders is usually
carried out by multidisciplinary teams which include clinical psychologists
and colleagues from other disciplines such as social work and psychiatry.
Children’s conduct problems require an assessment of their behaviour,
abilities, and family and school situations. The Achenbach System of
Empirically Based Assessment (ASEBA, Achenbach & Rescorla, 2000,
2001) and the Strengths and Difficulties Questionnaire (SDQ, Goodman,
2001) are widely used to assess conduct problems.
ASEBA parent, teacher and self-report rating scales contain over
100 items and yield a total problem score, scores for internalizing and
externalizing behaviour problems, and scores in various problem areas
including conduct problems. There are versions for school-aged children
and preschoolers. Computer scoring systems are available and
normative data are used to interpret scores. SDQ parent, teacher and
self-report rating scales contain only 25 items and yield a total problem
score, as well as scores for various problem areas, including conduct

Book 1.indb 65 06/03/2012 13:47

 66 C L I N I C A L P S Y C H O L O G Y : A N I N T R O D U C T I O N

problems. There are also SDQ norms to facilitate interpretation. The

brevity of the SDQ makes it very acceptable to parents and teachers.
To establish a DSM-IV-TR or ICD-10 diagnosis of oppositional
defiant disorder or conduct disorder, a structured interview for parents
and children may be administered, such as the troublesome behaviour
module of the Development and Well-Being Assessment (DAWBA,
Goodman et al., 2000). Abilities and achievements of children with
conduct problems, as well as their family and school situations, are
assessed in the same way as those of children with ADHD, mentioned
earlier. Assessment information is integrated into a formulation that is
used for treatment planning as illustrated in the case study of conduct
disorder described earlier. This should link predisposing, precipitating
and maintaining factors to the young person’s behavioural problems
and specify protective factors that may be drawn on during treatment. A
general clinical formulation model for conduct disorder and oppositional
defiant disorder is given in Figure 2.4.

Intervention
The material covered earlier in this chapter makes it clear that conduct
problems are complex. Personal genetic, neurobiological and psycho-

Figure 2.4 General formulation model for conduct disorder and oppositional defiant disorder

Book 1.indb 66 06/03/2012 13:47

 2 • CHILDHOOD BEHAVIOUR DISORDERS 67

logical characteristics of children and adolescents, and psychosocial

factors within the family and the wider system, may predispose young-
sters to develop conduct problems. Once these develop, they may
remain confined to the home in the case of oppositional defiant disorder
or spread to the community in the case of conduct disorder. The degree
to which conduct problems escalate depends on the degree to which
there are problem-maintaining factors within the individual, family,
school and peer group. Despite their complexity, conduct problems are
not completely refractory to treatment. Available evidence from empiri-
cal studies permits treatments of choice to be identified for preadoles-
cent behaviour problems and more pervasive difficulties in adolescence.
For circumscribed conduct problems, typical of children with oppo-
sitional defiant disorder, behavioural parent training is currently the
treatment for which there is greatest empirical support. In a meta-
analysis of over 70 studies, McCart et al. (2006) found that for children
under 12, parent training programmes were significantly more effective
than child-focused programmes. Behavioural parent training involves
coaching parents to target and reinforce their children’s prosocial
behaviour while extinguishing their antisocial behaviour (Forgatch &
Patterson, 2010; Webster-Stratton & Reid, 2010).
For pervasive conduct problems, typical of children with conduct
disorder, family therapy, multisystemic therapy and treatment foster
care are currently the treatments for which there is greatest empirical
support (Carr, 2009b). Family therapy involves helping parents,
adolescents and other family members develop patterns of interaction
that promote prosocial behaviour, better communication and family
problem-solving, and for conduct problems functional family therapy is
one of the approaches with a particularly strong evidence base (Sexton
& Alexander, 2003). Multisystemic therapy extends beyond the family
and includes intervention in the school and peer group and also at the
individual level, so that problem-maintaining factors in all of these
systems are modified (Henggeler & Schaeffer, 2010). Multisystemic
intervention may also involve addressing parents’ personal difficulties
such as depression or alcohol problems.
Where parents’ personal difficulties are too severe to permit them to
engage effectively in multisystemic treatment, treatment foster care is
the intervention of choice (Smith & Chamberlain, 2010). Here, the
conduct disordered youngster is placed with a specially trained foster
family who work collaboratively with the child’s natural parents in
implementing a behavioural programme that allows the youngster to
develop prosocial behaviour and disengage from patterns of antisocial
behaviour.
With respect to service development, it may be most efficient to offer
services for adolescent conduct disorder on a continuum of care (Carr,
2009a). Less severe cases may be offered family therapy. Moderately
severe cases and those that do not respond to circumscribed family
interventions may be offered multisystemic therapy. Extremely severe
cases and those that are unresponsive to intensive multisystemic
therapy may be offered treatment foster care. These conclusions are

Book 1.indb 67 06/03/2012 13:48

 68 C L I N I C A L P S Y C H O L O G Y : A N I N T R O D U C T I O N

consistent with international best practice guidelines (American Aca-

demy of Child and Adolescent Psychiatry, 2007b; NICE, 2006a).
There are many other treatments for conduct disorders besides
those highlighted in this chapter. Some are empirically untested so we
do not know if they are effective. Some have been tested and found to
be ineffective. And most importantly, there are those treatments that
have been tested and found to be harmful. There is now considerable
evidence that intervention programmes that bring youngsters with
conduct disorders together in groups lead to an increase in conduct
problems (Dishion & Dodge, 2005). This contamination process may
occur because youngsters reinforce each other’s deviant behaviour and
share a commitment to a deviant set of values and ideology. The fact
that interventions that aggregate conduct-disordered youngsters are
harmful unfortunately has not had a major impact on policies for dealing
with juvenile delinquents. Many delinquents are assessed and treated
in group-based residential settings. Such policies exacerbate rather
than ameliorate conduct problems.

Controversies
There are many controversies in the scientific study, assessment and
treatment of psychological problems in children and adolescents.

Dimensions or categories
With regard to scientific study, there is controversy over whether children’s
abnormal behaviour is best conceptualized in dimensional or categorical
terms. While the DSM and ICD diagnostic systems are clearly based
on a categorical conceptualization of children’s psychological difficulties,
most empirical studies point to the validity of dimensional models. For
example, factor analytic studies consistently show that common childhood
difficulties fall on the two dimensions of internalizing and externalizing
behaviour problems, which are normally distributed within the population
(Achenbach, 2009).
Children with diagnoses of oppositional defiant disorder, conduct dis-
order and ADHD represent a subgroup of cases with extreme external-
izing behaviour problems, while those with anxiety or depressive
disorders have extreme internalizing behaviour problems (Carr, 2006a).
Similarly, children with a diagnosis of intellectual disability fall at the
lower end of the continuum of intelligence, a trait is normally distributed
within the population (Carr et al., 2007). The dimensional approach is
clearly more scientifically valid than a categorical approach, and has the
potential to be less stigmatizing. On the other hand, categorical diag-
noses such as ADHD create a focus for pressure groups whose inter-
ests are served by reifying psychological difficulties as ‘psychiatric
illnesses’.

Book 1.indb 68 06/03/2012 13:48

 2 • CHILDHOOD BEHAVIOUR DISORDERS 69

Are psychological problems really ‘psychiatric illnesses’?

This brings us on to the area of assessment, in which there is a
controversy over whether ADHD, conduct disorder and other DSM and
ICD diagnoses are ‘real psychiatric illnesses’, invalid fabrications, or
spurious social constructions (Kutchins & Kirk,1999). Those who argue
that they are invalid fabrications point to the evidence for the
dimensionality of childhood psychological problems. Those who argue
that they are spurious social constructions point to the interests that are
served by defining them as ‘real psychiatric illnesses’.
Parents, health and educational professionals, the pharmaceutical
industry and society at large may all, in certain circumstances, derive
benefits from conceptualizing children’s psychological problems as ‘real
psychiatric illnesses’. For example, parents or schools may have
difficulty meeting children’s needs for intellectual stimulation, nurturance
and clear limit-setting, and so children in their care become aggressive
and disruptive. In response these parents or educational professionals
may prefer children in their care to receive a diagnosis of ADHD and a
prescription for stimulant therapy, rather than exploring ways to better
meet the children’s needs for intellectual stimulation, nurturance and
clear limit-setting. In such instances pharmaceutical companies may
support the diagnosis of ADHD, because they may stand to gain
financially from offering a pharmacological treatment for behaviour
problems.

Should treatment focus on the child or the context?

This brings us to controversies concerning the treatment of psychological
problems in children and adolescents. If children’s difficulties are
conceptualized as individual ‘psychiatric illnesses’, there is a risk that
the predominant focus for treatment will be on the individual child rather
than on the broader social context within which the child lives. That is,
the main emphasis will be on treating children’s problems with
medication and individual therapy to modify the ‘illness inside the child’,
with less emphasis on addressing important risk factors within the
child’s family, school and wider social context.
In the cases of oppositional defiant disorder and conduct disorder
this is particularly problematic, since the major risk factors that can
effectively be addressed in treatment are social, through interventions
such as parent training, family therapy, MST and treatment foster care.
In the case of ADHD, the strong emphasis on medication is problematic
because its effects are time limited to about 3 years (Swanson & Volkow,
2009). Also, stimulant medication may adversely affect growth and
cardiovascular functioning and lead to a variety of somatic complaints
including loss of appetite, headaches, insomnia and tics, which occur in
5–12% of cases (Breggin, 2001; Paykina et al., 2007; Rapport & Moffitt,
2002).

Book 1.indb 69 06/03/2012 13:48

 70 C L I N I C A L P S Y C H O L O G Y : A N I N T R O D U C T I O N

Summary
A wide variety of psychological problems may occur in child-
hood. This chapter focused on disruptive behaviour disorders,
which include ADHD, oppositional defiant disorder and con-
duct disorder. ADHD is characterized by inattention, hyperac-
tivity and impulsivity. The median prevalence rate for ADHD in
international epidemiological studies is 2.7%. Comorbid devel-
opmental language delays, specific learning difficulties, elimi-
nation disorders, conduct disorders and emotional disorders
are quite common. A poor outcome occurs for about a third of
cases who typically have secondary conduct and academic
problems.
ADHD is a one of the most heritable psychological disor-
ders. Extreme levels of overactivity and executive function
deficits, which are polygenetically determined, probably inter-
act with environmental factors (either intrauterine or psychoso-
cial) to give rise to the clinical syndrome of ADHD. Individuals
with ADHD show structural and functional neuroanatomical
abnormalities of the frontostriatal circuitry, which subserves
executive function, and the cerebellum, which subserves tem-
poral information processing. They also show a dysregulation
of the dopamine and noradrenergic and adrenergic systems.
Adjustment problems shown by youngsters with ADHD are in
part maintained by problematic relationships within the family,
school and peer group. Multimodal treatment includes behav-
ioural parent training, school-based contingency management,
self-regulation skills training, dietary control where food intoler-
ance is present, and stimulant therapy. In addition assessment
and treatment of comorbid problems may be required.
A distinction is made between oppositional defiant disorder
and conduct disorder, with the former reflecting a less perva-
sive disturbance than the latter; the central feature of both is
antisocial behaviour. The median prevalence rate for both
oppositional defiant disorder and conduct disorder in interna-
tional epidemiological studies is 3.7%. Children with conduct
problems are a treatment priority because the outcome for
more than half of these youngsters is very poor in terms of
criminality and psychological adjustment. In the long term the
cost to society of unsuccessfully treated conduct problems is
enormous.
Comorbidity for conduct disorders and both ADHD and emo-
tional problems such as anxiety and depression is very high,
particularly in clinical populations. Three classes of risk factor
increase the probability that conduct problems in childhood or
adolescence will escalate into later life difficulties:

Book 1.indb 70 06/03/2012 13:48

 2 • CHILDHOOD BEHAVIOUR DISORDERS 71

personal biological and psychological characteristics, problem-

atic parenting practices, and family disorganization. Biological
theories have focused on the roles of genetic factors, neurobio-
logical deficits, neurotransmitter dysregulation, neuroendocrine
factors, arousal levels, temperament, and neuropsychological
deficits in the aetiology of conduct problems. Classical psycho-
analytic theory points to superego deficits and attachment
theory points to insecure attachment in the development of
conduct disorders. Problems with social information processing
and social skills deficits are the principal factors highlighted in
cognitive theories of conduct problems.
Modelling and coercive family processes have been identi-
fied by social learning theory as central to the development and
maintenance of conduct difficulties. Systems theories highlight
the role of characteristics of family systems, broader social
network systems and societal systems in the aetiology and
maintenance of conduct problems, with oppositional defiant
disorders in pre-adolescent children whose problems are con-
fined to the home, behavioural parent training is the treatment
of choice. With older children and adolescents who present
with pervasive conduct problems, family therapy, multisystemic
therapy and treatment foster care are currently the treatments
for which there is greatest empirical support, and these may be
offered on a continuum of care depending on problem severity.
There is controversy over whether children’s abnormal
behaviour is best conceptualized in dimensional or categorical
terms. There is also controversy over whether DSM and ICD
diagnoses are ‘real psychiatric illnesses’, invalid fabrications or
spurious social constructions. Finally there is controversy over
whether children’s psychological problems are most usefully
conceptualized as individual ‘psychiatric illnesses’ or as aspects
of the broader social context within which the child lives.

Questions
● What are the main psychological disorders that occur in childhood?
● What are the main clinical features of ADHD, oppositional defiant
disorder and conduct disorder?
● How prevalent are the disruptive behaviour disorders?
● What are the main biological and psychological theories of disruptive
behaviour disorders and the main research findings relevant to
these theories?
● What are the main evidence-based approaches to the assessment
and treatment of disruptive behaviour disorders?
● Do you think it’s useful to conceptualize children’s behaviour
problems as ‘psychiatric illnesses’?

Book 1.indb 71 06/03/2012 13:48

 72 C L I N I C A L P S Y C H O L O G Y : A N I N T R O D U C T I O N

FURTHER READING
Professional
● Carr, A. (2006). Handbook of child and adolescent clinical psychology: A
contextual approach (second edition). London: Routledge.
● Weisz, J. & Kazdin, A. (2010). Evidence-based psychotherapies for chil-
dren and adolescents (second edition). New York: Guilford Press.

Self-help
● Barkley, R. (2000). Taking charge of ADHD: the complete authoritative
guide for parents (revised edition). New York: Guilford.
● Forehand, R. & Long, N. (1996). Parenting the strong-willed child: The
clinically proven five week programme for parents of two to six year olds.
Chicago: Contemporary Books.
● Forgatch, M. & Patterson, G. (1989). Parents and adolescents living to-
gether. Part 1. The basics. Eugene, OR: Castalia.
● Forgatch, M. & Patterson, G. (1989). Parents and adolescents living to-
gether. Part 2. Family problem solving. Eugene, OR: Castalia.

WEBSITES
● AACAP (American Academy of Child and Adolescent Psychiatry) prac-
tice parameters for the treatment of ADHD, conduct disorder and oppo-
sitional defiant disorder:
www.aacap.org/cs/root/member_information/practice_information/
practice_parameters/practice_parameters
● Achenbach System of Empirically Based Assessment (ASEBA):
www.aseba.org
● Incredible Years Programme:
www.incredibleyears.com
● NICE (National Institute for Clinical Excellence) guidelines for treating
ADHD:
http://guidance.nice.org.uk/topic/mentalhealthbehavioural
● Parents Plus Programme:
www.parentsplus.ie
● Parent–Child Interaction Therapy:
http://pcit.phhp.ufl.edu
● Strengths and Difficulties Questionnaire (SDQ):
www.sdqinfo.com

Book 1.indb 72 06/03/2012 13:48

 Eating disorders 3
Learning objectives
After studying this chapter you will be able to:
● give an account of the main clinical features of
anorexia and bulimia nervosa
● summarize the epidemiology of eating disorders
● list the risk factors for eating disorders
● outline the main biological and psychological
theories of eating disorders
● name the main evidence-based approaches to
assessment and treatment of eating disorders.

Introduction
Anorexia nervosa and bulimia nervosa are the main eating disorders of
concern in clinical psychology. They typically first occur during
adolescence. In both conditions there is an overevaluation of body
shape and weight, with self-worth being judged almost exclusively in
terms of these personal attributes. With anorexia, the primary feature is
the maintenance of a very low body weight, whereas with bulimia the
main feature is a cycle of binge eating and self-induced vomiting or
other extreme weight control measures including dieting, excessive
exercise, and laxative use. Diagnostic criteria for these two eating
disorders are given in Table 3.1.
Eating disorders are of concern because they are dangerous (Klump
et al., 2009; Mitchell & Crow, 2010). In chronic cases they lead to many

Book 1.indb 73 06/03/2012 13:48

 74 C L I N I C A L P S Y C H O L O G Y : A N I N T R O D U C T I O N

TABLE 3.1
Diagnostic criteria for anorexia and bulimia nervosa
DSM-IV-TR ICD-10
Anorexia nervosa
A. Refusal to maintain body weight at or above For a definitive diagnosis the following are required:
a minimally normal weight for age and A. Body weight is maintained at least 15% below that
height (weight loss or failure to gain weight expected (either lost or never achieved) or a
in a growth period leading to body weight Quetelet’s body mass index of 17. 5 or less (BMI =
less than 85% of that expected). weight (kg)/(height (m)2). Prepubertal patients may
B. Intense fear of gaining weight or becoming show failure to make the expected weight gain during
fat even though underweight. the period of growth.
C. Disturbance in the way in which one’s body B. The weight loss is self-induced by the avoidance of
weight or shape is experienced, undue fattening foods, self-induced vomiting, self-induced
influence of body weight or shape on self- purging, excessive exercise, use of appetite
evaluation, or denial of seriousness of the suppressants or diuretics.
current low body weight. C. There is a body image distortion in the form of a specific
D. In postmenarcheal females, amenorrhea psychopathology whereby a dread of fatness persists
(the absence of at least three consecutive as an intrusive, overvalued idea and the patient
menstrual cycles). imposes a low weight threshold on himself or herself.
Specify restricting type or binge eating–purging D. A widespread endocrine disorder involving the
type. hypothalamic–pituitary–gonadal axis is manifest in
women as amenorrhea and in men as a loss of sexual
interest and potency. There may also be elevated
levels of growth hormone, raised cortisol levels,
changes in the peripheral metabolism of the thyroid
hormone and abnormalities of insulin secretion.
E. If the onset is prepubertal, the sequence of pubertal
events is delayed or arrested (growth ceases; in girls
breasts do not develop and there is a primary
amenorrhea; in boys the genitals remain juvenile).
With recovery, puberty is often completed normally but
the menarche is late.
Bulimia nervosa
A. Recurrent episodes of binge eating. An For a definitive diagnosis all of the following are required:
episode of binge eating is characterized by A. There is a persistent preoccupation with eating and an
both of the following: irresistible craving for food; the patient succumbs to
1. Eating in a discrete period of time (e.g. episodes of overeating in which large amounts of food
within a 2 hour period) an amount of food are consumed in short periods of time.
that is definitely larger than most people B. The patient attempts to counteract the fattening effects
would eat during a similar period of time of food by one or more of the following: self-induced
and under similar circumstances. vomiting; purgative abuse; alternating periods of
2. A sense of lack of control over eating starvation; use of drugs such as appetite
during the episode (e.g. a feeling that one suppressants, thyroid preparations or diuretics. When
cannot stop eating or control what or how bulimia occurs in diabetic patients they may choose to
much one is eating). neglect their insulin treatment.
B. Recurrent inappropriate compensatory C. The psychopathology consists of a morbid dread of
behaviour in order to prevent weight gain, fatness and the patient sets herself or himself a
such as self-induced vomiting; misuse of sharply defined weight threshold, well below the
laxatives, diuretics, enemas, or other premorbid weight that constitutes the optimum or
medications; fasting or excessive exercise. healthy weight in the opinion of the physician. There is
C. The binge eating and inappropriate often but not always a history of an earlier episode of
compensatory behaviours both occur, on anorexia nervosa, the interval between the two
average, at least twice a week for 3 months. disorders ranging from a few months to several years.
D. Self-evaluation is unduly influenced by body This earlier episode may have been fully expressed or
shape and weight. may have assumed minor cryptic form with a
E. The disturbance does not occur exclusively moderate loss of weight and/or a transient phase of
during episodes of anorexia nervosa. amenorrhea.
Specify purging or non-purging type.

Note: Adapted from DSM-IV-TR (APA, 2000) and ICD-10 (WHO, 1992).

Book 1.indb 74 06/03/2012 13:48

 3 • EATING DISORDERS 75

medical complications including growth retardation, osteoporosis, gas-

trointestinal bleeding, dehydration, electrolyte abnormalities and cardiac
arrest. The mortality rate among women with anorexia is 12 times that
of the normal population, and eating disorders are associated with a
raised suicide risk. It is ironic in our western industrial culture, where
food is plentiful, that self-starvation and a pattern of bingeing and
purging are major problems affecting teenage girls.
In this chapter, after considering the classification, epidemiology and
clinical features of eating disorders, a variety of theoretical explanations
concerning their aetiology will be considered along with relevant empir-
ical evidence. Some comments on assessment and treatment will also
be made.

Case study of anorexia nervosa

Mar, a 14-year-old girl, was referred for treatment because her weight
had fallen continuously since she was about 12 years old. When
assessed she was 5 stone 11 pounds (37 kg) in weight and 5 feet
2 inches (1.57 m) tall. The normal weight range for a 14-year-old girl is
6 stone 8 pounds to 9 stone. Mar had a body mass index (BMI) of 15,
which is at the first percentile and significantly below the normal range.
BMI is an index of thinness which is calculated by dividing weight in
kilograms by height in metres squared. The normal range for BMI is
18.5–24.9. Mar had amenorrhea, a highly restrictive eating pattern of 2
years’ duration and a daily routine involving episodes of intensive
exercise. She had gone through an episode of self-induced vomiting
after mealtimes and occasional bingeing for about three months, but
this had ceased a year previously.

Presentation
In the intake interview Mar expressed a fear of becoming fat and said
she experienced her hips, buttocks, stomach and thighs to be consider-
ably larger than their actual size. That is, she had a distorted body
image, believing herself to be markedly larger than her actual size. She
continually ruminated about food and the number of calories associated
with each aspect of her diet. Her mood was generally low, and she had
on occasion experienced suicidal thoughts, but had never had frank
suicidal intentions. On the Eating Disorder Inventory (Garner, 2005),
Mar obtained extreme scores on the drive for thinness, body dissatis-
faction, ineffectiveness, perfectionism, and maturity fear subscales.
Mar held a range of rigid beliefs about the importance of controlling her
body shape.

Developmental history
Mar’s personal developmental history was within normal limits. Her
language and cognitive development had been advanced and Mar had
always been in the top 10% of her class in school for academic subjects.

Book 1.indb 75 06/03/2012 13:48

 76 C L I N I C A L P S Y C H O L O G Y : A N I N T R O D U C T I O N

Within the family, she was described by her parents, Roddy and Maggie,
as a model child. Mar had no previous behavioural or emotional
problems. She had good peer relationships and a circle of about four to
six good friends in her neighbourhood. The transition to secondary
school had been uneventful, as had her menarche.
Mar continued to do as well in secondary school as she had in
primary school, but towards the end of her first year she became
despondent about her weight. As a young teenager she was, according
to her mother, ‘well built’. Mar began dieting shortly before her 13th
birthday. She believed that she was not fitting in with her friends, who
by now were going to discos and beginning to take an interest in boys.
Her mother’s view was that she had been hurt by some critical comments
made by girls at her school about her weight.

History of the presenting problem

What began as normal dieting, which was supported wholeheartedly by
her parents, gradually became more and more intense around the time
that Bev, Mar’s older sister, went to college and her younger brother
Nick began school. Also, at that time there was increased conflict
between Maggie and Seamus (Bev’s father and Maggie’s first husband).
Most of the arguments were about financing Bev during her time at
college. Maggie and Seamus had separated when Bev was young, and
Bev had had little contact with her father since then. However, because
of the family’s limited financial resources, Maggie had asked Seamus to
help with supporting Bev through college. It was about this issue that
the conflict had arisen. Mar was a sensitive girl and worried about the
effect of this conflict on her mother.
Shortly after she started dieting, Mar began to lose weight rapidly,
and changed from being ‘well built’ to being quite slim. After about year
of dieting (and a year before the intake interview), Roddy, quite by
accident, had found Mar vomiting behind the toilet block when the family
were on holiday on a campsite. Maggie and Roddy were shocked by
this. They had seen programmes about bulimia on TV and knew that
secretive vomiting was a sign of an eating disorder. Mar said she had a
stomach upset, and denied that her vomiting was motivated by a fear of
fatness.
After the holiday, she was taken to the family doctor by the parents
for an assessment of her dieting and vomiting problems. The doctor
said that Mar had a mild eating problem, but provided she stopped
dieting all would be well. He saw her regularly over the course of the 12
months prior to a multidisciplinary assessment. During that period, he
advised the parents to take a low-key approach and encouraged Mar to
eat a healthy balanced diet and avoid bingeing and vomiting. He
impressed on her the dangers of developing an electrolyte imbalance
and cardiac problems if she persisted with the bulimic pattern. Mar
stopped the bulimic pattern but continued with dieting. Her weight
continued to fall drastically and her periods stopped about four months
before the assessment.

Book 1.indb 76 06/03/2012 13:48

 3 • EATING DISORDERS 77

Roddy and Maggie did not know what to do to stop this fanatical
dieting, so they tried a few different things. Maggie, who loved to cook,
made increasingly sumptuous meals to try to tempt Mar away from her
diet. She took a softly-softly approach, never raising her voice and
never being harsh or punitive. She looked to her mother, Mrs Fox, for
support and gradually felt more and more guilt. She was convinced that
the eating problem was a reflection on some mistake she had made as
a parent, and ruminated about this and the effects on Mar of her conflict
with Seamus. Roddy left the management of Mar’s eating problem to
Maggie, although occasionally he tried to convince Mar to eat. These
conversations usually ended in a heated argument, with Roddy shouting
at Mar and telling her she was breaking her mother’s heart, and then
storming out of the room.
Because Roddy’s attempts to get Mar to eat had been stressful and
unsuccessful, he had gradually stopped trying to encourage Mar to eat.
Mealtimes had become a nightmare, according to Roddy. He said he
now frequently played a round of golf after work and afterwards ate a
bar-meal at the golf club with his brother Mel.

Family history
Mar lived with her mother, Maggie, her father, Roddy, and her younger
brother, Nick, aged 7. Her older sister, Bev, aged 20, had moved out
2 years previously to go to college. Roddy’s brother and three sisters
and Maggie’s two brothers were all married with children, none of whom
had any significant psychological problems or eating disorders. Maggie’s
two brothers tended to deny the reality of Mar’s problem or to say it was
something she would grow out of. Roddy’s brother saw Mar’s behaviour
as defiance that required strict discipline. Roddy’s sisters thought that it
was a personal problem and that she might be depressed about
something.

Formulation
Mar was a 14-year-old girl who presented with anorexia nervosa and a
history of bulimia, the onset of which was precipitated by Mar’s entry into
adolescence, critical comments made by peers about her weight and
increased family stress. This stress was associated with her half-sister’s
move to college, conflict between her mother and her half-sister’s father,
and her younger brother’s entry into primary school. Mar’s personality
profile and weight-related issues predisposed her to developing ano-
rexia. She had a history of being ‘well-built’, was dissatisfied with her
weight and in adolescence had dealt with this initially through dieting and
later through a bulimic pattern of vomiting when she believed she had
overeaten. Her attempts at weight control were excessive because of
her personality profile. She was perfectionistic, but also believed herself
to be ineffective and so strived excessively to achieve her ideal weight.
Mar’s restrictive eating was maintained at an interpersonal level by
the inconsistent way in which her parents managed her refusal to eat a

Book 1.indb 77 06/03/2012 13:48

 78 C L I N I C A L P S Y C H O L O G Y : A N I N T R O D U C T I O N

Figure 3.1 Formulation of a case of anorexia nervosa

normal diet and maintain a normal body weight. Mar’s anorexia was
maintained at an intrapsychic level by her distorted body image, maturity
fears and need for control coupled with a sense of being powerless. It
was also maintained by the rigid thinking, obsession with food and
difficulty taking a normal perspective that accompanies the starvation
process. Important protective factors were the parents’ commitment to
engaging in family treatment, the availability of Mar’s supportive peer
group, who wanted her to recover and rejoin them, and Mar’s high
intelligence. This formulation is diagrammed in Figure 3.1.

Treatment
Mar and her family participated in outpatient family therapy for 6 months.
In the first stage Maggie and Roddy took responsibility for refeeding Mar
and helping her attain a normal body weight. Once she attained a body
weight in the normal range, she was encouraged to take control of her
diet and weight. This was monitored by the therapy team on a weekly
basis. Provided Mar did not fall below a BMI of 19, her parents agreed not
to interfere in the self-management of her diet and weight.
In the middle phase of therapy the focus was on helping the family
arrange for Mar to develop age-appropriate routines, pastimes and
responsibilities with increasing autonomy and privacy. Mar rekindled
her relationships with her friends, developed an interest in creative

Book 1.indb 78 06/03/2012 13:48

 3 • EATING DISORDERS 79

writing and began to go to dances and concerts, like a normal teenager.

The final phase of therapy helped the family anticipate situations where
relapses might occur and plan ways to manage such situations. Mar
continued to maintain a normal body weight after treatment, but
remained slim. She was very careful about her diet and exercise, so as
to avoid becoming overweight.

Epidemiology, course and outcome

Anorexia nervosa and bulimia nervosa are most common among female
adolescents and young women (Hoek, 2006; Keel, 2010). About 1–2%
of the adolescent and young adult female population suffer from eating
disorders. Anorexia is less common than bulimia. The average preva-
lence rates for anorexia nervosa and bulimia nervosa among young
females are about 0.3–0.5% and 1–4% respectively. The onset for ano-
rexia usually occurs in adolescence, and the peak age of onset for
bulimia is in later adolescence or young adulthood. Community studies
show that, contrary to earlier data from clinical studies, there is not a
significant relationship between eating disorders and social class.
Since 1960 there has been an increase in the incidence of eating
disorders in the UK and the USA, largely accounted for by increases in
rates of bulimia rather than anorexia. Since the 1990s in the UK, rates
of bulimia have begun to decline (Currin et al., 2005). While eating
disorders may be more common in western industrialised countries,
there is growing evidence of eating disorders in non-westernised
cultures. In clinical rather than community populations, anorexia nervosa
is commonly comorbid with mood and obsessive compulsive disorders,
while bulimia nervosa is commonly comorbid with drug abuse and
borderline personality disorder.
The outcome for eating disorders is poor for a significant minority of
cases (Steinhausen, 2002; Stice, 2002), but can be improved with early
intervention and evidence-based treatment (American Psychiatric
Association, 2006; NICE, 2004a). For anorexia nervosa about half of all
cases have a good outcome, a third have moderate outcome and a fifth
have a poor outcome. At 20-year follow-up, the mortality rate is about 6%
(with a range of 0–21% across studies). Starvation and suicide are the
primary causes of death. A poor prognosis is associated with lower
weight, a more chronic condition, the absence of a clear precipitating
stressful life event, bulimic symptoms, comorbid obsessive compulsive
disorder, problematic family relationships, dropping out of treatment and
lower social class. For bulimia nervosa about half of all cases have a
good outcome, a quarter have a moderate outcome and the remaining
quarter have a poor outcome. A poor prognosis in bulimia is associated
with later onset, a more chronic condition, more frequent bingeing and
vomiting, greater body dissatisfaction, higher perfectionism, comorbid
substance abuse, impulsive personality disorders, and lower social class.
Risk factors identified in an extensive review of longitudinal and
cross-sectional studies for eating disorders are given in Table 3.2
(Jacobi et al., 2004).

Book 1.indb 79 06/03/2012 13:48

 80 C L I N I C A L P S Y C H O L O G Y : A N I N T R O D U C T I O N

TABLE 3.2
Risk factors for eating disorders
Risk factors common to anorexia Risk factors unique to Risk factors unique to
and bulimia nervosa anorexia nervosa bulimia nervosa
Female Preterm birth/Birth trauma Childhood obesity
Adolescent Infant feeding and sleep Social phobia in
problems adolescence
Genetic factors High-concern parenting in Parental criticism
early childhood about weight, high
expectations and low
contact in adolescence
Pregnancy complications Obsessionality (OCD, Parental obesity in
OCPD) in adolescence adolescence
Child sexual abuse Perfectionism in Parental depression,
adolescence drug and alcohol abuse
in adolescence
Physical neglect in childhood Weight subculture
(dancer, model, athlete)
Gastrointestinal problems, picky eating and Acculturation
eating conflicts in childhood
Childhood anxiety disorder
Stressful life events in childhood and
adolescence
Weight concerns and dieting in adolescence
Low social support in adolescence
Low self-esteem
Ineffectiveness
Low interoception (difficulty interpreting internal
gastrointestinal and emotional stimuli)
Avoidant coping

Note: Based on C. Jacobi, C. Hayward, M. de Zwaan, H. C. Kraemer, & W. S. Agras (2004). Coming to terms with risk
factors for eating disorders: Application of risk terminology and suggestions for a general taxonomy. Psychological
Bulletin, 130, 19–65.

Clinical features
Historically anorexia nervosa was first described in modern medical
literature by Charles Lasègue in France in 1873 and by Sir William Gull
in the UK in 1874, and it was Gull who first used the term ‘anorexia
nervosa’. Both Lasègue and Gull described anorexia as a condition
characterized by emaciation, an inadequate and unhealthy pattern of
eating, and an excessive concern with the control of body weight and
shape. Attempts at subclassifying eating disorders led to the
establishment of bulimia nervosa as a separate diagnosis from anorexia
in 1979 by Gerard Russell in the UK. In the classification of eating
disorders in both DSM-IV-TR (American Psychiatric Association, 2000)
and ICD-10 (World Health Organization, 1992), this distinction between
anorexia nervosa and bulimia nervosa is a central organizing principle,
with the former being characterized primarily by weight loss and the
latter by a cyclical pattern of bingeing and purging.

Book 1.indb 80 06/03/2012 13:48

 3 • EATING DISORDERS 81

The distinction, while descriptively useful, does not take full account
of variations in eating problems seen in clinical practice. Many anorexic
clients present with bulimic symptoms and many bulimic clients develop
anorexia. The DSM contains a category – eating disorders not otherwise
specified – for the many ‘mixed cases’ seen in clinical practice that do
not meet the criteria for either anorexia or bulimia.
Eating disorders are characterized by distinctive clinical features in
the domains of behaviour, perception, cognition, emotion, social
adjustment and physical health (Agras, 2010). At a behavioural level,
restrictive eating is typical of anorexia. Clients report low calorific intake
and eating low-calorie foods over a significant time period. They may
cook for the family but not eat meals they prepare. Clients with anorexia
present as thin or emaciated. They may wear baggy clothes to conceal
the extent of their weight loss.
In contrast, clients with bulimia are typically of normal weight. A cycle
of restrictive eating, bingeing and compensatory behaviours is typical of
bulimia. These compensatory behaviours may include vomiting, using
diuretics and laxatives or excessive exercising. Usually particular types
of situation that are interpreted as threatening or stressful lead to a
negative mood state and precipitate bouts of bingeing. Such situations
include interpersonal conflicts, isolation, and small violations of a strict
diet such as eating a square of chocolate. Bingeing may also arise from
alcohol intoxication.
While bingeing brings immediate relief, it also leads to physical
discomfort and to guilt for not adhering to a strict diet. Purging relieves
both guilt and physical discomfort but may also induce shame and fear
of negative consequences of the binge–purge cycle. Relatives who live
with bulimic clients may describe specific routines they have developed
to conceal their vomiting and excessive exercise, for example running
the shower in the bathroom to mask the sound of them vomiting. In
addition to abnormal eating patterns, clients with eating disorders –
especially bulimia – may display a variety of self-destructive behaviours
including self-injury, suicide attempts and drug abuse. These behaviours
are often construed as self-punishments for not living up to perfectionistic
standards or attempts to escape from conflicts associated with self-
worth and individuation.
With respect to perception, in most clinical cases of eating disorder
there is a distortion of body image. The client perceives the body or
parts of the body such as the stomach, buttocks or thighs to be larger
than they are. People with eating disorders may also have low
interoception; that is, difficulty interpreting internal gastrointestinal and
emotional stimuli. This makes it difficult for them to know when it’s
appropriate to start and stop eating, and how to interpret their feelings
and emotions.
With respect to cognition, there is a preoccupation with food that is a
consequence of dietary restraint. Low self-esteem and low self-efficacy
are also common. Thus, many clients with eating disorders view them-
selves as worthless and powerless, and see achieving a slim body
shape and low body weight through dietary restraint as the route to an

Book 1.indb 81 06/03/2012 13:48

 82 C L I N I C A L P S Y C H O L O G Y : A N I N T R O D U C T I O N

increased sense of control over their lives and increased self-worth.

This process is often compounded by perfectionist tendencies and a
wish to attain exceptionally high standards. In bulimia, the repeated fail-
ure to sustain low-calorie intake leads to further self-criticism, and low
self-esteem and also strengthens the belief in lack of control. In ano-
rexia, starvation directly affects cognitive processes. There is an
increasing rigidity and inflexibility in thinking style and a gradual reduc-
tion in the capacity to concentrate. In all eating disorders, there may be
conflict concerning dependence and maturity. On one hand there may
be a fear of maturity and independence; on the other there may be a
wish to escape from parental control and the lack of autonomy and pri-
vacy that this entails.
With regard to emotional state, clients with eating disorders report an
intense fear of fatness. In anorexia, low mood may arise from a failure
to live up to perfectionist standards, and improvements in mood may
occur when the urge to eat is resisted. In bulimia depressed or irritable
mood may occur as a result of dietary restraint, or in response to life
stresses. Such episodes of low mood lead to bingeing, which brings
temporary relief. However, after binges, low mood may occur as a result
of the sense of failure that this entails. Suicide attempts occur in up to
20% of patients with anorexia and 25% of those with bulimia (Franko &
Keel, 2006). Suicidality in eating disorders is associated with depression,
substance abuse, and a history of child physical and sexual abuse.
With respect to interpersonal adjustment, withdrawal from peer
relationships, deterioration in family relationships, and poor educational
or vocational performance may all occur as a result of eating problems.
The health complications of anorexia involve an endocrine disorder
affecting the hypothalamic–pituitary–gonadal axis. This leads to amen-
orrhea; starvation symptomatology such as reduced metabolic rate,
bradycardia, hypotension, hypothermia, and anaemia; lanugo hair on
the back; delayed gastric emptying; electrolyte abnormalities; renal dys-
function; and zinc deficiency. In bulimia, erosion of dental enamel may
occur due to vomiting. Lesions on the back of the dominant hand may
develop if the hand is used to initiate vomiting. With both anorexia and
bulimia a particularly serious concern is that the client may develop
electrolyte abnormalities that may lead to a fatal arrhythmia.

Aetiological theories
Under normal circumstances hunger motivates people to eat until they
have the experience of ‘being full’ and most of the time their weight is
remarkably stable, as if homostatically governed. When people try to
slim through restrained eating, they experience chronic hunger and
negative affect, and become preoccupied with food. In response to
these negative experiences, most people give up dieting and return to
their usual eating habits and normal body weight. People who develop
anorexia, however, redouble their efforts to maintain a pattern of
restrained eating when they experience hunger, negative affect and
intense food preoccupation. In contrast, people who develop bulimia

Book 1.indb 82 06/03/2012 13:48

 3 • EATING DISORDERS 83

engage in bingeing when the negative effects of restrained eating and

life stresses make them feel bad, and later engage in compensatory
purging. Biological, psychodynamic, cognitive-behavioural and systemic
theories have been developed to explain the aetiology, course and
treatment of eating disorders.

Biological theories
Hypotheses have been proposed to explain the role of a number of
biological factors in the development and course of eating disorders.
These have focused on genetics, mood dysregulation and starvation-
related processes. Genetic and mood dysregulation hypotheses posit a
role for each of these factors in the aetiology of eating disorders, while
starvation theories are concerned primarily with the way in which the
biological sequelae of self-starvation contribute to the maintenance of
abnormal eating patterns.

Genetics
The genetic hypothesis proposes that a biological predisposition to
eating disorders is genetically transmitted and that individuals with this
predisposition when exposed to certain environmental conditions
develop an eating disorder. Evidence from twin and family studies
shows unequivocally that genetic predisposing factors contribute mod-
erately to the aetiology of eating disorders, and that they are 50–
83% heritable (Klump et al., 2009; Wade, 2010). Positive findings from
candidate gene studies focusing on serotonin, dopamine and other
neurotransmitter systems and on genes involved in body weight regula-
tion have not been substantiated in meta-analyses (Scherag et al.,
2010).
There is some evidence that appetite and satiety dysregulation
renders people vulnerable to the development of eating disorders, and
that this vulnerability may be polygenetically determined (Stice et al.,
1999). Collier and Treasure (2004) propose that genetic factors
contribute to temperamental dispositions that underpin the development
of personality traits associated with eating disorders. These may be
conceptualized as falling along a continuum from restrictive, anorexia-
like disorders to disinhibited, bulimic-like disorders. The predisposing
personality traits of perfectionism, harm avoidance and depression may
place people at risk for developing both restrained, anorexic-like and
disinhibited, bulimic-like eating disorders. Compulsivity and inflexibility
may be the personality traits that place people at specific risk for
developing restricting, anorexia-like disorders. Impulsivity and novelty
seeking may be the personality traits that place people at specific risk
for developing disinhibited, bulimia-like eating disorders. The assumption
in this proposal is that the biological basis for each of these personality
traits is polygenetically determined, and that through interaction with the
environment the traits develop and predispose the person to developing
an eating disorder.

Book 1.indb 83 06/03/2012 13:48

 84 C L I N I C A L P S Y C H O L O G Y : A N I N T R O D U C T I O N

Mood dysregulation
It has been proposed that eating disorders are an expression of an
underlying mood disorder (Vögele & Gibson, 2010). Depression is often
present in the family histories of people with eating disorders, along with
other mood regulation difficulties such as substance abuse and
borderline personality disorder. If anorexia and bulimia are fundamentally
mood disorders, then a plausible hypothesis is that eating disorders
arise from a dysregulation of the serotonergic neurotransmitter system
in those centres of the brain that subserve mood. Considerable evidence
suggests that abnormalities in the serotonergic neurotransmitter system
contribute to dysregulation of mood as well as appetite and impulse
control in eating disorders (Kaye, 2008).
The neurotransmitter dysregulation hypothesis has led to controlled
trials of antidepressants for eating disorders, mainly conducted with
young adults. Both selective serotonin re-uptake inhibitors (SSRIs) and
tricyclic antidepressants (TCAs) have been found to lead to short-term
improvements in bulimia, but have limited impact on anorexia nervosa
(McElroy et al., 2010; Wilson & Fairburn, 2007).

Starvation
The starvation hypothesis proposes that eating disorders follow a chronic
course because they are partly maintained by biological abnormalities
and related alterations in psychological functioning caused by starvation.
Evidence from studies of people with anorexia and bulimia and partici-
pants in starvation laboratory experiments show that the neuroendocrine
abnormalities and changes in gastric functioning that arise from experi-
mentally induced starvation are similar to those observed in patients with
eating disorders (Frichter & Pirke, 1995; Singh, 2002). More pronounced
changes occur in anorexia than in bulimia. Starvation-related neuroendo-
crine changes occur in the hypothalamic–pituitary–gonadal axis, which
governs reproductive functioning. They also occur in the hypothalamic–
pituitary–adrenal axis and the hypothalamic–pituitary–thyroid axis, which
govern mood, appetite, arousal and other vegetative functions.
In addition, there is evidence that starvation leads to delayed gastric
emptying and that this reduces hunger perception. Neuroimaging
studies show that anorexia and bulimia lead to reduced cortical mass,
with some degree of normalization after recovery (Kaye, 2008). One
implication of starvation theories is that a distinction should be made
between re-feeding programmes, which aim to reverse the starvation
process by helping patients regain weight to render them accessible to
psychological interventions, and later therapy in which the maintenance
of normal body weight and eating patterns is the principal goal. This
distinction is central to effective forms of therapy for anorexia.

Psychoanalytic theories
Psychoanalytic explanations of eating disorders focus on the role of
intrapsychic factors in the genesis and maintenance of self-starvation.

Book 1.indb 84 06/03/2012 13:48

 3 • EATING DISORDERS 85

Hilda Bruch (1973, 1978) argued that the psychodynamics that

underpins anorexia arises from early childhood experiences. Accord-
ing to Bruch, the mothers of anorexic girls adopt a parenting style in
which parental needs for control and compliance take primacy over
the child’s needs for self-expression and autonomy. The child has
difficulty in learning how to interpret need-related internal physiological
states and in developing a coherent sense of self separate from
caregivers.
In adolescence the fear of fatness, obsession with food and guilt for
eating are part of an attempt to manage a central conflict related to the
attainment of autonomy and a coherent sense of self. The youngster
experiences a fear of separation from parents and a fear of being overly
controlled by the parents; a fear of maturation, sexuality, intimacy and
independence; and a fear of having little control over the self or body
size (as a symbol of self). This conflict about autonomy is characterized
by low self-esteem coupled with perfectionistic strivings to improve the
self.
There is ample evidence for distorted body image, low interoception,
maturity fears, perfectionism, low self-esteem, the use of suppression
as a coping strategy and low self-directedness among people with
eating disorders (Aldeo et al., 2010; Cassin & von Ranson, 2005; Jacobi
& Fittig, 2010; Jacobi et al., 2004). There is also some evidence for
problematic parent–child relationships as precursors of eating disorders
(Jacobi & Fittig, 2010; Jacobi et al., 2004; Striegel-Moore & Bulik, 2007).
Over-concerned parenting in childhood is a risk factor for anorexia.
Parental criticism about weight, high expectations and low contact with
parents in adolescence are associated with bulimia.
Results of a small number of trials suggest that psychodynamic psy-
chotherapy may be effective as a treatment for eating disorders in
adults, but not adolescents (Thompson-Brenner et al., 2009). The
Maudsley group in their controlled trials of psychodynamic psychother-
apy with young adults, working within the context of Malan’s (1995)
psychodynamic therapy model, have found that a unique psychody-
namic focal hypothesis may be formed for each patient and that Bruch’s
themes typically characterize these focal hypotheses. Psychoanalytic
psychotherapy, as practised by the Maudsley group, aims to help the
patient gain insight into the way in which the psychodynamics of past
relationships with parents underpins the transference–countertransfer-
ence, the patient–therapist relationship and the relationships that the
patient has with other significant people in their life. In addition, psycho-
analytic psychotherapy facilitates the patient’s search for less destruc-
tive ways to assert autonomy from the parents and to develop a strong
sense of personal identity.

Cognitive-behavioural theories
There are a number of cognitive-behaviour therapy (CBT) approaches
to understanding and treating eating disorders (Wilson, 2010). A
particularly well developed model has been proposed by the Oxford

Book 1.indb 85 06/03/2012 13:48

 86 C L I N I C A L P S Y C H O L O G Y : A N I N T R O D U C T I O N

group led by Christopher Fairburn (2008). In this transdiagnostic model

Fairburn proposed that the over-evaluation of shape and weight and
their control is the core underlying cognitive cause of anorexia, bulimia
and ‘mixed’ eating disorders. That is, people with eating disorders judge
their self-worth in terms of their weight and shape and their capacity to
control these, rather than in terms of the quality of their close
relationships, their work performance or involvement in their pastimes.
They hold beliefs such as ‘I am only good if I am thin’ or ‘I can only be
happy if I control my eating and weigh seven stone’. These belief
systems motivate people with eating disorders to follow strict diets.
Those who develop anorexia are highly successful at dieting and
develop very low body weight. This state gives rise to the starvation
syndrome which involves a preoccupation with eating, a heightened
sense of being full, rigid obsessionality and social withdrawal. These
side-effects of the starvation process strengthen the core beliefs
associated with over-evaluation of shape and weight. In this way people
with anorexia become trapped in a vicious cycle whereby their over-
evaluation of shape and weight is strengthened by the side-effects of
starvation.
People who develop bulimia (like those with anorexia) also over-
evaluate their shape and weight and engage in strict dieting. However,
periodically, stressful life events lead to episodes of low mood, which
they cope with by bingeing. This temporarily improves their mood, but
afterwards they become self-critical for deviating from their strict diet,
and compensate for their bingeing by vomiting, taking laxatives
or exercising excessively. They then return to the practice of strict
dieting, motivated by their over-evaluation of shape and weight. This
continues until another stressful life event causes a drop in mood and a
repetition of the binge–purge cycle. Fairburn’s model is diagrammed in
Figure 3.2.
Fairburn’s (2008) model of CBT progresses through four stages over
20 sessions. In the first stage the therapist engages with the patient
though bi-weekly sessions over a period of a month, conducts an assess-
ment, collaboratively develops a formulation, provides psychoeducation
about eating disorders and the CBT model, arranges regular ‘in session
weighing’ and arranges for patients to start a pattern of regular eating. In
the second stage appointments are held weekly, progress is reviewed,
barriers to progress are identified, and the formulation is refined. In the
third stage the repetitive cycles of cognition and behaviour that maintain
the eating disorder are addressed. In the final stage, appointments are
held fortnightly and the focus is on maintaining gains and planning for
relapse prevention. Variations on this basic treatment model have been
developed for patients with severe weight loss or complex personal and
interpersonal problems, inpatients and younger patients, and for group
therapy.
Many controlled trials have shown that about 50% of young
adult patients with bulimia nervosa benefit from CBT (Wilson, 2010;
Wilson & Fairburn, 2007). Few trials of CBT with anorexia have been
conducted.

Book 1.indb 86 06/03/2012 13:48

 3 • EATING DISORDERS 87

Figure 3.2 Fairburn’s cognitive-behavioural model of eating disorders (adapted from C. Fairburn (2008). Cognitive
behaviour therapy and eating disorders. London: Guilford)

Systemic theories
Systemic theories underline the role of contextual factors in the devel-
opment and treatment of eating disorders. Sociocultural, developmental
and family systems formulations fall into this broad domain.

Sociocultural factors
Sociocultural theories highlight the role of broad cultural factors such as
the idealization of female thinness specific to particular societies, nota-
bly those prevalent in western industrialised nations, in predisposing
individuals to developing eating disorders (Nasser & Katzman, 2003).
Evidence supporting the sociocultural position allows the following con-
clusions to be drawn (Levine & Murnen, 2009; Levine & Smolak, 2010).
Epidemiological studies consistently show that eating disorders exist
internationally but are more prevalent in western societies where food is
plentiful, thinness is valued and dieting is promoted. Eating disorders
are more prevalent among groups under greater social pressure to
achieve the slim aesthetic ideal, such as dancers, models and athletes.
Westernization, modernization and exposure to transnational mass
media advocating the thin ideal are risk factors for eating disorders. The
prevalence of eating disorders is higher in ethnic groups that move from
a culture that does not idealize the thin female form to cultures that do.

Book 1.indb 87 06/03/2012 13:48

 88 C L I N I C A L P S Y C H O L O G Y : A N I N T R O D U C T I O N

While these findings point to the importance of sociocultural factors

in predisposing individuals to developing eating problems, not all dieters
develop anorexia or bulimia. Precipitating factors such as stressful life
events and the presence of other individual genetic, neurobiological,
psychological or family factors (mentioned elsewhere in the chapter and
listed in Table 3.2) probably contribute to the development of eating
disorders (Mazzeo & Bulik, 2009).

Life-cycle transitions and stress

It has been proposed that a build-up of stresses at particular points in
the individual and family life cycles may precipitate the onset of an eat-
ing disorder or prevent the rapid resolution of a potential eating disor-
der, particularly in cases where biological and psychosocial predisposing
factors are already present (e.g. Crisp, 1983; Dare, 1985; Serpell &
Troup, 2003). At an individual level, Crisp (1983) argues that when
youngsters have particular difficulties dealing with the physical and
emotional changes that coincide with the transition to adolescence, an
eating disorder may occur since it allows youngsters to avoid the chal-
lenges posed by adolescence. At a family level, Dare (1985) proposes
that the co-occurrence of a number of critical transitional stresses such
as the onset of puberty in a younger child, an older child leaving home,
or the loss of a grandparent may place excessive demands on family
members to develop new roles, routines and support systems. The
development of an eating disorder provides families with a period of
respite, where routines, roles and supports appropriate to a previous
stage of the family life-cycle may continue to be used so that families
may maintain the status quo rather than negotiating changes appropri-
ate to the next stage of the life-cycle. Both of these theories are sup-
ported by evidence for the association between eating disorders and
stressful life events in adolescence.
Serpell and Troup (2003) propose that childhood adversity (including
neglect, sexual abuse and family conflict), helplessness, low self-
esteem and rigid perfectionism predispose people to developing eating
disorders. In response to sociocultural pressures for thinness, these
four factors give rise to four intermediate predisposing factors: (1)
dietary restraint, (2) low shape and weight-based self-esteem, (3)
disgust at food and food-related body stimuli and (4) bodily shame.
When stressful life events that involve managing complex interpersonal
situations and relationships arise in people who have these vulnerability
factors, an eating disorder may occur. This complex developmental
theory is supported by evidence for a number of risk factors listed in
Table 3.2.

Family systems approaches

Family systems theories of anorexia point to a number of organizational
features that may be predisposing or maintaining factors for eating disor-
ders (le Grange & Rienecke Hoste, 2010). For example, Minuchin et al.

Book 1.indb 88 06/03/2012 13:48

 3 • EATING DISORDERS 89

(1978) characterized the families of teenagers with anorexia as enmeshed

and rigid, with a strongly overprotective attitude to the child. He also
argued that there was a lack of conflict resolution and an involvement of
children in parental conflicts. Selvini Palazzoli (1988) pinpointed the fol-
lowing features as typical of the anorexic family: an ethic of self-sacrifice,
limited parental leadership, blame-shifting since everything is done for
the good of others, unclear communication and secret alliances between
one parent and the anorexic child, and covert marital dissatisfaction.
Available empirical evidence indicates that there is not a single
dysfunctional family constellation (a psychosomatic family) that causes
anorexia and bulimia (Jacobi et al., 2004). Rather, a variety of patterns
of family organization are associated with eating disorders. Families of
youngsters with anorexia tend to be more controlled and organized,
while families of bulimic adolescents tend to be more chaotic, conflicted
and critical. These patterns of organization probably reflect families’
attempts to cope with eating disorders.
A group at the Maudsley Hospital in London have developed an
approach to family therapy for young teenagers with anorexia for which
there is considerable empirical support. The model, which was
manualized and popularized by James Lock (Lock et al., 2001),
underlines the value of the family as a central treatment resource in
facilitating recovery, rather than as an aetiological factor. The approach
is premised on the idea that young teenagers with anorexia are
regressed, and not capable of responsible autonomous eating. Rather
than being in control of their eating, they are controlled by their eating
disorder. That is, the starvation syndrome (mentioned in the section on
CBT above) prevents the young person from recovering. It is because
of this that parents play a central role in the recovery process. Therapists
support parents in treating their adolescents as if they were younger
children by refeeding them until a safe and stable weight has been
achieved. At this point they may safely transfer responsibility for
maintaining a healthy diet and weight to the adolescent.
Lock proposes that most children and teenagers can be treated
effectively as outpatients, unless their low weight poses significant
medical risks. Treatment typically spans about 20 sessions and lasts
from 6 months to a year. In the first stage of therapy the therapist forms
an alliance with the family, conducts a family assessment, offers
psychoeducation about the risks associated with anorexia, sets up a
routine for weighing the patient at the beginning of each session, and
supports the parents in helping the young person to eat in the therapy
session. In the second stage the aim is to help the parents gradually
transfer responsibility for eating responsibly to the adolescent and
explore the relationship between the anorexia and the adolescent’s
achievement of developmental tasks such as increasing autonomy
within the family. In the final stage of treatment the emphasis is on
consolidating the gains the parents and adolescent have made in
managing the adolescent’s growing autonomy, anticipating how the
family will manage the adolescent’s growing independence, and relapse
anticipation and prevention.

Book 1.indb 89 06/03/2012 13:48

 90 C L I N I C A L P S Y C H O L O G Y : A N I N T R O D U C T I O N

Evidence from a series of trials shows that family therapy is effective

with up to 90% of young adolescents with non-chronic anorexia (le
Grange & Rienecke Hoste, 2010; Lock et al., 2001).

Interpersonal therapy
Interpersonal theory was developed by Harry Stack Sullivan (1953),
who proposed that psychological problems are maintained by problem-
atic current life relationships. From this theory interpersonal therapy
(IPT) was developed as an effective treatment for depression. It was
then adapted for bulimia in young adults and shown to be an effective
treatment for this condition (Tanofsky-Kraff & Wilfley, 2010; Wilson &
Fairburn, 2007).
In IPT for bulimia, it is assumed that one or more of four categories
of interpersonal difficulties maintain the condition. These are: (1) grief
following bereavement or other losses, (2) role disputes within important
family or work relationships, (3) role transitions within the family or
workplace, and (4) interpersonal deficits, such as problems in making
and maintaining friendships. Interpersonal therapy alleviates bulimia by
helping clients resolve problems in these areas that maintain their
pattern of bingeing and purging.
IPT for bulimia involves three stages and spans 20 sessions
conducted over a period of 4 to 5 months. In the first stage the client is
engaged in treatment, current interpersonal problems are identified and
a treatment contract is established. In the middle stage the core
interpersonal problem that maintains the eating disorder is addressed.
In the final stage gains made are consolidated and clients are helped to
prepare to continue the work after termination of therapy.

Assessment
Assessment and treatment of eating disorders are usually carried out
by multidisciplinary teams that include professionals from clinical psy-
chology, psychiatry, psychiatric nursing, dietetics and other disciplines.
Assessment covers the client’s physical, nutritional and psychological
state (Anderson & Murray, 2010; Katzman et al., 2010). With teenagers
a family assessment is essential. With adults, interviews with involved
family members are important.
Psychometric instruments that may be useful in the assessment of
clients with eating disorder are the Eating Disorder Examination (EDE,
Fairburn et al., 2008) and the Eating Disorder Inventory (EDI-3, Garner,
2005). The EDE, which is considered the diagnostic gold standard, is a
detailed interview that allows DSM diagnoses of eating disorders to be
made with high reliability. The EDI-3 is a comprehensive self-report psy-
chological assessment instrument for assessing eating pathology and
related psychological traits such as perfectionism and ineffectiveness.
On the basis of the assessment a preliminary formulation may be drawn
up. This should link predisposing, precipitating and maintaining factors
to the abnormal eating pattern and specify protective factors that may
be drawn on during treatment. A general clinical formulation model for
eating disorders is given in Figure 3.3.

Book 1.indb 90 06/03/2012 13:48

 3 • EATING DISORDERS 91

Figure 3.3 General formulation model for eating disorders

Intervention
Intervention for eating disorders is multidisciplinary. It includes
management of the medical complications of eating disorders (Katzman
et al., 2010) coupled with psychological intervention. There is strong
evidence to support the effectiveness of family therapy for young
teenagers with non-chronic anorexia nervosa and CBT for bulimia in
young adults, following the models of these interventions outlined earlier
in the chapter (Hay & Claudino, 2010; le Grange & Rienecke Hoste,
2010; Wilson, 2010). The use of these treatments for these populations
is consistent with best practice guidelines (American Psychiatric
Association, 2006; NICE, 2004a).
In a review of available evidence, Eisler (2005) concluded that after
treatment, between a half and two-thirds of teenagers with anorexia
achieve a healthy weight. At 6 months to 6 year follow-up, 60–90%
have fully recovered and no more than 10–15% are seriously ill. Eisler
also noted that the negligible relapse rate following family therapy is
superior to the moderate outcomes for individually oriented therapies. It
is also far superior to the high relapse rate following inpatient treatment,
which is 25–30% following first admission, and 55–75% for second and
further admissions.
Thompson-Brenner et al. (2003) conducted a meta-analysis
of 26 studies involving 51 treatment conditions, of which 36 were

Book 1.indb 91 06/03/2012 13:48

 92 C L I N I C A L P S Y C H O L O G Y : A N I N T R O D U C T I O N

cognitive-behavioural or behavioural and 15 were some other form of

therapy. Across all treatments, the recovery rate was 40% after
treatment and 43% at 1 year follow-up. The recovery rate of 45% for
individual therapy was higher than that of 26% for group therapy. In this
meta-analysis there were no significant differences in outcome between
therapies, but more studies of CBT had been conducted than of any
other form of therapy, so it is the best validated. Of the other forms of
therapy that have been investigated, interpersonal therapy has been
shown to be as effective as CBT at 1 year follow-up.

Controversies
On of the major controversies within the field is between those who
advocate a biomedical conceptualization of eating disorders and the
feminist position (Maine & Bunnell, 2010). The biomedical approach,
with its focus on genetics and neurobiological aspects of eating disor-
ders, sees the individual woman as sick or defective, and its primary
aim is to cure the illness. In contrast, the feminist position construes
eating disorders as a gendered condition, and the relentless and self-
destructive pursuit of the thin ideal as a response to sociocultural pres-
sures generated by a male-dominated society.

Summary
Anorexia nervosa and bulimia nervosa typically occur first
during adolescence, principally among females. About 1–2%
of the adolescent and young adult female population suffer
from eating disorders. The average prevalence rates for
anorexia nervosa and bulimia nervosa among young females
are 0.3–0.5% and 1–4% respectively. In both conditions there
is an overevaluation of body shape and weight.
With anorexia, the primary feature is the maintenance of a
very low body weight; with bulimia a cycle of binge eating and
purging is the distinctive feature. In most clinical cases of eat-
ing disorder there is a distortion of body image, depressed or
irritable mood, and interpersonal adjustment problems. Eating
disorders entail significant health complications.
The outcome for eating disorders is poor for a significant
minority of cases. For anorexia nervosa about half of all cases
have a good outcome, a third have a moderate outcome and a
fifth have a poor outcome. At 20-year follow-up, the mortality
rate is about 6%. For bulimia nervosa about half of all cases
have a good outcome, a quarter have a moderate outcome and
the remaining quarter have a poor outcome.
Biological theories point to the role of genetics, mood dys-
regulation and starvation-related processes in the aetiology
and maintenance of eating disorders. Evidence from twin and

Book 1.indb 92 06/03/2012 13:48

 3 • EATING DISORDERS 93

family studies show unequivocally that genetic predisposing

factors contribute moderately to the aetiology of eating disor-
ders. Eating disorders have been conceptualized as mood dis-
orders associated with dysregulation of the seratonergic
system. Antidepressants have been found to lead to short-term
improvements in bulimia, but have no impact on anorexia
nervosa.
Starvation-related neuroendocrine changes occur in the
hypothalamic–pituitary–gonadal axis, which governs reproduc-
tive functioning, and the hypothalamic–pituitary–adrenal axis
and hypothalamic–pituitary–thyroid axis, which govern mood
and appetite. The starvation syndrome maintains restricted
eating. Bruch’s psychoanalytic theory proposes that over-
controlling parenting practices cause eating disorders and the
related problems of distorted body image, maturity fears, per-
fectionistic strivings, low self-esteem and low self-efficacy.
There is some evidence that focal psychodynamic psycho-
therapy can lead to improvement for adults with anorexia,
but not adolescents. Fairburn’s transdiagnostic CBT model
assumes that the over-evaluation of shape and weight and
their control is the core underlying cognitive cause of anorexia,
bulimia and ‘mixed’ eating disorders. About 50% of young
adults with bulimia benefit from individual CBT. Few trials of
CBT with people of any age with anorexia or with adolescents
with any eating disorder have been conducted.
Social and family factors may play a role in the aetiology of
anorexia. There is no single dysfunctional family constellation
that causes eating disorders. The Maudsley approach to family
therapy for adolescent eating disorders underlines the value of
the family as a central treatment resource in facilitating recov-
ery, rather than as an aetiological factor. Up to 90% of adoles-
cents with non-chronic anorexia can benefit from this approach.
IPT assumes that eating disorders are maintained by inter-
personal factors, notably grief, role disputes, role transitions
and interpersonal deficits. IPT alleviates bulimia by helping cli-
ents resolve problems in these areas that maintain their pattern
of bingeing and purging. IPT is as effective as CBT, but fewer
validation studies have been conducted. Assessment and
treatment of eating disorders is usually carried out by multidis-
ciplinary teams, with an initial focus on weight restoration for
anorexia and the development of a normal diet for bulimia.
Once weight and diet have been normalized, the focus should
shift to psychotherapy.
For young adolescents, family therapy is the treatment of
choice; for adult bulimics, CBT is the best validated treatment.
There is controversy over whether eating disorders are most
usefully conceptualized as biologically based medical conditions
or a gendered response to socio-cultural pressures for thinness.

Book 1.indb 93 06/03/2012 13:48

 94 C L I N I C A L P S Y C H O L O G Y : A N I N T R O D U C T I O N

Questions
● What are the main clinical features of anorexia nervosa and bulimia
nervosa?
● How prevalent are eating disorders?
● What are the main biological and psychological theories of eating
disorders and the main research findings relevant to these theories?
● What are the main evidence-based approaches to assessment and
treatment of eating disorders?
● What are your views on the controversy concerning the biomedical
and feminist views of eating disorders?

FURTHER READING
Professional
● Agras, W. (2010). The Oxford handbook of eating disorders. New York:
Oxford University Press.
● Carr, A. (2006). Handbook of child and adolescent clinical psychology
(second edition). London: Routledge (Chapter 17).
● Fairburn, C. (2008). Cognitive behaviour therapy and eating disorders.
London: Guilford.
● Lock, J., Le Grange, D., Agras, W., & Dare, C. (2001). Treatment manual
for anorexia nervosa: A family based approach. New York: Guilford.

Self-help
● Fairburn, C. (1995). Overcoming binge eating. London: Guilford.
● Lock, J. J. & Le Grange, D. (2004). Help your teenager beat an eating
disorder. London: Brunner-Routledge.

WEBSITES
● Academy for Eating Disorders:
www.aedweb.org
● APA (American Psychiatric Association) practice guidelines for treating
eating disorders:
www.guideline.gov/content.aspx?id=9318
● Beat (Beating Eating Disorders):
http://www.b-eat.co.uk
● Eating Disorders Resources:
http://edr.org.uk
● Eating Disorders Treatment:
http://eating-disorder.com
● NICE (National Institute for Clinical Excellence) guidelines for treating
eating disorders:
http://guidance.nice.org.uk/topic/mentalhealthbehavioural

Book 1.indb 94 06/03/2012 13:48

 Drug misuse 4
Learning objectives
After studying this chapter you will be able to:
● distinguish between drug experimentation and
harmful drug use
● name the main clinical features of drug dependence
● summarize the epidemiology of drug misuse
● list the risk factors for drug misuse
● outline the main biological, psychological and
integrative theories of drug misuse
● name the main evidence-based approaches to
assessment and treatment of drug misuse
● give a considered view on the pros and cons of harm
reduction strategies for addressing drug misuse.

Introduction
Habitual drug misuse in adolescence is of particular concern to clinical
psychologists because it may have a negative long-term effect on the
adolescent and an intergenerational effect on their children (Crome et
al., 2004; Heath et al., 2008; Kaminer & Winters, 2011). For the adoles-
cent, habitual drug misuse may negatively affect mental and physical
health, criminal and educational status, the establishment of auton-
omy from the family of origin and the development long-term intimate

Book 1.indb 95 06/03/2012 13:48

 96 C L I N I C A L P S Y C H O L O G Y : A N I N T R O D U C T I O N

relationships. The children of teenagers who engage in chronic and

harmful drug use may suffer from drug-related problems such as foetal
alcohol syndrome, intrauterine addiction or HIV infection.
In this chapter, after considering the classification, epidemiology and
clinical features of drug misuse, a variety of theoretical explanations
concerning the aetiology and maintenance of these conditions will be
considered along with relevant empirical evidence. Some comments on
the assessment and treatment of drug use will be made and relevant
controversies considered. Cases of drug misuse vary widely in their
presentation. Below two examples of very different types of case are
presented.

A case of harmful polydrug use

Carl, 18, and Betty, 19, referred themselves for treatment to an inner
city drug clinic in a public health service. Both were polydrug users and
had developed physiological dependence to opiates at the time of
referral.

History of the presenting problem

They both had been using drugs since about the age of 10 years, begin-
ning with cigarettes which they stole from their parents. They were part
of a peer group involved in experimental drug use. At 12 they both began
drinking alcohol. They stole beer from Carl’s father and wine from a
supermarket. They went on to experiment with benzodiazepines which
they stole from Betty’s mother, who had been prescribed these for anxi-
ety and sleep problems by the family doctor. They then used cannabis,
various solvents, and a variety of stimulants including amphetamines.
They progressed to opiates about a year before they first attended the
clinic. They had got to the stage where they could no longer finance their
drug-taking habits and had a series of bad debts. They requested evalu-
ation for placement on a methadone maintenance programme.
The couple lived together on welfare in a two-room apartment. They
had financed their drug habits through theft and prostitution. They were
part of a group of drug users who lived in Dublin’s inner city. Their whole
lifestyle centred around getting and using any drugs they could find, but
mainly opiates.

Developmental and family history

Betty and Carl had known each other from childhood. Both had a history
of academic and conduct problems at school. Their families were part
of a community and so their parents knew each other and discussed
Betty and Carl’s relationship. When the young couple began living
together about 6 months before the referral, their parents disapproved
of this. However, in both of the families their mothers were very loyal to
them and occasionally gave them financial assistance when it was clear
that they were showing withdrawal symptoms and needed a fix.

Book 1.indb 96 06/03/2012 13:48

 4 • DRUG MISUSE 97

Carl’s grandfather lived with Carl’s parents. Both he and Carl’s father
had a serious drink problem for which they had been unsuccessfully
treated over many years. Carl had four siblings, all of whom had drug
problems. Betty had three siblings, all but one of whom were using
drugs. However, Carl and Betty had the most serious drug problems of
the two families. They were both eldest children.

Formulation
Betty and Carl presented with habitual, harmful drug misuse and depen-
dence. This had evolved gradually out of an earlier pattern of pre-
adolescent experimental drug use, which may be viewed as a
precipitating factor. Both Betty and Carl were predisposed to develop
substance use problems because of their family role models, their aca-
demic difficulties, lack of career opportunities and other conduct prob-
lems. Their drug problems were maintained at a physiological level by
dependence and the related fear of withdrawal.
At a psychosocial level their drug problems were maintained through
involvement in a subculture and lifestyle that revolved around obtain-
ing and using drugs to the exclusion of almost all other activities. The
main protective factor was the couple’s loyalty to each other, and their
wish in the long term to have children. This formulation is diagrammed
in Figure 4.1.

Figure 4.1 Formulation of a case of harmful drug use

Book 1.indb 97 06/03/2012 13:48

 98 C L I N I C A L P S Y C H O L O G Y : A N I N T R O D U C T I O N

Treatment
The initial treatment plan for Betty and Carl involved detoxification fol-
lowed by either residential treatment in a therapeutic community or out-
patient methadone maintenance. Betty and Carl completed detoxification
and chose to enter the drug-free therapeutic community. However, they
dropped out and relapsed after about 6 weeks. They returned to the
inner-city clinic where they both commenced a methadone maintenance
programme with adjunctive counselling.
Over a period of a couple of years they engaged in a cycle in which
they periodically were detoxified, entered the therapeutic community,
dropped out, relapsed and recommenced methadone maintenance with
adjunctive counselling.

A case of early drug experimentation

Chas, aged 15, was referred for treatment to a private family therapy
institute when his parents found that he had been smoking cannabis
with his school friends at a party. He had smoked cannabis a couple of
dozen times over a 6-month period and had also taken LSD once. His
drug use occurred within the context of a peer group who were
experimenting with a range of drugs, and who associated drug use with
listening to and playing music.

Developmental history
Chas’ developmental history was within normal limits. He was a fine
student in the top stream of his school and had come second in his
class in the Junior Certificate. He was an able sportsman, an avid chess
player and musician. He loved to push himself to the limit in all of his
leisure activities and was clearly a risk taker. He had excellent social
skills and a wide circle of friends including a girlfriend with whom he had
being having a relationship for about 4 months. He had particularly
good relationships with his parents.

Family history
Neither of Chas’ parents smoked or drank alcohol, and both were solici-
tors. They worked long hours, but on a matter of principle would not send
Chas to boarding school (which was common practice among their
peers), believing strongly in the importance of family life. There was a
live-in nanny in their house who cared for Chas and his two younger sis-
ters, Triona, aged 8, and Briony, aged 10. The parents were guilt-ridden
when they brought the family for the intake interview. Both were of the
view that Chas’ drug misuse resulted from a failure to be sufficiently avail-
able for him during his adolescence due to their heavy work schedules.

Formulation
Chas presented with experimental rather than habitual drug use. The
onset was precipitated by availability of cannabis. Chas was predisposed

Book 1.indb 98 06/03/2012 13:48

 4 • DRUG MISUSE 99

to become involved in experimental drug use because of his tendency

for sensation seeking and risk taking. The drug use was maintained
through involvement in a drug-using peer group. The principal protective
factors were Chas’ good premorbid adjustment and the supportiveness
and stability of his family.

Treatment
In a series of family therapy sessions involving Chas and his parents,
the risks of abusing various types of drug were discussed. Other rec-
reational channels into which Chas could direct his energy were
explored. As part of this process, Chas and his father arranged a week-
end at an adventure sports centre in Donegal together. The parents
were supported in setting strict limits on drug use while Chas lived in
their house. In later sessions the focus moved to Chas’ career plans.

Comparison of cases
These two cases are very different. The first is a chronic and complex
case of habitual and harmful polydrug use and opiate dependence while
the second involves only recreational or experimental use of cannabis.
They differ along a number of dimensions including the pattern of drug-
using behaviour, the types of drug used, the impact of the drugs used,
the overall personal adjustment of the young people and the presence
of other personal or family-based problems and protective factors.
Clearly drug misuse itself is not always a unidimensional problem. It
may occur as part of a wider pattern of life difficulties. The definition and
classification of drug misuse is therefore a complex challenge.

Classification, epidemiology, risk factors and

protective factors
Within both DSM-IV-TR (American Psychiatric Association, 2000) and
ICD-10 (World Health Organization, 1992) a distinction is made between
drug dependence and harmful drug use. While substance abuse or
harmful drug use refers to drug taking that leads to significant dis-
tress, health problems or impairment, drug dependence refers to those
situations where there is a compulsive pattern of use involving physio-
logical changes associated with tolerance and withdrawal. Diagnostic
criteria for both conditions are given in Table 4.1.
Illegal drug use across the life span is common. In an Irish national
survey of over 8,000 15–64 year olds conducted in 2002, the lifetime
prevalence of illegal drug use was 19% (National Advisory Committee
on Drugs and the Drug and Alcohol Information and Research Unit,
2004). In a UK national survey of over 9,000 11–15-year-olds conducted
in 2001, the lifetime prevalence for illegal drug use was 29% (National
Centre for Social Research and the National Foundation for Educational
Research, 2002). In both surveys cannabis was the most commonly
used drug and prevalence was higher among older male teenagers.

Book 1.indb 99 06/03/2012 13:48

 100 C L I N I C A L P S Y C H O L O G Y : A N I N T R O D U C T I O N

TABLE 4.1
DSM-IV-TR and ICD-10 diagnostic criteria for drug abuse and dependence
DSM-IV-TR ICD-10
Substance abuse Harmful use
A. A maladaptive pattern of substance use leading A pattern of psychoactive substance abuse that is
to clinically significant impairment or distress as causing harm to health. The damage may be physical
manifested by one or more of the following (as in cases of hepatitis from the self-administration
occurring within a 12-month period: of injected drugs) or mental (e.g. episodes of
1. Recurrent substance abuse resulting in a depressive disorder secondary to heavy consumption
failure to fulfil major obligations at work, of alcohol).
school or home. The fact that pattern of use of a particular substance
2. Recurrent substance abuse in situations in is disapproved of by a culture or may have led to
which it is physically hazardous. socially negative consequences such as arrest or
3. Recurrent substance-related legal problems.
marital arguments is not in itself evidence of harmful
4. Continued substance use despite having use.
persistent or recurrent social or interpersonal
problems caused by or exacerbated by the
effects of the substance.
B. The symptoms have never met the criteria for
substance dependence for this type of
substance.
Substance dependence Dependence syndrome
A maladaptive pattern of substance abuse, leading A cluster of physiological, behavioural and cognitive
to clinically significant impairment or distress, as phenomena in which the use of a substance or a
manifested by three or more of the following class of substances takes on a much higher priority
occurring at any time in the same 12-month than other behaviours that once had greater value.
period: Three or more of the following in a 12-month period:
1. Tolerance defined by either (a) A strong desire or sense of compulsion to take the
(a) a need for markedly increased amounts of substance.
the substance to achieve intoxication (b) Difficulty in controlling substance taking behaviour
(b) markedly diminished effect with continued in terms of onset, termination or levels of use.
use of the same amount of the substance (c) A physiological withdrawal state when substance
2. Withdrawal as manifested by either of the use has ceased or been reduced as evidenced by:
following: the characteristic withdrawal syndrome for the
(a) the characteristic withdrawal syndrome for substance; use of the substance to avoid
the substance withdrawal symptoms.
(b) the same substance is taken to relieve or (c) Evidence of tolerance such that increased doses
avoid withdrawal symptoms of the substance are required in order to achieve
3. The substance is taken in larger amounts over a the effects originally produced by lower doses.
longer period than was intended. (e) Progressive neglect of alternative pleasures or
4. There is a persistent desire or unsuccessful interests because of psychoactive substance use,
efforts to cut down or control substance use. increased amount of time necessary to obtain or
5. A great deal of time is spent in activities take the substance or to recover from its effects.
necessary to obtain the substance, use the (f) Persisting with substance use despite clear
substance or recover from its effects. evidence of overtly harmful consequences such as
6. Important social, occupational or recreational harm to the liver through excessive drinking,
activities are given up or reduced because of depressive mood states consequent to periods of
substance use. heavy substance abuse, or drug-related
7. The substance use is continued despite impairment of cognitive functioning.
knowledge of having a persistent or recurrent
physical or psychological problem that is likely
to have been caused or exacerbated by the
substance.
Specify with or without physiological dependence.

Note: Adapted from DSM-IV-TR (APA, 2000) and ICD-10 (WHO, 1992).

Book 1.indb 100 06/03/2012 13:48

 4 • DRUG MISUSE 101

Experimentation with drugs in adolescence is common (Chung &

Martin, 2011; Frischer et al., 2004; Griffin, 2010; Weinberg et al., 2002).
Major US and UK surveys concur that by 19 years of age approximately
three quarters of teenagers have drunk alcohol; about half have tried
cigarettes and cannabis; and about a fifth have tried other street drugs
such as solvents, stimulants, hallucinogens or opiates. Between 5%
and 10% of teenagers under 19 have drug problems serious enough to
require clinical intervention.
Drug use reaches its peak in the early 20s, and most young adults
‘mature out’ of substance use as they approach their 30s (Jochman &
Fromme, 2010). This occurs partly because persistent drug use is
incompatible with role changes such as employment, marriage and
parenthood that occur in the 20s. Better outcomes occur in cases
where there is no comorbid psychopathology; an easy temperament
and low levels of sensation seeking and impulsivity; good social
problem-solving skills; positive family and school relationships; a longer
time in treatment; engagement in post-treatment aftercare; develop-
ment of negative attitudes to drug use and positive health-oriented val-
ues; and involvement with non-drug-using peers in the post-treatment
period (Catalano et al., 2011; Chung & Martin, 2011; Jochman &
Fromme, 2010).
About one third of adolescents who use drugs progress to chronic
drug abuse or dependence (Catalano et al., 2011). Risk factors in
multiple domains, listed in Table 4.2 are associated with the progression
from experimental drug use to harmful abuse or dependence. The
greater the number of risk factors, the higher the probability of developing
serious drug problems.

Clinical features
In clinical practice psychologists take account of significant behavioural,
physiological, affective, perceptual, cognitive and interpersonal features
when assessing and treating cases of adolescent drug misuse (Heath
et al., 2008; Kaminer & Winters, 2011; Scheier, 2010). These are sum-
marized in Table 4.3.
Drug misuse is associated with a wide variety of behaviour patterns.
These patterns may be described in terms of the age of onset, the
duration and frequency of drug use, and the range and amount of
substances used. Thus useful distinctions may be made between
adolescents who began using drugs early or later in their development;
between those who have recently begun experimenting with drugs and
those who have a chronic history of drug misuse; between daily users,
weekend users and occasional users; between those that confine their
drug misuse to a limited range of substances such as alcohol and
cannabis and those that use a wide range of substances; and between
those who use a little and those who use a great deal of drugs.
Chronic and extensive daily polydrug misuse with an early onset is
associated with more difficulties than experimental, occasional use of a
limited number of drugs with a recent onset. The former usually entails

Book 1.indb 101 06/03/2012 13:48

 102 C L I N I C A L P S Y C H O L O G Y : A N I N T R O D U C T I O N

TABLE 4.2
Risk factors for adolescent drug use
Domain Risk factor
Community • Availability of drugs
• Laws and norms favourable to drug use
• Media portrayals of drug use
• Transitions and mobility
• High crime rate, low cohesion and community disorganization
• Extreme economic deprivation
Family • Parental drug use
• Favourable parental attitudes to drug use
• Poor parenting skills (lack of rules, consequences and
supervision of children, and severe or inconsistent
punishment)
• Family conflict, child abuse and neglect, domestic violence
School • Academic failure in late primary school
• Lack of commitment to school
Peer group • Involvement with friends who use drugs
Self • Early and persistent antisocial behaviour
• Early onset of drug use
• Favourable attitude to drug use
• Alienation and rebelliousness
• Personality factors (sensation seeking, risk taking, impulsivity
and low harm-avoidance)

Note: Adapted from R. F. Catalano, K. P. Haggerty, J. D. Hawkins, & J. Elgin (2011).

Prevention of substance use and substance use disorders: Role of risk and protective factors.
In Y. Kaminer & K. C. Winters (Eds.), Clinical manual of adolescent substance abuse
treatment (pp. 30–31). Arlington, VA: American Psychiatric Publishing. At least two
longitudinal studies have provided evidence for each risk factor.

a constricted drug-focused lifestyle and multiple associated physical

and psychosocial problems, whereas the latter does not. A consistent
finding is that only a minority of youngsters progress from experimental
to habitual drug misuse and from the use of a single legal drug to multi-
ple legal and illegal drugs. However, most polydrug misusers began
with early use of ‘gateway’ drugs: nicotine, alcohol and cannabis.
Behavioural patterns of drug misuse evolve within specific contexts.
Drug-using behaviour often comes to be associated with particular
locations, times, modes of administering drugs, physiological and
affective states, control beliefs and social situations. With recreational,
experimental drug use, weekly oral drug taking at peer-group gatherings
while in a positive mood state may occur and young people may have
strong beliefs that they are in control of their drug-taking behaviour.
With habitual drug use, solitary daily injections to prevent withdrawal
and alleviate negative mood may occur. This type of drug use may be
accompanied by strong feelings of being unable to control the frequency
of drug use or to cut down on the amount taken.
Negative physiological features of drug use may be grouped into
those associated with intoxication, those that follow intoxication, those
associated with withdrawal following the development of dependence,
and medical complications that arise from drug misuse. Stimulants

Book 1.indb 102 06/03/2012 13:48

 4 • DRUG MISUSE 103

TABLE 4.3
Clinical features of drug use
Domain Features
Behaviour Drug-using behaviour
• Age of onset
• Duration and frequency of use
• Range of substances and amount used
• Change in pattern over time
Context of drug-using behaviour
• Solitary or social use
• Locations and times of use
• Modes of administering the drug (oral, nasal or injection)
• Physiological state (when seeking excitement or during withdrawal)
• Affective state (positive or negative)
• Beliefs about ability to control drug use
Negative Intoxication
physiological • Physical problems due to hyper-arousal (e.g. arrhythmias or dehydration)
effects • Physical problems due to hypo-arousal (e.g. stupor)
Following intoxication
• Exhaustion
• Dehydration
• Sleep and appetite disturbance
• Sexual dysfunction
Withdrawal
• Nausea, vomiting, muscle aches and discomfort following opioid use
• Sleep and appetite disturbance following stimulant use
• Seizures following sedative use
Long-term medical complications
• Poisoning and overdose Infections including hepatitis and HIV
• Liver and kidney damage
Negative During intoxication
emotional effects • Fear and anxiety due to unexpected effects of drugs (particularly hallucinogens)
Following intoxication and during withdrawal
• Depressed mood
• Irritability and anger
• Anxiety
Negative During intoxication
perceptual effects • Distressing hallucinations (with hallucinogens and some stimulants)
Following intoxication
• Brief flashbacks or protracted psychotic states (with hallucinogens and some
stimulants)
Negative • Impaired cognitive functioning
cognitive effects • Declining academic performance
Negative effects • Adolescent–parent conflict
on interpersonal • Adolescent–teacher conflict
adjustment • Induction into drug using peer subculture
• Social isolation
• Conflict with juvenile justice system
• Conflict with heath care system

Book 1.indb 103 06/03/2012 13:48

 104 C L I N I C A L P S Y C H O L O G Y : A N I N T R O D U C T I O N

(such as amphetamines and cocaine) and hallucinogens (such as LSD)

lead to physiological changes associated with increased arousal such
as tachycardia and blood pressure changes. In cases of extreme
intoxication cardiac arrhythmias and seizures may occur. On the other
hand, extreme intoxication following the use of alcohol, sedatives,
solvents and opioids leads to physiological changes associated with
reduced arousal such as drowsiness, stupor and coma. Withdrawal
from dependence-producing stimulants entails significant disruption of
sleep and increased appetite. Withdrawal from sedatives and alcohol is
particularly dangerous because, as part of a syndrome of autonomic
hyperactivity, grand mal seizures may occur. Withdrawal from opioids
leads to a syndrome characterized by nausea, vomiting, diarrhoea and
muscle aches.
There are a wide variety of medical complications associated with
drug misuse, ranging from injuries sustained while intoxicated, to liver
or kidney damage due to the toxicity of substances abused, to infections
including hepatitis and HIV arising from non-sterile injections. With all
street drugs there is a risk of death by intentional or accidental overdose
or poisoning due to impurities in the drug.
A central reason for many forms of drug use is to induce pharmaco-
logically a pleasant affective state. It is therefore not surprising that for
many drugs, including alcohol, stimulants, hallucinogens, and opioids,
elation is a central feature of initial intoxication. With sedatives, in con-
trast, intoxication leads to apathy. Many polydrug misusers refer to
drugs by their primary mood-altering characteristics. Thus, a distinction
is made between uppers and downers, and particular cocktails of drugs
or sequences of drugs are used to regulate mood in particular ways.
Negative mood states typically follow intoxication, for most classes of
drugs. This is particularly true for drugs such as opioids or cocaine that
lead to tolerance and dependence. The intense negative mood states
that characterize withdrawal syndromes associated with such addictive
drugs motivate habitual drug misuse. The health problems, financial
difficulties and psychosocial adjustment problems that evolve as part of
habitual drug use may also contribute to frequent and intense negative
mood states and paradoxically motivate drug users to use more drugs
to improve their mood state. Negative mood states typically include
some combination of depression, anxiety and anger.
At a perceptual level, some types of drugs, but particularly hallucino-
gens, lead to pronounced abnormalities during intoxication and with-
drawal. In the current decade, widely used hallucinogens include MDMA
(known as Ecstasy or E) and LSD (known as acid). The hallucinations
and perceptual distortions that occur during intoxication are not always
experienced as pleasant. In some situations they lead to great distress.
Brief flashbacks or enduring psychotic states that involve hallucinations
and perceptual distortions may occur following intoxication and these
invariably are experienced as distressing.
With respect to cognition, alcohol and most street drugs lead to
impaired concentration, reasoning and judgement during intoxica-
tion and withdrawal. Long-term regular drug misuse in many instances

Book 1.indb 104 06/03/2012 13:48

 4 • DRUG MISUSE 105

leads to chronic impaired cognitive functioning. The nature, extent and

reversibility of this impairment vary depending on the pattern of drug
misuse. With teenagers, the impaired cognitive functioning associated
with regular drug use may lead to a decline in academic performance.
Drug use may have a negative impact on interpersonal adjustment.
Within the family, drug use often leads to conflict or estrangement
between adolescents and their parents. At school, drug use may lead to
conflict between the adolescent and teachers both because of declining
academic performance and because of antisocial behaviour such as
theft or aggression associated with drug misuse. Young people who
use drugs within a peer-group situation may become deeply involved in
a drug-oriented subculture and break ties with peers who do not abuse
drugs. Some teenagers develop a solitary drug-using pattern and
become increasingly socially isolated as their drug using progresses.
Within the wider community, drug-related antisocial behaviour such
as aggression, theft and selling drugs may bring youngsters into contact
with the juvenile justice system. Drug-related health problems and drug
dependency may bring them into contact with the health service. Conflict
between drug users and health-care professionals may arise in
situations where youngsters expect to be offered prescribed drugs
(such as methadone) as a substitute for street drugs (such as heroin)
and this does not occur.
Drug misuse often occurs with comorbid psychological problems
including conduct disorder, ADHD, specific learning difficulties, mood
disorders, anxiety disorders, schizophrenia and bulimia. In dual diagno-
sis cases, the relationship between these comorbid psychological prob-
lems and drug use is complex (Phillips et al., 2010). Any or all of them
may precede drug use and contribute in some way to the development
of drug-using behaviour. In addition, drug use may precipitate or main-
tain some of these other psychological problems. For example, the use
of cannabis and hallucinogens may precipitate the onset of schizophre-
nia. Chronic polydrug misuse may lead to learning difficulties, and
chronic alcohol use can lead to amnesic syndrome. Amphetamine
usage may lead to anxiety problems. Drug dependence may lead to
chronic conduct problems such as assault and theft. Negative drug-
related experiences such as losses and drug-related accidents may
lead to mood disorder, which in turn may lead to further drug use. Drug
use is also an important risk factor for suicide in teenagers.

Theories
Some of the more clinically influential explanations for drug misuse will
be presented below. These have been classified into five categories.
Biological theories emphasize the role of genetic and physiological
factors in harmful drug use and the disease-like nature of addiction.
Intrapsychic deficit theories point to the importance of personal
psychological vulnerabilities in the aetiology of drug misuse. Cognitive-
behavioural theories underline the significance of conditioning and
other learning processes in the genesis of drug problems. Systemic

Book 1.indb 105 06/03/2012 13:48

 106 C L I N I C A L P S Y C H O L O G Y : A N I N T R O D U C T I O N

theories propose that drug use is strongly influenced by social factors

within the family and community. Integrative theories draw on concepts
from multiple domains to explain problematic drug use and inform
treatment.

Biological theories
Biological formulations are concerned with the disease-like nature of
drug addiction, the role of genetic and temperamental predisposing
factors in rendering some adolescents vulnerable to drug misuse, and
the centrality of neurobiological process to the maintenance of harmful
drug use and addictive behaviour.

The disease model

The self-help organization Narcotics Anonymous (NA), which is
modelled on Alcoholics Anonymous, takes the view that addiction is a
disease that can only be managed, not cured (Narcotics Anonymous,
2008). Within NA it is assumed that this disease is characterized by
abnormities of the central nervous system that give rise to uncontrollable
urges, cravings and loss of control over drug-using behaviour. According
to NA, complete abstinence and regular attendance at NA self-help
meetings are essential for managing the disease of addiction. NA self-
help meetings are convened and attended by other recovering drug
users. Within these meetings a 12-step programme is pursued. The 12
steps of Narcotics Anonymous are set out in Table 4.4.

TABLE 4.4
The 12 steps of Narcotics Anonymous
Step Principle
1 We admitted we were powerless over our addiction and that our lives had become unmanageable.
2 We came to believe that a power greater than ourselves could restore us to sanity.
3 We made a decision to turn our will and our lives over to God as we understood Him.
4 We made a searching and moral inventory of ourselves.
5 We admitted to God, to ourselves and to other human beings the exact nature of our wrongs.
6 We were entirely ready to have God remove all these defects of character.
7 We humbly asked Him to remove our shortcomings.
8 We made a list of all persons we had harmed, and became willing to make amends to them all.
9 We made direct amends to such people whenever possible, except when to do so would injure
them or others.
10 We continued to take personal inventory and when we were wrong, promptly admitted it.
11 We sought through prayer and meditation to improve our conscious contact with God as we
understood Him, praying only for knowledge of His will for the power to carry that out.
12 Having had a spiritual awakening as a result of these steps, we tried to carry this message to
addicts, and to practise these principles in all our affairs.

Note: Adapted from Narcotics Anonymous (2008). Narcotics Anonymous (sixth edition).
Chatsworth, CA: Narcotics Anonymous World Services (p. 17).

Book 1.indb 106 06/03/2012 13:48

 4 • DRUG MISUSE 107

In NA meetings addicts invoke spiritual help to manage their addic-

tion, and new members are teamed up with a sponsor to whom they can
turn for support when they are tempted to relapse. The 12-step approach
was developed in the US in 1935 by Bill Wilson, an alcoholic New York
stockbroker and Dr Robert Smith, an alcoholic physician. Their approach
and the international self-help organization – Alcoholics Anonymous –
that they founded were based on their own experiences of recovery
using principles of the Oxford Group, a non-denominational Christian
organization (Jaffe & Kelly, 2011). NA derives from this movement.
Long-term, regular attendance at NA meetings is incorporated into
some residential treatment programmes for adolescent drug users and
is the mainstay of long-term aftercare in many such programmes. The
Minnesota Model is a widely used example of this practice. It integrates
the 12-step approach with group and family therapy (Winters et al.,
2000). There is evidence from a few treatment outcome studies for the
effectiveness of such programmes for adolescents recovering from
drug dependence. Up to 53% of young people who participate in these
programmes remain abstinent compared with 27% of those who do not
(Jaffe & Kelly, 2011).
Evidence for a simple disease model as proposed by NA is lacking.
Adolescents who use drugs are a heterogeneous group, only one third
of whom go on to develop harmful drug use (Catalano et al., 2011).
Multiple social, psychological and biological factors are implicated in the
aetiology of ongoing harmful drug use within this subgroup. There is no
evidence for an underlying unitary disease process. Also, the disease
model cannot explain the fact that a proportion of very severe drug
users mature out of their addiction in middle age (Jochman & Fromme,
2010).

Genetics
Genetic theories of drug misuse, which propose that vulnerability to
addiction is inherited, are partly supported by the findings of twin, family
and adoption studies (Hasin & Katz, 2010). These show that a predis-
position to drug and alcohol misuse and dependence is moderately
heritable, particularly in males, but that genetic influences on experi-
mentation and recreational drug use are less pronounced. Over half of the
variance in the genetic predisposition to drug, alcohol and nicotine abuse
is shared, and not drug-specific.
However, genetic factors do influence individual differences in sensi-
tivity to, and tolerance for, specific drugs. For example, some males
are genetically predisposed to developing alcohol problems, and the
characteristic that is transmitted may be a low physiological and sub-
jective response to alcohol (Schuckit, 1994).

Temperament
The temperament hypothesis holds that youngsters who develop drug
and alcohol problems do so because they have particular temperamental
characteristics that are partially biologically determined, which predis-
pose them to developing poor self-control. Thus, they are apt to engage

Book 1.indb 107 06/03/2012 13:48

 108 C L I N I C A L P S Y C H O L O G Y : A N I N T R O D U C T I O N

in a range of risky behaviours including drug use. In support of this

hypothesis, difficult temperament in early childhood, sensation-seeking,
a low level of harm-avoidance and low self-control in adolescence have
consistently been related to teenage drug use (Wills & Ainette, 2010).
Youngsters with these temperamental characteristics engage in
dangerous novel experiences and risky rule-breaking behaviour of
which drug misuse is just one example. Related risky behaviours include
driving fast cars or motor bikes, playing high-contact sports, fighting and
theft.
Treatment programmes influenced by this position may aim to train
youngsters in self-control skills so that they can regulate their tendencies
to pursue novel and dangerous experiences including intoxication.
Alternatively they may help these adolescents to refocus their energy
into demanding and risky prosocial leisure or work activities. In some
cases participation in group residential programmes where youngsters
are challenged to take risks and master skills such as horse riding,
sailing or mountain climbing may be effective, although this is still a
controversial approach to treatment (Becker, 2010).
There is little evidence for the effectiveness of wilderness or adven-
ture therapy as a treatment for adolescent drug use. It may be that such
programmes lead to abstinence while young people are engaged in
treatment, but the risk of relapse after treatment is high unless the wil-
derness experience is coupled with evidence-based individual or family
interventions during and after the wilderness experience. A problem
with wilderness therapy, common to all group-based approaches, is
that it runs the risk of contagion effects, whereby groups of adolescent
drug users on such programmes reinforce each other’s positive atti-
tudes to drugs (Dishion & Dodge, 2005).

Neurobiological perspectives
Neurobiological theories of drug use propose that two main systems are
central to the development of harmful drug use and dependence
(Hutchison, 2010). The first is the incentive motivation network or
reward system, which includes the mesolymbic dopamine pathway
involving the ventral tegmental area and the nucleus accumbens. The
second is the control network or inhibitory system, which includes areas
of the prefrontal cortex. These are illustrated in Figure 4.2.
The reward system motivates people to seek things essential for
survival such as food, water and sexual mates. This is the system that
is activated when positive reinforcement occurs (described below). The
inhibitory system helps people consider the consequences of impulsively
seeking these sorts of things without regard to possible dangers of
doing so.
When adolescents repeatedly use drugs such as nicotine, alcohol,
cocaine or heroin, the reward system of the brain that is normally
activated to release dopamine by survival-relevant stimuli such as food,
water and sexual mates is ‘hijacked’ into responding as if drugs were
required for survival. With repeated use, drugs and cues associated
with their use take on increasingly greater motivational significance – a

Book 1.indb 108 06/03/2012 13:48

 4 • DRUG MISUSE 109

Figure 4.2 The reward system in the human brain. Note: The ventral tegmental area is
connected to both the nucleus accumbens and the prefrontal cortex via the pathways in the
diagram, and dopamine is the principal neurotransmitter involved in the reward system

process known as incentive sensitization – and drug use becomes

compulsive. Eventually with chronic use of addictive drugs such as
heroin or cocaine, people come to find drug use more rewarding than
anything else, and other activities become far less rewarding. Through
a combination of classical conditioning (described below) and incentive
sensitization, intense motivation to use drugs – experienced as urges or
cravings – comes to be activated by cues such as situations or people
associated with drug use, and causes relapse even after long periods of
abstinence. Loss of control over drug use is associated with greater
activation of the brain’s reward system relative to the control system
when exposed to cues associated with drug use.
Adolescence is a critical period of addiction vulnerability due to the
characteristics of the nervous system during this neurodevelopmental
stage (Chambers et al., 2003). During adolescence there is a relative
over-functioning of the incentive motivation network or reward system
and under-functioning of the control network or inhibitory system.
Adolescence is associated with increased impulsivity, risk-taking and
novelty seeking, and with experiencing novel stimuli as more strongly
reinforcing than in adulthood.
From an evolutionary perspective, this increased risk-taking and
novelty-seeking may have been adaptive because it motivated
adolescents to explore novel behaviours associated with adult roles.
Unfortunately, this neurodevelopmental stage renders adolescents
vulnerable to experimenting with drugs because drug taking is risky and
provides novel experiences. It also renders adolescents vulnerable to
addiction because the positive effects of drugs are experienced as more
reinforcing than at other stages of the life cycle.
As adolescents mature into adulthood, the inhibitory system’s effect
on the reward system increases, and consequently risk-taking behaviour

Book 1.indb 109 06/03/2012 13:48

 110 C L I N I C A L P S Y C H O L O G Y : A N I N T R O D U C T I O N

decreases. This process is facilitated by pruning of cortical synapses

and increased myelination, particularly in the frontal and temporal lobes,
which leads to an increase in the efficiency of neural circuitry between
the inhibitory system and the reward system. There is some evidence
that pruning and myelination are adversely affected by frequent drug
use in adolescence, which in turn may account for greater vulnerability
to addiction during the teenage years (Lubman & Yücel, 2008).
Neurobiological theories also propose that habitual drug use leads to
long-term drug-induced changes in the brain’s reward system (Shaham
& Hope, 2005). This neuroadaptation accounts for the phenomena of
tolerance, dependence, withdrawal, and the high rate of relapse among
recovered addicts. With tolerance, a gradual increase in drug dosage is
required for intoxication to occur. This increase in dosage in turn leads
to physiological dependence and the related phenomenon of unpleasant
or hazardous withdrawal symptoms when drug taking ceases abruptly.
An attempt to avoid this withdrawal syndrome maintains further drug
use. Extensive pharmacological evidence supports the hypothesis that
for certain classes of drugs, tolerance, dependence and withdrawal
occur. In particular these phenomena are associated with habitual use
of alcohol, opioids, stimulants (such as cocaine) and sedatives, but not
hallucinogens (such as cannabis, MDMA and LSD) (Kaminer & Marsch,
2011).
Neurobiological theories have led to the inclusion of detoxification in
treatment programmes for adolescents who have developed depend-
ence. These theories have also informed the development of pharma-
cological interventions such as methadone maintenance programmes
(Kaminer & Marsch, 2011). In such programmes, youngsters who have
developed opioid dependency are prescribed a daily dose of metha-
done as a substitute for street opioids. Methadone prevents withdrawal
symptoms from occurring, but does not give the ‘high’ associated with
heroin. People on methadone can function quite well socially and occu-
pationally, and avoid the dangers of procuring and using street drugs.
Methadone maintenance programmes typically include routine monitor-
ing of drug use through urinalysis and adjunctive counselling. They are
effective with a proportion of opioid-dependent adolescents.

Intrapsychic deficit theories

A number of theories account for drug misuse in terms of specific
intrapsychic vulnerabilities and deficits. Among the more clinically
influential are those that invoke personality traits, stress and coping
processes, learning difficulties and the challenges of identity formation
to explain the development of drug misuse.

Addictive personality
The idea that people are predisposed to develop drug problems or
addiction because they have particular personality traits or attributes is
often referred to as the addictive personality hypothesis. This is quite

Book 1.indb 110 06/03/2012 13:48

 4 • DRUG MISUSE 111

similar to the temperament hypothesis mentioned earlier, although the

addictive personality hypothesis also assumes that environmental
factors play a role in the development of personality.
There is some support for the addictive personality hypothesis. For
example, a meta-analysis of data on personality traits of adult drug
users showed that high levels of neuroticism and disinhibition and low
levels of conscientiousness and agreeableness characterize adult
substance use disorders (Kotov et al., 2010).

Stress and coping through self-medication

Stress and coping formulations propose that drugs are used to alleviate
negative affective states, and specific drugs are chosen because of their
unique effects. This theory is often referred to as the self-medication
hypothesis (Grunberg et al., 2011; Khantzian, 2003). From this perspec-
tive drugs use is conceptualized as a strategy for coping with negative
mood states or psychological disorders such as depression, posttrau-
matic stress disorder (PTSD) or psychosis that have arisen in response
to a range of current or past adversities such as abuse, neglect, bereave-
ment, armed combat or problematic parent–child relationships.
There are many versions of this broad hypothesis. For example, psy-
choanalytic theorists have argued that low levels of care and high levels
of criticism from primary caregivers in early childhood may lead to inse-
cure attachment, unmet dependency needs, harsh superego develop-
ment and low-self esteem. Drugs are used, according to this formulation,
to alleviate the negative mood states that arise from these detrimental
formative experiences (Wieder & Kaplan, 1969). Another variant of this
position proposes that where adolescents have suffered sexual abuse
or exposure to other traumatic events, drugs may be used to deal with
the symptoms of posttraumatic stress disorder or depression that have
arisen from these adverse experiences. A third variant is that teenagers
with a genetic vulnerability for psychosis may use drugs to cope with
prodromal psychotic symptoms.
There is little doubt that in a proportion of cases adolescents use
drugs to deal with stress, trauma and related psychopathology. In clini-
cal samples between 70% and 80% of cases have comorbid substance
use and other psychological disorders (Kaminer et al., 2011a). However,
in many cases drug use is not preceded by stress or psychopathology.
Rather stress and psychological difficulties arise as a result of harmful
drug use. Where drug use occurs with comorbid psychological disor-
ders such as PTSD, depression or psychosis, both the drug-use prob-
lem and the comorbid difficulties require treatment. There is no evidence
to suggest that treating comorbid disorders alleviates drug misuse or
addiction.

Learning difficulties
Another intrapsychic deficit that has been suggested to predispose
youngsters to developing drug misuse is learning difficulties. According

Book 1.indb 111 06/03/2012 13:48

 112 C L I N I C A L P S Y C H O L O G Y : A N I N T R O D U C T I O N

to this position, children who have learning difficulties and who experi-
ence academic failure at school do not develop a strong commitment to
achieving academic goals and turn to drug use as an alternative life-
style (Mason, 2010). Interventions that derive from this perspective aim
to provide adolescents with a school curriculum appropriate to their abil-
ity levels and a participative ethos that includes teenagers and their
parents in school activities so as to enhance commitment to academic
goals (Griffin & Botvin, 2010).

Identity formation
Erik Erikson (1950, 1968) argued that the lack of an established identity
during adolescence is a normative intrapsychic deficit and that partici-
pation in a drug-using subculture is one of a wide range of lifestyles that
may be explored during the adolescent’s search for adult identity and
autonomy from parental control. Recent studies have shown that young
people who consolidate their identities in early adulthood engage in less
drug use and other risky behaviours than those who have difficulty with
identity formation (e.g., Arnett, 2005; Schwartz et al., 2010).
Treatment programmes based on this position focus on facilitating
individuation and developing alternatives to drug taking as a route to
autonomy and identity formation. The treatment of chronic drug depend-
ence in drug-free therapeutic communities such as Synanon, Daytop
and Phoenix House in the US is consistent with this theoretical position
(DeLeon, 2000). Therapeutic communities facilitate the development of
drug-free lifestyles and identities by offering a context within which ado-
lescent can engage in structured community living and therapeutic
activities with ex-addicts who have successfully become drug-free.
Research on therapeutic communities has shown that they can be
effective for a proportion of young adult addicts who are motivated to
engage in treatment (DeLeon, 2000; Smith et al., 2006). Therapeutic
communities are probably not an appropriate intervention for young
adolescents.

Cognitive-behavioural theories
Cognitive-behavioural theories focus on the role of classical and
operant conditioning and cognitive processes in the maintenance of
drug misuse.

Operant conditioning
Operant conditioning or instrumental learning theories propose that
drug use is maintained initially by positive reinforcement associated
with the mood-elevating effects of drugs and later, in the case of
dependence-producing substances such as alcohol, cocaine or heroin,
by negative reinforcement, where drug use prevents aversive withdrawal
symptoms (e.g. O’Brien et al., 1992; Schulteis & Koob, 1996). Treatment
programmes based on this formulation include initial detoxification so

Book 1.indb 112 06/03/2012 13:48

 4 • DRUG MISUSE 113

drugs lose their negative reinforcement value, and the provision of

positive reinforcement for alternatives to drug-using behaviours.
The Adolescent Contingency Reinforcement Approach (A-CRA) is
an evidence-based therapy in which operant conditioning is the central
intervention (Dakof et al., 2011; Godley et al., 2006). With A-CRA,
therapists work with adolescents and their parents, both alone and in
conjoint sessions, to identify reinforcers or rewards that young people
value and that will improve the quality of their lives, and reduce drug
use. The process begins with a functional analysis of both drug using
and prosocial behaviour to identify situations that trigger drug use and
prosocial behaviours, and related reinforcers. Adolescents are helped
to set goals and plan prosocial activities to improve their quality of life
and, with their parents, arrangements are made for them to receive
reinforcement for doing so. Adolescents and parents engage in
communication, problem-solving, and relapse management skills
training. Homework assignments are set and reviewed in all sessions,
and drug use is monitored with regular urinalysis testing. A-CRA
typically spans about 3 months of weekly sessions. In a series of trials
A-CRA has been found to be effective for adolescents with a range of
drug use problems (Waldron & Turner, 2008).

Classical conditioning
Wikler (1973) has offered an explanation of relapse following detoxifica-
tion in people who have developed tolerance and dependence using a
classical conditioning framework. According to this position, certain
conditioned stimuli (CSs) or cues in the environments of drug users
elicit withdrawal symptoms and craving (conditioned responses or
CRs), because in the past these cues have been associated with with-
drawal symptoms that are conceptualized as unconditioned stimuli
(UCSs)
In cue exposure treatment, based on this formulation, exposure to
withdrawal and craving eliciting cues (CSs) without engaging in drug
taking leads to extinction of the CRs, particularly cravings. Adolescents
enter situations that elicit craving, observe videotapes or audiotapes of
such situations, or undergo imaginal exposure to such situations and
concurrently use a variety of coping strategies to tolerate their discomfort
and avoid drug-taking.
There is controversy about the effectiveness of cue exposure treat-
ment, and few studies have evaluated it in the treatment of adolescent
drug users (Conklin & Tiffany, 2002; Drummond et al., 1995).

Cognitive-behaviour therapy
Within cognitive-behaviour therapy (CBT) models, drug use is concep-
tualized as a set of learned behaviours and related cognitions (Kaminer
et al., 2011b). Drug-use behaviours, and related urges, cravings, beliefs
and expectations about the risks and benefits of drug use and the
degree to which drug use can be controlled, are assumed to be learned

Book 1.indb 113 06/03/2012 13:48

 114 C L I N I C A L P S Y C H O L O G Y : A N I N T R O D U C T I O N

through classical and operant conditioning as well as through cognitive

learning processes.
Witkiewitz and Marlatt (2004) argue that in high-risk situations, drug
users who have well-rehearsed coping strategies and use them
effectively develop increased self-efficacy beliefs and a decreased
probability of relapse. Those who have poor coping strategies are driven
to relapse by their low self-efficacy beliefs in their capacity to avoid
substance use and their expectations of a high from drug use. This
leads to the abstinence violation effect (AVE), where guilt and a sense
of loss of control predominate. With the AVE people may say to
themselves, ‘I’ve relapsed. I’ve let myself and my family down. I have no
control over my drug taking. There is no point in trying to stop now.’ This
failure experience in turn leads to an increased probability of a minor
slip becoming a major relapse.
CBT for drug use involves helping adolescents become motivated to
reduce or stop drug use and develop and implement skills and coping
strategies to avoid relapse. Motivational interviewing or motivational
enhancement therapy is the main intervention used to facilitate engage-
ment in treatment (Miller & Rollnick, 2002; Tevyaw & Monti, 2004). With
motivational interviewing the psychologist invites the young person to
describe their drug-using behaviour and consider the pros and cons of
continued drug use; gives normative feedback on the effects of the
young person’s drug use and options for changing drug-using behaviour;
invites the young person to make a decision about changing their drug
use; and supports their self-efficacy beliefs about reducing drug use.
CBT programmes help young people set drug-reduction goals, iden-
tify situational cues that elicit urges or cravings to use drugs, and
develop skills for drug refusal and strategies for coping with urges and
cravings to use drugs in risky situations where they might relapse. In
CBT programmes young people also develop skills for managing nega-
tive emotions including anger, anxiety and depression without recourse
to drug use. Finally, CBT programmes help young people develop com-
munication and problem-solving skills and use these to increase social
support and develop a drug-free lifestyle.
Results from a series of controlled trials support the effectiveness of
both individual and group-based CBT for adolescent drug use.
Furthermore, contagion effects common in group treatment of antisocial
youngsters have not been found in trials of CBT for adolescent drug
misuse (Dishion & Dodge, 2005). Mindfulness-based meditation as a
relapse prevention strategy has recently been incorporated into CBT for
drug use (Zgierska et al., 2009).

Systemic theories
Systemic theories of drug misuse propose that family problems and
challenges in the wider social system such as social disadvantage,
deviant peer-group membership and drug availability are central to the
aetiology of drug problems.

Book 1.indb 114 06/03/2012 13:48

 4 • DRUG MISUSE 115

Family systems approaches

The ideas that adolescent drug misuse is caused or maintained by
parental drug use, poor parenting skills and family disorganization are
some of the more important family systems hypotheses. Empirical
studies have established an association between each of these factors
and adolescent drug use (Kliewer, 2010). In families where parents use
drugs, adolescents may learn drug using behaviour patterns directly
through a process of modelling. They may acquire positive attitudes to
drugs through exposure to their parents’ permissive attitudes. Further-
more, parents’ drug-using behaviour may compromise their capacity to
parent their adolescents adequately. If parents do not jointly establish
clear rules prohibiting drug use and consistently apply clear conse-
quences for violating these rules, then adolescent drug use is more
likely to occur.
Parenting problems may occur within a broad pattern of family
disorganization associated with adolescent drug use. The pattern may
include parental psychological problems; lack of a clear parental alliance
and clear intergenerational boundaries between adolescents and
parents; poor family communication, problem-solving and conflict-
resolution skills; extreme family enmeshment or disengagement; and
difficulty addressing the family life-cycle transitions, especially that of
facilitating adolescent autonomy. Within such disorganized families drug
misuse may serve an organizing function, since it introduces certain
predictable routines into family life and provides a focus for parental
concern, which may increase family cohesion and prevent parental
separation.
Multidimensional family therapy (MDFT, Liddle, 2010), functional
family therapy (FFT, Waldron & Brody, 2010), brief strategic family
therapy (BSFT, Robbins et al., 2010) and multisystemic therapy (MST,
Henggeler & Schaeffer, 2010) are evidence-based approaches to
treating adolescent drug misuse based on systemic theory (Waldron &
Turner, 2008). All of these approaches involve working directly with
adolescents and their parents to improve family functioning as an
avenue to reducing adolescent drug misuse. Parents are helped to
establish clear rules prohibiting drug use and consistently apply clear
consequences for violating these rules.
These approaches also facilitate the development of positive family
relationships and good family communication, problem-solving and
conflict-resolution skills. There is a progression from initial engagement,
to becoming drug-free, to addressing family issues associated with fos-
tering adolescent development and autonomy, to disengagement,
where the emphasis is on planning for relapse prevention. With these
family-based approaches, treatment typically involves conjoint family
sessions, separate sessions with adolescents and parents, and ses-
sions with involved health, social service and juvenile justice profes-
sionals and school staff, as required. Evidence from controlled trials
shows that evidence-based family-oriented approaches are very effec-
tive for adolescent drug-use problems (Waldron & Turner, 2008).

Book 1.indb 115 06/03/2012 13:48

 116 C L I N I C A L P S Y C H O L O G Y : A N I N T R O D U C T I O N

Extrafamilial social problems

Hypotheses about extrafamilial social problems propose that social
disadvantage and deviant peer-group membership, as well as drug
availability, cause and maintain drug misuse.

Social disadvantage
Social disadvantage theories argue that neighbourhoods character-
ized by poverty, low socio-economic status, high population density
and high crime rates create a context within which drug misuse can
flourish. This is because drugs offer an escape from the multiple
stresses associated with this type of social environment; they are avail-
able in these environments; and they are socially sanctioned within a
crime-oriented subculture (Catalano et al., 2011; Gardner et al., 2010).
Social disadvantage theory entails the view that effective intervention
programmes support families, enhance educational and vocational
opportunities for young people, and strengthen communities. Evidence
from prevention studies supports the effectiveness of parent training
programmes during the prenatal, infancy, childhood and adolescent
stages of the life cycle; school-based and after-school programmes that
enhance social and academic competence; vocational programmes
that create youth employment opportunities linked to ongoing educa-
tion; and community-based programmes that strengthen community
cohesion and reduce alcohol and drug availability to young people
(Catalano et al., 2011).

Deviant peer-group membership

Problem-behaviour theory is an example of a formulation that links
drug misuse to deviant peer-group membership. This theory pro-
poses that drug use is one of a series of interrelated problem be-
haviours, which reflect adherence to unconventional attitudes held by
a deviant peer group (Catalano et al., 2011; Jessor & Jessor, 1977).
Adolescents engage in these behaviours to obtain acceptance from
their deviant peer group and for personal excitement. Young people
are predisposed to developing problem behaviours if they are alien-
ated from mainstream society. This may be reflected in their weak
attachments to parents, their rejection of authority, their valuing
independence more than academic achievement, and their lack of
religiosity. A wealth of survey data supports this theory (Andrews &
Hops, 2010).
Treatment programmes based on the hypothesis that deviant peer-
group membership is central to adolescent drug abuse provide residen-
tial peer-group-based treatment, within the context of a therapeutic
community, where the rejection of drug use is part of the therapeutic
community’s subculture. Therapeutic communities as a treatment for
drug use have been mentioned earlier, in the section on identify forma-
tion, where it was noted that they can be effective for a proportion of
young adult addicts, but may not be appropriate for young adolescents
(DeLeon, 2000; Smith et al., 2006).

Book 1.indb 116 06/03/2012 13:48

 4 • DRUG MISUSE 117

Availability
Hypotheses about availability suggest that lenient laws or inadequately
enforced laws concerning teenage use of nicotine, alcohol and street
drugs increase the probability of adolescent drug use. This type of the-
ory has few treatment implications but suggests important avenues for
prevention. Prevention programmes, according to this view, should pro-
mote stricter drug-related legislation, and the enforcement of laws
affecting availability of drugs to teenagers. The availability hypotheses
has largely been supported by empirical tests, and prevention pro-
grammes based on it have been moderately effective (Toumbourou et
al., 2007).

Social norms
That social norms may contribute to the development of drug misuse is
a widely held view. There is strong evidence from empirical studies for
a causal link between exposure to favourable media attitudes to nicotine,
alcohol and illicit drug use and drug-using behaviour (Nunez-Smith et
al., 2010). One implication of this position is that the risks of drug use
may be reduced by policies and legislation that prohibit positive media-
based messages about nicotine, alcohol and drug use (Snyder &
Nadorff, 2010).

Integrative theories
Two important integrative theories that draw on concepts from multiple
domains are Prochaska and DiClemente’s transtheoretical stages of
change model (Prochaska et al., 1992) and West’s (2006) synthetic
model of motivation and addiction.

Transtheoretical stages of change model

From an analysis of 24 schools of psychotherapy, Prochaska and
DiClemente identified five stages of therapeutic change which they
labelled pre-contemplation, contemplation, preparation, action and
maintenance (Prochaska et al., 1992). They also found, by surveying
clients and therapists engaged in therapy, that specific techniques were
maximally effective in helping clients make the transition from one stage
of change to the next.
The techniques identified in this survey fall into the categories of
support, belief exploration and consulting to behavioural change. In
most schools of therapy there tends to be a progression from support,
to belief-system exploration, to behavioural change consultation.
Prochaska and DiClemente have applied their transtheoretical stages
of change model and related interventions to the treatment of addictive
behaviours including drug use (DiClemente, 2003). According to this
model, in the pre-contemplation stage, the provision of support creates
a climate within which adolescents may ventilate their feelings and
express their views about their drug problems and life situation. Such

Book 1.indb 117 06/03/2012 13:48

 118 C L I N I C A L P S Y C H O L O G Y : A N I N T R O D U C T I O N

support facilitates movement from the pre-contemplation to the contem-

plation stage.
Facilitating the exploration of beliefs about the pros and cons of
modifying drug use, according to the model, may promote movement
from the contemplation to the planning stage. In the transition from the
planning to the action stage the most useful interventions are helping
adolescents examine various action plans for reducing drug use, and
facilitating the development of an emotional commitment to change. In
moving from the action to the maintenance stage the focus is on helping
adolescents integrate positive changes into their lives and avoidance or
management of relapses.
Prochaska and DiClemente argue that five principal categories of
factors are involved in symptom maintenance: situational maintaining
factors, maladaptive cognitions, interpersonal conflicts, family conflicts
and intrapsychic conflicts. These factors are hierarchically organized,
with earlier factors being more responsive to change than later factors.
Effective therapy follows one of three strategies once the person has
passed through to the action stage. The first strategy is to target the
situations that maintain drug use and only shift to the cognitive level or
higher levels if no change occurs. The second strategy is to focus on
the family systems level, which is the key level within the hierarchy
typically involved in maintaining drug use. A third strategy is to target all
levels, by, for example, offering individual work to alter maladaptive
cognitions and intrapsychic conflicts associated with drug use; peer-
group work and social skills training to target interpersonal conflicts or
deviant peer-group membership; and family work to address family
conflicts and drug misuse maintaining family interaction patterns.
The central prediction of this model is that stage-specific interventions
will be more effective than those that are not stage-specific. Little
research has been conducted to test this hypothesis with adolescent
drug users, and results from studies of adults are mixed (West, 2006).
However, the theory has been very influential clinically and has informed
the development of procedures such as harm reduction (Marlatt &
Witkiewitz, 2010) and motivational interviewing (Macgowan & Engle,
2010), where the aim is not to promote abstinence or reduction in drug
use, but to prevent drug-related harm and facilitate movement towards
planning and action stages. Needle exchanges and provision of safe
injection sites are examples of harm-reduction interventions. Motivational
interviewing has been described above in the section on CBT.

West’s synthetic theory of motivation and addiction

Robert West (2006), a major critic of the stages of change model,
proposed that addiction is not a matter of conscious choice and
progression through invariant stages, but a reward-seeking behaviour
over which a person has lost control. It arises from abnormalities in the
motivational system, many of which are not conscious, or abnormalities
in the physical and social environment that are conducive to prioritizing
drug use. Abnormalities in the motivational system may be caused by

Book 1.indb 118 06/03/2012 13:48

 4 • DRUG MISUSE 119

drug use, for example withdrawal symptoms and the acquired drive to
seek drugs to alleviate these, or they may be due to predisposing factors
such as negative affectivity or impulsivity.
West explains drug addiction in terms of his synthetic theory of moti-
vation, which is also referred to as PRIME theory. PRIME is an acronym
for plans, responses, impulses and inhibitory forces (felt as urges),
motives (felt as wants or needs) and evaluative beliefs. According to
PRIME theory, adolescents’ conscious plans and evaluations influence
their drug use through motives, and motives influence drug use through
impulses which are determined in large part by non-conscious pro-
cesses. The motivational system that underpins drug use is influenced
by past experiences through non-conscious processes such as habitu-
ation and sensitization, classical and operant conditioning, and con-
scious processes such as cognitive learning. However, it is also
influenced by stimuli in the immediate internal and external environ-
ment. Therefore, an adolescent’s motivation to use drugs is inherently
unstable and changes from moment to moment.
Treatment based on this model capitalizes on the instability of the
motivational system by bolstering the adolescent’s motivation to
exercise restraint or temporarily suppress the forces driving drug use
and addressing relevant predisposing factors. This may be done by, for
example, modifying relevant emotional or environmental factors such
as negative mood states induced by stressful life events, drug availability,
peer pressure to use drugs, or family disorganization. According to
West‘s model, treatment sessions should be scheduled close together
so that they have a cumulative effect in altering the adolescent’s
feelings, impulses and beliefs that motivate them to use drugs.
West’s formulation integrates a vast body of animal and human
research on the psychology, sociology and neurobiology of addiction,
and offers an alternative to the oversimplified, but intuitively appealing,
stages of change model described earlier. However, it has not yet led to
the development of treatments for adolescent drug use.

Assessment
Assessment of adolescents with drug problems may be conducted
by multidisciplinary teams that include clinical psychologists and medi-
cal staff, and should involve interviews with the adolescent and parents
or carers. Brief questionnaires such as the Personal Experience
Screening Questionnaire (PESQ, Winters, 1991) may be used to screen
for drug use. Comprehensive questionnaires such as the Per-
sonal Experience Inventory (PEI, Winters & Henly, 1989) and compre-
hensive structured interviews such as the Global Appraisal of Individual
Needs (GAIN, Dennis, 1998) may be used for a more thorough assess-
ment of drug use severity and personal, family and school-related
adjustment problems.
Physical examination and regular urinalysis may be included in the
assessment of adolescents with drug problems. Physical examina-
tion facilitates the identification and treatment of drug-related physical

Book 1.indb 119 06/03/2012 13:48

 120 C L I N I C A L P S Y C H O L O G Y : A N I N T R O D U C T I O N

Figure 4.3 General formulation model for adolescent drug misuse

complications including hepatitis and HIV infection. Awareness of the

extent of physical problems may motivate adolescents and their
families to engage in treatment. Regular urinalysis provides reliable
information on relapse, which is critical for effective treatment of habit-
ual drug users. A formulation is drawn up that integrates assessment
information; highlights predisposing, precipitating, maintaining and pro-
tective factors; and indicates whether the drug problem reflects tran-
sient experimentation or a more entrenched pattern of habitual drug
misuse. This formulation is used to guide intervention. A general clinical
formulation model for adolescent drug misuse is given in Figure 4.3.

Treatment
Treatment of adolescent drug use should aim to engage the adolescent
and parents or carers in therapy, motivate them to use therapy to
work towards reducing adolescent drug use, and address the young
person’s personal, family- and school-related difficulties. Reviews of
treatment outcome studies show that family-oriented approaches
such as MDFT, FFT, BSFT, MST and A-CRA, and individual ap-
proaches such as CBT, combined with motivational interviewing are
effective interventions for adolescent drug use (Dakof et al., 2011;

Book 1.indb 120 06/03/2012 13:48

 4 • DRUG MISUSE 121

Kaminer et al., 2011b; Waldron & Turner, 2008; Williams & Chang,
2000). Literature reviews consistently show that for adolescents living
with their parents, evidence-based family-oriented treatment
programmes are the treatment of choice for drug problems because
they have the best outcome, involve the young person’s family as a
treatment resource, and modify family problems that may be maintaining
adolescent drug use (e.g., Williams & Chang, 2000). Family-based
approaches have been shown to be effective for engaging adolescent
drug users and their networks in therapy, for reducing drug misuse, for
improving associated behaviour problems, for improving overall family
functioning and for preventing relapse.
Where there are significant obstacles to involving families in
treatment, CBT combined with initial motivational interviewing is the
intervention of choice. Motivational interviewing facilitates engagement
in therapy and through CBT young people develop skills to reduce drug
use, communicate, problem-solve and deal with relapses. Where
adolescents have developed physiological dependence, psychological
interventions may be combined with initial detoxification or with long-
term pharmacological interventions such as methadone maintenance
for opioid dependence (Kaminer & Marsch, 2011). For chronic drug
problems with a high risk of relapse, long-term aftercare though regular
attendance at 12-step NA meetings may prevent relapse (Jaffe & Kelly,
2011). This overall approach to treatment of adolescent drug use is
consistent with international best practice guidelines (American
Academy of Child and Adolescent Psychiatry, 2005; Department of
Health 2007; NICE, 2008b).

Controversies
A central controversy in the field of adolescent drug use concerns the
stability over time of the motivation to use drugs. In the stages of change
model, Prochaska and DiClemente argue that motivation to cease drug
use evolves through a series of relatively stable and sequential stages
of change from pre-contemplation through contemplation, planning and
action to maintenance (DiClemente, 2003; Proschaska et al., 1992).
In contrast, Robert West (2006) argues that motivation to cease drug
use is inherently unstable. He has put forward the following arguments
against the stages of change model. The precise boundaries of any of
the stages of change are arbitrarily drawn in research studies; for
example, a person is in the planning stage if their plans apply to the next
30 days. There is no evidence that stages are always stable and that
progression through them is invariably orderly. There is also no evidence
that drug users’ attempts to quit are always guided by conscious,
coherent plans, and much evidence that unconscious processes,
classical and operant conditioning, erratic impulses, and highly specific
environmental cues affect the development and cessation of drug use.
In West’s (2006) synthetic theory of addiction he proposes that abnor-
malities of the motivational system are central to addiction, that the
motivational system is inherently unstable, and that important aspects

Book 1.indb 121 06/03/2012 13:48

 122 C L I N I C A L P S Y C H O L O G Y : A N I N T R O D U C T I O N

of the motivation to use or abstain from drugs are governed by un-

conscious learning processes and impulses. According to West, inter-
ventions should not stimulate adolescents to think about what ‘stage’
they are in or be matched to such stages, but rather they should put
maximum tolerable pressure on the young person to cease drug use.
A related controversy concerns harm-reduction programmes such as
needle exchanges, safe injection sites, and the provision of free tests of
the quality of MDMA sold at raves. Advocates of harm-reduction
programmes argue that in the absence of highly effective treatments
that all drug users and addicts are highly motivated to use, mortality or
morbidity due to using street drugs of unknown quality under adverse
conditions may be reduced by pragmatic and humane harm-reduction
interventions (Marlatt & Witkiewitz, 2010). Critics of this approach argue
that harm-reduction interventions send a message to adolescents that
drug use is acceptable (Leshner, 2008).

Summary
Habitual drug misuse in adolescence is of particular concern to
clinical psychologists because it may have a negative long-
term effect on adolescents and an intergenerational effect on
their children. A conservative estimate is that between 5% and
10% of teenagers under 19 have drug problems serious
enough to require clinical intervention.
A distinction is made between drug dependence and drug
misuse. While drug misuse refers to using drugs in such a way
that the person is harmed, drug dependence refers to those
situations where there is a compulsive pattern of use that may
involve physiological changes that accompany the phenomena
of tolerance and withdrawal. Drug misuse is associated with a
wide variety of behaviour patterns which may be described in
terms of the age of onset, the duration of drug misuse, the
frequency of use, the range of substances used, and the
amount used.
Physiological features of drug misuse may be grouped into
those associated with intoxication, those that follow intoxica-
tion, those associated with withdrawal following the develop-
ment of dependence, and medical complications that arise. At
an affective level, negative mood states typically follow the
euphoria of intoxication for most classes of drugs. At a percep-
tual level, some types of drug, but particularly hallucinogens,
lead to pronounced abnormalities during intoxication and with-
drawal. With respect to cognition, most street drugs lead to
impaired concentration, reasoning and judgement during intox-
ication and withdrawal. Long-term regular drug misuse in many
instances leads to impaired cognitive functioning. Drug misuse

Book 1.indb 122 06/03/2012 13:48

 4 • DRUG MISUSE 123

may have an impact on interpersonal adjustment leading to

family, school and peer-group-based difficulties.
Drug misuse often occurs with comorbid psychological
problems including conduct disorder, ADHD, specific learning
difficulties, mood disorders, anxiety disorders, psychosis and
bulimia. The relationship between these comorbid psychological
problems and drug misuse is complex. Explanations for drug
misuse focus on biological factors, intrapsychic deficits,
cognitive-behavioural learning processes, social factors and
multiple factors from these four domains.
Biological formulations are concerned with the disease-
like nature of drug addiction, the role of genetic and tempera-
mental predisposing factors in rendering some adolescents
vulnerable to drug misuse, and the centrality of neurobiologi-
cal processes to the maintenance of harmful drug use and
addictive behaviour. Biological theories have informed the
development of pharmacological treatments for drug prob-
lems such as detoxification and methadone maintenance, and
have been endorsed by the self-help movement Narcotics
Anonymous to justify its claims that addiction is a medical
disease.
With regard to theories that emphasize the role of intra-
psychic vulnerabilities and deficits, among the more clinically
influential are those that invoke personality traits, stress and
coping processes, learning difficulties and the challenges of
identity formation to explain the development of drug misuse.
These perspectives have informed the development of a range
of psychotherapeutic approaches to drug misuse including
drug-free therapeutic communities. Cognitive-behavioural
theories explain drug problems and their treatment in terms of
classical and operant conditioning and various cognitive learn-
ing processes. CBT, motivational interviewing, contingency
management and cue-exposure treatments for dug misuse
developed within the cognitive-behavioural tradition.
Systemic theories of drug misuse propose that family prob-
lems and challenges in the wider social system, such as social
disadvantage, deviant peer-group membership and drug avail-
ability are central to the aetiology of drug problems. Family
therapy and community-oriented approaches to the prevention
of drug use are based on systemic theories.
With regard to integrative theories, Prochaska and
DiClemente propose that the motivation to cease drug use
evolves through a series of sequential stages and effective
intervention must be matched to the adolescent’s readiness to
change. In contrast, West’s synthetic theory of addiction pro-
poses that the motivational system is inherently unstable, and
that effective interventions place maximum tolerable pressure
on the young person to cease drug use.

Book 1.indb 123 06/03/2012 13:48

 124 C L I N I C A L P S Y C H O L O G Y : A N I N T R O D U C T I O N

The assessment of adolescents with drug problems should

be multidisciplinary and involve both medical and psychologi-
cal evaluation. Treatment of adolescent drug use should aim to
engage the adolescent and parents or carers in therapy, moti-
vate them to use therapy to work towards reducing adolescent
drug use, and address the young person’s personal, family-
and school-related difficulties. Evidence-based family therapy
is the treatment of choice for adolescent drug problems. There
is controversy about the value of harm-reduction interventions
for drug problems, with one group proposing that such inter-
ventions improve public health while another argues that they
give adolescents the message that drug misuse is acceptable.

Questions
● What are the principal differences between drug experimentation
and harmful drug use?
● What are the areas that need to be covered when offering a
comprehensive description of the clinical features of an adolescent
with drug problems?
● How prevalent is drug misuse?
● What are the main risk factors for drug misuse?
● What are the main biological, psychological and integrative theories
of drug misuse and the main research findings relevant to these
theories?
● What are the main evidence-based approaches to the assessment
and treatment of drug misuse?
● Are harm-avoidance strategies for addressing drug misuse justified?
● Should parents be included in the treatment of adolescent drug
problems?

FURTHER READING
Professional
● Carr, A. (2006). Handbook of child and adolescent clinical psychology: A
contextual approach (second edition). London: Routledge (Chapter 16).
● Kaminer, Y. & Winters, K. (2011). Clinical manual of adolescent sub-
stance abuse treatment. Arlington, VA: American Psychiatric Publishing.
● Weisz, J. & Kazdin, A. (2010). Evidence-based psychotherapies for chil-
dren and adolescents (second edition). New York: Guilford Press.

WEBSITES
● AACAP (American Academy of Child and Adolescent Psychiatry) prac-
tice parameters for the treatment of substance use disorders:
www.aacap.org/cs/root/member_information/practice_information/
practice_parameters/practice_parameters

Book 1.indb 124 06/03/2012 13:48

 4 • DRUG MISUSE 125

● BSFT manual for Adolescent Drug misuse:

http://archives.drugabuse.gov/txmanuals/bsft/bsftindex.html
● Chestnut Health Systems manuals for MDFT, CBT, A-CRA and GAIN
are available:
www.chestnut.org/LI/cyt/products
● Drugscope, UK:
www.drugscope.org.uk
● Drug Treatment Centre Board, Ireland:
www.addictionireland.ie
● Gilbert Botvin’s Life Skills Training drug misuse prevention programme:
www.lifeskillstraining.com
● Howard Liddle’s Multidimensional Family Therapy (MDFT):
www.miami.edu/ctrada
● Jim Alexander and Tom Sexton’s Functional Family Therapy (FFT):
www.fftinc.com
● José Szapocznik’s Brief Strategic Family Therapy (BSFT):
www.bsft.org
● Narcotics Anonymous:
www.na.org
● National Institute on Drug Abuse, USA:
www.nida.nih.gov
● National Treatment Agency for Substance Misuse, UK:
www.nta.nhs.uk
● NICE (National Institute for Clinical Excellence) guidelines for treating
drug misuse:
http://guidance.nice.org.uk/Topic/MentalHealthBehavioural
● Scott Henggeler’s Multisystemic Therapy (MST):
http://mstservices.com
● Substance Abuse and Mental Health Services Administration, USA:
www.samhsa.gov

Book 1.indb 125 06/03/2012 13:48

 5 Anxiety disorders

Learning objectives
After studying this chapter you will be able to:
● distinguish between separation anxiety, phobias,
generalized anxiety disorder, panic disorder,
posttraumatic stress disorder and obsessive compulsive
disorder in terms of their main clinical features
● summarize the epidemiology of anxiety disorders
● list the risk factors for anxiety disorders
● outline the main biological and psychological
theories of anxiety disorders
● name the main evidence-based approaches to
assessment and treatment of anxiety disorders
● give a considered view on the medicalization of fear.

Introduction
While normal fear is adaptive and prevents people from entering threat-
ening situations, with anxiety disorders people develop irrational fears of
situations that do not threaten their survival (Antony & Stein, 2009a).
They also develop non-adaptive behavioural patterns associated with
avoidance of feared situations or experiences. For people with anxiety
disorders, their fears are accompanied by intense physiological arousal
shown by some or all of the following features: accelerated heart rate,
sweating, trembling, sensations of shortness of breath or smothering,

Book 1.indb 126 06/03/2012 13:48

 5 • ANXIETY DISORDERS 127

feelings of choking, chest pain, nausea, numbness or tingling, and chills

or hot flushes. The person may also experience dizziness, derealization
(feelings of unreality) or depersonalization (feelings of being detached
from the self).
Within DSM-IV-TR (American Psychiatric Association, 2000) and
ICD-10 (World Health Organization, 1992), distinctions are made between
a variety of anxiety disorders based on the developmental timing of their
emergence, the classes of stimuli that elicit the anxiety, the pervasive-
ness and topography of the anxiety response, and the role of clearly iden-
tifiable factors in the aetiology of the anxiety. The following are the
principal anxiety disorders described in DSM-IV-TR and ICD-10.
● Separation anxiety
● Phobias
● Generalized anxiety disorder
● Panic disorder
● Posttraumatic stress disorder
● Obsessive compulsive disorder
Descriptions of these conditions and case examples are given below.
This is followed by a consideration of the clinical features, epidemiology,
risk factors, course, theoretical explanations, assessment and treatment
of anxiety disorders.

Separation anxiety disorder

With separation anxiety disorder, which occurs most commonly in chil-
dren, a recurrent and persistent fear is aroused when separa-
tion from parents or caregivers is anticipated (American Psychiatric
Association, 2000; Furr et al., 2009; Pine & Klein, 2008; World Health
Organization, 1992). Separation anxiety disorder is characterized by
persistent, excessive worry about losing, or about possible harm be-
falling, a parent. In some instances nightmares about these issues
may occur. Separation anxiety is also characterized by recurrent head-
aches, stomach-aches, nausea and vomiting. There may be a refusal
to sleep without being near parents, and although not the only
cause of school refusal, it is one of the most common causes.

Case example of separation anxiety

Barry, aged 11, was referred because he had not attended school for
2 months, following the Easter holidays in the year prior to his entry to
secondary school. The family doctor could find no organic basis for the
abdominal pain or headaches of which he periodically complained,
particularly on the mornings when his mother asked him how his health
was. Barry’s friends visited him at weekends and he went cycling with
them regularly. But on Monday mornings he was unable to get to school
both because of the abdominal pains and also because of a sense of
foreboding that something dangerous might happen to his mother. If
forced to go to school, he would become tearful or aggressive.

Book 1.indb 127 06/03/2012 13:48

 128 C L I N I C A L P S Y C H O L O G Y : A N I N T R O D U C T I O N

Family history
While there was no serious threat to Barry’s mother’s health, she had a
variety of complaints including rheumatism and epilepsy which compro-
mised her sense of well-being. Her epilepsy was usually well controlled,
but she had experienced a number of grand mal fits in the 6 months
prior to Barry’s referral. Barry was one of four children and all had his-
tories of school refusal. Barry’s three brothers aged 20, 25 and 30 all
lived at home and had few friends or acquaintances. His eldest brother
ran a computer software business from his bedroom. All of the boys had
very close relationships with their mother and distant relationships with
their father. The father, Martin, who was a healthy man, ran a grocery
shop and worked long hours. He left early in the morning and returned
late at night. He was very concerned for Barry’s welfare and believed
that his wife mollycoddled the boy. However, he was reluctant to chal-
lenge her because he did not want to upset her. The parents had a
history of marital discord and over the year prior to the referral had
strongly disagreed about how to handle Barry’s separation anxiety.
Two of Barry’s maternal uncles had psychological adjustment
difficulties and both had been on medication, although details of their
problems were unavailable. These uncles had lived at home with their
mother until her death. They, Barry’s mother and her sister Gina had
very close relationships with their mother, Mary, but distant relationships
with their father. Barry’s mother’s parents had also quarrelled about
how best to manage the children, with Mary being lenient and her
husband being strict. Thus, the pattern of relationships in Barry’s
mother’s family of origin and Barry’s family were very similar.
At school, Barry was very popular, particularly because he generously
shared candy and sweets from his father’s shop with his peers. He had
complained of bullying once or twice and on one occasion said the gym
teacher victimized him.
Psychometric assessment showed that Barry was of high average
intelligence and his attainments in reading, spelling and arithmetic were
consistent with his overall level of ability. His school reports were good
and he was in the top third of his class with respect to ability.
Formulation
Barry presented with separation anxiety disorder and school refusal.
Barry’s anticipation of the transition to secondary school in the autumn
and his awareness of his mother’s worsening health may have precipi-
tated the onset of these problems. Predisposing factors in this case
include a possible genetic vulnerability to anxiety, a multigenerational
history of mother–child over-involvement and the modelling experience
of seeing his three brothers develop separation anxiety and subsequent
school refusal.
The separation anxiety and school refusal were maintained by
parental conflict about the management of these problems, the mother’s
over-concern and the father’s limited involvement in the management of
Barry’s difficulties. They may also have been maintained by the
availability of an active social life within the house involving frequent

Book 1.indb 128 06/03/2012 13:48

 5 • ANXIETY DISORDERS 129

Figure 5.1 Formulation of a case of separation anxiety disorder

contact with his mother, three brothers and friends who regularly visited
him.
Protective factors included Barry’s good premorbid adjustment, the
parents’ commitment to become jointly involved in Barry’s treatment,
the school’s commitment to help Barry overcome his school refusal,
and Barry’s membership of a supportive peer group, whose members
wanted him to overcome his problems. This formulation is diagrammed
in Figure 5.1.

Treatment
Treatment involved a series of family sessions and home–school liaison
meetings of the parents and school staff. Martin, the father, agreed to
drive Barry to school regularly for a month, and the school staff agreed
for a teacher to meet Barry in the car park and bring him into the
classroom, where he was to sit with two peers and work on a special
project for 20 minutes before class started each day. Concurrently,
weekly family sessions were held in which progress was assessed, a
reward system for school attendance was set up, and the transition to
secondary school was discussed.
Arrangements were also made for the mother to attend a series of
consultations for her epilepsy, which became better controlled, and for
Barry to be given some psychoeducation about his mother’s seizure
disorder, its treatment and prognosis. Barry returned to school and
moved to secondary school in the autumn. His recovery, however, was
incomplete and he later relapsed and required further treatment.

Book 1.indb 129 06/03/2012 13:48

 130 C L I N I C A L P S Y C H O L O G Y : A N I N T R O D U C T I O N

Phobias
Phobic anxiety is the intense fear that occurs when one is faced with an
object, event or situation from a clearly defined class of stimuli which is
out of proportion to the danger posed by the stimulus (American
Psychiatric Association, 2000; Blackmore et al., 2009; Hofmann et al.,
2009; World Health Organization, 1992). Exposure to the phobic
stimulus, or anticipation of exposure, may lead to a panic attack in
adults or to excessive crying, tantrums, freezing or clinging in children.
In phobias there is persistent avoidance of phobic stimuli or they are
endured with intense distress, and this interferes significantly with
personal, social or academic functioning.
Specific phobias are subdivided in DSM-IV-TR into those associated
with animals, injury (including injections), features of the natural envi-
ronment (such as heights or thunder) and particular situations (such as
elevators or flying). Specific phobias are distinguished from social pho-
bias and agoraphobia. With social phobia, anxiety is aroused by social
situations such as public speaking or eating in public, where there is the
possibility of scrutiny by others and humiliation or embarrassment as a
result of acting inappropriately. With agoraphobia there is a fear of pub-
lic places, such as standing in a queue or travelling on public transport,
and so these situations are avoided. Agoraphobia often occurs when
panic attacks have spontaneously occurred in public places, and these
places are avoided in case attacks recur. Panic attacks are discussed
in more detail below.

Case example of a specific phobia

Nora, aged 9, was referred because of her fear of the dark. She wanted
to go on a camping trip with the Brownies but was frightened because
she would have to sleep in complete darkness. This was something she
had never done. She always slept with the light on in her bedroom and
with the door open and the landing light on. Her developmental history
was within normal limits and she had never experienced a traumatic
incident in the darkness. Her parents had tried to convince her to sleep
with the light off, but she became so distressed on these occasions that
they had stopped making such attempts and believed that she would
eventually grow out of the darkness phobia.
Nora was an only child and there was no family history of anxiety
disorders or adjustment problems, nor was there a developmental
history of a particularly traumatic incident.
Treatment
This uncomplicated specific phobia was treated with in vivo, parent-
assisted systematic desensitization. That is, with support from her
parents, on successive nights Nora was helped to cope with sleeping in
an increasingly darker bedroom at home. The level of illumination was
decreased by leaving the light outside her room illuminated and gradually
closing over the door further on successive nights. After a month of this
treatment programme, Nora’s darkness phobia had improved sufficiently

Book 1.indb 130 06/03/2012 13:48

 5 • ANXIETY DISORDERS 131

for her to go camping and successfully sleep in a dark tent for three
nights without experiencing undue anxiety.

Generalized anxiety disorder

When individuals experience generalized anxiety, they have an ongoing
apprehension that misfortunes of various sorts will occur (American
Psychiatric Association, 2000; Bitran et al., 2009; Hazlett-Stevens et al.,
2009; World Health Organization, 1992). Their anxiety is not focused on
one particular object or situation. There is also difficulty controlling the
worrying process, and a belief that worrying is uncontrollable.
Generalized anxiety disorder is characterized by nervousness, rest-
lessness, difficulty relaxing, feeling on edge, being easily fatigued, con-
centration difficulties, irritability, tearfulness, sleep disturbance and
signs of autonomic overreactivity such as trembling, sweating, dry-
mouth, light-headedness, palpitations, dizziness and stomach discom-
fort. DSM-IV-TR and ICD-10 require some but not all of these features
to be present.

Case example of generalized anxiety disorder

Margie, aged 10, was referred because of excessive tearfulness in school
which had been gradually worsening over a number of months. The
tearfulness was unpredictable. She would often cry when spoken to by
the teacher or while playing with her friends during break time. In the
referral letter her family doctor described her as a worrier, like her mother.

Presentation
In the intake interview Margie said that she worried about many routine
daily activities and responsibilities. She worried about doing poorly at
school, that she had made mistakes which would later be discovered,
that her friends wouldn’t like her, that her parents would be disappointed
with the way she did her household jobs, that she would be either too
early or too late for the school bus, that there would be no room for her
on the bus and that she would forget her schoolbooks. She worried
about her health and had frequent stomach aches.
She also had wider ranging fears about the safety of her family. She
worried that the house would be struck by lightening, that the river would
break its banks and flood the low lying fens where she lived and her
house would be washed away. She had concerns about the future and
worried that she would fail her exams, be unable to find a satisfactory
job, and would fail to find a marital partner or would marry an unsuitable
person. She reported feeling continually restless and unable to relax.

Family history
Margie was the eldest of four children and the only girl in the family. The
family was very close-knit. Both of the parents showed symptoms of
anxiety in the intake interview and the mother had been treated with
benzodiazepines for anxiety over a number of years. The parents

Book 1.indb 131 06/03/2012 13:48

 132 C L I N I C A L P S Y C H O L O G Y : A N I N T R O D U C T I O N

regularly discussed their worries about their own health and safety and
their own concerns about the uncertainty of the future.
The father, Oliver, worked with an insurance company, and frequently
discussed at the family dinner table accidents and burglaries that had
befallen his clients. Margie regularly participated in these conversations,
being the eldest child. The parents’ chief concern was about Margie’s
tearfulness, which they viewed as unusual. Her worries and fears they
saw as quite legitimate. Margie had a couple of close friends with whom
she played at the weekends, but she spent a lot of time in her parents’
company.

Formulation
Margie presented with a generalized anxiety disorder. No clear-cut pre-
cipitating factor for the condition was apparent. It had gradually evolved
over the course of Margie’s development. However, the referral was
precipitated by episodes of tearfulness at school. Predisposing factors
in this case included a possible genetic vulnerability to anxiety and
exposure to a family culture marked by a concern with safety and an
over-sensitivity to danger. Ongoing involvement in parental conversa-
tions about potential threats to the well-being of family members possi-
bly maintained the condition along with inadvertent reinforcement of
Margie’s tearfulness at school, where crying was responded to with
considerable concern.
Protective factors in this case included good premorbid adjustment,
particularly at school, the parents’ and school’s commitment to resolving
the problem and the availability of peer-group support. This formulation
is diagrammed in Figure 5.2.

Figure 5.2 Formulation of a case of generalized anxiety disorder

Book 1.indb 132 06/03/2012 13:48

 5 • ANXIETY DISORDERS 133

Treatment
Treatment in this case involved family work focusing on helping
Margie and her parents reduce the amount of time they spent talking
about danger and threats to their health and safety, and increase
the amount of time they spent engaged in activities and conversa-
tions focusing on Margie’s strengths and capabilities. The parents were
also helped to coach Margie in relaxation skills and mastery-oriented
coping self-statements. Some reduction in anxiety and tearfulness
occurred, and Margie showed some improvement in her adjustment in
school.

Panic disorder
With panic disorder there are recurrent unexpected panic attacks; an
ongoing primary fear of further attacks; and a secondary fear of losing
control, going crazy, having a heart attack or dying (American Psychiatric
Association, 2000; Ballenger, 2009; Hofmann et al., 2009; World Health
Organization, 1992). Panic attacks are experienced as acute episodes
of intense anxiety which reach a peak within 10 minutes. They are char-
acterized by autonomic hyperarousal shown by some of the following:
palpitations, sweating, trembling or shaking, shortness of breath, feel-
ings of choking or smothering, chest pain or discomfort, nausea or
abdominal distress, dizziness, chills or hot flushes, parasthesias,
(numbness or tingling sensations), derealization (feelings of unreality)
and depersonalization (feelings of being detached from oneself).
People with panic disorder come to perceive normal fluctuations in
autonomic arousal as anxiety-provoking, since they believe that such
fluctuations may signal the onset of a panic attack. During a panic attack
there is typically an urge to escape from the situation in which the attack
occurred and to avoid such situations in future. Panic attacks typically
occur in public settings such as in queues or on public transport, and
escaping from these situations usually alleviates acute autonomic
arousal. Thus, secondary agoraphobia often develops whereby the
person fears leaving the safety of the home in case a panic attack
occurs in a public setting.

Case example of panic disorder

Sandra, a 15-year-old girl, was referred because of anxiety about sitting
exams. She lived with her grandparents, Ruth and Josh. She slept and
ate well and appeared to be happy. However, she would not leave the
house to socialize or attend college. A tutor from the local technical
college at which she was enrolled had regularly brought school work to
her for about 9 months. The imminence of her GCSE state exams,
which were due to be held at the college, precipitated the referral. She
wanted to overcome her anxiety so that she could travel to college and
sit her exams, which she had felt unable to complete the previous year
due to anxiety.

Book 1.indb 133 06/03/2012 13:48

 134 C L I N I C A L P S Y C H O L O G Y : A N I N T R O D U C T I O N

History of the presenting problem

In a preliminary interview, conducted at her grandparents’ house where
she lived, Sandra described a fear of leaving the safety of her home and
how the distress she experienced increased the further away from her
home she travelled. The anxiety began during her mock O-Level school
exams a year previously. She had a panic attack and left the exam hall.
She ran to her grandparents’ house after this incident and subsequent
attempts to return to school led to further panic attacks. During the
attacks she couldn’t catch her breath and felt dizzy. She also felt as if
she were out of her body (depersonalization) and as if the world was
dream-like (derealization). She then feared she would die. The initial
attack lasted no more than a few minutes. Subsequent attacks were
similar to the first.
Her family and the college staff, after some preliminary ineffective
attempts to help her get out and about, gave up trying. On many
occasions, when she found herself any distance from the house, she
would begin to panic and run back quickly. This led to the symptoms of
panic abating. One staff member at the college visited her and taught
her some relaxation exercises. He suggested she use these to help her
cope with attempts to leave the house, but she found them of little
benefit. Eventually she settled for a house-bound life.
On a couple of occasions, when she had sufficient courage to visit
her friends, she had panic attacks. At these times she was frightened of
accepting a cup of hot tea because she believed she might not be able
to finish the tea without scalding herself, should she experience a panic
attack and need to escape from the situation quickly. She said she
would not like to offend her friends by not finishing her tea. Sandra was
also frightened of going on buses or in cars on the motorway and of
queuing at the bank. She worried that she might have a panic attack in
these situations and not be able to get home safely.

Family history
Sandra’s parents were divorced. Her father, Des, was a police officer in
London and had separated from her mother, Lynn, when Sandra was 7
years old. Lynn lived near the grandparents, in a rural village about a
3-hour drive from London. Lynn cohabited with Jeff, whom she had met
while hospitalized for depression. She had an extensive history of
psychiatric treatment for anxiety and depression.
Sandra’s mother and grandparents were preoccupied with physical
illness and psychological problems, and regularly discussed threats to
each other’s well-being. They shared a view, based on Lynn’s experi-
ences, that psychological problems ran a chronic course and were
unresponsive to psychological treatments, because they were due to
biological factors.
There were a number of distinctive family relationships in this case.
Sandra had very close relationships with her mother and grandparents.
The mother and grandmother were involved in regular conflicts over the
suitability of Jeff as a partner for Lynn. Sandra’s brother, Paul, who
attended university, visited her occasionally with his friends and she

Book 1.indb 134 06/03/2012 13:48

 5 • ANXIETY DISORDERS 135

envied his lifestyle. He rarely joined in the conversations about illness at

the grandparents’ house. He was a drama enthusiast and Sandra would
help him rehearse his lines when he visited. For Sandra, this was a
welcome break from the regular conversation about ill-health at her
grandparents’ house. Sandra had four or five friends who lived locally,
and two of these visited regularly.

Formulation
Sandra presented with panic disorder with agoraphobia, initially precipi-
tated by participation in a school examination. The principal predisposing
factors were a genetic vulnerability to anxiety from the mother’s side of
the family and a family culture that focused on illness, fear and danger.
Multiple unsuccessful treatments and the experience of negative rein-
forcement afforded by escaping from threatening situations maintained
the agoraphobic, avoidant behaviour. Other maintaining factors included
the father’s lack of involvement in attempts to help Sandra recover, com-
bined with the grandparents’ and mother’s over-involvement with Sandra.
This maintained Sandra’s anxiety and prevented recovery because it led
to her continued involvement in conversations about illness, fear and
danger, and a pessimistic biomedical view of anxiety.
However, Sandra’s good premorbid adjustment, her positive relation-
ship with her brother who was a good role model for recovery, her two
positive close peer relationships, and a desire for vocational progression
were important protective factors in this case. The family and the school
also were supportive of treatment that might help Sandra sit her exams.
This formulation is diagrammed in Figure 5.3.

Figure 5.3 Formulation of a case of panic disorder with agoraphobia

Book 1.indb 135 06/03/2012 13:48

 136 C L I N I C A L P S Y C H O L O G Y : A N I N T R O D U C T I O N

Treatment
Treatment in this instance began with family work involving the grand-
parents, the mother and, on a couple of occasions, the father, to reduce
the amount of illness and anxiety-focused conversation to which Sandra
was exposed and to challenge the beliefs that psychological problems
were unresponsive to psychological treatments. This was followed with
in vivo systematic desensitization coupled with a brief trial of clomi-
parmine (Anafranil).
In vivo systematic desensitization involved Sandra being supported
to make increasingly longer outings from her house, while concurrently
using relaxation exercises to help her to manage the anxiety these out-
ings evoked. Sandra could not tolerate the side-effects of clomiparmine,
so the medication was discontinued. It was also arranged for her to sit
exams at school in a private room. Following this, work placements at a
crèche and at an old folks’ home were arranged by the college staff.
While Sandra made a good recovery, she suffered periodic relapses
and re-referred herself for a number of further episodes of treatment
over the following 2 years.

Posttraumatic stress disorder

Posttraumatic stress disorder (PTSD) occurs following a catastrophic
trauma such as child abuse, rape, torture, a terrorist attack, armed
combat, a natural or man-made disaster, or a serious accident that
was perceived to be potentially life-threatening for oneself or others.
PTSD is characterized by (1) recurrent intrusive traumatic memories;
(2) intense anxiety in response to these memories and ongoing hyper-
arousal in anticipation of their recurrence; and (3) attempts to regulate
anxiety and hyper-arousal by avoiding cues that trigger traumatic
memories and attempts to suppress these memories when they intrude
into consciousness (American Psychiatric Association, 2000; Ehlers,
2009; Friedman, 2009; World Health Organization, 1992).
Recurrent, traumatic memories include flashbacks, nightmares, or
repetitive trauma-themed play in the case of children. These occur in
response to internal (psychological) or external (environmental) cues
that symbolize the traumatic event or aspects of it. Because they antici-
pate the recurrence of traumatic memories, people with PTSD experi-
ence chronic hyper-arousal which may lead to difficulty concentrating,
hyper-vigilance, irritability or sleep difficulties.
In PTSD, avoidance of trauma-related situations and attempts to
suppress traumatic memories may initially be relatively unsuccessful
and lead to an increase in the frequency and intensity of flashbacks.
However, in chronic cases, frequent, recurrent attempts to keep trauma-
related memories out of consciousness often result in emotional numb-
ing and an inability to recall traumatic memories. With emotional
numbing, not only are trauma-related emotions such as anxiety and
anger excluded from consciousness, but also tender feelings such as
love and joy are no longer experienced. PTSD may lead to restricted
involvement in normal activities and a sense of foreshortened future.

Book 1.indb 136 06/03/2012 13:48

 5 • ANXIETY DISORDERS 137

Case example of PTSD

Margaret, a 25-year-old woman, was referred because of recurrent night-
mares and erratic behaviour at work. She was employed as a cashier in
a petrol station in a busy suburban area. On two occasions while she was
at work, a man armed with a hypodermic syringe filled with blood, which
he claimed was HIV-infected, had coerced her into handing over the con-
tents of the cash register. She subsequently suffered from nightmares
and daytime flashbacks. She also suffered from a high level of general-
ized physiological arousal and was anxious and short-tempered at work.
She attempted to deal with the nightmares and flashbacks by putting
them out of her mind and thinking about other things, but found that this
was becoming less and less effective. When she became flooded with
feelings of anxiety she would become inappropriately aggressive to
customers at work and was frightened that she would lose her job
because of this. At home her relationships with her mother and sisters
had deteriorated.

Treatment
Treatment involved Margaret writing down accounts of her dreams and
flashbacks and organizing these into a sequence from the least to the
most threatening. She was also invited to alter the endings to these
scenarios so that she emerged victorious rather than victimized at the
conclusion of each of them. For example, in one scenario, rather than
the aggressor successfully attacking her with the HIV-infected syringe,
she imagined him shrinking to half his size and then she overpowered
him easily.
In therapy sessions, Margaret was imaginally exposed to these
scenarios, beginning with the least threatening and concluding with the
most threatening, until she could vividly imagine each of them without
being overwhelmed with anxiety. During the imaginal exposure ses-
sions, she was helped to enter a state of deep relaxation and then
listened to the account of the scenario that the psychologist read to her.
She coped with the anxiety that listening to these traumatic scenes
evoked by using relaxation and deep breathing exercises in which she
had been coached, and also by concluding each imagined scenario by
emerging victorious rather than victimized. Her symptoms abated over
a 6-month period.

Obsessive compulsive disorder

Obsessive compulsive disorder (OCD) is a condition typically character-
ized by distressing obsessions on one hand and compulsive rituals that
reduce anxiety associated with obsessions on the other (American
Psychiatric Association, 2000; Mathews, 2009; World Health Organiza-
tion, 1992; Zohar et al., 2009). Obsessions are recurrent, persistent
and stereotyped thoughts, images or impulses. They cause significant
anxiety because they are experienced as involuntary, uncontrollable and
senseless, and concern issues such as danger, violence and obscenity.

Book 1.indb 137 06/03/2012 13:48

 138 C L I N I C A L P S Y C H O L O G Y : A N I N T R O D U C T I O N

For example, there may be fears of contamination, of violently assaulting

or raping others, or that a catastrophe may occur unless symmetry or
order is maintained.
Compulsions are repetitive, ritualistic, stereotyped behaviours such
as hand-washing, ordering and checking or mental acts such as praying,
counting, or repeating words silently, which people feel compelled to
perform to regulate anxiety caused by obsessions. Compulsions are
either unrealistic ways to avert imagined dangers entailed by obsessions
or are clearly excessive. They are not inherently enjoyable and are
usually recognized as pointless, and repeated attempts are made to
resist them.

Case example of obsessive compulsive disorder

April, a 35-year-old woman, was referred because gradually over a
2-year period she had developed some unusual habits, beliefs and feel-
ings. With respect to her behaviour, she scrubbed the floors and walls
of the kitchen, bathroom and toilet every day. On one occasion she put
a full set of new bathroom towels in the dustbin after a student lodger
had used them once. On another occasion she put all the crockery from
her kitchen and the family’s Sunday dinner which she had cooked in the
dustbin.
She prevented the children from playing anywhere that they might
fall and cut themselves, including the playground. She took an hour to
go to bed each night because she had to return downstairs repeatedly
to check that the doors were locked and the fire was extinguished. She
had been an affectionate person, but now balked if her friends tried to
embrace or kiss her.
With respect to her beliefs, she was frightened that she or her
children or husband would catch HIV and develop AIDS. She feared
that the student lodger, her friends, or germs from the crockery might
infect her with the HIV virus. She was also frightened that a burglar
might break in if she did not lock up at night, stab her with a needle and
infect herself or the children with the HIV virus.
With respect to her mood, she felt anxious much of the time and had
difficulty sleeping. She also felt sad and empty. She was embarrassed,
because she knew that her extreme fears of HIV infection were unfounded.

Family history
April was brought up by strict parents with whom she continued to have
close contact. She had trained as a nurse but now was a homemaker
with a caring and successful husband and two healthy children. She
devoted herself fully to the welfare of her children and her husband.
Before the onset of her problems, in every way she described herself as
an exemplary wife and mother.
While on duty as a nurse she pricked her finger with a needle, and
this led to her first thought of HIV infection. Her HIV test was negative,
but she could not accept this and developed the obsessional belief that
she, her children and her husband would get AIDS. The belief became

Book 1.indb 138 06/03/2012 13:48

 5 • ANXIETY DISORDERS 139

stronger when her husband changed job, her youngest child went to
play school and she took in a lodger.
Her family and friends responded to her condition in the following
ways. Her husband helped with her cleaning and checking rituals and
reinforced them. Her children did not object to over-protection. Her friends
were very understanding of her lack of physical affection. Her sisters
discussed her fear of AIDS with her regularly in a sympathetic manner.

Formulation
April presented with OCD which was precipitated by her pricking her
finger with a hypodermic needle and recent life stresses including her
husband’s change of jobs, her children starting preschool and taking in
a lodger. She was predisposed to developing OCD by two main factors.
First, she came from a family where control and cleanliness were
valued. Second, because of her nursing training she was highly aware
of the risk of possible infection with the HIV virus.
The OCD was maintained in the following way. She found that her
compulsions to clean, discard food, over-protect the children, and check
the security of the house every night relieved her anxiety, so she repeated
these actions compulsively. Her family and friends reinforced her obses-
sional thoughts and her husband participated in her compulsive behav-
iour by, for example, checking the security of the house at her request.
There were two protective factors in this case deserving mention.
April was very intelligent and able to take on board a formulation of her
problem and understand its relevance to treatment. Her husband was
prepared to be involved and enlist family help in combating the
compulsions. This formulation is diagrammed in Figure 5.4.

Figure 5.4 Formulation of a case of obsessive compulsive disorder

Book 1.indb 139 06/03/2012 13:48

 140 C L I N I C A L P S Y C H O L O G Y : A N I N T R O D U C T I O N

Treatment
April was treated with a multimodal programme that included anti-
depressant medication and a spouse-assisted behaviour therapy
programme of exposure and response prevention. She drew up a list of
situations that elicited her obsessions, from the least to the most
anxiety-provoking. She planned to expose herself to these situations in
order of increasing provocativeness and not engage in compulsions
while doing so (with her husband’s support) until her anxiety abated.
For example, she lay in bed, allowed herself to worry about the security
of the house, and prevented herself from returning downstairs to check
that the doors were locked and the fire extinguished, while her husband
talked reassuringly with her, until her anxiety abated. She responded
well to treatment, which was carried out over a 3-month period.

Clinical features of anxiety disorders

The clinical features of the six types of anxiety disorder described above
are presented in Table 5.1. In the table clinical features are classified
into the domains of perception, cognition, affect, arousal, behaviour and
interpersonal adjustment. With respect to perception, the disorders
differ in the classes of stimuli that elicit anxiety.
With separation anxiety, the stimulus is separation from parents. For
phobias it is specific creatures (e.g. animals), events (e.g. injury), or
situations (e.g. meeting new people) that elicit anxiety. With generalized
anxiety disorder, the person interprets many aspects of their environ-
ment as potentially threatening. In panic disorder, somatic sensations of
arousal such as tachycardia are perceived as threatening since they are
expected to lead to a full-blown panic attack. With PTSD, internal and
external cues that remind the person of the trauma that led to the condi-
tion elicit anxiety. With OCD, stimuli that evoke obsessional thoughts
elicit anxiety. For example, potentially dirty situations may evoke obses-
sional ideas about cleanliness, and anxiety about contamination.
Cognitions in all six anxiety disorders have the detection and/or
avoidance of danger as the central organizing theme, and the belief that
danger-related thoughts have become uncontrollable. With separation
anxiety, children believe that they or their parents will be harmed if
separation occurs. With phobias, the person believes that contact with
the feared object or creature, or entry into the feared situation, will result
in harm such as being bitten by a dog in the case of dog phobia or being
negatively judged by strangers in the case of social phobia. With
generalized anxiety, people catastrophize about many features of their
environment. For example they may fear that the house will burn down,
their car will crash, they will be punished for wrongdoing, their friends
will leave them, and so forth. They also believe that the worrying process
has become uncontrollable.
In panic disorder, there is a belief that further panic attacks will occur
and that these may be fatal. Often individuals also believe that provided
they remain within the safety of the home, the panic attacks are less

Book 1.indb 140 06/03/2012 13:48

Book 1.indb 141
TABLE 5.1
Clinical features of anxiety disorders
Separation anxiety Phobias Generalized Panic disorder Posttraumatic stress Obsessive compulsive
disorder anxiety disorder disorder (PTSD) disorder (OCD)
Perception • Separation from • Specific objects, • The whole • The recurrence of • Cues that remind the • Specific situations,
parents or events or environment is panic attacks is seen person of the trauma such as those
caregivers is situations are perceived as as threatening are perceived as involving dirt, are
perceived as perceived as threatening • Attention is directed threatening. perceived as
threatening threatening • The person is inwards and benign • Flashbacks, threatening and elicit
hyper-vigilant, somatic sensations hallucinations or obsessional thoughts
scanning the are misinterpreted as illusions may occur
environment for threatening because where aspects of the
threats to well- they are seen as trauma are
being signalling the onset of reperceived
a panic attack
Cognition • The child • The person • The person • The person believes • Recurrent • Involuntary,
believes that believes that catastrophizes that the panic attacks uncontrollable uncontrollable
harm to the contact with the about many minor may lead to loss of memories of the obsessional thoughts,
parent or the self phobic object or daily events control, insanity, a trauma occur images or impulses
will occur entry into the • There is a belief heart attack or death • The person tries to elicited by
following phobic situation that the worrying distract themselves environmental cues
separation will lead to process is from recalling these intrude into
• This belief seems catastrophe uncontrollable traumatic memories consciousness and
to occur • This belief seems or to suppress them may involve themes
involuntarily and to occur • A belief in a of contamination, sex
is experienced as involuntarily and foreshortened future or aggression
uncontrollable is experienced as may develop • The person tries to
uncontrollable exclude these
thoughts from
consciousness

(Continued)
5 • ANXIETY DISORDERS
141

06/03/2012 13:48
Book 1.indb 142
TABLE 5.1
(Continued)
Separation anxiety Phobias Generalized Panic disorder Posttraumatic stress Obsessive compulsive
disorder anxiety disorder disorder (PTSD) disorder (OCD)
Affect • Intense fear or • Intense fear or • A continual • During panic attacks • Against a background • The obsessions cause
anger occurs anger is moderately high intense fear occurs of hyper-arousal, anxiety because they
when separation experienced if level of fear is and between attacks a periodic intrusive are experienced as
is anticipated, contact with the experienced – moderate level of fear episodes of intense uncontrollable and
during separation feared object or free-floating of recurrence is fear, horror or anger senseless
or following situation is anxiety experienced like those that
separation anticipated or occurred during the
occurs trauma are
experienced
• In chronic cases the
person may become
emotionally blunted
and unable to
experience tender
emotions
• Depression may
occur
Arousal • Episodes of • Episodes of • Continual hyper- • Episodes of extreme • Episodes of extreme • Ongoing moderate
hyper-arousal hyper-arousal or arousal occurs hyper-arousal occur hyper-arousal occur hyper-arousal occurs
occur with panic attacks with trembling, with palpitations, against a background • Hyper-arousal occurs
recurrent occur when sweating, dry- sweating, trembling, of moderate hyper- when cues elicit
abdominal pain, exposed to the mouth, light- shortness of breath, arousal with obsessions and
142 C L I N I C A L P S Y C H O L O G Y : A N I N T R O D U C T I O N

headaches, feared object or headedness, feelings of choking or difficulties compulsions are

nausea or situation palpitations, smothering, chest concentrating and resisted
vomiting • Sleep problems if dizziness, and pain, nausea, relaxing
• Sleep problems imminent stomach dizziness, chills or hot • Sleep problems
exposure to the discomfort flushes, parasthesias,
phobic object is • Sleep problems derealization and
anticipated depersonalization
• Between attacks there
is moderate hyper-
arousal
• Sleep problems

06/03/2012 13:48
Book 1.indb 143
Behaviour • Separation is • The phobic object • As worrying • Secondary • Children may cling to • Motivated by a wish to
avoided or or situation is intensifies, social agoraphobia may parents and refuse to reduce the anxiety
resisted avoided activities become develop where the sleep alone aroused by
• The child refuses • If exposed to the restricted person avoids public • Teenagers and adults obsessional beliefs,
to go to school phobic object or places in case the may use drugs or individuals engage in
• The child refuses situation, crying, panic attacks occur alcohol to block the compulsive rituals
to sleep alone tantrums, away from the safety intrusive thoughts and which they believe will
• If forced to freezing or of home emotions prevent a catastrophe
separate, crying, clinging may • Suicidal attempts may from occurring or
tantrums, occur in children occur undo some potentially
freezing or threatening event that
clinging may has occurred
occur • These rituals are
usually runrealistic or
excessive
Interpersonal • Peer • With specific • Peer relationships • If agoraphobia • Complete social • Members of the
adjustment relationships may phobias, may deteriorate develops secondary to isolation may occur if individual’s family or
deteriorate interpersonal • Occupational or the panic attacks, the trauma was social network may
• Academic problems are academic social isolation may solitary become involved in
performance may confined to performance may occur • Where the trauma helping the person
deteriorate phobic situations deteriorate was shared, the perform compulsive
• Agoraphobia and individual may confine rituals and
social phobia interactions to the inadvertently reinforce
may lead to group that shared the them
social isolation trauma • Social, educational
and occupational
functioning may
become impaired

Note: Features are based on ICD-10 (World Health Organization, 1992) and DSM-IV-TR (American Psychiatric Association, 2000) descriptions of anxiety disorders.
5 • ANXIETY DISORDERS
143

06/03/2012 13:48
 144 C L I N I C A L P S Y C H O L O G Y : A N I N T R O D U C T I O N

likely to occur, and so secondary agoraphobia develops. With PTSD,

there is a belief that provided the memories of the trauma are excluded
from consciousness, the danger of re-experiencing the intense fear,
distress and horror associated with the trauma that led to PTSD can be
avoided. With OCD, the most common obsessions are with dirt and
contamination; catastrophes such as fires, illness or death; symmetry,
order and exactness; religious scrupulosity; disgust with bodily wastes
or secretions such as urine, stools or saliva; unlucky or lucky numbers;
and forbidden sexual thoughts. There is also the belief that engaging in
specific rituals will neutralize the threat posed by specific obsession-
related stimuli.
In all six of the anxiety disorders listed in Table 5.1 the beliefs about
threat and danger are accompanied by affective states, characterized
by feelings of tension, restlessness and uneasiness. If one is compelled
to approach feared stimuli, or in the case of OCD prevented from exe-
cuting a compulsive ritual, outbursts of anger may occur. For example,
children with separation anxiety may have aggressive tantrums if forced
to remain at school without their parents. In PTSD, in addition to the
affective experiences of uneasiness and tension, an affective experi-
ence of emotional numbing, arising from attempts to exclude all affec-
tive material from consciousness, may develop.
The patterning of physiological arousal varies depending on the
frequency with which contact with feared stimuli occurs. With sepa-
ration anxiety, hyper-arousal occurs only when separation is imminently
anticipated. With specific phobias it occurs only in the presence of the
feared object. With generalized anxiety disorder, there is a pattern of
ongoing continual hyper-arousal. With panic disorder and PTSD there
is a moderate level of chronic hyper-arousal, punctuated by brief
episodes of extreme hyper-arousal. These occur in panic disorder
during panic attacks and in PTSD when memories of the traumatic event
intrude into consciousness. With OCD, specific obsession-related cues
evoke acute and intense episodes of arousal.
The extent to which physiological arousal finds expression in somatic
symptoms varies across conditions. For example, recurrent abdominal
pain and headaches are especially common in separation anxiety; full-
blown panic attacks with sweating, trembling, shortness of breath, feel-
ings of choking or smothering, chest pain, nausea, dizziness, chills or
hot flushes, parasthesias, derealization and depersonalization are most
common during panic attacks; whereas sleep problems occur in most
anxiety disorders.
Avoidance behaviours characterize all anxiety disorders. With
specific phobias, avoidance may lead to only a moderate constriction in
lifestyle. For example, a person may refuse to engage in sports or
athletics or to ride a bicycle because of an injury phobia. However, with
separation anxiety, generalized anxiety disorder, panic disorder and
PTSD, avoidance behaviour may lead the person to become house-
bound. With PTSD, individuals may use alcohol or drugs to regulate
negative affect and suppress traumatic memories. With OCD, indivi-
duals engage in compulsive rituals to regulate anxiety associated with

Book 1.indb 144 06/03/2012 13:48

 5 • ANXIETY DISORDERS 145

obsessional thoughts. Common compulsions include washing, repeating

an action, checking, removing contaminants, touching, ordering and
collecting.
Interpersonal relationships are affected by each of the anxiety disor-
ders in different ways. With simple phobias interpersonal difficulties
arise only in those situations where the individual refuses to conform or
co-operate with normal social activities so as to avoid the feared stimuli.
For example, a brief episode of marital conflict may occur if one partner
refuses to get in an elevator at a shopping mall because of claustropho-
bia. Separation anxiety, panic disorder, generalized anxiety and PTSD
may prevent young people from attending school or adults from attend-
ing work, and in all of these conditions family relationships and friend-
ships may be seriously compromised. With OCD, family members may
attempt to reduce the sufferer’s anxiety by participating in compulsive
rituals or in other instances they may increase anxiety by punishing
the individual for his or her compulsive behaviour. In extreme cases,
compulsive behaviour may become so frequent and intense that the
person’s lifestyle becomes constricted.

Epidemiology, risk factors and course

Anxiety disorders are more prevalent than any other category of psy-
chological disorders. The lifetime prevalence rate in adults for all
DSM-IV anxiety in the US National Comorbidity Survey Replication was
28.8% (Kessler et al., 2005). Across a wide range of epidemiological
studies there is a consensus that phobias are the most prevalent anxi-
ety disorders and that OCD is the least prevalent (Kessler et al., 2009;
Furr et al., 2009). Lifetime prevalence estimates for phobias range from
6% to 12%, whereas those for OCD fall below 3%. The lifetime preva-
lence rate of generalized anxiety disorder is 1–6%, and of panic disor-
der in adults and separation anxiety in children is 2–5%. The prevalence
of PTSD in national representative samples ranges from less than 1%
or 2% in western European countries to almost 8% in the US. This wide
variability is due to the fact that PTSD rates are dependent on both the
prevalence of trauma exposure within specific countries and the vulner-
ability of populations within these countries to developing PTSD symp-
toms. In populations exposed to terrorism the prevalence of PTSD is
12–16% (DiMaggio & Galea, 2006).
Comorbidity among anxiety disorders is quite high, and up to a third
of people with one anxiety disorder also suffer from another (Kessler et
al., 2009). Anxiety disorders may also occur comorbidly with mood
disorders in children and adults, substance use disorders in adolescents
and adults, and disruptive behaviour disorders in children (Furr et al.,
2009; Huppert, 2009; Zahradnik & Stewart, 2009). Where substance
misuse occurs, often alcohol or drugs are used for self-medication to
manage anxiety.
Comorbidity between anxiety disorders and personality disorders is
very common, and the highest level of comorbidity occurs with Cluster

Book 1.indb 145 06/03/2012 13:48

 146 C L I N I C A L P S Y C H O L O G Y : A N I N T R O D U C T I O N

C personality disorders (avoidant, dependent, and obsessive compulsive

personality disorders) (Brandes & Bienvenu, 2009). There is a strong
association between OCD and eating disorders. A significant proportion
of people with eating disorders such as anorexia nervosa also suffer
from OCD (Halmi, 2010).
There are clear age and gender differences in the prevalence of
anxiety disorders (Antony & Stein, 2009a; Furr et al., 2009; Kessler et
al., 2009). Across most available studies, the modal age of onset of
separation anxiety disorder and specific phobias is in childhood,
whereas that of other anxiety disorders tends to be in adolescence or
adulthood. In children and adults more females than males suffer from
anxiety disorders. The main exception to this finding is that equal
numbers of males and females suffer from OCD.
Anxiety disorders follow a recurring episodic course with a gradual
reduction in prevalence over the course of the life cycle (Kessler et al.,
2009). While most anxious adults have a history of childhood anxiety
disorders, most children with anxiety disorders do not grow up to have
anxiety or depression in adulthood (Pine & Klein, 2008).
A number of risk factors are associated with the development of
anxiety disorders. These include a family history of anxiety disorders
or psychopathology, a behaviourally inhibited temperament, neuroti-
cism, a personal history of psychopathology, a history of over-
controlling or critical parenting, a history of family conflict and violence,
and a history of stressful life events (Antony & Stein, 2009b; Pine &
Klein, 2008). In this context, behaviourally inhibited temperament is the
tendency, present from birth, to become nervous and withdraw from
unfamiliar stimuli and situations. Neuroticism is a personality trait that
develops over the life-span characterized by the tendency to experi-
ence negative affect including anxiety, depression and hostility.
For PTSD, additional risk factors include trauma severity, dissociative
experiences immediately following the trauma, low social support and
high life stress following the trauma, and low socio-economic status,
educational level and intelligence (Ehlers, 2009; Ozer et al., 2003). In
this context dissociative experiences refer to abnormalities of perception,
memory or identity such as derealization (seeing the world as dream-
like), depersonalization (viewing the self from an external perspective)
or inability to recall important personal information. For children, parental
PTSD is also a risk factor for developing the condition (Pine & Klein,
2008).

Aetiological theories
Theoretical explanations for anxiety disorders, related research and
interventions have been developed within biological, psychoanalytic,
cognitive-behavioural, and family systems traditions. Vulnerability to
anxiety disorders has also been studied by temperament and trait theo-
rists, and from an experimental psychopathology perspective to identify
information-processing biases associated with anxiety disorders.

Book 1.indb 146 06/03/2012 13:48

 5 • ANXIETY DISORDERS 147

Biological theories
Biological theories point to the role of genetic factors and neurobiological
abnormalities in the aetiology of anxiety disorders.

Genetics
The genetic hypothesis proposes that anxiety disorders develop where
a person with an inherited vulnerability to anxiety is exposed to
threatening or stressful environmental stimuli at critical developmental
stages when they are primed or prepared to develop fears. Results of
twin and family studies of anxiety disorders partially support the genetic
hypothesis, with twin studies yielding moderate heritability estimates
ranging from about 25% to 60%, with most in the 30–40% range, for
phobias, panic disorder, and vulnerability to PTSD and OCD (Afifi et al.,
2010; Gelernter & Stein, 2009; Hettema et al., 2001).
There is also support for the proposal that sensitivity to particular
classes of stimuli emerges at particular developmental stages (De Silva
et al., 1977). For example, it was mentioned in the section on epidemiol-
ogy that vulnerability to developing specific phobias and separation
anxiety is highest during childhood, whereas vulnerability to social pho-
bias, panic disorder, generalized anxiety disorder and OCD more
commonly emerges in adolescence.
The genetic hypothesis also entails the view that a dysfunctional bio-
logical factor which underpins the process of regulating stress responses
is genetically transmitted in families where anxiety disorders occur.
Many candidate genes for anxiety disorders have been investigated;
few have been identified; and where significant associations between
candidate genes and anxiety disorders have been found, very few con-
sistent replication studies are available. The search for candidate genes
has focused in large part on those whose products affect neurotransmit-
ters thought to be involved in the aetiology of anxiety disorders. Two
candidate genes – which affect the serotonin and dopamine systems –
deserve mention because consistent support has been found for a link
between them and anxiety disorders.
The short (rather than the long) allele variant of the 5-HTTLPR poly-
morphism, which regulates expression of the serotonin transporter
gene (which is called 5HTT or SLC6A4), is a risk factor for PTSD and
significantly increases the chances of developing PTSD following
trauma (Xie et al., 2009). In response to stress or trauma, people with
the short allele variant of 5-HTTLPR show decreased serotonin re-
uptake, increased amygdala neuronal activity, and increased hypotha-
lamic–pituitary–adrenal (HPA) axis reactivity. The amygdala is a brain
structure within the limbic system (which includes the amygdala, hip-
pocampus, insula and parts of the anterior cingulated cortex) located in
the medial temporal lobes that subserves the processing of emotional
information and memories. The HPA axis is a major part of the neuroen-
docrine system involving the hypothalamus, the pituitary gland located
below the hypothalamus, and the adrenal glands (located on top of the

Book 1.indb 147 06/03/2012 13:48

 148 C L I N I C A L P S Y C H O L O G Y : A N I N T R O D U C T I O N

kidneys), which controls stress reactions and other processes including

the immune system, sexuality and digestion.
At a behavioural level, these neurobiological processes associated
with the short allele variant of 5-HTTLPR subserve increased atten-
tional bias to threat, enhanced fear conditioning and stress sensitivity
(Caspi et al., 2010). However, the short allele variant of 5-HTTLPR
seems to be a general vulnerability factor for stress-related psychologi-
cal disorders, rather than a specific vulnerability factor for PTSD. For
example, it is also a vulnerability factor for depression and borderline
personality disorder.
A specific allele of the Val158Met polymorphism of the catechol-O-
methyltransferase COMT gene is a risk factor for panic disorder (Maron
et al., 2010). The COMT gene encodes an enzyme that breaks down
dopamine, weakening its signal. People with panic disorder are more
likely to have the COMPT allele associated with less efficient dopamine
breakdown. The consequent higher levels of dopamine in the limbic sys-
tems of such people with panic disorder may subserve their increased
sustained attention to salient stimuli, even when these stimuli are anxiety
provoking.

Neurobiology
The neurobiological hypothesis is that anxiety disorders are charac-
terized by neuroanatomical, neurotransmitter and neuroendocrine
abnormalities. There is considerable support for this hypothesis from
neuroimaging, psychophysiological and pharmacological studies,
although current knowledge of these abnormalities is incomplete (Britton
& Rauch, 2009; Khan et al., 2009; Martin et al., 2009).
However, there is a consensus about certain aspects of the neuro-
biology of anxiety disorders. With the exception of OCD, which has
distinct neurocircuitry mentioned below, anxiety disorders are asso-
ciated with abnormalities in brain structures that subserve processing
information about danger, fear conditioning and fear responses, pri-
marily the limbic system. Within this system, overactivity of the amyg-
dala during exposure to feared stimuli is central to anxiety disorders.
Excessive activity in the limbic system which subserves the experience
of fear and anxiety is normally inhibited by the orbitofrontal cortex, which
subserves impulse control, and the prefrontal cortex, which subserves
executive functions such as planning and decision-making. In anxiety
disorders, communication between the limbic system and the frontal
cortex is impaired and so persistent limbic overactivity occurs when
one is exposed to anxiety-provoking stimuli.
There is evidence for dysregulations of neurotransmitters, notably
GABA (gamma-amino-butyric-acid) and serotonin, which facilitate com-
munication between the limbic system and the frontal cortex – the brain
structures centrally involved in anxiety disorders. The efficiency of
both of these neurotransmitter systems is reduced in anxiety disord-
ers, and increased by anti-anxiety drugs (Dent & Bremner, 2009;
Mathew & Hoffman, 2009; Pollack & Simon, 2009; Stewart et al., 2009;
van Ameringen et al., 2009).

Book 1.indb 148 06/03/2012 13:48

 5 • ANXIETY DISORDERS 149

Selective serotonin reuptake inhibitors (SSRIs) such as fluoxetine

(Prozac) target the serotonergic neurotranmitter system, and benzodi-
azepines such as diazepam (Valium) target the GABA neurotransmitter
system. In the normal brain, GABA is usually released once arousal
reaches a certain level and decreases the experience of anxiety, but
this process is less efficient in people with anxiety disorders. Benzo-
diazepines reduce anxiety by binding to GABA neuroreceptors.
Unfortunately, benzodiazepines are addictive, and so long-term use for
the treatment of anxiety disorders is not regarded as best practice.
Dopamine, noradrenaline, glutamate and other neurotransmitter sys-
tems may also be dysregulated in anxiety disorders, although their roles
are less clearly understood.
Genetic vulnerability to anxiety disorders involves genes whose
action affects the efficiency of neurotransmitter systems associated
with anxiety, as was noted above in the discussion of genetic factors.
Evidence from a small number of neuroimaging studies shows that
psychological interventions, such as cognitive behaviour therapy,
normalize neurobiological functional abnormalities associated with
anxiety disorders (Frewen et al., 2008a).
In anxiety disorders there is evidence for the dysregulation of neuro-
peptides in the limbic system, notably corticotropin-releasing factor
(CRF). CRF is associated with HPA axis hyperactivity. Such hyperactiv-
ity is a central neurobiological feature of anxiety disorders, and is asso-
ciated with the release of the stress steroid cortisol which is elevated in
people with anxiety disorders (Khan et al., 2009).
The neurobiology of OCD differs from that of other anxiety disorders.
With OCD there are abnormalities in the functioning of circuits which
link the basal ganglia, the prefrontal cortex (particularly orbitofontal and
anterior cingulate regions) and the thalamus, which is referred to as the
cortico-striatal–thalamic circuit. Overactivity of the prefrontal cortex and
thalamus subserves the initiation and maintenance of obsessional
worrying, and overactivity of the basal ganglia subserves stereotyped
compulsive behaviour patterns typical of people with OCD. Surgical
disruption of the cortico-striatal–thalamic circuit alleviates chronic OCD,
although this invasive treatment is used only in cases resistant to
psychotherapy or medication (Aouizerate et al., 2006; Stewart et al.,
2009; Zohar et al., 2009). SSRIs are the most common pharmacological
intervention in both adults and children for OCD because, the condition
is associated with inefficient functioning of the serotonin neurotransmitter
system (Rapoport & Shaw, 2008; Zohar et al., 2009).

Temperament, traits, cognitive biases

and coping strategies
Temperament, traits, cognitive bias and coping strategy theories
propose that anxiety disorders develop in people who have specific
anxiety-prone dispositions. Temperamental characteristics are biologi-
cally based behavioural attributes present from birth. In support of this

Book 1.indb 149 06/03/2012 13:48

 150 C L I N I C A L P S Y C H O L O G Y : A N I N T R O D U C T I O N

view there is a substantial body of longitudinal research which shows

that infants with a temperament characterized by behavioural inhibition
– nervousness and avoidance of unfamiliar stimuli and situations – are
at risk for developing anxiety disorders (Kagan, 2010).
Personality traits are cross-situationally stable psychological charac-
teristics determined by both genetic and environmental factors. There is
a growing consensus that a five-factor model of personality traits is
probably the most parsimonious (John et al., 2008). The ‘Big 5’ per-
sonality traits are neuroticism, extraversion, openness to experience,
conscientiousness and agreeableness. In a meta-analysis Kotov et al.
(2010) found that all anxiety disorders were strongly associated with the
personality trait neuroticism; all disorders except specific phobias were
associated with low conscientiousness; and all anxiety disorders except
simple phobias and generalized anxiety disorder were associated with
high levels of introversion. High neuroticism entails emotional instability
and distress; low conscientiousness is the tendency not to follow
through on plans; and introversion involves social withdrawal.
A number of lower-order traits have been found to correlate with spe-
cific anxiety disorders. These include anxiety sensitivity, fear of nega-
tive evaluation, intolerance of uncertainty, perfectionism, thought–action
fusion and alexithymia (Starcevic & Berle, 2006). Because correlational
evidence on these traits comes from cross-sectional studies, it is not
clear whether they are predisposing vulnerability factors or correlates of
anxiety disorders. In a meta-analysis, Naragon-Gainey (2010) found
that anxiety sensitivity correlated .4–.6 with all anxiety disorders and
most strongly with panic disorder. Anxiety sensitivity refers to the ten-
dency to fear somatic, cognitive and social anxiety-related symptoms.
Fear of negative evaluation by others in social situations is correlated
with social phobia (Weeks et al., 2005). Intolerance of uncertainty is
associated most strongly with generalized anxiety disorder (Dugas et
al., 2004). People with a high level of intolerance for uncertainty believe
uncertainty is undesirable and should be avoided, and have difficulties
functioning well in uncertain situations, especially where stressful
events may occur. Perfectionism and thought–action fusion are strongly
correlated with OCD (Berle & Starcevic, 2005; Egan et al., 2011).
Perfectionism is the tendency to adhere to very high standards and
experience distress if these standards are not reached. With thought–
action fusion, there are beliefs that thoughts and actions are inextricably
linked, that immoral thoughts are equivalent to immoral acts, and that
that thoughts about specific events increase the likelihood of such
events occurring. Alexithymia, which refers to difficulty identifying and
labelling feelings, is strongly correlated with PTSD (Frewen et al.,
2008b).
Research from experimental psychopathology has consistently
shown that people with anxiety disorders show a range of information-
processing biases (McNally & Reese, 2009). They have an attentional
bias for threatening information, as shown by the tendency to take longer
to name the colours of threatening words than the colours of positive or
neutral words in the emotional Stroop test. In this test individuals read

Book 1.indb 150 06/03/2012 13:48

 5 • ANXIETY DISORDERS 151

randomized lists of all three types of words printed in different colours.

People with anxiety disorders also show a bias towards threatening
interpretations of ambiguous situations in studies where they are asked
to write interpretations of descriptions of situations such as ‘You are
awoken by a noise at night’. People with panic disorder have a memory
bias favouring recall of threatening information, in studies where they
memorize threatening and non-threatening stimuli. It is still unclear
whether these information-processing biases are correlates of anxiety or
predispositions that confer vulnerability to anxiety disorders.
Certain coping strategies are associated with anxiety disorders. In a
meta-analysis, Aldao et al. (2010) found that anxiety disorders were
associated with the use of rumination, avoidance and suppression as
coping strategies. They also found negative correlations between
anxiety and a number of adaptive coping strategies including problem-
solving, acceptance and reappraisal.

Psychoanalytic theories
In anxiety disorders, according to classical psychoanalytic theory,
defence mechanisms are used to keep unacceptable sexual or aggres-
sive impulses and moral anxiety about their expression from entering
consciousness (Busch et al., 2010). The unacceptable impulses and
related moral anxiety become transformed into neurotic anxiety. In pho-
bias, the unacceptable impulse is repressed and the neurotic anxiety
into which it is transformed is displaced onto a substitute object which
symbolizes the original object about which the unacceptable impulses
were felt. The key defence mechanism is displacement. Thus, when
people say that they are frightened of a particular object or situation, the
psychoanalytic hypothesis is that they are frightened about something
else, but have displaced their fear from the original taboo object or
event onto a more socially acceptable target. In Freud’s original state-
ment of this hypothesis, in the Little Hans case, where the boy had a
horse phobia, he argued that the taboo fear was castration anxiety, and
this fear of the father was displaced onto horses (Freud, 1909a). In
generalized anxiety disorders, the defences break down and the person
becomes overwhelmed with anxiety as the unacceptable impulses con-
tinually intrude into consciousness and seek expression. Anxiety about
taboo objects is displaced onto every available target.
Within psychoanalytic theory it is proposed that the unacceptability of
certain impulses, and habitual ways of defending against these, are
learned early in childhood in relationships with parents. In adulthood
these same defences and habitual ways of interacting with parents tend
to be deployed in relationships with significant people in the person’s
life (including partners, colleagues and therapists), a phenomenon
referred to as transference. From a psychoanalytic perspective, OCD is
explained as the sequelae of toilet training battles (Freud, 1909b).
According to classical psychoanalytic theory, children evolve through
oral, anal and phallic stages of development, with gratification being
principally derived from these differing bodily areas as development

Book 1.indb 151 06/03/2012 13:48

 152 C L I N I C A L P S Y C H O L O G Y : A N I N T R O D U C T I O N

occurs. During the anal phase of development, according to psycho-

analytic theory, children become angry with their parents’ insistence
that they use the toilet in an appropriate way. Attempts to express these
aggressive impulses are met with sanctions from the parents and so the
aggression is repressed. When these repressed sexual–aggressive
impulses attempt to find expression, this causes anxiety. The aggres-
sive impulses and thoughts are displaced and substituted by less unac-
ceptable thoughts or impulses. When these intrude into consciousness,
they are experienced as ego-alien because they have been disowned
or isolated. The anxiety is managed by carrying out a compulsive ritual
to undo or cancel out the undesirable impulse. Because the source of
this tendency towards compulsions is theorized to have arisen during
the anal developmental phase, it has become commonplace in popular
culture to refer to meticulous people as ‘anal’.
In psychoanalytic treatment, the aim is to interpret the defence, the
repressed forbidden feelings and the associated neurotic anxiety.
These three elements (the defence, the hidden feeling, and the associ-
ated anxiety) are referred to as the triangle of conflict (Ezriel, 1952).
During psychoanalytic treatment attention is drawn to the parallels
between the way in which the person manages current problematic
relationships with other significant people in their lives such as their
peers, work colleagues or partners; the current relationship with the
therapist; and past relationships with the parents. These three sets of
relationships are referred to as the triangle of person (Menninger, 1958).
Because the tendency to replicate relationship patterns from childhood
in adult life with friends, colleagues and therapists is referred to as
transference, interpretations that point to these replications, within the
triangle of person, are referred to as transference interpretations. The
triangle of conflict and the triangle of person are presented in Figure
5.5. Interpretations based on these are offered tentatively, at a stage in
the therapy when a strong working alliance has been established, and
within the context of a coherent psychodynamic case formulation
(Malan, 1995; McCullough-Vaillant, 1997).
The idea of displacement is clinically useful when working with
anxious patients. In my clinical experience, people worried about one
thing may say that they are worried about another. However, there is no
evidence to support the idea that all anxiety disorders represent
displacement of anxiety associated with psychosexual developmental
conflicts. There is some limited evidence from a small number of
controlled trials that short-term psychodynamic therapy is effective for
anxiety disorders (Leichsenring, 2009). For example, in a controlled
trial, Milrod et al. (2007) found that panic-focused psychodynamic
psychotherapy was more effective than applied relaxation training in the
treatment of panic disorder, and in another controlled trial Leichsenring
et al. (2009) found that short-term psychodynamic psychotherapy was
as effective as cognitive-behavioural therapy in the treatment of
generalized anxiety disorder.

Book 1.indb 152 06/03/2012 13:48

 5 • ANXIETY DISORDERS 153

Figure 5.5 Psychodynamic triangles of conflict and person (based on Ezriel, H. (1952). Notes on psychoanalytic group
therapy: II. Interpretation. Research Psychiatry, 15, 119. Menninger, K. (1958). Theory of Psychoanalytic Technique.
London: Imago. Malan, D. (1995). Individual Psychotherapy and the Science of Psychodynamics. London: Arnold.
McCullough-Vaillant, L. (1997). Changing Character: Short-Term Anxiety Regulating Psychotherapy for Restructuring
Defences, Affects and Attachments. New York: Basic Books.)

Cognitive-behavioural theories
Theories developed within the cognitive-behavioural tradition (which
includes both behavioural and cognitive formulations) point to the
importance of conditioning and cognitive learning processes in the
development of anxiety disorders.

Behavioural approaches
Behavioural theories of anxiety disorders, such as Mowrer’s (1939) two-
factor theory, propose that anxiety and associated avoidance of feared
objects, situations or memories are learned though the processes of
classical and operant conditioning. With classical conditioning, it is

Book 1.indb 153 06/03/2012 13:48

 154 C L I N I C A L P S Y C H O L O G Y : A N I N T R O D U C T I O N

proposed that a person becomes frightened of a neutral object, situation

or memory that was present during a trauma or exposure to a highly
anxiety-provoking stimulus. The classically conditioned fear response
to the previously neutral stimulus does not extinguish because the
person’s avoidant behaviour is negatively reinforced each time the
previously neutral stimulus is avoided. In behavioural psychology,
negative reinforcement is the term used to describe the strengthening
of a response that leads to escaping from an aversive situation, such as
the experience of anxiety.
Eysenck (1979) added the concepts of biological preparedness,
incubation and constitutional vulnerability to Mowrer’s theory. He
proposed that as a result of evolutionary processes, people are
biologically prepared at specific developmental stages to develop
phobias through one-trial classical conditioning to specific classes of
stimuli such as snakes, spiders, injuries and natural hazards (De Silva
et al., 1977). He also proposed that conditioned fears are strengthened
through incubation, a positive feedback process, in which fear itself
reinforces fear of the phobic stimulus. That is, each time a person is
briefly exposed to or briefly recalls the feared stimulus, or the trauma
associated with it, the conditioned fear is strengthened, because the
person becomes afraid of the experience of anxiety. This whole process
occurs outside of cognitive control. Finally, Eysenck proposed that
some people are constitutionally vulnerable to developing anxiety
disorders through having high levels of neuroticism and introversion, a
hypothesis supported by meta-analytic data from personality trait
studies of people with anxiety disorders (Kotov et al., 2010).
Behavioural treatment for anxiety disorders involves exposure to
stimuli that elicit anxiety until habituation occurs and the anxiety
response is extinguished (Moscovitch et al., 2009). Systematic
desensitization and flooding (also referred to as implosion therapy) are
two commonly used behavioural procedures. With systematic
desensitization, a procedure developed by Joseph Wolpe (1969) in
South Africa, clients in a deeply relaxed state are exposed to increasingly
anxiety-provoking stimuli, with progression to the next stimulus occurring
once habituation to the present one has occurred. With flooding (or
implosion), a technique developed by Thomas Stampfl (Stampfl &
Levis, 1968), clients are exposed for a prolonged period (often lasting a
number of hours) to their most anxiety-provoking stimuli until anxiety
responses are extinguished. With these exposure-based behavioural
interventions, anxiety-provoking stimuli may be presented in vivo (real
life), in virtual reality using computer simulations, or using mental
imagery where the psychologist invites the client to close their eyes and
imagine the feared object or situation.
In all behavioural treatment programmes, prior to exposure clients are
given detailed psychoeducation about their anxiety disorder, a formulation
which explains how it developed and is maintained, the proposed
exposure-based treatment plan, and training in relaxation skills or other
coping strategies for use during exposure to help them tolerate exposure
to the feared object or situation until their anxiety responses are

Book 1.indb 154 06/03/2012 13:48

 5 • ANXIETY DISORDERS 155

extinguished, although in Stampfl’s original implosion therapy protocol he

encouraged clients to feel maximum anxiety (Stampfl & Levis, 1968). For
separation anxiety disorders, children are exposed to separation from
parents, usually through supported attendance at school. For phobias,
exposure is arranged to feared objects or situations. For panic disorder,
clients are exposed to physiological sensations of hyper-arousal
(interopceptive exposure) by directing attention to their heart rate and
respiration. If they have secondary agoraphobia, they are also exposed
to public places that they typically avoid. For generalized anxiety disorder,
clients are exposed to feared objects and situations and are also helped
to plan and practise worrying to desensitize them to their fear of
uncontrollable rumination. For PTSD, clients are exposed to cues that
evoke flashbacks or to traumatic memories. For OCD, exposure treatment
is referred to as exposure and response prevention, because clients are
exposed to cues (such as dirt) that elicit obsessions, and are helped to
prevent themselves from engaging in their anxiety-reducing compulsions
until their anxiety responses extinguish. A large body of research supports
the effectiveness of exposure-based treatment programmes for adults
and children with anxiety disorders (Moscovitch et al., 2009; Olatunji
et al., 2010; Rapee et al., 2009).

Cognitive approaches
According to Aaron T. Beck’s cognitive theory, anxiety disorders occur
when threatening stressful life events reactivate danger-oriented cognitive
schemas. It is proposed that these schemas were formed early in child-
hood through exposure to traumatic or adverse experiences and
parenting practices that sensitized the individual to threat, danger and
personal vulnerability and encouraged avoidant coping (Clark & Beck,
2010a). These threat-oriented schemas contain beliefs, attitudes and
assumptions about threat and vulnerability relevant to personal safety
such as ‘The world is dangerous, so I must continually be on guard’ or
‘My health is ailing so any uncomfortable somatic sensation must reflect
serious ill health’. These threat-oriented schemas also direct the identi-
fication, interpretation and evaluation of experience and underpin anxiety-
maintaining cognitive distortions such as minimizing safety-related
events, maximizing threat-related negative events and catastrophizing
about the future. These schemas dominate the biased, threat-sensitive
way people with anxiety experience themselves in the world.
Anxious people are more likely to attend to threat-oriented rather
than safety-oriented objects, events and situations, and to interpret
ambiguous situations in a threatening rather than a positive way
(McNally & Reese, 2009). On a moment-to-moment basis this tendency
finds expression through the experience of danger-oriented negative
automatic thoughts. For example, a person with panic disorder who
notices their heartbeat and respiration may have the negative automatic
thought ‘These are signs that I’m going to have a panic attack, I must be
going crazy’; or a person with OCD who notices a speck of dirt on their
cutlery may think ‘That dirt contains germs, so if I use the cutlery I may

Book 1.indb 155 06/03/2012 13:48

 156 C L I N I C A L P S Y C H O L O G Y : A N I N T R O D U C T I O N

become infected and die’. These negative automatic thoughts cause

anxious arousal, which in turn motivates avoidant coping that alleviates
anxiety and reinforces avoidant coping.
According to cognitive theory, over time, the repetition of these types
of micro-event in which ambiguous stimuli evoke threat-oriented
negative automatic thoughts that elicit anxiety and motivate avoidance
strengthen threat-oriented schemas and weaken personal control over
anxiety, particularly the capacity to access more adaptive non-threat-
oriented schemas.
Cognitive therapy helps clients challenge their negative automatic
thoughts and underlying core beliefs, attitudes and assumptions about
the dangerousness of the situations in which they feel anxiety. This
involves clients monitoring fluctuations in anxiety levels in threatening
situations, accessing the negative automatic thoughts and beliefs that
underpin these fluctuations, and challenging these thoughts and beliefs
by generating safe rather than danger-oriented interpretations of situ-
ations and engaging in ‘behavioural experiments’ such as exposure
to feared situations to check out whether the catastrophes they fear
actually occur.
Cognitive therapy, like behaviour therapy, uses exposure procedures
to treat anxiety disorders, but explains their effectiveness in terms of their
effects on threat-oriented schemas rather than extinction of conditioned
responses. Beck’s theory is supported by evidence which shows that
anxiety is associated with a threat-sensitive cognitive style (McNally &
Reese, 2009) and also by the results of treatment outcome studies with
adults and children which support the efficacy of cognitive-behavioural
approaches to treatment (Olatunji et al., 2010; Rapee et al., 2009).
In a meta-analysis of 108 studies of cognitive behaviour therapy
involving all types of anxiety disorder, Norton and Price (2007) found
that cognitive restructuring and exposure therapy alone, in combination,
or combined with relaxation training were all equally effective treatments
for anxiety disorders. Cognitive-behaviour therapy is as effective as
medication such as SSRIs in the treatment of anxiety disorders.
However, its effects are more enduring (Hollon et al., 2006). These
more enduring effects are probably due to significant changes in
psychological processes that maintain anxiety disorders such as the
extinction of conditioned responses, the preferential accessing of non-
threat-oriented schemas and the use of non-avoidant coping strategies.
Attempts have been made to integrate the cognitive theory of anxiety
disorders with current knowledge about the neurobiology of anxiety.
Clark and Beck (2010b) have proposed that activation of negative
cognitive schemas is subserved by amygdala hyperactivity and avoidant
coping is subserved by hypoactivity of the frontal cortex. In contrast, the
process of challenging negative automatic thoughts and actively coping
with anxiety-provoking situations is subserved by increased activity in
the frontal cortex and a gradual reduction in amygdala activity. There is
some evidence that cognitive therapy gradually normalizes the
neurobiological abnormalities that typify anxiety disorders (Frewen et
al., 2008a).

Book 1.indb 156 06/03/2012 13:48

 5 • ANXIETY DISORDERS 157

Family systems theory

Systemic theories of anxiety disorders propose that family interaction is
central to the aetiology of anxiety disorders and that this provides a
rationale for family therapy as a treatment for anxiety (e.g., Bloch et al.,
1994; Combrinck-Graham, 1986; Dadds et al., 1992; Perlmutter, 1996).
According to this position, individuals develop anxiety disorders when
they are socialized in families where parents (and other caregivers)
elicit, model and inadvertently reinforce anxiety-related beliefs and
behaviours. Furthermore, trauma, stressful life events and family life-
cycle transitions in either the family of origin or the family of procreation
precipitate the onset of anxiety disorders. These disorders are main-
tained by patterns of family interaction that reinforce anxiety-related
beliefs and avoidant behaviour.
Family belief systems that promote anxiety involve ideas such as –
unknown situations should be routinely interpreted as dangerous
because it’s better to be safe than sorry; the future will probably entail
many hazards, catastrophes and dangers; inconsequential events in
the past will lead to dangerous threatening consequences at unexpected
times in the future; fluctuations in autonomic arousal should be
interpreted as the onset of full-blown anxiety attacks; minor symptoms
are reflective of serious illness; and testing out the validity of any of
these beliefs will lead to more negative consequences than continuing
to assume that they are true. Through observing parents and other
significant family members articulate these types of danger-oriented
belief and engaging in family interactions premised on them, individuals
come to internalize them and develop danger-saturated belief systems.
Parental modelling of avoidant coping and inadvertent reinforcement
of children’s danger-saturated beliefs and avoidant behaviour are the
main behaviour patterns that promote anxiety. When children observe
parents coping with perceived threats by avoiding rather than confronting
them, they adopt similar coping strategy themselves. Such anxiety-
related beliefs and avoidant coping are inadvertently reinforced when
parents acknowledge their validity and do not challenge them.
Family life-cycle transitions, such as starting school, moving house,
birth of a sibling, having children, changing jobs and family stresses
such as child abuse, marital discord, illness, injury or bereavement may
precipitate the onset of anxiety disorders. In such situations, the
individual interprets the transition or stress as a major threat and copes
by engaging in avoidant behaviour.
Parents (in the case of children) or partners (in the case of adults)
may inadvertently maintain an individual’s anxiety-related beliefs and
avoidant behaviour by sympathizing with their irrational fears, accepting
their danger-saturated view of the situation, and condoning their avoid-
ant behaviour as a legitimate coping strategy. Parents’ and partners’
own danger-saturated belief systems and personal adjustment prob-
lems, if such are present, may prevent them from providing the person
with the anxiety disorder with opportunities to develop the skills required
to confront and master feared situations. So, for example, in families

Book 1.indb 157 06/03/2012 13:48

 158 C L I N I C A L P S Y C H O L O G Y : A N I N T R O D U C T I O N

where there are marital problems, parental depression, parental alcohol

abuse or some other difficulty, the parents may avoid facing these dif-
ficulties and focus their attention instead on reassuring an anxious child
or arranging extensive medical investigations for anxiety-related
somatic complaints. The patterns of family interaction that evolve in
such situations may inadvertently maintain the child’s anxiety and rein-
force the parents’ avoidance of their own marital or personal difficulties.
Commonly, family members are not consciously aware of the
secondary gains associated with these problem-maintaining patterns of
interaction. Where adults develop anxiety disorders, their partners may
become involved in rituals that help them avoid feared situations and
this process may allow the couple to avoid dealing with unresolved
marital conflicts over issues such as the distribution of power within the
marriage.
Family therapy for children with anxiety disorders aims to support
parents and children in creating opportunities within which children can
develop the skills required to confront and master feared situations.
Couples therapy for cases in which one partner has an anxiety disorder
involves helping the couple to work as a team and jointly enter situations
that are increasingly anxiety-provoking for the person with the anxiety
disorder, and remain in these until the anxiety subsides. The non-
symptomatic partner’s role in such programmes is to provide support
and encourage the symptomatic partner to engage in active coping
strategies. Family therapy also aims to reduce danger-oriented family
cultures by encouraging family members in their conversations and
behaviour to focus more on bravery and positive accomplishments and
less on danger and avoidance.
There is substantial evidence, mainly from cross-sectional studies,
that the parents of most children with anxiety disorders have anxiety
disorders or other psychological problems themselves; that modelling
plays an important role in the transmission of anxiety patterns from
parents to children; that anxiety disorders are associated with an over-
controlling parenting style, a negative or critical style and styles that
foster insecure attachment, such as not responding to children’s distress
signals; and that stressful family circumstances, especially child abuse
and marital discord, are associated with anxiety (Bögels & Brechman-
Toussaint, 2006; Degnan et al., 2010; Hudson & Rapee, 2009; Rapee
et al., 2009; van der Bruggen et al., 2008). There is also evidence that
in adulthood, anxiety disorders, notably PTSD, can lead to significant
relationship difficulties, which in turn may reduce the support available
to the partner with the anxiety disorder and thereby maintain it (Taft
et al., 2011).
Comparative trials have shown that family-based interventions are
effective for childhood anxiety disorders, but are not always more
effective than individual CBT (Bögels & Brechman-Toussaint, 2006;
Rapee et al., 2009). In a review of 12 studies of couples-based treat-
ment for panic disorder for agoraphobia, Byrne et al. (2004) concluded
that couples-based exposure therapy was as effective as individually
based CBT.

Book 1.indb 158 06/03/2012 13:48

 5 • ANXIETY DISORDERS 159

An integrative perspective
In clinical practice an integrative approach to conceptualizing and
treating anxiety disorders is useful. Distinctions may be made between
predisposing, precipitating, maintaining and protective factors, and
insights and related evidence associated with the various theories
reviewed above may be integrated into this formulation framework.
A range of personal and family factors may predispose people to
develop anxiety disorders. Personal factors include a genetic vulnera-
bility to anxiety, a behaviourally inhibited temperament, a threat-
oriented cognitive bias, attachment insecurity and personality traits
such as neuroticism, introversion, low conscientiousness, anxiety sen-
sitivity, fear of negative evaluation, intolerance of uncertainty, perfec-
tionism, thought–action fusion, and alexithymia. Family factors that may
predispose people to develop anxiety disorders include growing up in a
stressful family with anxious parents who adopt controlling or critical,
unsupportive parenting styles and foster a threat-oriented family cul-
ture, or families characterized by domestic violence and child abuse. All
of these predisposing factors sensitize children to threat, and support
the development of avoidant coping.
The onset of anxiety disorders may be precipitated by trauma, life-
cycle transitions or stressful life events that threaten the individual’s safety
or security. Once anxiety disorders occur they may be maintained by a
range of processes. These include a threat-oriented cognitive style,
hyper-vigilance, and ruminative and avoidant coping strategies and
defence mechanisms. Avoidant coping maintains anxiety through the
process of negative reinforcement (getting relief from avoiding feared situ-
ations), and prevents individuals from testing out danger-oriented beliefs.
Anxiety disorders may also be maintained by interacting with family mem-
bers who support these processes and/or who adopt threat-sensitive
belief systems and avoidant coping styles. Protective factors include per-
sonal attributes and social relationships that support actively coping with
feared stimuli, and challenging danger-saturated belief systems.

Assessment
Through careful clinical interviewing of clients and members of their
families, the symptoms of anxiety, situations in which they occur and
relevant history are obtained. A diagnosis is given in accordance with
the criteria outlined in ICD-10 and DSM-IV-TR. A formulation explaining
the symptoms entailed by the diagnosis may be developed in which the
relevant predisposing, precipitating, maintaining and protective factors
are outlined. A general clinical formulation model for anxiety disorders
is given in Figure 5.6.
The best available structured interview for assessing anxiety
disorders is the Anxiety Disorders Interview Schedule for DSM-IV, for
which both adult and child versions are available (ADIS, Brown et al.,
1994; Silverman & Albano, 1996). A range of standardized self-report
instruments and rating scales may be used to assess specific anxiety

Book 1.indb 159 06/03/2012 13:48

 160 C L I N I C A L P S Y C H O L O G Y : A N I N T R O D U C T I O N

Figure 5.6 General formulation model for anxiety disorders

disorders or specific traits associated with them in children and adults

(Carr, 2006a; Carr & McNulty, 2006; Hunsley & Mash, 2008). During the
process of assessment and treatment, patients and family members
may be invited to keep daily records of fluctuations in feelings of anxiety,
related thoughts, related avoidant behaviours and the circumstances
surrounding these fluctuations.

Treatment
The discovery that exposure therapies effectively alleviate anxiety is
one of the most important contributions that psychologists have made
to the treatment of anxiety disorders. Another important discovery is
that briefly exposing patients with anxiety disorders to threatening
stimuli sensitizes them to these stimuli and increases anxiety. Thus,
non-directive permissive approaches to counselling people with anxiety
disorders may actually exacerbate rather than alleviate their anxiety.
Many of us who work clinically with people who suffer from anxiety
come across clients whose anxiety has worsened as a result of
participation in well-intentioned, non-directive counselling.
Current best practice is to take a stepped-care approach to the
treatment of anxiety disorders. For people with mild or non-chronic
anxiety disorders, guided self-help approaches may be taken. Meta-

Book 1.indb 160 06/03/2012 13:48

 5 • ANXIETY DISORDERS 161

analyses of controlled trials have shown that both bibliotherapy and

computer-based guided self-help are effective for people with anxiety
disorders recruited through media advertisements (Andrews et al.,
2010; Cuijpers et al., 2010; Salloum, 2010). Fear Fighter is a particularly
well researched computer-based programme for the treatment of panic
disorder and phobias in adults (www.fearfighter.com).
Psychological treatment may be offered to cases that do not respond
to self-help. For all of the anxiety disorders, cognitive-behaviour therapy
protocols have been developed and positively evaluated in adults
(Barlow et al., 2007; Franklin & Foa, 2007; Najavits, 2007) and children
(In-Albon & Schneider, 2007; Watson & Rees, 2008). While the evidence
base for CBT anxiety disorder programmes is vast, there is also strong,
though less extensive, evidence for the effectiveness of systemic
therapy for a number of anxiety disorders including separation anxiety
disorder and OCD in children, and panic disorder with agoraphobia in
adults (Carr, 2009b, 2009c). There is some evidence from a small
number of controlled trials for the effectiveness of psychoanalytic
psychotherapy in the treatment of generalized anxiety disorder and
panic disorder in adults (Leichsenring, 2009).
Process studies of a range of different types of psychotherapy for
anxiety show that a better outcome occurs where there is a strong
therapeutic alliance, a structured and intensive approach to treatment
that involves psychoeducation, challenging danger-oriented beliefs,
exposure to feared situations until habituation occurs, the provision of
training in coping strategies, fostering social and family support and
good compliance with exposure-based homework assignments
between sessions (Stiles & Wolfe, 2006; Woody & Ollendick, 2006). A
number of client characteristics influence the outcome of psycho-
therapy for anxiety disorders (Newman, Crits-Christoph et al., 2006;
Newman, Stiles et al., 2006). A poorer outcome is associated with more
severe symptoms; comorbid depression, substance use, interpersonal
problems and personality disorders; an external locus of control; a his-
tory of problematic relationships with parents; low socio-economic sta-
tus; and low expectations of therapeutic success.
In adults, pharmacological therapy is appropriate where there is limited
response to psychotherapy, or where patients express a preference for
medication rather than psychological intervention. For most anxiety disor-
ders, SSRIs are the medication of choice. Benzodiazepines, once popu-
lar, are not now widely used except on a short-term basis, because of the
potential for addiction. For chronic OCD that is unresponsive to both psy-
chological and pharmacological intervention, psychosurgery that disrupts
the cortico-striatal–thalamic circuit that subserves OCD symptomatology
may be considered, because there is some evidence for its effectiveness
(Aouizerate et al., 2006; Stewart et al., 2009; Zohar et al., 2009).
Evidence from meta-analyses supports the effectiveness of SSRIs
for childhood anxiety disorders (Bridge et al., 2007). However, because
selective serotonin reuptake inhibitors may increase suicide risk, they
should be used very cautiously, and only with frequent clinical monitoring
in cases where there is no response to psychological intervention (Rudd
et al., 2009).

Book 1.indb 161 06/03/2012 13:48

 162 C L I N I C A L P S Y C H O L O G Y : A N I N T R O D U C T I O N

This overall approach to the management of anxiety disorders in

children and adults is consistent with international best practice guide-
lines (American Academy of Child and Adolescent Psychiatry, 2007c,
2009, 2010; American Psychiatric Association, 2004a, 2007, 2009;
NICE, 2005a, 2005b, 2006b, 2011).

Controversies
There are many controversies in the scientific study and clinical
treatment of anxiety disorders. The medicalization of fear and courage
is one deserving particular mention (Breggin, 1991). Within ICD-10 and
DSM-IV-TR, anxiety disorders are framed as medical conditions
requiring treatment, and in practice in many instances pharmacological
treatment is favoured because it is more convenient to offer than non-
pharmacological alternatives. An alternative viewpoint is that this way of
conceptualizing fundamental human experiences such as fear and
courage further disempowers people who are already feeling frightened
and powerless. For example, if a person has repeated panic attacks
and develops a constricted lifestyle because they are afraid of having a
panic attack while away from the safety of their home, it may lead them
to believe that they are truly powerless to control their fear if their fear is
defined as an illness requiring pharmacological treatment. A further
aspect of this argument is that for many years addictive pharmacological
treatments, such as diazepam (Valium) or other benzodiazepines, were
routinely prescribed for anxiety disorders.
Those who are critical of the medicalization of experiences such as
fear and courage would argue that if a person can understand that panic
attacks develop from the misinterpretation of bodily sensations and
hyperventilation, then they may use this knowledge and their own cour-
age to take control of their fear. In this way they are empowered to be
courageous rather than disempowered by being defined as ill. Those
who are critical of the medicalization of distress would argue, in the
same vein, that a person given a diagnosis of PTSD and prescribed
medication to manage the recurrent traumatic memories may also
become disempowered. They may develop a belief that they are power-
less to control recurrent traumatic memories of experiences such as
road traffic accidents, assault with a deadly weapon, or involvement in
war or combat. In contrast, if they are helped to understand that trau-
matic memories of life-threatening events must be repeatedly recalled,
processed and integrated into people’s overall views of themselves,
then this opens up a range of non-pharmacological procedures which
trauma survivors may follow to help them take control of recurrent, intru-
sive distressing memories.
In order to further our understanding of apparently irrational fears,
post-traumatic distress and courage, continued scientific study is
essential. The use of diagnoses such as PTSD and panic disorder may
be valuable in this context. However, it is also valuable to study fear,
distress and courage as normal psychological process. It may be fruitful
too to study the social processes that underpin the medicalization and

Book 1.indb 162 06/03/2012 13:48

 5 • ANXIETY DISORDERS 163

the medical treatment of fear in clinical practice and to explore the

degree to which these, and alternative conceptualizations of fear,
empower clients to be courageous.

Summary
Normal fear is an adaptive response to potential threats to
safety while anxiety is a similar non-adaptive response to situ-
ations that are not threatening. In DSM-IV-TR and ICD-10 a
number of anxiety disorders are defined which differ in the
stimuli that elicit anxiety and associated types of avoidant
response. With separation anxiety, separation from parents
elicits anxiety and is avoided. Consequently school refusal
often occurs. For phobias specific creatures, events or situ-
ations elicit anxiety and these circumscribed situations are
avoided. With generalized anxiety disorder, many aspects of
the environment elicit anxiety; the process of apparently uncon-
trollable worrying also is experienced as anxiety-provoking;
and a wide range of situations are avoided. In panic disorder,
somatic sensations of arousal are perceived as a threatening
prelude to a panic attack, and public situations in which panic
attacks previously occurred are avoided, leading to secondary
agoraphobia in many cases. With PTSD, cues that trigger
flashbacks to traumatic events that precipitated the condition
elicit anxiety; these cues are avoided; and recollections of the
trauma are suppressed. With OCD, stimuli that evoke obses-
sional thoughts (such as dirt) elicit anxiety, and compulsive
behaviour (such as hand washing) alleviate this anxiety.
At a clinical level anxiety disorders involve selective attention
to potential threats, threat-oriented cognition, abnormal levels of
physiological arousal, avoidance behaviour, and the disruption
of interpersonal relationships so that the individual’s lifestyle
becomes constricted. In a major US study the lifetime preva-
lence rate for all anxiety disorders was about 29%. With the
exception of OCD, more females than males suffer from anxiety
disorders. The typical age of onset of separation anxiety disor-
der and specific phobias is in childhood, whereas other anxiety
disorders typically first occur in adolescence or adulthood. Up to
a third of people with one anxiety disorder also suffer from
another. There is considerable comorbidity with other disorders,
notably substance misuse, disruptive behaviour, and personality
and eating disorders. Risk factors for anxiety disorders include a
family history of anxiety disorders or psychopathology; a behav-
iourally inhibited temperament; neuroticism; a personal history
of psychopathology; a history of significant family conflict or vio-
lence; and a history of stressful life events.

Book 1.indb 163 06/03/2012 13:48

 164 C L I N I C A L P S Y C H O L O G Y : A N I N T R O D U C T I O N

Theoretical explanations for anxiety disorders and related

treatments have been developed within biological, trait theory,
psychoanalytic, cognitive-behavioural, and family systems tra-
ditions. Genetic studies show that anxiety disorders are about
30–40% heritable. Candidate genes that affect the serotoner-
gic and dopaminergic neurotransmitter systems partly explain
this genetic vulnerability. With the exception of OCD, anxiety
disorders are associated with overactivity within the limbic sys-
tem, especially the amygdala, which subserves the processing
of fear-related information, and inadequate inhibition of this by
the frontal cortex, which subserves rational evaluation of poten-
tially threatening situations. In OCD, overactivity of the prefron-
tal cortex and thalamus subserves the initiation and maintenance
of obsessional worrying, and overactivity of the basal ganglia
subserves the repetition of compulsive behaviour patterns. In
anxiety disorders there is dysregulation of neurotransmitter
systems that facilitate communication between brain structures
involved in these conditions. Pharmacological treatments such
as SSRIs and benzodiazepines aim to rectify these dysregu-
lated neurotransmitter systems. Dysregulation of neuropep-
tides, notably CRF, also occurs in anxiety disorders and this is
associated with HPA axis hyperactivity and the release of the
stress steroid, cortisol.
A variety of traits are associated with all anxiety disorders,
including the temperamental characteristic behavioural inhibi-
tion, neuroticism, conscientiousness and introversion. Asso-
ciations have been found between specific cognitive traits and
specific anxiety disorders including anxiety sensitivity and
panic disorder; fear of negative evaluation and social phobia;
intolerance of uncertainty and generalized anxiety disorder;
perfectionism and OCD; thought–action fusion and OCD; and
alexithymia and PTSD. People with anxiety disorders also
show information processing biases favouring the detection
and recall of threat-oriented material and the interpretation of
ambiguous situations as threatening.
Psychoanalytic theories propose that defence mechanisms,
such as displacement and undoing, are used to keep unac-
ceptable sexual or aggressive impulses and moral anxiety
about their expression from entering consciousness. Treatment
involves the interpretation of defences, related neurotic anxiety
and repressed unacceptable unconscious impulses. Cognitive-
behavioural theories of anxiety point to the role of conditioning,
especially negative reinforcement, and cognitive learning pro-
cesses, especially the development and elaboration of threat-
oriented cognitive schemas, in the development of anxiety
disorders. CBT for anxiety disorders involves exposure to
feared stimuli until extinction of anxiety occurs, cognitive
restructuring, and relaxation and coping skills training. Family

Book 1.indb 164 06/03/2012 13:48

 5 • ANXIETY DISORDERS 165

systems theories highlight the roles of family belief systems

and interaction patterns in the development and maintenance
of anxiety disorder and the significance of family life-cycle tran-
sitions in precipitating the onset of these conditions. Family
therapy aims to reduce the danger-oriented family culture and
facilitate parents (in the case of anxious children) and partners
(in the case of anxious adults) in helping individuals with anxi-
ety disorders enter feared situations and cope with these.
In clinical practice an integrative approach to assessment
and treatment of anxiety disorders may be taken. Assessment
of anxiety symptoms and relevant personal and family history
informs the development of a formulation that explains the aeti-
ology and maintenance of the condition. This formulation
guides treatment. A stepped care approach to treatment is
considered best practice, with guided self-help being offered in
the first instance and progression to evidence-based psycho-
logical and/or pharmacological interventions where required.
There is a substantial evidence base for the effectiveness of
CBT, and a smaller evidence base for the effectiveness of sys-
temic and psychoanalytic approaches for anxiety disorders.
SSRIs are the pharmacotherapy of choice for most anxiety dis-
orders and are as effective as psychotherapy in the short term,
but their effects are not as enduring as those of psychological
intervention. There is controversy about the medicalization of
fear and courage.

Questions
● What are the main clinical features of separation anxiety, phobias,
generalized anxiety disorder, panic disorder, posttraumatic stress
disorder and obsessive compulsive disorder?
● How prevalent are anxiety disorders?
● What are the risk factors for anxiety disorders?
● What are the main biological and psychological theories of anxiety
disorders and the main research findings relevant to these theories?
● What are the main evidence-based approaches to assessment and
treatment of anxiety disorders?
● Is the medicalization of fear justified?

FURTHER READING
Professional
● Antony, M. & Stein, M. (2009). Oxford handbook of anxiety and related
disorders. New York: Oxford University Press.
● Carr, A. (2006). Handbook of child and adolescent clinical psychology:
A contextual approach (second edition). London: Routledge (Chapters
12–13).

Book 1.indb 165 06/03/2012 13:48

 166 C L I N I C A L P S Y C H O L O G Y : A N I N T R O D U C T I O N

● Carr, A. & McNulty, M. (2006). Handbook of adult clinical psychology: An

evidence based practice approach. London: Brunner-Routledge (Chapters
11–15).
● Clark, D. A. & Beck, A. T. (2010). Cognitive therapy of anxiety disorders.
New York: Guilford Press.
● Ollendick, T. & March, J. (2003). Phobic and anxiety disorders in children
and adolescents: A clinical guide to effective psychosocial and pharma-
cological interventions. Oxford: Oxford University Press.

Self-help
● Antony, M. & Swinson, R. (2000). The shyness and social anxiety
workbook: Proven, step-by-step techniques for overcoming your fear.
Oakland, CA: New Harbinger.
● Antony, M., Craske, M. & Barlow, D. (2006). Mastering your fears and
phobias: Workbook (second edition). Oxford: Oxford University Press.
● Barlow, D. H. (2006). Master your anxiety and panic: Workbook (fourth
edition). Oxford: Oxford University Press.
● Craske, M., & Barlow, D. (2006). Mastery of your anxiety and worry:
Workbook (second edition). Oxford: Oxford University Press.
● Foa, E. B. & Wilson, R. (2001). Stop obsessing! How to overcome your
obsessions and compulsions (revised edition). New York: Bantam Books.
● Herbert, C. & Wetmore, A. (1999). Overcoming traumatic stress: A self-
help guide using cognitive behavioural techniques. London: Robinson.
● Last, C. (2006). Help for worried kids. New York: Guilford.
● Rapee, R., Spense, S., Cobham, V., & Wignal, A. (2000). Helping your
anxious child: A step-by-step guide for parents. San Francisco: New
Harbinger.

WEBSITES
● American Academy of Child and Adolescent Psychiatry’s practice
parameters for the treatment of anxiety disorders, PTSC and OCD:
www.aacap.org/cs/root/member_information/practice_information/
practice_parameters/practice_parameters
● American Psychiatric Association’s practice guidelines for treating panic
disorder, PTSD and OCD:
http://psychiatryonline.org/guidelines.aspx
● Anxiety Alliance, UK:
www.anxietyalliance.org.uk
● Anxiety Disorders Association of America:
www.adaa.org
● Anxiety UK:
www.anxietyuk.org.uk
● Fearfighter computer-based CBT programme for anxiety:
www.fearfighter.com
● National Institute for Clinical Excellence guidelines for treating anxiety
disorders, PTSD and OCD:
http://guidance.nice.org.uk/topic/mentalhealthbehavioural
● NHS:
www.nhs.uk/Conditions/Anxiety/Pages/Introduction.aspx

Book 1.indb 166 06/03/2012 13:48

 Depression 6
Learning objectives
After studying this chapter you will be able to:
● give an account of the main clinical features of
depression and distinguish it from normal sadness
● distinguish between major depressive disorder,
bipolar disorder, dysthymia and cyclothymia
● summarize the epidemiology of depression
● list the risk factors for depression and for suicide
● outline the main biological and psychological
theories of depression
● name the main evidence-based approaches to
assessment and treatment of depression
● do the right thing if a friend is suicidal
● give a considered view on antidepressants,
electroconvulsive therapy and gender differences in
the prevalence of depression.

Introduction
Feelings of happiness and sadness are adaptive. Many behaviour pat-
terns that lead to happiness, such as socializing with others, becoming
absorbed in productive work and developing longstanding friendships,
are important for the survival of the species. Sadness, which commonly

Book 1.indb 167 06/03/2012 13:48

 168 C L I N I C A L P S Y C H O L O G Y : A N I N T R O D U C T I O N

follows loss of valued relationships, skills, personal characteristics,

objects and events, may also be adaptive, in that it reminds us to take
care of things we value in future so that we don’t lose them again.
Sadness also signals to others that we require care and elicits support
from others, which soothes our emotional pain.
Extreme mood states such as mania and depression are less
adaptive. There is no doubt that during periods of mania or hypomania
some individuals with bipolar disorder, which is characterized by
episodes of mania and depression, produce highly creative work (Silvia
& Kaufman, 2010). However, this is done at a high cost. Inevitably
people who suffer from bipolar disorder run the risk of dangerous risk-
taking, dehydration and exhaustion during manic episodes.
Seasonal affective disorder (or winter depression, as it is colloquially
known) may be linked phylogenetically to hibernation and this may have
been adaptive for our cave-dwelling ancestors (Montañés et al., 2006).
However, nowadays depression seems to fulfil no adaptive function.
Despite this, it is a highly prevalent condition, affecting up to 25% of the
population (Kessler & Wang, 2009). Because of its prevalence, the main
focus in this chapter will be on major depressive disorder, although
reference will be made to other mood problems such as bipolar disorder.
From Table 6.1, in which the diagnostic criteria for a depressive
episode from DSM-IV-TR (American Psychiatric Association, 2000) and

TABLE 6.1
Criteria for a major depressive episode
DSM-IV-TR ICD-10
A. Five or more of the following symptoms have been present during In a typical depressive episode the
the same 2-week period nearly every day and this represents a individual usually suffers, for a
change from pervious functioning; at least one of the symptoms is period of at least 2 weeks, from
either (1) depressed mood or (2) loss of interest or pleasure. depressed mood, loss of interest
Symptoms may be reported or observed. and enjoyment and reduced
1. Depressed mood. In children and adolescents can be irritable energy leading to increased
mood. fatiguability and diminished activity.
2. Markedly diminished interest or pleasure in almost all daily Marked tiredness after only slight
activities. effort is common. Other common
3. Significant weight loss or gain (of 5% per month) or decrease or symptoms are:
increase in appetite. In children consider failure to make 1. Reduced concentration and
expected weight gains. attention
4. Insomnia or hypersomnia. 2. Reduced self-esteem and
5. Psychomotor agitation or retardation. confidence
6. Fatigue or loss of energy. 3. Ideas of guilt and unworthiness
7. Feelings of worthlessness, excessive guilt. 4. Bleak and pessimistic views of
8. Poor concentration and indecisiveness. the future
9. Recurrent thoughts of death, suicidal ideation or suicide attempt. 5. Ideas or acts of self-harm or
B. Symptoms do not meet criteria for mixed episode of mania and suicide
depression. 6. Disturbed sleep
C. Symptoms cause clinically significant distress or impairment in 7. Diminished appetite.
social occupational, educational or other important areas of The lowered mood varies little from
functioning. day to day, is often unresponsive
D. Symptoms not due to the direct effects of a drug or a general to circumstances and may show a
medical condition such as hypothyroidism. characteristic diurnal variation as
E. The symptoms are not better accounted for by uncomplicated the day goes on.
bereavement.

Note: Adapted from DSM-IV-TR (APA, 2000), ICD-10 (WHO, 1992).

Book 1.indb 168 06/03/2012 13:48

 6 • DEPRESSION 169

ICD-10 (World Health Organization, 1992) are given, it may be seen

that depression is not simply ‘feeling sad’. Major depressive disorder is
a recurrent condition characterized by episodes of low mood and loss of
interest in pleasurable activities along with other symptoms such as
poor concentration, fatigue, pessimism, suicidal thoughts, and sleep
and appetite disturbance. Depression is a major public health concern
because it radically reduces quality of life, has huge economic costs in
terms of reduced productivity of the national work force, and has
adverse effects on the mental health and adjustment of children of
depressed parents (Garber, 2010; Kessler & Wang, 2009). This chapter
will consider the clinical features, epidemiology, risk factors, course,
theoretical explanations, assessment and treatment of depression. Risk
factors for suicide will also be discussed.

Case example of major depression

May, a single woman in her early thirties, was referred for counselling
by her family doctor. She insisted on being seen by the psychologist at
her house, since she had been bedridden for 2 years. May’s first episode
of depression occurred in her mid-twenties, after her first and only
significant romantic relationship ended. She said that her boyfriend,
Rob, had ‘broken her heart’. This first depressive episode lasted almost
a year. During this time May spent most of her days in bed. She had
little energy and no desire to get up and engage with life. Unfortunately,
during this depressive episode she lost her job as a teacher.
May lived in a small maritime town about 250 miles from the village
where she grew up. Her mother came to stay with her during her first
episode of depression. At her family doctor’s suggestion, May attended
a series of counselling sessions. These helped her to recover. Shortly
after her recovery, May’s counsellor left the district. After a few months
and a series of disappointing and unsuccessful attempts to rekindle old
college friendships, May relapsed. She spent most of the next 2 years
in bed. Once again, her energy level dropped, she lost interest in all
activities, felt very sad and empty, and believed that there was little
point in trying to recover. For much of this period, May refused to see
anyone except her mother and the family doctor.

Personal and family history

May was born and brought up until the age of 8 in a small rural village.
She moved house when she was 8 years old and lost a number of close
friends through the change of address. This was particularly stressful
for her because she had difficulty making new friends, and felt lonely
much of the time afterwards. Before moving house, May had relied on
her childhood friends to make living with her parents bearable. When
she lost this support, she felt very isolated. May’s home life was
unbearably stressful because she and her mother were regularly beaten
brutally by May’s father. Her mother would not talk to her about this, nor
would she protect May from the beatings. May lived in this violent family

Book 1.indb 169 06/03/2012 13:48

 170 C L I N I C A L P S Y C H O L O G Y : A N I N T R O D U C T I O N

situation until she left home to go to college at the age of 18. During her
childhood and teenage years May spent a lot of time studying to distract
herself from the unhappy home atmosphere.
On the positive side, May had a good relationship with her cousins
and some happy childhood memories of staying at their seaside house.
She made a couple of good friends at college with whom she went on
holidays to Greece in her early 20s. When May left college, she began
work as a teacher and loved her job. She got on well with children and
was admired by her colleagues for this.
Within May’s extended family there was a history of mood and
alcohol problems. Her aunt and a cousin had suffered from depression.
She also had an uncle with a drink problem, which may have been
related to a difficulty with mood regulation.

Presentation
May presented with profound feelings of sadness and emptiness, a loss
of interest in her career and friendships and an inability to experience
pleasure. Notable features of her behaviour were the fact that she lived
a constricted housebound lifestyle, was unable to concentrate and com-
plained of forgetfulness. May also experienced early morning waking,
had diurnal variation of mood, with her mood being worse in the morn-
ing, had little appetite and marked weight loss, and refused to take anti-
depressant medication. From time to time she thought about killing
herself, but never planned in a detailed way to end her life and never
made a suicide attempt.
She held a distinctly negative view of herself, the world and the future.
She talked about herself in self-deprecating ways. For example, she said
‘I’m no good as a teacher. I’ve lost my job because of this illness. I’m no
good as a woman. I’ll never be married. I’m no good as a person. I’m dirty
and worthless and I’m rotting inside. I deserve to be hurt.’ She viewed the
world as a bleak place. What follows are some of her beliefs about her
world: ‘My father is no good. He beat me as a child and beat my mother.
He is the reason why I am ill. I can’t change the past, so I will be ill forever.
My mother is no good. I would recover if she were not here looking after
me. She interferes in my life and tries to control me. I have no friends so
there is no point in recovery. Other people deserve to be hurt. Whatever
pleasant things I have experienced were few and far between. For
example, my holiday in Greece. I had no control over either the good or
bad things that happened to me, so I cannot control my recovery.’
May’s view of the future was also dark. For example, she said: ‘There
is no point in recovery because other people will only take advantage of
me. You can’t trust anyone because they will abandon you. I have been
unfortunate in the past, so I will always be unfortunate. There is no light
at the end of the tunnel.’

Formulation
May presented with the symptoms of major depressive disorder: low
mood, diurnal variation in mood, loss of interest and pleasure in daily

Book 1.indb 170 06/03/2012 13:48

 6 • DEPRESSION 171

activities, poor concentration, appetite and sleep disturbance, energy

loss, worthlessness, pessimism and suicidal ideation. She had experi-
enced two episodes of major depression, each precipitated by the loss
of valued relationships. The first episode was triggered by her losing her
boyfriend and the second by her failing to renew old friendships, the
loss of her counsellor and the loss of work relationships. For other
people these types of event might not have led to depression, but for
May the losses were particularly stressful because biological and
psychological predisposing factors had rendered her especially vul-
nerable to depression.
May’s family history of mood disorders suggested that she might
have had a genetic biological vulnerability to developing depression.
Her negative childhood experiences of violence and loss of supportive
friends after moving house probably rendered her psychologically
vulnerable to developing depression, since these led her to view herself,
other people and the future in a pessimistic way. Once May’s mood
dropped, it was maintained by this negative way of interpreting events.
In addition to this cognitive maintaining factor, at behavioural and
interpersonal levels May’s constricted lifestyle also maintained her
depression. Her lifestyle reduced opportunities for engaging in pleasant
activities, forming relationships, and finding employment. The absence
of these opportunities confirmed May’s negative view of herself, her
world and her future. She was locked into a vicious cycle.
Eventually this had taken its toll on May’s appetite, circadian rhythms
and activity level. She slept poorly, awoke early, ate little and rarely
exercised. These sleeping, eating and activity problems may also have
maintained May’s depressed mood. However, there were protective
factors in this case. May had a history of good premorbid adjustment,
and strong support for her recovery from both her mother and her family
doctor. This formulation is diagrammed in Figure 6.1.

Intervention
Following assessment, May was helped to understand this formulation.
She engaged in a multimodal treatment programme involving cognitive-
behavioural interventions, family therapy and antidepressant medica-
tion. Behaviour therapy helped her alter her self-defeating patterns of
behaviour; engage in regular exercise and pleasant activities; and
expand her constricted lifestyle. Cognitive therapy helped her to chal-
lenge her pessimistic thinking style and view the world in more positive
terms. Family therapy helped May’s mother reduce her inappropriate
over-involvement with May and her father apologize for the violence to
which May had been subjected and exposed to as a child.
Antidepressant medication aimed to normalize the dysregulated
serotonergic neurotransmitter system that was presumed to underpin
May’s depressive symptoms. Over a period of months she increased
her activity level, developed a more positive thinking style, achieved
greater autonomy from her parents and began to engage in a more
normal lifestyle.

Book 1.indb 171 06/03/2012 13:48

 172 C L I N I C A L P S Y C H O L O G Y : A N I N T R O D U C T I O N

Figure 6.1 Formulation of a case of depression

Major depression is a recurring episodic condition, so May was not

‘cured’ by this multimodal programme. While she gradually began to
enjoy a better quality of life, she continued to struggle to maintain a posi-
tive mood state and was vulnerable to relapse when faced with subse-
quent life stresses, particularly those involving loss of valued relationships.

Clinical features
Table 6.1 gives diagnostic criteria for episodes of major depression from
DSM-IV-TR (American Psychiatric Association, 2000) and ICD-10 (World
Health Organization, 1992). Within both systems depressive episodes
may be classified in terms of severity and with respect to the presence or
absence of melancholic or somatic features and psychotic features.

Severity
With regard to symptom severity, episodes of depression may be
subclassified as mild, moderate or severe, depending on the number of
symptoms present and the degree of impairment.

Melancholia
With regard to melancholic or somatic features, in severe depression
where there is a loss of pleasure in all activities (referred to as anhedonia)

Book 1.indb 172 06/03/2012 13:48

 6 • DEPRESSION 173

and a lack of reactivity to pleasant stimuli along with diurnal variation in

mood, and sleep and appetite disturbance, the DSM codes such
episodes as having melancholic features. In the ICD this presentation is
referred to as the somatic syndrome. Historically there was a view that
these symptoms reflected an ‘endogenous’, genetically determined and
biologically based form of depression, as distinct from a ‘reactive’
depression arising from exposure to stressful life events and
environmental adversity (Monroe et al., 2009).
This distinction between endogenous and reactive depression has
not been supported by research, which shows that all episodes of
depression are preceded by stressful life events, and that in any given
case some combination of genetic vulnerability and environmental
adversity contributes to the development of depression (Parker, 2009).

Psychotic depression
In both DSM and ICD, if mood-congruent delusions and hallucinations
are present, then depressive episodes are described as having
psychotic features. Mood-congruent delusions are strongly held,
extremely pessimistic beliefs that have no basis in reality, such as the
belief of an innocent person that he or she is guilty of many wrongs and
so deserves to die. In depression, mood-congruent hallucinations are
usually auditory and involve hearing voices in the absence of external
stimuli, which say depressing things, such as that the patient is a failure,
guilty of wrongdoing, or evil.
A range of clinical features of children, adolescents and adults with
major depressive disorders have been identified through research and
clinical observation (e.g., Bech, 2009; Brent & Weersing, 2008; Gotlib &
Hammen, 2009; Nolen-Hoeksema & Hilt, 2009a). A classification of
common clinical features of depression into the domains of perception,
cognition, mood, somatic state, behaviour and relationships is given in
Table 6.2. When depressive episodes occur, clinical features may be
linked by assuming that depressed individuals have usually suffered a
loss of some sort: a loss of an important relationship, a loss of some
valued attribute such as athletic ability or health, or a loss of status.

Perception
With respect to perception, having suffered a loss, depressed individuals
tend to perceive the world as if further losses are probable. Depressed
people selectively attend to negative features of the environment. This
in turn leads them to engage in depressive cognitions and unrewarding
behaviour patterns which further entrench their depressed mood. In
severe depression, individuals may report mood-congruent auditory
hallucinations. We may assume that this severe perceptual abnormality
is present when individuals report hearing voices criticizing them or
telling them depressive things, as noted above. Auditory hallucinations
also occur in schizophrenia. However, the hallucinations that occur in
schizophrenia are not necessarily mood-congruent.

Book 1.indb 173 06/03/2012 13:48

 174 C L I N I C A L P S Y C H O L O G Y : A N I N T R O D U C T I O N

TABLE 6.2
Clinical features of depression
Perception Perceptual bias towards negative events
Mood-congruent hallucinations†
Cognition Negative view of self, world and future
Over-general memory
Cognitive distortions
Inability to concentrate
Indecision
Suicidal ideation
Suicidal intention*
Excessive guilt*
Mood-congruent delusions†
Mood Depressed mood
Irritable mood
Anxiety and apprehension
Distinct quality of depressed mood*
Loss of interest in pleasurable activities (anhedonia)*
Lack of emotional reactivity*
Somatic state Fatigue
Diminished activity
Loss of appetite or overeating
Aches and pains
Early morning waking*
Diurnal variation of mood (worse in morning)*
Change in weight*
Loss of interest in sex*
Behaviour Psychomotor retardation or agitation*
Depressive stupor†
Relationships Deterioration in family relationships
Withdrawal from peer relationships
Poor work or educational performance

*These features are associated with melancholic depression and are referred to as vegetative
features or the somatic syndrome. †These features occur in psychotic depression.

Cognition
With respect to cognition, depressed individuals describe themselves,
the world and the future in negative terms. They evaluate themselves as
worthless and are critical of their occupational and social accomplish-
ments. Often this negative self-evaluation is expressed as guilt for not
living up to certain standards or letting others down. They see their world,
including family, friends and work or school as unrewarding, critical and
hostile or apathetic. They describe the future in bleak terms and report
little if any hope that things will improve. Where they report extreme hope-
lessness and this is coupled with excessive guilt for which they believe
they should be punished, suicidal ideas or intentions may be reported.
Extremely negative thoughts about the self, the world and the future may
be woven together in severe cases into depressive delusional systems.
In addition to the content of the depressed individual’s thought being
bleak, they also display logical errors in their thinking and concentration

Book 1.indb 174 06/03/2012 13:48

 6 • DEPRESSION 175

problems. Errors in reasoning are marked by a tendency to maximize

the significance and implications of negative events and minimize the
significance of positive events. They also have over-general autobio-
graphical memories. That is, they have difficulty remembering specific
happy events in detail (which might lighten their mood), but rather
remember both positive and negative past episodes in their lives in
global over-general ways. In addition they have concentration, attention
and decision-making problems that lead to difficulties managing occu-
pational, academic or leisure activities demanding sustained attention
and decisiveness.

Affect
With respect to affect, low mood, diurnal variation in mood and anhedo-
nia are key features of depression. Depressed mood is usually reported
as a feeling of sadness, emptiness, loneliness or despair. Diurnal vari-
ation in mood is particularly common in severe depression, with mood
being worse in the morning. During an episode of major depression as
a person moves from mild to moderate to severe depression, the
increasing number and intensity of symptoms may lead to intense anxi-
ety. That is, fears are experienced such as ‘Will this get worse? Am I
stuck in this living hell for ever? Will I ever be myself again? Will I be
able to prevent myself from committing suicide to escape?’ Irritability
may also occur, with the person expressing anger at the source of their
loss, for example anger at a deceased loved one for abandoning the
grieving person, or anger at health professionals for being unable to
alleviate the depression.

Somatic state
Changes in somatic state associated with depression include loss of
energy, disturbances of sleep and appetite, weight loss or failure to
make age-appropriate weight gain, pain symptoms and loss of interest
in sex. Typically, depressed people have difficulty sleeping and eat little
due to appetite loss. These symptoms are referred to as vegetative
features. With regard to sleep disturbance, depressed people may have
difficulty going to sleep, wake frequently during the night, or suffer from
early-morning waking. Usually, they report having racing thoughts and
engaging in depressive rumination when they can’t sleep. In atypical
cases of depression people may sleep too much due to constant
feelings of exhaustion and eat excessively due to increased appetite or
because eating may temporarily reduce their distress.
Headaches and medically unexplained chest, back or abdominal
pain are other somatic features of depression. For some patients, these
pain symptoms are the first to be reported to their family doctors, and
only when medical investigations of these complaints are negative is
depression considered as a possible diagnosis. All of the somatic fea-
tures of depression mentioned above are consistent with research find-
ings, discussed below, that dysregulation of neurobiological, endocrine

Book 1.indb 175 06/03/2012 13:48

 176 C L I N I C A L P S Y C H O L O G Y : A N I N T R O D U C T I O N

and immune functions is associated with depression and that sleep

architecture is also affected.

Behaviour
At a behavioural level, depressed individuals may show either reduced
and slowed activity levels (psychomotor retardation) or increased but
ineffective activity (psychomotor agitation). They typically fail to engage
in activities that would bring them a sense of achievement or connect-
edness to family or friends. Where individuals become immobile, this is
referred to as depressive stupor. Fortunately this is rare.
One risky behavioural complication of depression is self-harm. A dis-
tinction is made between suicidal behaviour and non-suicidal deliberate
self-harm. With suicidal behaviour, self-harm is primarily motivated by
the intention to end one’s life. With non-suicidal deliberate self-harm,
there are other motivations. People may cut or burn themselves to dis-
tract themselves from their depressive feelings. They may take non-
lethal overdoses to elicit care from family or friends or to gain admission
to hospital and remove them from stressful situations.

Relationships
At an interpersonal level, depressed individuals report a deterioration in
their relationships with family, friends, colleagues, school teachers and
other significant figures in their lives. They describe themselves as
lonely and yet unable or unworthy to take steps to make contact with
others. Ironically, when depressed people try to overcome their loneli-
ness by talking to others, they tend to drive them away through their
pessimistic, self-centred talk and depressive behaviour.

Classification
In DSM-IV-TR and ICD-10, mood disorders are primarily classified in
terms of polarity (unipolar versus bipolar conditions) and course
(episodic versus continuous conditions). Distinctions are made between
● major depressive disorder
● bipolar disorder
● dysthymia
● cyclothymia.
Major depressive disorder and bipolar disorder are episodic conditions,
with the former characterized by episodes of low mood, negative
cognition, and sleep and appetite disturbance and the latter characterized
in addition by episodes of mania in which elation, grandiosity, flight of
ideas and expansive behaviour occur. Dysthymia and cyclothymia are
less severe non-episodic chronic and continuous conditions, with
dysthymia being characterized by depressive symptomatology and
cyclothymia being characterized by similar but less extreme mood
fluctuations than bipolar disorder.

Book 1.indb 176 06/03/2012 13:48

 6 • DEPRESSION 177

The distinctions between unipolar and bipolar conditions and between

episodic and persistent disorders that are central to the classification of
mood disorders in ICD-10 and DSM-IV-TR have subordinated earlier
classification systems, which made primary distinctions between psy-
chotic and neurotic, endogenous and reactive, and overt and masked
depression (Farmer & McGuffin, 1989; Kendell, 1976; Parker, 2009).
With the psychotic/neurotic and endogenous/reactive classification sys-
tems, it was assumed that psychotic and endogenous depressions were
more severe than neurotic and reactive depressions, with the more
severe conditions being due to genetic and biological factors and requir-
ing treatment with medication or electroconvulsive therapy, and the less
severe conditions being due to environmental factors and requiring
treatment with psychotherapy (Parker, 2009). However, evidence from
stressful life-event research shows that all episodes of depression,
regardless of quality or severity, are preceded by stressful life events
and in that sense are reactive (Monroe et al., 2009). Treatment outcome
research has shown that only about two out of three cases of depres-
sion respond to available treatments; that symptom type or severity
does not always predict which patients will respond to physical or psy-
chological interventions; and that for most patients multimodal therapy
involving a combination of medication and psychotherapy is most effec-
tive (Paykel & Scott, 2009). The older psychotic/neurotic and endog-
enous/reactive distinctions have been incorporated into DSM-IV-TR and
ICD-10, insofar as depressive episodes may be specified as having
either psychotic features or melancholic/somatic features, typical of
what formerly was referred to as endogenous depression.
With regard to the overt/masked distinction, this was introduced to
take account of adults whose depression was masked by medically
unexplained symptoms such as headaches and chest pains (Hoogenhout
et al., 2010) or children whose depression was masked by conduct
problems (Carlson & Cantwell, 1980). Adult cases that would formerly
have been described as having masked depression are classified in
DSM-IV-TR and ICD-10 as having a somatoform disorder, a condition
characterized by multiple medically unexplained symptoms. What would
formerly have been referred to as masked depression in children is clas-
sified as comorbid depression and conduct disorder in DSM-IV-TR and
as depressive conduct disorder in ICD-10.

Epidemiology, course and risk factors

Major depression is the most common mood disorder, with a lifetime
prevalence rate of 6–25% in international community studies (Kessler &
Wang, 2009). In the US National Co-morbidity Survey Replication the
lifetime prevalence of DSM-IV major depression was 16.6%, whereas
the lifetime prevalence of dysthymia was 2.5% and of bipolar disorder
was 3.9% (Kessler et al., 2005). Depression is less common among
prepubertal children than adolescents and adults (Brent & Weersing,
2008). In children, equal numbers of boys and girls have depression,
but this changes in adolescence and by adulthood, compared with men,

Book 1.indb 177 06/03/2012 13:48

 178 C L I N I C A L P S Y C H O L O G Y : A N I N T R O D U C T I O N

about twice as many women have depression (Nolen-Hoeksema & Hilt,

2009b).
Comorbid disorders occur in most cases of depression. In the US
National Comorbidity Replication Survey, 59% of depressed participants
had comorbid anxiety disorders and 24% had comorbid substance use
disorders (Kessler & Wang, 2009). In clinical samples of depressed
patients, comorbid personality disorders occur in 50–85% of inpatients
and 20–50% of outpatients (Klein et al., 2009). The highest level of
comorbidity occurs with cluster C personality disorders (avoidant,
dependent, and obsessive compulsive personality disorders).
Depression follows a chronic relapsing course, with up to 80% of
people having recurring episodes, and in community samples the
median duration of episodes is about 5 or 6 weeks (Kessler & Wang,
2009). In clinical samples episodes typically last for 5–6 months; the
majority of cases recover from a depressive episode within a year;
about half of all patients continue to have fluctuating residual symptoms
between episodes; for less than 10% recovery does not occur and
chronic depressive symptoms persist; and most cases relapse within 5
years (Angst, 2009; Boland & Keller, 2009).
As more depressive episodes occur, there are decreases in inter-
episode intervals and a reduction in the amount of stress required to
trigger the onset of further depressive episodes, an issue discussed
below under stress theories (Boland & Keller, 2009).
Risk factors for depression include a family history of mood disor-
ders, female gender, low socio-economic status involving economic
and educational disadvantage, an adverse early family or institutional
environment, a depressive temperament, a negative cognitive style,
deficits in self-regulation, high levels of life stress, and low levels of
social support from family and friends (Garber, 2010; Hammen et al.,
2010).
Risk factors for recurrent major depressive episodes identified in the
US Collaborative Depression Study of over 500 patients include a his-
tory of three or more prior episodes, comorbid dysthymia (often called
double depression), comorbid anxiety and substance use disorders,
long duration of individual episodes, poor control of symptoms by anti-
depressant medication, onset after 60 years of age, a family history of
mood disorder, and being a single female (Boland & Keller, 2009).
For a subgroup of people who suffer from depression, deficits in
visually processing light and the season of the year are risk factors for
depression (Rosenthal, 2009). These people, who experience regularly
recurring depressive episodes in the autumn and winter, with remission
in the spring and summer, are said to have seasonal affective disorder.
They develop symptoms in the absence of adequate light and respond
favourably to enhanced environmental lighting, often referred to as ‘light
therapy’ (Golden et al., 2005).
In community samples about 3.4% of people with a major depressive
disorder commit suicide; the rate in clinical samples is about 15%; and
about 60% of completed suicides (studied by psychological autopsy)
are depressed (Berman, 2009).

Book 1.indb 178 06/03/2012 13:48

 6 • DEPRESSION 179

Aetiological theories
Theoretical explanations for depression and related treatments have
been developed within biological, psychoanalytic, cognitive-behavioural
and family systems traditions. Much research on depression has been
guided by these theories. In addition, research on depression has been
informed by psychological constructs such as stress, temperament,
personality traits, cognitive biases, coping strategies and interpersonal
styles. A number of influential theories, hypotheses and related treat-
ments and research findings from these areas will be briefly reviewed
below.

Biological theories
Biological theories of depression point to the role of genetic factors in
rendering people vulnerable to the development of mood disorders, and
to the role of structural and functional brain abnormalities; dsysregula-
tion of neurotransmitter, neuroendocrine and immune systems; and
sleep architecture and circadian rhythm abnormalities in the aetiology
of depression. There is considerable support for biological theories from
neuroimaging, pharmacological, psychophysiological and other neuro-
biological studies, although current knowledge of these abnormalities is
incomplete (Davidson et al., 2009; Hamilton et al., 2011; Levinson,
2009; Sullivan et al., 2000; Thase, 2009). However, there is a consen-
sus about certain aspects of the neurobiology of depression which will
be presented below.

Genetics
The genetic hypothesis proposes that depression develops where a
person with an inherited vulnerability to mood disorders is exposed to
stressful life events. Results of twin, adoption and family studies show
that a predisposition to depression is genetically transmitted. Major
depression is about 40% heritable (Sullivan et al., 2000), whereas bipo-
lar disorder is about 70% heritable (Edvardsen et al., 2008). Precisely
what biological characteristics are genetically transmitted and the
mechanisms of transmission are still largely unknown. However, results
of studies on structural and functional brain abnormalities, neurotrans-
mitter dysregulation, endocrine abnormalities, immune system dysfunc-
tion, sleep architecture and circadian rhythm abnormalities in some
cases suggest that a biological vulnerability to dysregulation of one or
more of these systems is probably inherited. It is also probable that the
vulnerability is polygenetically transmitted, since the results of family
studies cannot easily be accounted for by simpler models of genetic
transmission.
Many candidate genes for depression have been investigated; few
have been identified; and where significant associations between can-
didate genes and depression have been found, very few consistent rep-
lication studies are available (Levinson, 2009; Shyn & Hamilton, 2010).
The search for candidate genes has focused in large part on those

Book 1.indb 179 06/03/2012 13:48

 180 C L I N I C A L P S Y C H O L O G Y : A N I N T R O D U C T I O N

whose products affect neurotransmitters thought to be involved in the

aetiology of mood disorders, notably serotonin and noradrenaline.
One candidate gene that affects the serotonin system deserves
mention because consistent support has been found for the link between
it and vulnerability to depression. A common polymorphism (5-HTTLPR)
in the promoter region of the serotonin transporter gene (5HTT or
SLC6A4) regulates gene expression. In a large meta-analysis, Karg et
al. (2011) found that the short (rather than the long) allele variant of the
5-HTTLPR polymorphism increases the risk of developing depression
under stress, particularly in the case of child abuse and severe medical
problems. This increased stress sensitivity for these types of life event
probably occurs because of decreased serotonin re-uptake and
increased amygdala neuronal activity in response to stress. The vulner-
ability associated with the short allele variant of the 5-HTTLPR polymor-
phism is not specific to depression. It also renders people vulnerable to
PTSD and borderline personality disorder. This is because the seroton-
ergic neurotransmitter system subserves a range of stress-related emo-
tional processes including both depression and anxiety.

The limbic system and dorsolateral prefrontal cortex

Depression is associated with abnormalities in the functioning of brain
structures that subserve the experience and expression of emotions,
primarily the limbic system (which includes the amygdala, hippocampus,
insula and parts of the anterior cingulate cortex), and those that
subserve self-regulation, primarily the dorsolateral prefrontal cortex. In
depressed people the limbic system (especially the amygdala and
anterior cingulate cortex) is overactive, while the dorsolateral prefrontal
cortex is underactive (Hamilton et al., 2011). The overactive limbic
system probably subserves the ongoing experience of intense negative
emotions, while the underactive dorsolateral prefrontal cortex probably
subserves a deficit in regulating these negative emotional experiences
through reappraisal and purposeful problem-solving.
There is some preliminary evidence that successful psychological
and pharmacological treatments normalize these abnormalities in dif-
ferent ways. Psychological interventions such as cognitive therapy
probably ameliorate depression by increasing activity in the prefrontal
cortex, whereas antidepressant medication probably alleviates depres-
sion by decreasing limbic system overactivity (Clark & Beck, 2010;
Thase, 2009).

Neurotransmitters
There is evidence for hypoactivity of the serotonergic and noradrener-
gic neurotransmitter systems in neuroanatomical centres associated
with depression (Thase, 2009). Originally depletion of serotonin and
noradrenaline was thought to cause depression, but now a more com-
plex dysregulation of these systems involving a reduction in the sensi-
tivity of postsynaptic receptor sites is hypothesized to be the critical
difficulty. The efficiency of these neurotransmitter systems is reduced in
depression, and increased by antidepressant drugs (Gitlin, 2009).

Book 1.indb 180 06/03/2012 13:48

 6 • DEPRESSION 181

Four main classes of antidepressant medication have been devel-

oped: tricyclic antidepressants (TCAs), monoamine oxidase inhibitors
(MAOIs), selective serotonin reuptake inhibitors (SSRIs), and novel or
dual action antidepressants (Gitlin, 2009). TCAs such as imipramine
(which has the trade name Tofranil) increase the sensitivity of dysfunc-
tional receptor sites to serotonin and noradrenaline. MAOIs such as
phenelzine (which has the trade name Nardil) prevent the enzyme –
monoamine oxidase – from breaking down neurotransmitters in the
synaptic cleft and lead to an increase in neurotransmitter levels.
TCAs and MAOIs were developed in the 1950s and were widely
used until the 1980s, when they were largely replaced in clinical practice
by SSRIs and novel or dual-action antidepressants. SSRIs such as
fluoxetine (which has the trade name Prozac) prevent serotonin from
being reabsorbed into the presynaptic membrane and so increase
levels of this neurotransmitter. Novel and dual action antidepressants
operate in a variety of ways. For example venlafaxine (with the trade
name Effexor), which is a dual-action antidepressant, prevents both
noradrenaline and serotonin from being reabsorbed into the presynaptic
membrane and so increases levels of both of these neurotransmitters.
Results of meta-analyses of controlled trials show that for severe
depression the positive effects of antidepressants are substantial, but
for mild or moderate depression their effects are negligible (Fournier et
al., 2010). Furthermore, there is no evidence that the newer antidepres-
sants, such as the SSRIs, are any more effective than the older ones,
such as the TCAs, although some have fewer side-effects (Gitlin, 2009).
Antidepressant side-effects are discussed below in the section on con-
troversies. There is consistent evidence that genetic vulnerability to
depression involves genes whose action affects the efficiency of the
serotonin neurotransmitter system, which is associated with depres-
sion, as was noted above in the discussion of genetic factors.

Neuroendocrine and immune systems

Hypothalamic–pituitary–adrenal (HPA) axis overactivity is a central
aspect of the stress response. The HPA axis is a major part of the
neuroendocrine system3 involving the hypothalamus, the pituitary
gland located below the hypothalamus, and the adrenal glands (located
on top of the kidneys), which controls stress reactions and other
processes including the immune system, sexuality and digestion. The
HPA axis is activated by noradrenaline and inhibited by serotonin
neurotransmission.
There is evidence for the dysregulation of neuropeptides, notably
corticotropin-releasing factor (CRF), in the limbic system of depressed
people. CRF is released in response to stress and is associated with
HPA axis hyperactivity. CRF release and increased HPA axis activity
result in elevated levels of the stress steroid cortisol and disruption of
normal cortisol circadian rhythms (Thase, 2009). Elevated cortisol
arising from HPA axis overactivity in turn compromises the efficiency of
the immune system, rendering depressed patients more susceptible to
inflammatory diseases including arthritis and atherosclerosis (Glassman

Book 1.indb 181 06/03/2012 13:48

 182 C L I N I C A L P S Y C H O L O G Y : A N I N T R O D U C T I O N

& Miller, 2007). Such illnesses in turn are additional stresses that may
maintain or exacerbate depression.

Sleep architecture and circadian rhythms

Depression is associated with a disruption of sleep architecture and
circadian rhythms. Sleep disturbance, which includes difficulty falling
asleep, broken sleep and early-morning waking, is a core symptom of
depression. Psychophysiological studies show that abnormal sleep
architecture underpins depressive sleep disturbance (Thase, 2009).
Depressed people spend more time in rapid eye movement (REM)
sleep and less time in slow-wave sleep. They also show shorter REM
onset latency. Up to 60% of depressed people temporarily recover fol-
lowing sleep deprivation, although they relapse after even a brief sleep
(Hemmeter et al., 2010). Antidepressants regularize abnormal sleep
architecture, probably by normalizing serotonin and noradrenaline
neurotransmitter systems, which are dysregulated in depression and
regulate sleep architecture. Light therapy, which artificially extends
exposure to daylight during short winter days to the duration of long
summer days is an effective treatment for seasonal affective disorder,
suggesting that seasonal depression is associated with disrupted
circadian rhythms (Monteleone et al., 2010).
In summary, there is considerable support for a neurobiological the-
ory of depression. Major depressive disorder is about 40% heritable.
Vulnerability to depression is probably polygenetic, and so far the only
candidate gene for which there is consistent evidence is one that affects
the efficiency of the serotonegic neurotransmitter system. Dysregulations
of this system and the noradrenergic system occur in depression. Both
neurotransmitter systems are involved in a range of other neurobiologi-
cal features of depression including overactivity of the limbic system
and underactivity of the dorsolateral prefrontal cortex; HPA axis overac-
tivity, elevated cortisol levels and reduced immune system efficiency;
and disturbed sleep architecture characterized by increased REM and
reduced slow-wave sleep. These neurobiological abnormalities occur
more commonly in severe depression. Antidepressant medication,
which is effective for severe but not mild or moderate depression, allevi-
ates depression by increasing the efficiency of serotonergic and
noradrenergic neurotransmitter systems.

Stress theories
Stress theories propose that depression develops following exposure to
stress. There are variations on this theme, for example diathesis–stress
theories propose that depression only follows exposure to stress in
people who have specific biological or psychological attributes that
render them vulnerable to stressful life events, and the most vulnerable
require the least stress for depression to occur (e.g., Joiner & Timmons
2009; Joormann, 2009; Levinson, 2009). Stress-generation theory pro-
poses that people with certain personal attributes inadvertently generate
excessive stress, which in turn leads to depression (Liu & Alloy, 2010).

Book 1.indb 182 06/03/2012 13:48

 6 • DEPRESSION 183

A substantial body of research shows that the onset, course and

severity of depression are associated with stress, including acute and
chronic stressful life events and recent and early life adversity and loss
(Goodman & Brand, 2009; Hammen, 2009; Harkness & Lumley, 2008;
McLeod et al., 2007; Monroe et al., 2009). Early life stress such as
rejection and hostility, child abuse, parental depression and parental
death may cause childhood depression and render people vulnerable to
further episodes of depression in adulthood. In adulthood loss of
important relationships, roles and resources may precipitate initial
episodes of depression and relapse in recovered patients, or may delay
recovery during treatment. Higher levels of stress are associated with
more severe depressive symptoms.
As the number of episodes of depression increases, the amount of
stress required to precipitate a relapse decreases (Boland & Keller,
2009). This may be due to the neurobiological process of kindling
(Monroe & Harkness, 2005) and the cognitive process of rumination
(McLaughlin & Nolen-Hoeksema, 2011). According to cognitive theory,
minor stresses, which might normally lead to small negative mood
changes, may give rise to chronic rumination and catastrophizing in
people who have previously had depressive episodes, and this
rumination and catastrophizing may lead to major negative mood
changes and the onset of further episodes of depression. According to
kindling theory, multiple episodes of depression probably render the
neurobiological systems that maintain depression more vulnerable to
depressogenic changes in response to minor stresses.
Depressed people are not passive recipients of environmental stress,
but play an active role in stress generation. Available research indicates
that those more likely to generate stress leading to depression are
female, have been exposed in early life to child abuse or chronic
adversity and have depressive cognitive styles (discussed below in the
section on cognitive and behavioural theories) (Liu & Alloy, 2010).

Temperament, traits, cognitive biases, coping

strategies and interpersonal styles
Hypotheses that variables such as temperament, personality traits,
cognitive biases, coping strategies and interpersonal style render
people vulnerable to depression when they encounter stress and
adversity, or maintain depression, will be considered below.

Temperament
The Temperament and Character Inventory has been used in much of
the research on temperament and depression (Cloninger et al., 1993).
This instrument includes four dimensions of temperament: harm
avoidance, reward dependence, novelty seeking and persistence. The
structure of temperament in this model has been inferred from genetic
studies of personality. Three of the temperamental dimensions are

Book 1.indb 183 06/03/2012 13:48

 184 C L I N I C A L P S Y C H O L O G Y : A N I N T R O D U C T I O N

hypothesized to be related to specific neurotransmitter systems of the

brain. It is proposed that harm avoidance is subserved by the serotonin
system; reward dependence by the noradrenaline system; and novelty
seeking by the dopamine system. In a meta-analysis, Kampman and
Poutanen (2011) found that the harm avoidance temperamental
dimension was strongly associated with current depressive symptoms,
and improvements in harm avoidance occurred in treatment studies of
major depressive disorder. This finding is consistent with evidence for
the central role of dysregulation of the serotonergic neurotransmitter
system in depression.
In Watson and Clark’s model of temperament a distinction is made
between positive and negative emotionality. They have found that
depressed people tend to have high levels of negative emotionality and
low levels of positive emotionality (Watson, 2009). In this model negative
emotionality is the temperamental dimension that underpins the
personality trait neuroticism, whereas the personality trait extraversion
is underpinned by the temperamental dimension of positive emotionality.
The role of these personality traits in depression will now be considered.

Personality traits
In a major meta-analysis, Kotov et al. (2010) investigated correlations
between depression and the ‘Big 5’ personality traits: neuroticism,
extraversion, conscientiousness, openness and agreeableness. They
found that neuroticism was the personality trait most strongly associ-
ated with major depressive disorder. There were significant but smaller
negative correlations between depression and both extraversion and
conscientiousness. Thus, the typical personality trait profile of people
with major depressive disorder was characterized by a high level of
neuroticism (which entails negative emotionality and distress), introver-
sion (which involves social withdrawal and a lack of positive emotional-
ity) and low conscientiousness (where there is a tendency not to follow
through on plans). It is not clear whether this personality profile predis-
poses people to depression, whether it occurs as a result of depression,
or whether depression and the personality profile are the result of some
independent factor.
Within both the psychoanalytic and cognitive-behavioural traditions
there are hypotheses about the association between specific personality
dimensions and vulnerability to depression when one is faced with spe-
cific types of stressor. Within the psychoanalytic tradition, Blatt (2004)
has proposed that distinctions may be made between dependent and
self-critical, perfectionistic forms of depression. Within the cognitive-
behavioural tradition, Beck et al. (1983) distinguished between socio-
tropic and autonomous depressives. In these formulations it is proposed
that people with high levels of dependence or sociotropy have strong
needs for relatedness and so are vulnerable to depression when faced
with loss of important relationships, whereas people with high levels of
perfectionistic self-criticism or autonomy have strong needs for self-
definition through achievement and so are vulnerable to depres-
sion when faced with failure. Extensive research has shown that the

Book 1.indb 184 06/03/2012 13:48

 6 • DEPRESSION 185

personality traits of dependence/sociotropy and self-criticism/autonomy

are correlated with depression (Klein et al., 2009; Luyten et al., 2005).
A number of lower-order traits have been found to correlate with
depression. These include low self-esteem (Orth et al., 2008), perfec-
tionism (Egan et al., 2011), shame and guilt (Kim et al., 2011).

Cognitive biases
Research from experimental psychopathology has consistently found
that people with depression show a range of information-processing
biases before, during and between depressive episodes at the levels of
attention, memory and reasoning that render them vulnerable to depres-
sion and maintain low mood during depressive episodes (Joormann,
2009). People with depression are more likely to selectively attend to,
and remember, negative information about the self and the world
(Peckham et al., 2010; Phillips et al., 2010). Over-general autobio-
graphical memory – the tendency to remember generalities but not spe-
cific details of past events – is also a well established characteristic of
depression, with greater over-general memory being predictive of more
severe future depressive symptoms (Sumner et al., 2010). In depres-
sion there is also a bias towards pessimistic interpretations of situ-
ations, known as depressive cognitive style (Haeffel et al., 2008).
Depressive cognitive style and its relationship to helplessness will be
discussed below under cognitive and behavioural theories.
Alongside depression-specific cognitive biases that confer vulnera-
bility to depression, a number of general cognitive deficits arise as a
result of depression. In a meta-analysis, McDermott and Ebmeier
(2009) found significant correlations between depression severity and a
range of cognitive functions including processing speed, episodic mem-
ory and executive function, but not semantic or visuo-spatial memory.

Coping strategies
Certain coping strategies are associated with depression. In a meta-
analysis, Aldao et al. (2010) found that depression was strongly associ-
ated with the use of rumination as a coping strategy. With rumination,
depressed people repeatedly recycle negative and depressive thoughts
and have difficulty disengaging from them. Depression was also corre-
lated, although less strongly, with the use of avoidance and suppres-
sion as coping strategies. Aldao et al. (2010) found negative correlations
between depression and a number of adaptive coping strategies includ-
ing problem-solving, acceptance and reappraisal.

Interpersonal styles
Distinctive interpersonal styles are associated with the development
and maintenance of depression. In line with Bowlby’s (1980) attachment
theory, there is evidence that depression is associated with an insecure
attachment style arising from child-rearing experiences that interfered
with the development of attachment security, such as parental rejection,

Book 1.indb 185 06/03/2012 13:48

 186 C L I N I C A L P S Y C H O L O G Y : A N I N T R O D U C T I O N

child abuse and neglect, and loss of a parent through bereavement

(Bakermans-Kranenburg & van IJzendoorn, 2009; Dozier et al., 2008).
Depressed people tend to have higher levels of dependency and
sociotropy, both of which are associated with strong needs for interper-
sonal closeness, as noted above in the section on personality traits
(Klein et al., 2009).
Compared with non-depressed people, depressed people have
social skills deficits (Joiner & Timmons, 2009). In both quality and con-
tent their speech is more negative. They talk more slowly and quietly
and with less modulation about more negative things, with a greater
focus on the self and a reduced focus on the concerns of others. Their
non-verbal behaviour is more negative. They engage in less eye con-
tact, show fewer positive emotional facial expressions and more ani-
mated negative facial expressions. They also engage in more
reassurance seeking and negative feedback seeking than people with-
out depression. Some of these skills deficits predate the onset of
depressive episodes and remain after remission.
The interpersonal style of depressed people has a number of conse-
quences (Joiner & Timmons, 2009). It leads to low mood and distress in
others who interact with depressed people (known as the depression
contagion effect). This in turn may lead others to avoid them, or act in
critical, hostile and blaming ways towards them. This negative response
involving criticism and hostility, or responding in an over-involved way
towards a depressed family member, is referred to as expressed emo-
tion. Depressed people who live in family situations characterized by
high levels of expressed emotion, which is very stressful for the
depressed person, have been found to relapse more rapidly than those
whose families respond to them in a low-key way (Hooley, 2007).

Psychoanalytic theories
Of the many psychoanalytic theories of depression that have been
developed, reference will be made here to Freud’s (1917) original posi-
tion, Bibring’s (1965) ego-psychological model and Blatt’s (2004) object
relations formulation. These theories have been selected because they
are illustrative of psychodynamic explanations, and Blatt’s model has
been singled out for attention because, unlike many psychodynamic
theories, considerable effort has gone into empirically testing it.

Freud’s classical psychoanalytic theory

In Freud’s (1917) psychoanalytic theory he proposed that depression
arose from self-directed anger which occurred in response to loss of a
valued person or attribute. He argued that following a major loss in adult
life such as bereavement (referred to as object loss), regression to the
earliest stage of development – the oral stage – occurs. In this regressed
state the person functions psychologically like an infant and so a
distinction between the self and the lost object is not made. The lost
object is introjected and experienced as part of the self. In depression,

Book 1.indb 186 06/03/2012 13:48

 6 • DEPRESSION 187

aggression at the introject of the lost object for bringing about a state of
abandonment is experienced as self-directed anger or the self-criticism
that characterizes depressed people.
People whose primary caregivers either failed to meet their depend-
ency needs during the oral phase and so neglected them, or were over-
indulgent and so did not provide them with opportunities to learn
self-sufficiency, are predisposed to developing depression according to
this model. When they lose a loved one, they feel the loss more acutely
than others and are more likely to regress, introject the lost object and
experience retroflexive anger. Freud proposed that the loss of valued
personal attributes (such as career status) as well as the loss of valued
people could symbolize object loss. In Freud’s structural personality
theory he distinguished between the unconscious id, which represented
sexual and aggressive instincts; the superego, which represented the
internalization of societal norms and standards; and the ego, which rep-
resented conscious functions that attempted to reconcile and balance
the instincts of the id, the standards set by the superego and the
demands of day-to-day life.
In depression, the superego is the psychological structure that directs
anger at the ego. Because the superego, which is not fully developed in
children, is the psychological structure necessary for directing anger at
the ego, the traditional psychoanalytic position entails the view that
children are unable to experience depression. This view is unsupported
by available epidemiological data. However, Freud’s position was
important in drawing attention to the significance of loss in depression,
a hypotheses that has been supported by subsequent research
(Goodman & Brand, 2009; Monroe et al., 2009).
There is also good evidence that self-directed anger, in the form of
guilt and shame, is strongly associated with depression (Kim et al.,
2011). Finally, Freud pointed out the importance of early life experi-
ences in creating a vulnerability to depression, an idea that is central to
modern psychodynamic, attachment and cognitive theories of depres-
sion, and one that has considerable empirical support (Bakermans-
Kranenburg & van IJzendoorn, 2009; Blatt, 2004; Goodman & Brand,
2009; Joormann, 2009).

Bibring’s ego-psychology theory

Bibring (1965), a later psychodynamic ego psychologist, explained
depression as the outcome of low self-esteem which resulted from per-
ceiving a large discrepancy between the self as it is and the ideal self.
Internalization of harsh, critical parental injunctions or perfectionistic
parental injunctions during early childhood accounted for the develop-
ment of a particularly unrealistic ego-ideal, which in psychoanalytic
theory is an aspect of the superego. A substantial body of evidence
supports the view that low self-esteem is an important correlate and in
some instances a precursor of depression, and in some but not all
cases this is associated with a history of critical or punitive parenting
(Blatt, 2004; Orth et al., 2008).

Book 1.indb 187 06/03/2012 13:48

 188 C L I N I C A L P S Y C H O L O G Y : A N I N T R O D U C T I O N

Blatt’s psychoanalytic theory of two types of depression

It was noted in the section on personality traits that Blatt (2004) distin-
guished between two types of depression associated with two distinct
types of early parent–child relationships that engender vulnerability to
depression when faced with two distinct types of stress in later life. A
vulnerability to stresses involving loss of attachment relationships is
central to the anaclitic or dependent type of depression, and this has its
roots in early experiences of neglectful parenting or loss of parents. A
vulnerability to stresses involving loss of autonomy and control is cen-
tral to the introjective or self-critical perfectionistic type of depression,
and this has its roots in early experiences of critical, punitive parenting.
This distinction between depression associated with disruption of
interpersonal relationships and that associated with threats to master-
ing important achievement-oriented tasks has been made by many
theorists, but has found its clearest articulation in Blatt’s work. Dependent
and self-critical types of depression may be assessed with Blatt’s
Depressive Experiences Questionnaire. A growing body of evidence
using this instrument has shown that in adults, these subtypes of
depression are associated with the recall of different childhood experi-
ences, which have led to the development of different types of depres-
sive object-relations that are typically activated in later life by different
types of stressful life event, and lead to the use of different types of
defence mechanism (Blatt, 2004).
Children who experience either neglectful parenting or the loss of a
parent develop internal working models for later life relationships in
which expectations of abandonment are a central feature. For such indi-
viduals, denial and repression are the most common defence mecha-
nisms employed to deal with perceived threats. These individuals are
particularly vulnerable in later life to stressful events that involve the
disruption of relationships such as rejection or bereavement. When they
develop a mood disorder it is characterized by a preoccupation with the
themes of abandonment, helplessness and a desire to find someone
who will provide love. On the other hand, children exposed to critical
and punitive parenting develop internal working models for relation-
ships in which the constructs of success and failure or blame and
responsibility are central organizing features. Projection or reaction for-
mation are the most common defences used by such individuals. In
teenage years and adulthood they are particularly vulnerable to experi-
ences of criticism, failure or loss of control. Their mood disorders are
characterized by a sense of self-criticism, inferiority, failure, worthless-
ness, anger and guilt.

Psychodynamic treatment of depression

Short-term psychodynamic psychotherapy and long-term psychoanalysis
are the principal treatments that have been developed within the psycho-
analytic tradition. In short-term psychodynamic psychotherapy, which
may last for about 20 sessions, the focus is on the main depression-

Book 1.indb 188 06/03/2012 13:48

 6 • DEPRESSION 189

maintaining, self-defeating defences and the therapist plays quite an

active role in facilitating therapeutic change. In long-term psychoanalysis
the focus is less circumscribed, and the therapist takes a less active
stance, which encourages the development to transference.
Certain practices are common to most psychoanalytic approaches to
depression (Blatt, 2004; McCullough-Vaillant, 1997). Self-defeating
defences repeatedly used by patients to regulate anxiety associated
with unacceptable unconscious feelings are explored. (The triangle of
conflict in Figure 5.5 in Chapter 5 guides the exploration of defences,
anxiety and repressed impulses.) Blatt’s twin themes of dependency
and self-criticism typically emerge as central to these repetitive self-
defeating and depression-maintaining patterns.
Therapists point out the parallels between the way patients repeat
these patterns which were learned in early parent–child attachment
relationships with important people in their current lives and with the
therapist. (The triangle of person in Figure 5.5 in Chapter 5 guides the
exploration of parallels between relationships with parents, the therapist
and significant others.) This process is referred to as transference inter-
pretation, because it involves interpreting how patterns learned in one
context are transferred to other contexts. Through repeated transfer-
ence interpretations patients learn to mentalize – that is, to understand
the mental state of themselves and others – in these depression-
maintaining repetitive patterns (Allen et al., 2008). The analytic relation-
ship also provides patients with a forum within which they can repeatedly
work through the intense depressive and angry feelings, and related
anxieties that underpin their problematic defences and ways of manag-
ing relationships, rooted in their early attachment experiences.
Developing skill at mentalizing and working through previously unac-
ceptable unconscious feelings frees patients to explore more adaptive
ways of living their lives. This may involve developing more realistic
standards for self-evaluation and/or more trusting ways of engaging in
relationships.
In a meta-analysis of 23 studies involving over 1300 cases, Driessen
et al. (2010) found that short-term psychodynamic psychotherapy was
an effective treatment for depression in an outpatient context. It is as
effective at one-year follow-up as other therapeutic approaches, includ-
ing CBT, which has the largest evidence base and is often popularized
as the only effective psychotherapy for depression. In the UK, Lemma
et al. (2011) have developed a manual for short-term psychodynamic
psychotherapy for depression – dynamic interpersonal therapy (DIT) –
which integrates practices used in previous trials that support the effec-
tiveness of short-term psychodynamic psychotherapy.

Cognitive and behavioural theories

Of the many behavioural theories of depression, Lewinsohn’s (Lewinsohn
& Gotlib, 1995) is particularly important because it has led to a consider-
able amount of research on the effectiveness of behavioural treatments

Book 1.indb 189 06/03/2012 13:48

 190 C L I N I C A L P S Y C H O L O G Y : A N I N T R O D U C T I O N

for depression. Cognitive theories of depression developed by Beck et

al. (1979) and Abramson et al. (1978) are among the most important and
influential in the field. They have spawned an extraordinary amount of
research on psychological processes in depression and the effective-
ness of cognitive therapy. For these reasons, the theories of Lewinsohn,
Beck and Abramson will be considered in this section.

Lewinsohn’s behavioural theory

In Lewinsohn’s behavioural theory, he proposes that depression is
maintained by a lack of response-contingent positive reinforcement
(RCPR) (Lewinsohn & Gotlib, 1995). This occurs because people with
depression lack the social skills for eliciting rewarding interactions from
others. In the 12-session, group-based Coping with Depression pro-
gramme based on this model, clients learn social skills necessary for
increasing the rate of response-contingent positive reinforcement in
their lives. In addition they learn to arrange their lives so that they are
more active, engage in more pleasant events and have more opportuni-
ties for using social skills to obtain RCPR. The Coping with Depression
programme also includes relaxation and coping skills training so that
clients are better able to deal with negative emotions arising from
stressful events. A meta-analysis of the programme supports its effec-
tiveness with outpatient adolescents and adults (Cuijpers et al., 2009a).

Beck’s cognitive theory

According to Beck’s cognitive theory, depression occurs when life
events involving loss occur and reactivate negative cognitive schemas
formed early in childhood as a result of early loss experiences (Beck,
2005, 2008; Beck et al., 1979). These negative schemas entail negative
assumptions such as ‘I am only worthwhile if everybody likes me’.
Negative assumptions may be assessed with the Dysfunctional Attitudes
Scale (Weissman & Beck, 1978). When activated, depressive schemas
underpin the occurrence of negative automatic thoughts, such as ‘No
one here likes me’, and cognitive distortions, such as ‘all-or-nothing
thinking’. When a depressed person experiences a drop in mood in a
particular situation, according to Beck’s theory, this mood change is due
not to the situation but to the negative automatic thought that the
situation elicited. The low mood and related depressive behaviour that
occur in such situations make it more likely that similar situations will
recur. These episodes also reinforce depressive schemas. A diagram
of Beck’s model is presented in Figure 6.2.
Negative schemas have their roots in loss experiences in early
childhood, including
● loss of parents or family members through death, illness or separation
● loss of positive parental care through parental rejection, criticism,
severe punishment, over-protection, neglect or abuse
● loss of personal health

Book 1.indb 190 06/03/2012 13:48

 6 • DEPRESSION 191

Figure 6.2 Cognitive-behavioural model of depression

● loss of positive peer relationships through bullying or exclusion from

peer groups
● the expectation of loss, for example where a parent was expected to
die of chronic illness.
According to Beck, two negative schemas that contain latent attitudes
about the self, the world and the future are of particular importance in
depression. The first relates to interpersonal relationships and the
second to personal achievement. He referred to these as sociotropy
and autonomy, as mentioned earlier in the section on personality traits.
Individuals who have negative self-schemas where sociotropy is the
central organizing theme define themselves negatively if they perceive
themselves to be failing to maintain positive relationships. Thus their
core assumption about the self may be ‘If I am not liked by everybody,
then I am worthless’. Individuals who have negative self-schemas
where autonomy is the central organizing theme define themselves

Book 1.indb 191 06/03/2012 13:48

 192 C L I N I C A L P S Y C H O L O G Y : A N I N T R O D U C T I O N

negatively if they perceive themselves to be failing in achieving work-

related goals. Thus their core assumption about the self may be ‘If I am
not a success and in control, then I am worthless’.
When faced with life stresses, individuals vulnerable to depression
because of early loss experience and the related development of nega-
tive self-schemas become prone to interpreting ambiguous situations in
negative, mood-depressing ways. The various logical errors that they
make are referred to as cognitive distortions and include the following.
● All-or-nothing thinking (or dichotomous thinking). Thinking in extreme
categorical terms. For example, ‘Either I’m a success or a failure’.
● Mental filter (or selective abstraction). Filtering out positive aspects
of the situation, selectively focusing on the negative aspects of a
situation, and drawing conclusions from these. For example, ‘I made
a mistake earlier today so everything I did today was wrong’.
● Over-generalization. Generalizing from one instance to all possible
instances. For example, ‘I failed that stats exam so I’ll never be any
good at stats’.
● Magnification or minimization. Exaggerating or under-emphasizing
the significance of events. For example, ‘He said she didn’t like me
so that must mean she hates me’, or ‘He said he likes me, but he
probably doesn’t mean it’.
● Personalization. Attributing negative feeling of others to the self. For
example, ‘He looked really angry when he walked into the room, so
I must have done something wrong’.
● Emotional reasoning. Taking feelings as facts. For example, ‘I feel
like the future is black so the future is hopeless’.
● Discounting the positives. Believing that positive personal charac-
teristics or achievements do not count in overall self-evaluation. For
example. ‘I passed that exam, but that was just good luck, I’m really
no good at stats’.
● Mind reading. Assuming that others are reacting negatively to you
without having evidence for this. For example, ‘Her silence means
that she doesn’t like me’.
● Fortune telling. Predicting that things will turn out badly without hav-
ing evidence to support this. For example, ‘I will probably not enjoy
the party’.
● Catastrophizing. Erroneously predicting extreme distress on the
basis of limited evidence. For example, ‘My heart is racing. I must be
going to have a heart attack’.
● Labelling. Identifying completely with situational shortcomings. For
example, ‘I didn’t just make a mistake, I proved that I’m a complete
fool’.
● ‘Should’ and ‘must’ statements. Making absolute statements about
how the self or others ought to be. For example, ‘I should always be
perfect and he should be loving’.
Depressed individuals interpret situations in terms of their negative
cognitive schemas and so their automatic thoughts are characterized
by these depressive cognitive distortions. Automatic thoughts are self-

Book 1.indb 192 06/03/2012 13:48

 6 • DEPRESSION 193

statements that occur without apparent volition when an individual

attempts to interpret a situation so as to respond to it in a coherent way.
In cognitive therapy, clients learn to monitor situations where nega-
tive mood changes occur; to identify negative automatic thoughts that
lead to these decreases in mood; to generate alternative positive inter-
pretations of situations in which negative mood changes occur; and
to evaluate the validity of these positive and negative views of mood-
altering situations. This may involve reflecting on available evidence, or
generating evidence by carrying out behavioural tasks and checking the
impact of these. For example, attempting to complete successfully a
task where failure is expected.
Meta-analyses have shown that with adults, cognitive therapy is as
effective as antidepressant medication in alleviating depressive symp-
toms, and more effective in relapse prevention (Butler et al., 2006;
Hollon et al., 2006), and that CBT is effective in treating depressed ado-
lescents (Harrington, 1998; Maag et al., 2009). Meta-analyses also
show that CBT self-help programmes involving either bibliotherapy or
computer-based interventions are effective for treating mild to moderate
depression (Andrews et al., 2010; Gregory et al., 2004).
Beck (2008) has proposed a neurobiological explanation for the
effectiveness of CBT. He argues that the generation of negative auto-
matic thoughts is subserved by overactivity in the limbic system, par-
ticularly the amygdala, and underactivity of the prefrontal cortex. This
pattern of underactivity and overactivity of these brain regions arises
from both genetic factors and loss experiences in early life. Cognitive
therapy alleviates depression by facilitating an increase in activity in the
prefrontal cortex (by encouraging patients to reappraise situations in
which they have negative mood changes) which in turn downregulates
the overactive limbic system.

Learned helplessness theory

According to learned helpless theory, depression arises when a person
repeatedly fails to control the occurrence of aversive stimuli or has
repeated experiences of failure at valued tasks and adopts a cognitive
style that involves making internal, global, stable attributions for these
failures and external, specific, unstable attributions for success
(Abramson et al., 1978). For example, saying ‘I failed an exam because
I’ve always been useless at school’ is an internal, global, stable attribu-
tion for failure. On the other hand, saying ‘I failed the exam because the
questions were unexpected and I was tired that day’ involves attributing
failure to partially external, specific and unstable factors.
Attributional style is assessed with the Attributional Style Ques-
tionnaire (Peterson & Villanova, 1988). The Penn Resiliency Programme,
in which young people are trained in learned optimism, is based on the
learned helplessness model (Gillham et al., 2008). In this programme,
participants learn to attribute success to internal, global, stable factors,
and failure to specific, unstable factors that may be changed by using
coping and problem-solving skills that are included in the programme

Book 1.indb 193 06/03/2012 13:48

 194 C L I N I C A L P S Y C H O L O G Y : A N I N T R O D U C T I O N

curriculum. The Penn Resiliency Programme rests on the assumption

that if people can develop an optimistic cognitive style, they will be less
vulnerable to depression. A meta-analysis has confirmed the effective-
ness of this programme in preventing depression in at-risk young
people (Brunwasser et al., 2009).

Family systems theory

Family systems theories of depression highlight the importance of
family-based stress, support, belief systems and interaction patterns in
the aetiology and maintenance of depression. What follows is one
example of such a theory that I have elaborated in greater detail
elsewhere (Carr, 2006b). Both genetic and environmental factors con-
tribute to the development of depressive conditions. The amount of
stress required to precipitate the onset of an episode of depression is
proportional to the genetic vulnerability. That is, little stress may pre-
cipitate the onset of an episode in individuals who are genetically vul-
nerable to the condition, whereas a great deal of stress may be
necessary to precipitate the disorder in individuals without a family his-
tory of depression.
A variety of family factors may predispose people to developing
depression. Both loss experiences and exposure to stresses in early life
that prevent needs for safety and security from being met may render
individuals vulnerable to developing depression in adolescence and
adulthood. Loss experiences include death of a parent, unsupported
lengthy separations from parents, and parental psychological absence
for extended periods, for example through parental depression. Stresses
that prevent needs for safety and security from being met include child
abuse, neglect, multiplacement experiences, parental conflict and
violence, family disorganization and long-term exposure to a pessimistic
family culture.
Episodes of major depression may be precipitated by stressful family
life-cycle transitions, such as the birth of children, bereavements or
divorce. Loss experiences associated with the disruption of significant
relationships or failure to achieve valued goals may precipitate episodes
of depression. For example, family relationships may be disrupted
through conflict and criticism, threats of separation, violence, infidelity
and violations of trust. Failure to achieve valued goals include exam
failure, work-related performance difficulties, unemployment, and seri-
ous illnesses or injury.
Depression may be maintained by particular types of personal and
family belief systems, notably those characterized by a preoccupation
with past losses, a negative view of the self as valueless and powerless,
and pessimism and hopelessness about the future. Such depressive
belief systems may lead to a reduction in activities and an avoidance of
participation in relationships that might disprove these depressive
beliefs or lead to a sense of pleasure and optimism.
Depression may be maintained by particular patterns of family inter-
action. Where a teenager becomes depressed, parents may take

Book 1.indb 194 06/03/2012 13:48

 6 • DEPRESSION 195

conflicting positions on how best to respond, with one parent treating

the adolescent as an ill child and the other treating the young person as
a disobedient teenager, and the parents engaging in repetitive conflicts
about how best to deal with their adolescent. This triangulation process
prevents parents from jointly supporting their teenager’s recovery.
Where an adult becomes depressed and behaves in increasingly help-
less ways, their partner may respond by increasingly engaging in care-
taking, so that the entire relationship becomes dominated by interactions
involving helplessness and caregiving. This process disrupts the
couple’s capacity to meet each other’s needs for desired levels of
intimacy and autonomy.
This family systems conceptualization of depression is supported by
evidence on the role of genetic factors and early life stress in predisposing
people to developing depression; recent life stress in precipitating the
onset of depressive episodes; and both pessimistic belief systems and
negative patterns of family interaction in maintaining depression (Beach
et al., 2009; Garber, 2010; Hammen et al., 2010; Joiner & Coyne, 1999;
Kaslow et al., 2009).
Effective systemic interventions for depression help family members
understand how episodes of depression develop and the role of family
belief systems and patterns of family interaction in maintaining depres-
sion. They also empower family members to develop more adaptive
belief systems and supportive interaction patterns. Systemic interven-
tions include family therapy, where therapists conduct sessions with
whole families; couples therapy, where marital or cohabiting partners
attend therapy sessions together; and individual interpersonal therapy,
where interpersonal issues are the central focus of therapy conducted
with depressed individuals. Evidence from controlled trials and meta-
analyses support the effectiveness of these various approaches to sys-
temic therapy (Beach et al., 2009; Carr, 2009a, 2009b; Kaslow et al.,
2009).

An integrative approach
In clinical practice an integrative approach to conceptualizing depression
is useful. Distinctions may be made between predisposing, precipitating,
maintaining and protective factors. Insights and related evidence
associated with the various theories reviewed above may be integrated
into the following formulation framework.
A range of personal, family and community-based factors may pre-
dispose people to developing depression. Personal factors include a
genetic vulnerability to depression and a depressive temperament; loss
and failure experiences and related depressive cognitive schemas, low
self-esteem and a depressive cognitive style; attachment insecurity, a
depressive interpersonal style and social skills deficits; and personality
traits, particularly perfectionism, neuroticism, introversion and low con-
scientiousness. Family factors that predispose to depression include
separations and bereavements, child abuse, excessive parental criti-
cism, family adversity, and growing up in a family where parents suffer

Book 1.indb 195 06/03/2012 13:48

 196 C L I N I C A L P S Y C H O L O G Y : A N I N T R O D U C T I O N

from depression or other psychopathology. With respect to the commu-

nity and the wider social context, socio-economic status and social and
educational disadvantage are important predisposing factors for depres-
sion. All of these personal, family and community-based predisposing
factors sensitize individuals to loss.
The onset of depression may be precipitated by stressful life events,
particularly those that involve loss or failure. Once an episode of depres-
sion occurs it may be maintained by a range of processes including a
depressive cognitive style; self-defeating behaviour and a lifestyle with
few opportunities for pleasant events or positive reinforcement; rumina-
tive and avoidant coping; and problematic relationships with family,
friends and colleagues. Protective factors in cases of depression include
personal attributes and social relationships that support developing
a more active and positive lifestyle and challenging pessimistic belief
systems.

Assessment
Through careful clinical interviewing of individuals and members of their
families, the symptoms of depression and relevant history are obtained.
A diagnosis is given in accordance with the criteria outlined in ICD-10
and DSM-IV-TR, and a formulation explaining the symptoms entailed
by the diagnosis may be given in which the relevant predisposing,
precipitating, maintaining and protective factors are outlined. A general
clinical formulation model is given in Figure 6.3.
Validated structured interviews for diagnosing depression that may
be used in clinical practice include the mood disorders module of the
Structured Clinical Interview for DSM-IV Axis I Disorders (SCID, First et
al., 1996) for adults and the depression module of the Development and
Well-Being Assessment (DAWBA, Goodman et al., 2000) for children.
Depressive symptom severity may be rated with the Hamilton Rating
Scale (HRS, Hamilton, 1967) and the Children’s Depression Rating
Scale (CDRS, Polanski & Mokros, 1999). Self-reported symptom
severity may be assessed with the Beck Depression Inventory II
(BDI-II, Beck et al., 1996) and the depression scale of the Beck Youth
Inventories II (BYI-II, Steer et al., 2005). A range of standardized self-
report instruments and rating scales may be used to assess personal
characteristics such as cognitive style, and environmental factors such
as stressful life events in adults and children (Dougherty et al., 2008;
Persons & Fresco, 2008). During the process of assessment and
treatment patients and family members may be invited to keep daily
records of fluctuations in mood, related thoughts and behaviour, and
the circumstances preceding and following these fluctuations.

Suicide risk
A central concern when evaluating depression is the assessment of
suicide risk (Hawton & Fortune, 2008; Hawton & Taylor, 2009). This is
because depression is one of the most important risk factors for suicide.

Book 1.indb 196 06/03/2012 13:48

 6 • DEPRESSION 197

Figure 6.3 General formulation model for depression

In conducting this type of risk assessment, interviews are conducted

with the depressed person and members of their family to develop an
understanding of their current circumstances, and the extent to which
the risk factors listed in Table 6.3 are present.
A key feature of suicide risk assessment is determining whether the
person is actively planning to end their life (referred to as suicidal inten-
tion) or alternatively is experiencing thoughts of their own death, without
planning how to bring this about (referred to as suicidal ideation).
Suicidal intention is the most important risk factor for suicide and may
be assessed with the Beck Scale for Suicide Ideation (Beck & Steer,
1991). Where it is judged that a person is at risk of suicide, international
best practice guidelines advise that arrangements be made for constant
supervision of the person until their level of risk decreases (American
Academy of Child and Adolescent Psychiatry, 2001; American Psy-
chiatric Association, 2003; NICE, 2004b). This supervision may be pro-
vided by the family in the home or, where that is not possible, in a
hospital. If a person judged to be at high risk of suicide refuses to be
admitted to hospital (and that is the only viable option for ongoing super-
vision), then they may be involuntarily admitted to hospital. Legislation
and practical procedures for involuntary hospital admission vary from

Book 1.indb 197 06/03/2012 13:48

 198 C L I N I C A L P S Y C H O L O G Y : A N I N T R O D U C T I O N

TABLE 6.3
Risk and protective factors for suicide
Risk factors Domain Protective factors
• Suicidal intention Suicidal • Suicidal ideation (not intention)
• Advanced planning intention and • Acceptance by adolescent of no-suicide
• Precautions against discovery ideation contract
• Lethal method • Acceptance by parents and carers of
• Absence of help-seeking suicide monitoring contract
• A final act
Availability of lethal methods Method Absence of lethal methods
lethality
• Loss of parents or partner by death, Precipitating • Resolution of interpersonal conflict with
separation or illness factors parents or partner that precipitated
• Conflict with parents or partner attempted suicide
• Involvement in judicial system • Acceptance and mourning of losses that
• Severe personal illness precipitated attempted suicide
• Major exam failure • Physical and psychological distancing
• Unwanted pregnancy from peers or others who precipitated
• Imitation of other suicides imitative attemptive suicide

Suicide attempted to serve the function of: Motivation Capacity to develop non-destructive
• escaping an unbearable psychological coping styles or engage in treatment to be
state or situation better able to:
• gaining revenge by inducing guilt • regulate difficult psychological states
• inflicting self-punishment • modify painful situations
• gaining care and attention • express anger assertively
• sacrificing the self for a greater good • resolve conflicts productively
• mourn losses
• manage perfectionistic expectations
• solicit care and attention from others
• cope with family disorganization
• High level of hopelessness Personality- • Low level of hopelessness
• High level of perfectionism based factors • Low level of perfectionism
• High level of impulsivity • Low level of impulsivity
• High levels of hostility and aggression • Low levels of hostility and aggression
• Inflexible coping style • Flexible coping style
• Depression Disorder- • Absence of psychological disorders
• Alcohol and drug abuse related • Absence of physical disorders
• Conduct disorder factors • Absence of multiple comorbid chronic
• Antisocial personality disorder disorders
• Borderline personality disorder • Capacity to form therapeutic alliance
• Epilepsy and engage in treatment for
• Chronic painful illness psychological and physical disorders
• Multiple comorbid chronic disorders
• Previous suicide attempts Historical • No history of previous suicide attempts
• Loss of a parent in early life factors • No history of loss of a parent in early life
• Previous psychiatric treatment • No history of previous psychiatric
• Involvement in the juvenile justice treatment
system • No history of involvement in the juvenile
justice system

Book 1.indb 198 06/03/2012 13:48

 6 • DEPRESSION 199

Risk factors Domain Protective factors

• Family history of suicide attempts Family factors • No family history of suicide attempts
• Family history of depression • No family history of depression
• Family history of drug and alcohol abuse • No family history of drug and alcohol
• Family history of assaultive behaviour abuse
• Disorganized unsupportive family • No family history of assaultive behaviour
• Family deny seriousness of suicide • Well-organized supportive family
attempts • Family has low stress
• Family has high stress and crowding • Family has high social support
• Family has low social support and is
socially isolated
• Male Demographic • Female
• Social class 5 factors • Social class 2, 3 or 4
• White (not black) in US • Black (not white) in US
• Weak religious commitment • Strong religious commitment
• Early summer

country to country. In the UK and Ireland such admissions are usually

made by a psychiatrist.
If you have a friend who you think may be at risk of suicide, the most
useful thing you can do is to help them contact their family doctor (or
staff at their university health centre) to talk about the things that are
bothering them.

Treatment
Research on the psychological treatment of depression has shown that
relatively brief structured interventions of up to 20 sessions over 6
months are effective in helping about two-thirds of adolescents and
adults recover from a depressive episode (Carr, 2009a). Comparative
trials and meta-analyses have shown that CBT, psychodynamic and
systemic interventions are equally effective, although both the drop-out
rate and the evidence base for CBT are larger (Cuijpers et al., 2008).
The development of a strong therapeutic alliance and the adoption of
an approach that modifies depression-maintaining factors underpin
effective psychotherapy for depression (Castonguay et al., 2006; Follette
& Greenberg, 2006). There is evidence from meta-analyses that guided
self-help with books, or computer-based instruction on CBT approaches
to mood management and simple interventions that lead to increased
activity and physical exercise levels, often referred to as behavioural
activation, can effectively reduce depressive symptoms, especially in
people with mild to moderate depression (Andrews et al., 2010; Daley et
al., 2009; Gregory et al., 2004; Mazzucchelli et al., 2009).
In the short term, psychotherapy and antidepressant medication are
equally effective in patients with moderate depression, but in the long
term relapse rates are lower for psychotherapy and multimodal pro-
grammes that include psychotherapy (Vittengl et al., 2007). This is prob-
ably because through psychotherapy people learn relapse prevention
skills. Multimodal programmes, which may be offered by multidisciplinary

Book 1.indb 199 06/03/2012 13:48

 200 C L I N I C A L P S Y C H O L O G Y : A N I N T R O D U C T I O N

teams including clinical psychologists and physicians, that combine psy-

chotherapy and medication are more effective than either intervention
alone (Cuijpers et al., 2009b).
Mindfulness-based cognitive therapy, which combines cognitive
behavioural methods with mindfulness meditation, is particularly effec-
tive at delaying relapse in people with a history of chronically relapsing
depression (Baer, 2003). This is probably because through mindfulness
training people learn to ‘let go’ of negative thoughts and avoid ruminat-
ing about them. For patients with seasonal affective disorder, light
therapy – where the day is artificially lengthened by placing bright lights
in the home – has been shown in a meta-analysis to be effective (Golden
et al., 2005). For patients who do not wish to use conventional anti-
depressants there is some evidence for the effectiveness of St John’s
wort (Hypericum), although meta-analytic results are inconclusive
(Linde et al., 2005).
About a third of people with moderate to severe depression do not
respond to routine psychological intervention or medication. Evidence
for the effectiveness of combining various pharmacological interventions
to treat these patients is mixed, although this practice is widespread
(Zajecka & Goldstein, 2009). For severe treatment-resistant depression,
electroconvulsive therapy (ECT) is widely used, although there is
controversy (discussed below) about this because of its negative impact
on memory and the relatively brief duration of its effectiveness
(Carpenter et al., 2009; Read & Bentall, 2010).
Current best practice is to take a stepped-care approach to the treat-
ment of depression. For people with mild to moderate depression, a
guided self-help approach may initially be taken. Brief structured CBT,
psychodynamic or systemic psychological treatment may be offered to
cases that do not respond to self-help. This may be offered alone or in
combination with antidepressants, depending on patient preferences.
Fluoxetine may be effective for depression in children and adolescents,
although it is less effective in young people than in adults (Bridge et al.,
2007). Because SSRIs may increase suicide risk, they should be used
very cautiously with young people, and only with frequent clinical moni-
toring in cases where there is no response to psychological intervention
(Rudd et al., 2009). For chronic relapsing depression, mindfulness-
based CBT may be offered to delay or prevent relapse. For severe
depression, hospitalization may be necessary.
This overall approach to the management of depression in young
people and adults is consistent with international best practice guide-
lines (American Academy of Child and Adolescent Psychiatry, 2007d;
American Psychiatric Association, 2010; NICE, 2005c, 2009a).

Controversies
There are many controversies in the scientific study and clinical treat-
ment of mood disorders. Three that deserve mention here concern the
use of antidepressants and ECT as well as explanations given for the
high rate of depression in women compared with men.

Book 1.indb 200 06/03/2012 13:48

 6 • DEPRESSION 201

Antidepressants
Antidepressant medication, while widely used, is controversial because
of its questionable efficacy and side-effects. Initial enthusiasm for SSRIs
as a panacea for depression was tempered by results of Turner et al.’s
(2008) meta-analysis, which showed that the high level of effectiveness
of antidepressants reported in academic journals was largely the result
of journals publishing only trials with positive results and rejecting
studies in which antidepressants were shown to be no more effective
than placebos. Subsequent meta-analyses showed that compared with
placebos, the effects of TCAs and SSRIs were negligible for mild to
moderate depression; however, for severe depression their effects are
substantial (e.g., Fournier et al., 2010).
Antidepressants may have negative side-effects, some of which are
troublesome while others are risky or dangerous. Loss of sexual desire
and impotence, weight gain, nausea, sedation or activation, and dizzi-
ness are some of the more troublesome, with different types of anti-
depressant having different side-effect profiles (Gitlin, 2009). For de-
pressed pregnant women, antidepressant treatment may create health
risks for their offspring (Udechuku et al., 2010). MAOIs are particularly
dangerous antidepressants, and are used only with conscientious
patients who can follow strict dietary instructions, because patients on
MAOIs develop high blood pressure and suffer hypertensive crises if
they do not exclude foods that contain thyramine (such as cheese) from
their diets. Antidepressants may increase suicide risk in patients under
25 years, although results of meta-analyses suggest that the benefits
may outweigh the risks (Bridge et al., 2007).

Electroconvulsive therapy
ECT is controversial because of the brevity of its antidepressant effects
and its negative side-effects on memory functioning. In ECT seizures
are induced by briefly passing an electric current through the brain via
electrodes applied to the scalp. ECT is conducted under general anaes-
thetic, and muscle relaxants are used to prevent body spasms. A typical
course of ECT involves 6–12 twice-weekly sessions. Low-dose and
brief-pulse ECT applied to the non-dominant cerebral hemisphere is
sometimes used as an alternative to high-dose bilateral administration
to reduce the negative effect of ECT on memory and other cognitive
functions.
In a large meta-analysis, Carney et al. (2003) found that ECT was
more effective than a placebo (simulated ECT) and antidepressants.
They also found that the most effective form was bilateral and high dose
rather than unilateral and low dose. However, it was precisely this type
of ECT that they found led to greatest memory loss. ECT led to short-
term disorientation and temporary loss of memory for recent events
(anterograde amnesia) and also for distant autobiographical memories
(retrograde amnesia).
A more recent meta-analysis concluded that ECT’s effects on
cognitive function are not all negative. Semkovska and McLoughlin

Book 1.indb 201 06/03/2012 13:48

 202 C L I N I C A L P S Y C H O L O G Y : A N I N T R O D U C T I O N

(2010) found that after 15 days, processing speed, working memory,

anterograde memory, and some aspects of executive function improved
beyond baseline levels. The current ‘mainstream’ position reflected in
international best practice guidelines for psychiatrists is that ECT is the
treatment of choice for severe depression that does not respond to
antidepressants and psychotherapy (American Academy of Child and
Adolescent Psychiatry, 2004; American Psychiatric Association, 2001a;
NICE, 2009a; Royal College of Psychiatrists, 2005). In deciding on the
frequency, dosage, and unilateral or bilateral administration, the benefits
in terms of effectiveness must be balanced against the costs in terms of
memory impairment.
In contrast to this ‘mainstream’ position, Read and Bentall (2010)
propose that ECT should never be used. They conducted a thorough
review of studies on the effectiveness of ECT and its side-effects. They
found that ECT is effective only for a brief duration, and then only for
some patients when ratings of effectiveness are made by psychiatrists
who have a vested interest in showing that ECT is effective. They also
found that ECT leads to retrograde and anterograde amnesia and a
slight but significant increased risk of death. In view of this cost–benefit
analysis of ECT, they concluded that its use cannot be scientifically
justified. In a qualitative study of patients’ negative experiences of ECT,
Johnstone (1999) concluded that for some patients ECT leads to fear,
shame and humiliation and reinforces experiences of worthlessness
and helplessness associated with depression.

Gender and depression

The finding that twice as many women as men are diagnosed with
depression, whereas in childhood the prevalence of depression is the
same for boys and girls, has led to a variety of conflicting explanations
(Nolen-Hoeksema & Hilt, 2009b). One view is that the higher rate of
depression in women arises from the societal inequalities that favour
men over women and the oppressive sex-roles into which women fall
when they enter long-term heterosexual relationships. A second view is
that with the transition to adolescence, females undergo biological
changes that render them vulnerable to depression. A third view is that
women are more likely than men to acknowledge and report personal
distress and so receive a diagnosis of depression.
This controversy about the reasons for high rates of depression in
women has led to the development of complex explanations, and a
wealth of empirical data, which show that multiple personal and
contextual predisposing, precipitating and maintaining factors account
for the gender difference in depression (Nolen-Hoeksema & Hilt, 2009b;
Shibley-Hyde et al., 2008). Results of twin studies show that different
genetic factors render teenage girls vulnerable to depression compared
with boys. Also, girls have higher levels of the personality trait –
neuroticism – that is a vulnerability factor for depression.
Both biological and environmental factors precipitate the onset of
depression in females, and the nature and patterning of these is different

Book 1.indb 202 06/03/2012 13:48

 6 • DEPRESSION 203

for females compared with males. With regard to biological precipitating

factors, uniquely female hormonal changes associated with puberty,
the menstrual cycle, the postpartum period and the menopause trigger
depression in genetically vulnerable women, mainly by affecting oestro-
gens that in turn affect the serotonin neurotransmitter system which
subserves mood regulation. With regard to environmental precipitating
factors, females experience more independent stressful life events than
males and elicit more stressful life events (such as interpersonal rejec-
tion) from others. With regard to maintaining factors, females ruminate
more than males and interpret stressful events in a more pessimistic
way than males. Also, female social roles within society are more
oppressive than male roles and this may maintain depression. Collec-
tively, the aggregation of these factors may partly explain the higher
rates of depression in women.

Summary
Major depressive disorder is a recurrent condition, characterized
by episodes of low mood and loss of interest in pleasurable
activities along with other symptoms such as poor concentration,
fatigue, pessimism, suicidal thoughts and sleep and appetite
disturbance. Depressive episodes can vary in severity from
mild to severe, and melancholic or psychotic symptoms may
be present in severe cases.
The clinical features of depression include selective attention
to negative features of the environment, a pessimistic cognitive
style, low mood, somatic symptoms, psychomotor retardation
or agitation and a deterioration in relationships. Loss is often
the core theme linking these clinical features: loss of an
important relationship, loss of some valued attribute such as
health, or loss of status, for example through unemployment.
Major depression is distinguished from bipolar disorder, where
there are also episodes of elation, and from dysthymia, which
is a milder, non-episodic mood disorder.
Depression is a relatively common disorder with a lifetime
prevalence of about 17%. More adults than children and more
women than men suffer from depression. It follows a chronic
relapsing course, with up to 80% of people having recurring
episodes. About 3.4% of people with a major depressive disor-
der commit suicide.
Theoretical explanations for depression and related treat-
ments have been developed within biological, psychoanalytic,
cognitive-behavioural and family systems traditions. Biological
theories of depression point to the role of genetic factors in
rendering people vulnerable to the development of mood

Book 1.indb 203 06/03/2012 13:48

 204 C L I N I C A L P S Y C H O L O G Y : A N I N T R O D U C T I O N

disorders, and to the role of structural and functional brain

abnormalities; dsysregulation of neurotransmitter, neuroendo-
crine and immune systems; and sleep architecture and circa-
dian rhythm abnormalities in the aetiology of depression.
Psychoanalytic theories of depression, from Freud’s initial for-
mulation to the present time, point to the role of loss of valued
relationships, self-directed anger, self-criticism, and low self-
esteem in the aetiology of depression. Behavioural theories
propose that a lack of response-contingent positive reinforce-
ment causes depression. Cognitive theories propose that
depression arises when stressful life events reactivate depres-
sive schemas that developed as a result of early loss experi-
ences. Systemic theories point to the role of family factors in the
aetiology and maintenance of depression.
Research on stress shows that depression develops follow-
ing exposure to stress and that people with certain personal
attributes inadvertently generate excessive stress, which in
turn leads to depression. Temperamental characteristics such
as harm avoidance, high negative emotionality and low posi-
tive emotionality; personality traits such as high neuroticism,
low extraversion and low conscientiousness; a pessimistic
cognitive style; the use of rumination, avoidance and suppres-
sion as coping strategies; and an interpersonal style character-
ized by limited social skills, attachment insecurity, reassurance
seeking and negative feedback seeking all play a role in the
aetiology of depression.
Assessment of depression should address depressive symp-
toms; relevant predisposing, precipitating and maintaining fac-
tors; and suicide risk. A stepped-care approach to treatment is
usually taken. Patients who do not respond to guided self-help
may be offered multimodal programmes by multidisciplinary
teams which include antidepressant and psychological therapy.
Evidence-based psychodynamic, cognitive-behavioural and
system approaches are equally effective. There are controver-
sies about the effectiveness of antidepressants, the use of ECT
for severe depression, and the reasons for the large gender dif-
ferences in depression.

Questions
● Is depression the same as feeling sad?
● What are the main clinical features of depression?
● What are the differences between major depressive disorder, bipolar
disorder, dysthymia and cyclothymia?
● How prevalent is depression in men and women?

Book 1.indb 204 06/03/2012 13:48

 6 • DEPRESSION 205

● What is your view on the controversy about explanations for gender

differences in depression?
● What are the risk factors for depression?
● What are the risk factors for suicide?
● What are the main biological and psychological theories of depres-
sion and the main research findings relevant to these theories?
● What are the main evidence-based approaches to assessment and
treatment of depression?
● What should you do if you think your friend is suicidal?
● Is the use of antidepressants justified in all cases of depression?
● What are the arguments for and against the use of electroconvulsive
therapy for treatment-resistant depression?

FURTHER READING
Professional
● Gotlib, H. & Hammen, C. (2009). Handbook of depression (second edi-
tion). New York: Guilford Press.
● Nolen-Hoeksema, S. & Hilt, L. M. (2009). Handbook of depression in
adolescents. New York: Routledge.

Self-help
● Burns, D. (1999). Feeling good: The new mood therapy. New York:
Avon.
● Burns, D. (1999). The feeling good handbook (revised edition). New
York: Plume.
● Gilbert, P. (2000). Overcoming depression: A self-help guide using cog-
nitive behavioural techniques (revised edition). London: Robinson.
● Greenberger, D. & Padesky, C. (1995). Mind over mood: Changing how
you feel by changing the way you think. New York: Guilford.
● Williams, M., Teasdale, J., Segal, Z. & Kabat-Zinn, J. (2007). The mind-
ful way through depression: Freeing yourself from chronic unhappiness.
New York: Guilford.

WEBSITES
● American Academy of Child and Adolescent Psychiatry’s practice param-
eters for the treatment of depression, bipolar disorder and suicidal behav-
iour in young people:
www.aacap.org/cs/root/member_information/practice_information/
practice_parameters/practice_parameters
● American Psychiatric Association’s practice guidelines for treating
depression and bipolar disorder:
http://psychiatryonline.org/guidelines.aspx
● Beating the Blues computer-based CBT programme for depression:
www.beatingtheblues.co.uk
● Depression Alliance (UK):
www.depressionalliance.org

Book 1.indb 205 06/03/2012 13:48

 206 C L I N I C A L P S Y C H O L O G Y : A N I N T R O D U C T I O N

● Depression and Bipolar Support Alliance (USA):

www.dbsalliance.org
● NICE. National Institute for Clinical Excellence guidelines for treating
depression and bipolar disorder:
http://guidance.nice.org.uk/topic/mentalhealthbehavioural

Book 1.indb 206 06/03/2012 13:48

 Schizophrenia 7
Learning objectives
After studying this chapter you will be able to:
● give an account of the main clinical features of
schizophrenia and distinguish it from the popular
conception of a ‘split personality’
● distinguish between paranoid, hebephrenic,
catatonic and undifferentiated schizophrenia in
terms of their clinical features
● summarize the epidemiology of schizophrenia
● list the risk factors for schizophrenia
● outline the main biological and diathesis–stress
theories of schizophrenia
● name the main evidence-based approaches to
assessment and treatment of schizophrenia
● describe some of the controversial issues concerning
schizophrenia.

Introduction
The term schizophrenia refers to a collection of seriously debilitating
conditions characterized by positive and negative symptoms and
disorganization (Mueser & Jeste, 2008). Hallucinations and delusions
are the principal positive symptoms of schizophrenia.

Book 1.indb 207 06/03/2012 13:48

 208 C L I N I C A L P S Y C H O L O G Y : A N I N T R O D U C T I O N

Hallucinations involve experiencing sensations in the absence of

external stimuli. For example, with auditory hallucinations – which are
the most common type in schizophrenia – people report hearing voices
that others cannot hear. Delusions are strongly held, unfounded, cultur-
ally alien beliefs. For example, with persecutory delusions, individuals
may believe that a group of people are conspiring to harm them.
The negative symptoms of schizophrenia include flattened affect,
alogia and avolition. With flattened affect there is limited emotional
expression. With alogia there is impoverished thought which is inferred
from speech. Brief, concrete replies are given to questions (referred to
as poverty of speech), or speech production is normal but it conveys
little information due to repetition, or being overly concrete or overly
abstract (referred to as poverty of content). With avolition there is a lack
of goal-directed behaviour. Negative symptoms typically give rise to a
restricted lifestyle involving little activity, little social interaction with
others and little emotional expression. In schizophrenia, disorganization
may affect both speech and behaviour. Disorganized, illogical, incoher-
ent speech reflects an underlying formal thought disorder. Disorganized
catatonic behaviour in schizophrenia includes the virtual absence of
spontaneous activity or excessive purposeless activity.
The diagnostic criteria for schizophrenia are given in Table 7.1. From
the criteria it is clear that schizophrenia is a debilitating condition that
compromises the capacity to carry out normal activities. Schizophrenia
is a chronic relapsing disorder with incomplete remission between epi-
sodes (Hafner & an der Heiden, 2008). The symptoms of schizophrenia
typically first appear in late adolescence or early adulthood, wax and
wane over the life course, and have a profound long-term effect on
patients and their families.
Schizophrenia is the most debilitating of all psychological disorders,
affecting people’s capacity to live independently, make and maintain
satisfying relationships, engage in family life, parent children effectively,
work productively and enjoy leisure activities. Rates of unemployment,
homelessness and imprisonment are very high among people with
schizophrenia. Although just under 1% of people suffer from schizo-
phrenia, the World Health Organization has ranked it as second only to
cardiovascular disease in terms of overall disease burden internation-
ally (Murray & Lopez, 1996).
Despite these gloomy facts, scientific advances in our understanding
of schizophrenia, and advances in both pharmacological and psycho-
logical approaches to treatment, are making it increasingly possible for
people with schizophrenia to live far more productive lives than were
previously possible (Mueser & Jeste, 2008). In this chapter there will be
a consideration of the clinical features, epidemiology, risk factors,
course, theoretical explanations, assessment and treatment of schizo-
phrenia. First, however, let us consider a case example.

Case example of schizophrenia

Julian was referred for assessment and advice by his family doctor. His
parents were worried about him because he had been behaving

Book 1.indb 208 06/03/2012 13:48

 7 • SCHIZOPHRENIA 209

TABLE 7.1
Diagnostic criteria for schizophrenia
DSM-IV-TR ICD-10
A. Characteristic symptoms. Two or more of the A minimum of one very clear symptom (or two or more
following, each present for a significant portion of less clear-cut) belonging to any one of the groups
of time during a 1-month period (or less if (a) to (d) and at least two of the symptoms (e) to (h)
successfully treated): should have been present most of the time during a
(1) delusions period of 1 month or more.
(2) hallucinations (a) thought echo, thought insertion or withdrawal and
(3) disorganized speech (e.g. frequent thought broadcasting
derailment or incoherence) (b) delusions of control, influence, or passivity, clearly
(4) Grossly disorganized or catatonic behaviour referred to body or limb movements or specific
(5) Negative symptoms, affective flattening, thoughts
alogia or avolition (c) hallucinatory voices giving a running commentary
Only one criterion A symptom required if on the patient’s behaviour, or discussing the patient
delusions are bizarre or hallucinations consist of among themselves, or other types of hallucinatory
a voice keeping up a running commentary on the voice coming from some part of the body
person’s behaviour or thoughts or two or more (d) persistent delusions of other kinds that are
voices conversing with each other culturally inappropriate and completely impossible,
B. Social/occupational dysfunction. For a such as religious or political identity, or
significant portion of the time since the onset of superhuman powers and abilities
the disturbance, one or more major areas of (e) persistent hallucinations in any modality, when
functioning such as work, interpersonal accompanied either by fleeting or half-formed
relations, or self-care are markedly below the delusions without clear affective content, or by
level achieved prior to onset or with children a persistent overvalued ideas, or when occurring
failure to achieve the expected level of every day for weeks or months on end
interpersonal, academic or occupational (f) breaks or interpolations in the train of thought,
achievement resulting in incoherence or irrelevant speech or
C. Duration. Continuous signs of the disturbance neologisms
persist for at least 6 months (g) catatonic behaviour, such as excitement, posturing,
D. Not due to schizoaffective or mood disorder or waxy flexibility, negativism, mutism or stupor
E. Not due to substance use or general medical (h) negative symptoms such as marked apathy,
condition paucity of speech, and blunting or incongruity of
F. If there is autism or a pervasive developmental emotional responses, usually resulting in social
disorder, then prominent delusions and withdrawal and lowering of social performance
hallucinations of 1 month’s duration must be (i) a significant and consistent change in the overall
present. quality of some aspects of personal behaviour,
manifest as loss of interest, aimlessness, idleness,
a self-absorbed attitude and social withdrawal

Note: Adapted from DSM-IV-TR (APA, 2000) and ICD-10 (WHO, 1992, 1996).

strangely since returning to his rural home after studying in London for
a year. Julian had failed his exams and said he came home to ‘sort his
head out’. Since his return, Julian’s parents had noticed that he lacked
concentration and his conversation was incoherent much of the time.
Also, his behaviour was erratic and unpredictable.
His parents became particularly concerned when he went missing
some weeks prior to the referral. After searching for a few hours, they
found him 35 miles from their home, exhausted, dehydrated and
dressed in only his sports shorts, singlet and running shoes. Apparently
Julian believed he had to complete a secret mission in the east. While
jogging that morning, he headed eastwards towards the rising sun. He
thought he might jump onto the car ferry when he reached the coast,
cross the sea to Holland, and continue east towards India on his secret

Book 1.indb 209 06/03/2012 13:48

 210 C L I N I C A L P S Y C H O L O G Y : A N I N T R O D U C T I O N

mission. According to the family doctor, Julian’s account of this episode

was not coherent.
Since the episode, Julian has spent much of the time in his room
muttering to himself, often becoming quite distressed. When his parents
spoke to him, they found it hard to make sense of what he said.

Family history
Julian was the 19-year-old son of a prominent farmer in a rural English
village. The family lived in a large mansion on an extensive estate.
Julian’s father managed the farm; he had a traditional authoritarian
manner and a positive, if distant, relationship with Julian. While he was
centrally involved in the search for Julian, once he found his son,
Julian’s father returned to work and left the care of Julian to his wife.
Julian’s mother was an artist. She dressed flamboyantly, behaved in
a theatrical manner and held eccentric, unconventional beliefs. For
example, she held conspiracy theories about many issues, was inter-
ested in eastern mysticism and believed that faith healing and alterna-
tive medicine were preferable to traditional western medicine. This
personal style affected how she treated Julian after the ‘running east’
episode. She engaged him in intense conversations about the mystical
meaning of the psychotic experiences that led to him trying to make his
way to India on foot. Rather than taking Julian to the accident and emer-
gency department of the local hospital for assessment, she brought him
to a faith healer and then a homeopathist. It was only after these inter-
ventions failed to soothe his distress that she brought Julian to the fam-
ily doctor, who made the referral to the community mental health team.
In the preliminary assessment interview that we conducted with Julian
and both of his parents, Julian’s mother responded to him with intense
emotional overinvolvement (an index of high expressed emotion asso-
ciated with relapse in schizophrenia; Hooley, 2007).
With regard to the extended family, according to Julian’s parents
there was no family history of psychological disorder. However, some
members of the mother’s well-to-do family were odd or eccentric,
especially her brother, Sedrick, and her uncle, William Junior. William’s
eccentricities led him into serious conflict with his father, and Sedrick’s
odd behaviour underpinned his highly conflictual, childless marriage.

Developmental history
Julian grew up on the family farm and went to school locally. His devel-
opment was essentially normal. His academic performance at school
was above average. He had many friends in his local village, and was a
popular child and adolescent. Julian was excellent at cricket. He had no
psychological problems before going to university in London at 18.
Julian’s first term at college was successful academically and
socially. However, the occasional experimental cannabis use that
had begun the summer before going to college turned to regular use
once Julian moved to London. During his time at university Julian also

Book 1.indb 210 06/03/2012 13:48

 7 • SCHIZOPHRENIA 211

experimented with LSD on a few occasions. In the final term of his first
year at college, Julian developed an intense fear of exam failure. He
began to have difficulty studying effectively and often had difficulty
sleeping. He stopped attending classes regularly and increasingly spent
time alone. Julian was relieved to return home after sitting his exams.
His parents described him as quiet and thoughtful during the time he
spent at home prior to the ‘running east’ episode.

Presentation
Julian presented with delusions, hallucinations, disorganized speech
and anxiety. He was reluctant to be interviewed because he believed he
had urgent business to attend to in Holland and further afield in India.
He showed signs of being anxiously distressed throughout the interview.
He explained that his path was to the east. He believed he was being
called there by an unknown source. He knew this because of the sign
he had seen while out jogging on the morning of the ‘running east’
episode. The way an old cart wheel caught the sunlight and cast a
shadow on the red-brick wall of a barn against which it leaned made a
distinctive pattern. This pattern was a special sign for him indicating that
he should go east, first to Holland and then all the way to India. When
he questioned this idea, a clear authoritative voice said that he should
leave at once.
At this point in his narrative, he stopped in mid-sentence. He showed
thought blocking, and lost the thread of what he was saying. When
asked to continue his story, he began to giggle. When asked what was
amusing, he said that he could hear someone say something funny.
Julian then spoke about a number of unconnected topics in an incoherent
way before experiencing thought blocking again.
Later he said that he must go soon because people would try to
prevent him. He had heard them talking about him the day before. Julian
said they had tried to put bad ideas into his head. He described being
frightened by this and by periodic sensations that everything was too
loud and too bright and coming at him. He said ‘it was like doing acid
[LSD] all the time … a really bad trip’.

Formulation
Julian presented with auditory hallucinations, delusions, thought disor-
der, anxiety and a significant deterioration in social and occupational
functioning which had been present for more than a month – symptoms
consistent with an ICD-10 diagnosis of schizophrenia. He also showed
a complete lack of insight. He was unable to appreciate that the voices
he heard were hallucinations and his delusional beliefs were unfounded.
Among the important precipitating factors were the experience of
recent exam pressure and Julian’s transition from living at home to
living in London and attending college. The principal predisposing
factors were a possible genetic vulnerability to psychosis and a history
of hallucinogenic drug use. We suspected that there was a genetic

Book 1.indb 211 06/03/2012 13:48

 212 C L I N I C A L P S Y C H O L O G Y : A N I N T R O D U C T I O N

Figure 7.1 Formulation of a case of schizophrenia

vulnerability in this case because of the odd, eccentric behaviour of his

mother and uncles, suggestive of a high level of the trait schizotypy
(Lenzenweger, 2010).
His condition was maintained, we suspected, by a high level of
maternal expressed emotion characterized principally by emotional
over-involvement. Also, his mother inadvertently reinforced his delu-
sions through engaging him in long conversations about them. Protective
factors in this case were good premorbid adjustment and strong family
support. This formulation is diagrammed in Figure 7.1.

Treatment
The treatment plan included antipsychotic medication and family work
to reduce parental expressed emotion, with an initial brief period of hos-
pitalization. Julian did recover from this first psychotic episode. With
medication, his hallucinations and delusions decreased considerably.
Through family psychoeducation, his parents developed an under-
standing of his condition and of his need for a ‘low-key’ approach to
interacting with him as he recovered.
However, there were obstacles to this multimodal treatment pro-
gramme being as effective as possible. Julian did not like the side-
effects of his medication, especially weight gain and reduced sexual
functioning, and so had poor medication adherence. He also became
depressed during remission, when he thought about the many losses

Book 1.indb 212 06/03/2012 13:48

 7 • SCHIZOPHRENIA 213

that followed from his condition. He was unable to continue his university
education, and so could not pursue the career in law he had dreamed
of. He found it difficult to maintain friendships or to commit to engaging
regularly in sports. When he felt low, Julian would smoke cannabis to lift
his spirits.
Julian’s mother found it difficult to accept his diagnosis, and continued
to believe that there was a spiritual or mystical explanation for his
psychotic symptoms. She said she sometimes thought he was not an ill
young man, but a gifted seer or a ‘chosen one’. She often engaged
Julian in intense, distressing conversations about these issues. In the
years that followed his initial assessment, poor medication adherence,
ongoing cannabis use and exposure to high levels of expressed emotion
led Julian to relapse more frequently than might otherwise have been
the case.

Clinical features
A range of clinical features associated with schizophrenia have been
identified through research and clinical observation (Mueser & Jeste,
2008). A classification of these in the domains of perception, cognition,
emotion, behaviour, social adjustment and somatic state is given in
Table 7.2.

TABLE 7.2
Clinical features of schizophrenia
Perception • Breakdown in perceptual selectivity
• Hallucinations
Cognition • Delusions
• Confused sense of self
• Lack of insight
• Formal thought disorder
• Cognitive impairment (IQ, attention, memory, executive
function, psychomotor speed)
Emotion • Prodromal anxiety and depression
• Inappropriate, flattened or blunted affect
• Postpsychotic depression
Behaviour • Prodromal excitation (sleeplessness, impulsivity,
overactivity, compulsivity)
• Impaired goal-directed behaviour
• Excited or retarded catatonic behaviour
Social adjustment • Poor self-care and hygiene
• Poor educational or work performance
• Withdrawal from peer relationships
• Deterioration in family relationships
Somatic state • Comorbid substance use
• Comorbid health problems (CPOD, obesity, heart
disease, HIV/AIDS, Hepatitis B & C)
• Unhealthy lifestyle (poor diet, obesity, little exercise,
smoking)

Book 1.indb 213 06/03/2012 13:48

 214 C L I N I C A L P S Y C H O L O G Y : A N I N T R O D U C T I O N

Perception
At a perceptual level, individuals with schizophrenia describe a break-
down in perceptual selectivity, with difficulties in focusing on essential
information or stimuli to the exclusion of accidental details or back-
ground noise. Everything seems to be salient, and it is difficult to distin-
guish figure from ground. During an acute psychotic state, internal
stimuli such as verbal thoughts are experienced as auditory hallucina-
tions that have the same sensory quality as the spoken word.
Auditory hallucinations may be experienced as loud thoughts, as
thoughts being repeated by another person aloud (thought echo), as
voices speaking inside the head or as voices coming from somewhere
in the outer environment. Auditory hallucination may occur as a third-
person commentary on the patient’s action, as a voice speaking in the
second person directly to the patient, or as two or more people talking
or arguing. Patients may perceive voices to vary along a number of
dimensions. Voices may be construed as benign or malevolent, control-
ling or impotent, all-knowing or knowing little about the person, and the
person may feel compelled to do what the voice says or not.
Hallucinations that are perceived to be malevolent, controlling, all-
knowing and which the individual feels compelled to obey are far more
distressing than those that are not construed as having these attributes.
While auditory hallucinations are the most common in schizophrenia,
hallucinations may occur in other sensory modalities. Somatic halluci-
nations often occur in schizophrenia, with patients reporting feelings of
electricity in their body or things crawling under their skin. These may
be given delusional interpretations. For example, a patient reported that
the television was activating a transmitter in her pelvis and she could
feel the electricity from this causing insects to grow and move around
under her skin. Visual hallucinations – seeing visions – are relatively
rare in schizophrenia, but common in temporal lobe epilepsy.

Cognition
Delusions are the most prominent cognitive clinical features of schizo-
phrenia. Delusions are false, idiosyncratic, illogical and stubbornly
maintained erroneous inferences drawn to explain unusual experi-
ences, such as hallucinations. For example, a patient with auditory
hallucinations in which she heard an authoritative voice giving her
commands to gather the children to her inferred that she had been
chosen by God to prepare all children for the second coming of Christ.
Delusions may arise not only from hallucinations, but also from un-
usual feelings associated with psychosis. Persecutory delusions may
develop from feelings of being watched. Delusions of thought insertion
or thought withdrawal may develop as explanations for feelings that
thoughts are not one’s own, or that one’s thoughts have suddenly dis-
appeared. Factor analyses show that delusions fall into three broad
categories: delusions of influence (including thought withdrawal or in-
sertion, and beliefs about being controlled); delusions of self-significance
(including delusions of grandeur or guilt); and delusions of persecution

Book 1.indb 214 06/03/2012 13:48

 7 • SCHIZOPHRENIA 215

(Vahia & Cohen, 2008). Delusions may vary in the degree of convic-
tion with which they are held (from great certainty to little certainty),
the degree to which the person is preoccupied with them (the amount
of time spent thinking about the belief), and the amount of distress
they cause.
Particular sets of delusions may entail a confused sense of self,
particularly paranoid delusions where individuals believe that they are
being persecuted or punished for misdeeds, or delusions of control
where there is a belief that one’s actions are controlled by others.
During a psychotic episode there is usually lack of insight and
impaired judgement. That is, patients believe that the content of their
hallucinations and delusions is legitimate, and they have difficulty enter-
taining the idea that these experiences and beliefs arise from a clinical
condition. Between psychotic episodes, insight may improve and
patients may move towards accepting that their hallucinations and delu-
sions are symptoms of schizophrenia.
The speech of patients with schizophrenia is difficult to understand
because of abnormalities in the underlying form of thought. Formal
thought disorder is characterized by tangentiality, derailment, incoher-
ence, thought blocking, loss of goal and neologisms. With tangentia-
lity, answers given to questions are off the point. With derailment,
sentences make sense, but little meaning is conveyed by sequences of
sentences because there is a constant jumping from one topic to
another, with very loose associations between topics and little logic
to what is said. With incoherence, sentences are incorrectly formed so
they do not make sense. With thought blocking, the person abruptly
stops in mid-sentence and is unable complete their train of thought.
With loss of goal there is a difficulty in following a logical train of thought
from A to B. With neologisms, new words are made up that have an
idiosyncratic meaning for the patient.
Cognitive impairment or deterioration occurs in schizophrenia. This
may be either general or specific. With general cognitive deterioration,
there is a reduction in overall IQ with many cognitive functions nega-
tively affected. With specific cognitive impairment one or more of the
following functions may be impaired: attention, memory, cognitive flex-
ibility, social cognition and executive function, particularly the capacity
to follow through on a planned course of action. Cognitive impairment is
a better predictor of disability and vocational functioning than positive
symptoms.

Emotions
At an emotional level, during the prodromal phase, before an acute
psychotic episode, anxiety or depression may occur in response to
initial changes in perceptual selectivity and cognitive inefficiency. A key
part of relapse prevention is for patients to learn how to identify and
manage prodromal changes in affect.
During acute psychotic episodes, anxiety or depression may occur in
response to hallucinations, delusions, formal thought disorder and other

Book 1.indb 215 06/03/2012 13:48

 216 C L I N I C A L P S Y C H O L O G Y : A N I N T R O D U C T I O N

distressing symptoms. Inappropriate affect may be present particularly

in hebephrenic schizophrenia, where the individual responds not to the
external social context but to internal stimuli such as auditory hallucina-
tions, for example by laughing wildly. Flattened or blunted affect may
occur, particularly in chronic cases. During remission following an epi-
sode of psychosis, the sense of loss that comes with increased insight
into the reality of the condition may give rise to post-psychotic depres-
sion.

Behaviour
At a behavioural level, prodromal excitation may occur prior to an acute
psychotic episode, characterized by sleep disturbance, impulsive be-
haviour, and overactivity which may include compulsive behaviour.
During acute psychotic episodes, avolition occurs, with impairment of
goal-directed behaviour.
In chronic cases catatonic behaviour may occur, with impairment in
the capacity to initiate and organize voluntary movement and posture.
Catatonia may be either retarded or excited. Excessive purposeless
motor activity is the hallmark of excited catatonia and may include
stereotypies (repetitive actions), echolalia (repeating words said by
others) or echopraxia (imitating the actions of others). With retarded
catatonic behaviour there is a marked reduction in purposeful activity.
Patients may show immobility, mutism, adopt unusual postures for long
periods of time, and display waxy flexibility (allowing one’s limbs to be
manipulated like a warm candle) or negativism (resisting attempts to
have one’s limbs moved).

Social adjustment
In schizophrenia there a marked deterioration in social adjustment. The
capacity for self-care, dressing appropriately, grooming and personal
hygiene deteriorates, so that people with schizophrenia often look
dishevelled and unkempt. A significant decline in performance in
educational and work settings occurs. There is a withdrawal from
regular socializing with friends and difficulty in making and maintaining
new relationships. A deterioration in relationships with family members
also occurs. Schizophrenia has a negative impact on parent–child,
marital and sibling relationships.

Somatic state
About half of all people with schizophrenia have comorbid substance
use disorders and almost three-quarters have significant health prob-
lems. The most common health problems include chronic obstructive
pulmonary disease (COPT), which is usually due to smoking; heart
disease and diabetes due to obesity; HIV/AIDS and hepatitis B and C
due to unsafe sex and intravenous drug use. The substance use and
medical problems so common in schizophrenia are essentially lifestyle

Book 1.indb 216 06/03/2012 13:48

 7 • SCHIZOPHRENIA 217

problems. On the positive side, schizophrenia is associated with

reduced rates of cancer and rheumatoid arthritis (Tandon et al., 2008a).

Classification
To take account of the marked variability in symptomatology among
people with schizophrenia, various subtypes have been defined. Also,
a number of psychotic conditions that closely resemble schizophrenia
have been identified, and referred to as schizophrenia spectrum
disorders. Schizophrenia subtypes and spectrum disorders are consid-
ered in this section. In ICD-10 (World Health Organization, 1992) and
DSM-IV-TR (American Psychiatric Association, 2000), four main sub-
types of schizophrenia are distinguished:
● paranoid
● catatonic
● hebephrenic or disorganized
● undifferentiated.
Where paranoid delusions predominate, a diagnosis of paranoid schiz-
ophrenia is given. Cases in which either retarded or excited catatonic
behaviour is the principal feature are classified as having catatonic
schizophrenia. Cases are classified as hebephrenic in the ICD-10 and
disorganized in the DSM-IV-TR when inappropriate or flat affect is the
principal feature and where there is disorganized behaviour and speech.
In both ICD-10 and DSM-IV-TR, when cases do not fall into any of the
three categories just mentioned, they are classified as undifferentiated.
While distinctions between the four main subtypes of schizophrenia
have been useful for describing different clinical presentations and date
back to Emil Kraepelin’s (1899) work, research has shown that these
subtypes are not consistently differentiated by family history, course,
prognosis or treatment response.
In contrast to the lack of success in validating subtypes of schizophre-
nia, there has been considerable progress in identifying other conditions
that share a very similar pattern of family history, course, prognosis and
treatment response to schizophrenia. These include disorders that have
the same symptomatology as schizophrenia, but are of briefer duration
(such as schizophreniform disorder); those with the same symptomatol-
ogy as schizophrenia in addition to the symptoms of a mood disorder
(schizoaffective disorder); and those characterized by chronic mild
schizophrenia-like symptoms (such as schizotypal, schizoid and para-
noid personality disorders). These conditions, along with schizophrenia,
constitute schizophrenia spectrum disorders (Mamah & Barch, 2011).
Research on the shared aetiology, course and treatment response of
these disorders and factor analytic studies of their symptomatology
suggest that the distribution of psychotic symptoms within the population
more closely approximates dimensions than disease-like categories.
The three principal dimensions are those involving positive symptoms,
negative symptoms and disorganization, mentioned in the opening
paragraph of this chapter (Rietkerk et al., 2008).

Book 1.indb 217 06/03/2012 13:48

 218 C L I N I C A L P S Y C H O L O G Y : A N I N T R O D U C T I O N

Epidemiology, course, outcome and risk factors

Reviews of international epidemiological studies allow a number of
conclusions to be drawn about the epidemiology of schizophrenia.
Under 1% of the population suffer from schizophrenia, and the lifetime
risk of this condition is about 0.7% (Saha et al., 2005). More men than
women suffer from schizophrenia: the male–female ratio is about 1.4:1
(McGrath et al., 2004). The onset of schizophrenia is earlier in males
(20–28 years) than in females (28–32 years) (Murray & Van Os, 1998).
The rates of schizophrenia are similar across countries and cultures
when similar diagnostic criteria are used (Mueser & Duva, 2011).
Schizophrenia follows a distinctive course although there is consid-
erable variability across cases (Jablensky, 2009; Jobe & Harrow, 2010;
Mueser & Duva, 2011, Tandon et al., 2009). The onset of schizophrenia
typically occurs in late adolescence or early adulthood and may be
acute or insidious. Typically the onset takes place over 5 years, starting
with negative and depressive symptoms, followed by cognitive and
social impairment and finally positive symptoms. Longitudinal studies
suggest that there is an early deterioration phase that extends over
5–10 years, a stabilization phase and a final gradual improvement
phase. For 50–70% of cases the condition follows a chronic relapsing
course, typically with incomplete remission between episodes. However,
up to 40% of patients show one or more periods of complete recovery
with good adjustment for at least a year, and 4–20% show complete
remission.
Psychotic episodes may last from 1 to 6 months, although some
extend to a year. They are usually preceded by a prodromal period of a
number of weeks. Psychotic episodes may be shortened and the
severity of symptomatology ameliorated through early detection and the
use of pharmacological and psychological treatment as outlined below.
Inter-episode functioning may vary greatly, and better inter-episode
functioning is associated with a better prognosis. The duration of
remission between episodes may be lengthened through the use of
maintenance medication and psychosocial interventions to reduce
stress and improve coping and illness management.
With treatment, usually positive symptoms (hallucinations and
delusions) abate between episodes but negative symptoms (blunted
affect, alogia and avolition) are relatively enduring and are more likely
to persist during remission. In the stabilization phase of schizophrenia
positive symptoms becoming less prominent, while negative symptoms
and cognitive deficits become more prominent. The lifespan of people
with schizophrenia is about 9 years shorter than that of the general
population, and this is partly accounted for by the high rate of suicide
during the first 10 years of the disorder and the high rate of comorbid
medical disorders mentioned earlier. About half of all people with
schizophrenia attempt suicide or self-harm, and about 10% commit
suicide (Heisel, 2008; Schennach-Wolff et al., 2011).
Risk factors for schizophrenia are listed in Table 7.3 (Lenzenweger,
2010; Murray & Castle, 2009; Tandon et al., 2008b). The greatest risk

Book 1.indb 218 06/03/2012 13:48

 7 • SCHIZOPHRENIA 219

TABLE 7.3
Risk factors for schizophrenia
Genetic factors
Positive family history of psychosis
Personality
Schizotypy
Prenatal and perinatal factors
Maternal flu infection or malnutrition in first or second trimester
Father over 35 years
Obstetric complications (low birth weight, prematurity, resuscitation)
Birth in late winter or early spring
Demographic factors
Male
Unmarried
Urban dwelling
Migrant
Low SES
Life history factors
Trauma history
Cannabis use

factor for schizophrenia is a family history of psychosis. This probably

finds subclinical expression as schizotypy, a personality trait in which
the central feature is a disorganized thinking style similar to (although
much milder than) that shown in schizophrenia (Lenzenweger, 2010).
Other risk factors make a small but significant contribution to overall
risk within the context of that associated with genetic vulnerability.
However, at present there is no consensus on how these risk factors
operate. Prenatal and perinatal risk factors, such as maternal flu infec-
tion and obstetric complications, probably have a negative direct or indi-
rect effect on the development of the nervous system in line with the
neurodevelopmental hypothesis mentioned below, rendering those
genetically predisposed even more neurobiologically vulnerable to psy-
chosis (Murray & Lewis, 1987). Trauma exposure and most demo-
graphic risk factors (being an unmarried, low-SES urban migrant) are
associated with higher levels of stress and lower levels of social
support, which increase the risk of psychosis in the genetically vulner-
able according to diathesis–stress conceptualizations of the condition
(Zubin & Spring, 1977). It is probable that the mechanism by which can-
nabis use affects schizophrenia is neurobiological rather than social–
environmental (Barkus & Murray, 2010).
In the short term, relapse is more likely in cases where there is heavy
cannabis use, poor treatment adherence, frequent contact with family
members who display high expressed emotion (criticism, hostility and
emotional over-involvement) and exposure to acute stressful life events
(Jablensky, 2009).
Longitudinal studies show that the risk factors listed in Table 7.4 are
associated with poorer outcome (Bota et al., 2011; Jablensky, 2009;
Jobe & Harrow, 2010). A poor outcome is associated with substance

Book 1.indb 219 06/03/2012 13:48

 220 C L I N I C A L P S Y C H O L O G Y : A N I N T R O D U C T I O N

TABLE 7.4
Risk factors for a poor outcome in schizophrenia
Early stage
Early age of onset
Insidious onset
Poor premorbid adjustment
Longer duration of untreated psychosis
Substance use
Lack of an identifiable precipitating stressor prior to hospitalization
Personality traits
Trait anxiety (and HPA axis hyperactivity)
External locus of control
Symptom profile
Severe negative symptoms (blunted affect, alogia, avolition)
Severe cognitive impairment
Lack of depressive symptoms
Lifestyle
Poor treatment adherence
Substance use
Social context
Single
Few friends
Stressful life events
Frequent contact with family members who display high expressed emotion
(over-involvement and criticism)
Living in a developing country

use and a longer period of untreated psychosis in people who have

poor premorbid adjustment and an early insidious onset with no clear
stressful life event preceding their first treated episode. A high level of
trait anxiety, which is probably subserved by hypothalamic–pituitary–
adrenal (HPA) axis overactivity and an external locus of control, is the
main personality trait associated with poor outcome. People with this
stress-sensitive profile are more reactive to stressful life-events,
including those associated with living in a developing country, and
family-based stress associated with high levels of expressed emotion,
all of which are also risk factors for poor outcome. A poorer outcome
occurs for those who are single and have few friends – factors which
suggest low levels of social support. The symptom profile predictive of
a poor outcome is marked by severe negative symptoms, cognitive
impairment and lack of depressive symptoms.
A favourable outcome in schizophrenia is associated with a range of
factors (Bota et al., 2011). These include good premorbid adjustment,
and a brief duration of untreated psychosis characterized by an acute
onset in response to precipitating stressful life events. A family history
of affective disorder (rather than schizophrenia) or little psychopathology
and a personal symptom profile in which there are affective as well as
psychotic features are also predictive of a good prognosis. A better
outcome occurs for those who have a favourable life situation to return
to following discharge from hospital.

Book 1.indb 220 06/03/2012 13:48

 7 • SCHIZOPHRENIA 221

Aetiological theories
Historically, research on schizophrenia has followed from two principal
traditions founded by the German psychiatrist Emile Kraepelin (1899)
and the Swiss psychiatrist Eugen Bleuler (1911). Kraepelin defined the
condition, which he named ‘dementia praecox’, as principally character-
ized by a constellation of observable symptoms (such as delusions,
hallucinations and thought disorder) and a chronic course due to an
underlying degenerative neurological condition. In contrast, Bleuler,
who coined the term ‘schizophrenia’, conceptualized the condition as a
disturbance in a circumscribed set of inferred psychological processes.
He speculated that the capacity to associate one thought with another,
to associate thoughts with emotions, and to associate the self with real-
ity were impaired or split. Hence the term ‘schizophrenia’ (from the
Greek words for split and mind).
Bleuler proposed that the four primary symptoms of schizophrenia
were loosening of associations (difficulty in thinking straight), incongru-
ous or flattened affect, impaired goal-directed behaviour or ambiva-
lence due to conflicting impulses, and autism or social withdrawal. The
emphasized words in the last sentence are sometimes referred to as
Bleuler’s ‘four As’. Bleuler argued that positive symptoms such as delu-
sions and hallucinations were secondary to these central psychological
difficulties. For Bleuler, the symptoms of schizophrenia such as delu-
sions and hallucinations represented the person’s attempt to cope with
the world despite disruption of central psychological processes. While
Kraepelin conceptualized schizophrenia as being distributed within the
population as a discrete disease-like category, Bleuler viewed the dis-
turbed psychological processes that he proposed underpinned schizo-
phrenia as on a continuum with normal psychological functioning. These
different views were precursors of the modern categorical and dimen-
sional approaches to understanding schizophrenia (Linscott & Van Os,
2010).
Up to the late 1970s, Bleuler’s tradition, associated with a broad
definition of schizophrenia, predominated in the US whereas in the UK,
Ireland and Europe, Kraepelin’s narrower definition held sway. Following
the landmark US–UK diagnostic study (US–UK Team, 1974) that
highlighted the extraordinary differences between the way schizophrenia
was defined in America and Britain, there has been a gradual move
towards developing an internationally acceptable set of diagnostic
criteria. The narrowing of the gap between the North American and
European definitions of schizophrenia is reflected in the marked
similarity between the diagnostic criteria for the disorder contained in
current versions of the ICD and DSM presented in Table 7.1.
Modern research on schizophrenia has also been guided by two
broad groups of theories. The first, in the tradition of Kraepelin, has
been concerned largely with the role of biological factors in the aetiol-
ogy and maintenance of the disorder. The second group of theories,
in the tradition of Bleuler, has addressed the role of psychological fac-
tors in schizophrenia. In the following section, biological theories of

Book 1.indb 221 06/03/2012 13:48

 222 C L I N I C A L P S Y C H O L O G Y : A N I N T R O D U C T I O N

schizophrenia and related research findings will be considered. This will

be followed by a consideration of the stress-vulnerability or diathesis–
stress approaches to conceptualizing schizophrenia and research find-
ings of relevance to this position.

Biological theories
Biological theories of schizophrenia point to the role of genetic and
neurodevelopmental factors in rendering people vulnerable to the
development of psychosis, and to the role of structural and functional
brain abnormalities; dsysregulation of neurotransmitter systems; and
sleep architecture and eye movement abnormalities in the aetiology of
schizophrenia. There is considerable support for biological theories
from neuroimaging, pharmacological, psychophysiological and other
neurobiological studies, although current knowledge of these abnor-
malities is incomplete (Bora et al., 2011; Downar & Kapur, 2008; Eyler,
2008; Fatemi & Folsom, 2009; Glatt, 2008; Harrison, 2009; Hollis, 2008;
Keshavan et al., 2008; Murray & Castle, 2009; Ritsner & Gottesman,
2011; Stewart & Davis, 2008). However, there is a consensus about
certain aspects of the neurobiology of schizophrenia, which will be pre-
sented below.

Genetics
The genetic hypothesis proposes that schizophrenia arises primarily
from an inherited vulnerability to psychosis. Results of twin, adoption
and family studies show that a predisposition to schizophrenia spectrum
disorders is genetically transmitted. Schizophrenia is about 80% heri-
table (Glatt, 2008; Sullivan et al., 2003). The lifetime risk for developing
schizophrenia is proportional to the number of shared genes. For
monozygotic twins the risk is 48%; for dizygotic twins the risk is 17%; for
children of an affected parent the risk is 13%; for grandchildren the risk
is 5%; and for members of the general population the risk is about 1%
(Ritsner & Gottesman, 2011). It is also probable that the vulnerability is
polygenetically transmitted, since the results of family studies cannot
easily be accounted for by simpler models of genetic transmission.
Many candidate genes for schizophrenia have been investigated;
some have been identified; and where significant associations between
candidate genes and schizophrenia have been found, a growing number
of consistent replication studies are available (Harrison, 2009; Ritsner &
Gottesman, 2011). Candidate genes for which consistent evidence is
available affect the growth and organization of neurones in the brain,
the development of synapses, and glutamate and dopamine neuro-
transmission. Candidate genes include neurreulin 1 (NRG1) and
disrupted-in-schizophrenia-1 (DISC1), which have multiple roles
in brain development, synapse formation and synaptic signalling;
catechol-O-methyltransferase (COMT), which regulates dopamine
signalling in the frontal cortex; D-amino acid oxidase activator
(DAOA) and dysbindin (DTNBP1), which affect glutamate signalling;

Book 1.indb 222 06/03/2012 13:48

 7 • SCHIZOPHRENIA 223

regulator of G-protein signalling 4 (RGS4) and calcineurin (PP3CC),

which affect dopamine and glutamate neurotransmission. The mecha-
nisms by which candidate genes give rise to the symptoms of schizo-
phrenia through altering the structure and functioning of the nervous
system are currently a focus for intensive research internationally
(Bertram, 2008).
Despite evidence for the role of genetic factors in schizophrenia, many
people who develop schizophrenia have no relatives that suffer from the
condition, and some people with a genetic predisposition to schizophrenia
do not develop psychotic symptoms. It is therefore likely that environmental
factors also contribute to the development of schizophrenia.

Neurodevelopment and neuropathology

The neurodevelopmental hypothesis proposes that prenatal and peri-
natal factors (often referred to as obstetric complications) interact with a
genetic vulnerability to psychosis to give rise to atypical neuroanatomi-
cal development initially in infancy, and later in adolescence, and this
culminates in the emergence of schizophrenia (Fatemi & Folsom, 2009;
McGlashen & Hoffman, 2000; Murray & Lewis, 1987).
In normal development, synaptic connections within the brain
increase up to 2 years, decline gradually before puberty and then
decrease markedly in adolescence. This sharp decline is due to synap-
tic pruning, which involves the elimination of superfluous synapses. It
coincides with the emergence of sophisticated cognitive skills in early
adolescence such as the capacity for abstract reasoning. According to
the neurodevelopmental hypothesis, the synaptic pruning process is
excessive in schizophrenia, leading to a fragmented brain and conse-
quent psychotic symptoms (McGlashen & Hoffman, 2000). Excessive
pruning is expected to have a more profound effect where fewer syn-
apses were formed during early brain development due to an adverse
intrauterine environment associated with obstetric complications.

Obstetric complications
A growing body of evidence supports the link between obstetric com-
plications and schizophrenia (Ellman & Cannon, 2008). Obstetric
complications that have been investigated with reference to the neuro-
developmental hypothesis include maternal infection with influenza or
rubella during early pregnancy, maternal malnutrition during early preg-
nancy, diabetes mellitus, smoking during pregnancy, bleeding during
pregnancy, problematic labour or delivery, anoxia or asphyxia at birth,
low birth weight, small head circumference, and congenital malforma-
tions. About 20–30% of patients with schizophrenia have a history of
obstetric complications, compared with 5–10% of the unaffected popula-
tion. Lack of oxygen to the foetus – foetal hypoxia – is involved in many
obstetric complications associated with psychosis. Cases with a history
of obstetric complications show an earlier onset of schizophrenia and
more pronounced neuroanatomical abnormalities, as predicted by the
neurodevelopmental hypothesis.

Book 1.indb 223 06/03/2012 13:48

 224 C L I N I C A L P S Y C H O L O G Y : A N I N T R O D U C T I O N

Neuroanatomy
In support of the neurodevelopmental hypothesis, five neuroanotomical
abnormalities have consistently emerged in neuroimaging and post-
mortem studies of schizophrenia (Bora et al., 2011; Keshavan et al.,
2008; Stewart & Davis, 2008). The first abnormality is reduced overall
brain volume and enlargement of the cerebral ventricles (particularly
the left ventricle) associated with brain atrophy. The second abnormal-
ity concerns the reduced size of, and activation within, the frontal lobes.
The dorsolateral prefrontal cortex is particularly affected, where there is
also increased neuronal packing density. This abnormality may under-
pin cognitive deficits (IQ, executive function, attention and memory).
The third abnormality is reduced temporal lobe volume including reduc-
tions in the size of the amygdala and hippocampus, structures that sub-
serve emotional processing and memory. The fourth abnormality is
decreased thalamic volume, and disorganization of the thalamocortical
pathways. The thalamus plays a central role in attention, and in filtering
and relaying information to various areas of the brain including the pre-
frontal cortex. The fifth abnormality is disorganization of white matter
tracts and reduced connectivity between many areas of the brain.
A detailed understanding of how these neuroanatomical abnormalities
give rise to the symptoms of schizophrenia is a focus of ongoing
research. Many of the structural brain abnormalities listed here precede
the onset of psychosis, and in some cases they progress over the
course of the schizophrenia (Chan et al., 2011).

Psychophysiology
Results of studies which show that schizophrenia is associated with
abnormalities in a number of psychophysiological indices reflective of
abnormal neurobiological processes also support the neurodevelop-
mental hypothesis (Javitt et al., 2008; Keshavan et al., 2008). Sleep
architecture assessed by electroencephalogram (EEG) is abnormal in
schizophrenia. Total sleep time and time during non-rapid eye move-
ment (REM) sleep is reduced, as is REM sleep latency. Evoked poten-
tials, which are detected with scalp electrodes during visual or auditory
tasks, are abnormal in schizophrenia, indicating impairments in neuro-
biological processes subserving visual and auditory perception and
information processing. Eye movements, especially those involved in
smooth pursuit tracking of a moving target, are abnormal in schizophre-
nia, indicating impairments in neurobiological processes subserving
occulomotor control. These evoked potential and eye movement abnor-
malities are highly heritable and present prior to the onset of acute
psychosis.

Neurotransmitters
Neurotransmitter dysregulation hypotheses attribute psychotic
symptoms to neurotransmission problems. Dysregulations of the dopa-
mine and glutamate neurotransmitter systems have been found in

Book 1.indb 224 06/03/2012 13:48

 7 • SCHIZOPHRENIA 225

schizophrenia (Downar & Kapur, 2008). Genes that affect both of these
neurotransmitter systems have been implicated in the aetiology of the
condition, as was noted above in the section on genetics.

Dopamine
The dopamine hypothesis arose from observations that medications,
such as chlorpromazine, that block dopamine D2 receptors alleviate
psychotic symptoms; and amphetamines, which release dopamine,
induce paranoid psychosis (Seeman, 2011). The original dopamine
hypothesis, which attributed psychotic symptoms to an excess of
dopamine, has inspired extensive research and the development of a
range of antipsychotic medications for schizophrenia; over time it has
been supplanted by more sophisticated formulations.
Available evidence indicates that overactivity of the mesolimbic
dopamine pathway subserves positive symptoms (hallucinations and
delusions), and underactivity of the mesocortical dopamine pathway
subserves negative symptoms (blunted affect, alogia and avolition) and
cognitive impairment (Downar & Kapur, 2008). First-generation anti-
psychotic medications such as chlorpromazine, which block dopamine D2
receptors, alleviate positive symptoms in most cases, but have no effect
on negative symptoms. In contrast, newer second-generation anti-
psychotic medications, such as clozapine, block dopamine D2 receptors
in the mesolymbic but not the mesocortical pathway, and so alleviate
positive symptoms and some negative symptoms.
Downar and Kapur (2008) have proposed the following explanation
to link dysregulation of the dopamine system to psychotic symptoms.
Dopamine is the neurotransmitter that gives salience to neural networks
associated with thoughts or perceptions. Overactivity of the mesolimbic
dopamine pathway probably results in many thoughts and perceptions
being misinterpreted as highly salient or important. Thus, thoughts are
misinterpreted as ‘voices’, and fleeting ideas that might otherwise be
ignored are misinterpreted as being very important and so are developed
into delusional belief systems. Antipsychotic medications that block
dopamine D2 receptors reduce this tendency to misinterpret unimportant
perceptions and thoughts as highly salient. However, delusions that
have already formed may need to be re-evaluated, which is what occurs
in cognitive therapy.
In contrast to the overactive mesolymbic dopamine pathway, the
underactive mesocortical dopamine pathway reduces the salience with
which certain perceptions, thoughts, feelings and motives are experi-
enced. This accounts for the negative symptoms (blunted affect, alogia
and avolition) and cognitive impairment that occur in schizophrenia.

Glutamate
The glutamate hypothesis proposes that underactivity of N-methyl-D-
asparate (NMDA) glutamate receptors underpins the symptoms and
cognitive impairment shown in schizophrenia (Downar & Kapur, 2008;
Harrison, 2009; Lin et al., 2011). Low glutamate levels have been found
in the cerebrospinal fluid of people with schizophrenia. Drugs that

Book 1.indb 225 06/03/2012 13:48

 226 C L I N I C A L P S Y C H O L O G Y : A N I N T R O D U C T I O N

reduce the efficiency of NMDA glutamate receptors (such as phencycli-

dine (PCP) or ‘angel dust’) induce psychotic symptoms. Drugs that
increase the efficiency of NMDA glutamate receptors, such as glycine,
alleviate psychotic symptoms, particularly negative symptoms.
Glutamate is the major excitatory neurotransmitter in the central
nervous system and NMDA receptors play a central role in attention,
perception and cognition. Reduced glutamate activity in the prefrontal
cortex may account for negative symptoms and cognitive impairment in
schizophrenia. The NMDA glutamate receptor also plays an important
role in the development of the nervous system, for example by influenc-
ing synaptic pruning, mentioned earlier in the section on neurodevelop-
ment. Thus, dysfunction of NMDA glutamate receptors may account for
some of the neuroanatomical abnormalities associated with schizo-
phrenia.
From a theoretical perspective, the dopamine and glutamate theo-
ries are not sophisticated enough to account for all of the symptoms of
schizophrenia and its response to antipsychotic medication. Contrary to
predictions derived from the dopamine and glutamate hypotheses,
antipsychotic medication does not immediately reduce symptoms,
although it immediately affects neurotransmission. About a third of
patients do not respond to antipsychotic medication. No antipsychotic
medication eliminates all symptoms. Dopamine-2 antagonists primarily
affect positive symptoms and have little impact on negative symptoms.
Drugs that increase the efficiency of NMDA glutamate receptors prima-
rily affect negative symptoms.
Current neurotransmitter-based hypotheses will ultimately be
replaced by more complex and integrated formulations involving a
number of neurotransmitter systems, which can explain the anomalies
listed above.

Two-syndrome hypothesis
In an attempt to integrate results from diverse clinical, genetic and
neurobiological studies, Crow (1985) proposed the two-syndrome
hypothesis. He argued that a distinction may be made between type 1
schizophrenia, which is a genetically inherited disease marked by a
dysregulation of the mesolimbic dopamine system and characterized by
positive symptoms, and type 2 schizophrenia, which is a neurodevelop-
mental disorder arising from prenatal or perinatal insults, resulting in
neuroanatomical abnormalites and marked by chronic negative symp-
toms. Type 1 schizophrenia, he proposed, has an acute onset, clear
precipitants, predominantly positive symptoms, a good response to
antipsychotic medication and good inter-episode adjustment. Type 2
schizophrenia, he argued, is characterized by poor premorbid function-
ing, an insidious onset, a chronic course, neuropsychological deficits,
predominantly negative symptoms and a poor response to medication.
The two-syndrome hypothesis fits a good proportion of available data
but is probably an oversimplification, since many cases show aspects of
both syndromes.

Book 1.indb 226 06/03/2012 13:48

 7 • SCHIZOPHRENIA 227

Antipsychotic medication
The most widely used and most effective pharmacological treatments
for psychosis are dopamine-2 antagonists. A distinction is made
between first- and second-generation, or typical and atypical anti-
psychotic medication. Both are dopamine-2 antagonists. Treatment
with second-generation antipsychotic medications such as risperidone,
olanzapine and clozapine is currently the first-line approach to pharma-
cological intervention for psychotic conditions, although clozapine is
reserved for treatment-refractory cases due to its problematic side-
effects detailed below (Kutscher, 2008; Tandon et al., 2010).
First- and second-generation antipsychotics are equally effective,
but they differ in their side-effect profiles (Dolder, 2008). With regard to
effectiveness, about half to two-thirds of patients respond to anti-
psychotics, and their main effects are on positive symptoms, with
limited effects on negative symptoms and cognitive impairment. With
regard to side-effects, rates of extrapyramidal side-effects (such as
parkinsonism) and tardive dyskinesia (an irreversible neurological
movement disorder) are lower for second-generation antipsychotic
medication. However, for second-generation antipsychotics, obesity,
raised cholesterol and risk of diabetes are more common. In schizo-
phrenia, ideally the lowest possible dose of medication should be used
in order to reduce side-effects and enhance quality of life.
Clozapine is an extremely effective second-generation antipsychotic,
and has a positive impact on suicidal and aggressive behaviour as well
as psychotic symptoms (Sajatovic et al., 2008). However, because of its
dangerous side-effects, clozapine is reserved for use in treatment-
refractory cases or those where there are high risks of suicide or
aggression. Clozapine may cause a severe reduction in white blood cell
count (agranulocytosis), and this can result in severe infections that
may be fatal. For patients on clozapine, routine monitoring of white
blood cell count is best practice.
Typically patients with schizophrenia continue to take antipsychotic
medication throughout their lives. Where patients show low adherence
in taking oral medication daily, they may be administered long-lasting
slow-release depot injections (Cunningham-Owens & Johnstone, 2009;
Leucht et al., 2011).

Stress-vulnerability theory
Stress-vulnerability or diathesis–stress theories propose that schizo-
phrenia occurs when neurobiologically vulnerable individuals are
exposed to psychosocial stress (Walker et al., 2008; Zubin & Spring,
1977). Neurobiological vulnerability may be due to genetic and/or pre-
natal and perinatal factors that impact on the integrity of the central
nervous system.
A substantial body of research shows that the onset, course and
severity of schizophrenia are associated with psychosocial stress and
trauma (Bebbington & Kuipers, 2008; Phillips et al., 2007; Tandon et al.,

Book 1.indb 227 06/03/2012 13:48

 228 C L I N I C A L P S Y C H O L O G Y : A N I N T R O D U C T I O N

2008b; Walker et al., 2008). Physical and sexual child abuse, family
violence and serious injury render people vulnerable to the develop-
ment of psychosis and there is a dose–response relationship, with
greater levels of trauma being predictive of more severe symptoms
(Shevlin et al., 2008). Low socio-economic status, migration to a new
country and living in an urban rather than a rural setting all confer risk
for the development of schizophrenia, and all entail increased stressful
demands on coping resources.
The onset of schizophrenia is typically triggered by a build-up of
stressful life events (illness, injury, life transitions, loss, etc.). Following
the onset of schizophrenia, a number of stresses associated with the
experience of psychosis and the response of others to it may compromise
recovery. For most patients psychotic symptoms are intrinsically
stressful, both as they are occurring and later, during remission, when
insight develops and patients realize that their psychotic symptoms
were due to a major and often life-long psychological disorder.
Highly emotional family responses to psychosis involving criticism
and hostility on one hand or excessive sympathy and emotional over-
involvement on the other (referred to as expressed emotion) are very
stressful and have been shown in numerous studies to reduce
significantly the time to relapse in patients stabilized on antipsychotic
medication (Hooley, 2007). Social stresses resulting from psychosis
including the loss of friendships, the development of a constricted
lifestyle, the experience of stigma and consequent social isolation may
all compromise recovery. Occupational impairment due to psychosis
may lead to a reduction in financial resources and SES, and recovery
may be impeded by these factors. Higher levels of stress are associated
with more severe psychotic symptoms.
HPA axis overactivity is a central aspect of the stress response. The
HPA axis is a major part of the neuroendocrine system involving the
hypothalamus, the pituitary gland located below the hypothalamus, and
the adrenal glands (located on top of the kidneys), which controls stress
reactions and other processes including the immune system. In
schizophrenia, dysregulation of the HPA axis has been found, for
example, in studies of cortisol levels (Bradley & Dinan, 2010; Walker et
al., 2008). Raised cortisol levels indicative of HPA axis hyperactivity are
more common in first-episode psychosis.
Heightened physiological arousal associated with HPA overactivity
probably exacerbates psychotic symptoms, particularly positive symp-
toms such as hallucinations, delusions and thought disorder. Elevated
cortisol arising from HPA axis overactivity compromises the efficiency of
the immune system and increases vulnerability to cardiovascular and
metabolic disease, common in schizophrenia. Such illnesses in turn are
additional stresses that may maintain or exacerbate psychosis.

Multimodal interventions
Multimodal interventions based on the stress-vulnerability model involv-
ing antipsychotic medication and psychological therapies aim to equip

Book 1.indb 228 06/03/2012 13:48

 7 • SCHIZOPHRENIA 229

people with schizophrenia and their families with the resources to con-
trol psychotic symptoms, reduce environmental stress, enhance social
support and work towards recovery. In a large meta-analysis of 106
studies of interventions for schizophrenia, Mojtabai et al. (1998) found
that after an average of 17 months, the relapse rate for patients with
schizophrenia who received psychological therapy plus medication was
20% lower than that of those who received medication only. The relapse
rate in patients treated with medication only was 52% and that for
patients treated with medication combined with psychological therapy
was 32%.
Family therapy, cognitive-behaviour therapy, cognitive remediation
therapy, social skills training and vocational rehabilitation are among
the range of evidence-based psychological interventions that have
been developed to help people with schizophrenia and their families
achieve these aims (Kern et al., 2009; Tandon et al., 2010). Brief
descriptions of these are presented below.

Family therapy
About half of medicated clients with schizophrenia relapse, and relapse
rates are higher in unsupportive or stressful family environments, char-
acterized by high levels of expressed emotion which involves criticism,
hostility or emotional over-involvement (Barrowclough & Lobban, 2008).
High levels of expressed emotion arise from family members’ apprais-
als of the controllability of psychotic symptoms. Family members who
express high levels of criticism or hostility tend to view patients as hav-
ing a high degree of control over their psychotic symptoms and there-
fore hold patients responsible for their difficulties. In contrast, those who
express high levels of emotional over-involvement tend to attribute
patients’ symptoms to uncontrollable factors and so view patients as
helpless victims of a psychiatric illness. Low expressed emotion occurs
where family members have an accurate understanding of psychosis
and skills for managing the condition within a family context.
The aim of psychoeducational family therapy is to reduce family
stress and enhance family support so as to delay or prevent relapse
and rehospitalization, and also to promote recovery. This is achieved by
helping family members understand schizophrenia within a stress-
vulnerability framework and develop knowledge and skills to manage
the condition. Psychoeducational family therapy may take a number of
formats including therapy sessions with single families; therapy sessions
with multiple families; group therapy sessions for relatives; or parallel
group therapy sessions for relative and patient groups.
Family therapy may be conducted in clinical settings or in patients’
homes. It involves psychoeducation based on the stress-vulnerability
models of schizophrenia with a view to helping families understand and
manage the symptoms of schizophrenia, antipsychotic medication,
related stresses and early warning signs of relapse. Psychoeducational
family therapy also helps families develop communication and problem-
solving skills, reduce destructive expressions of anger and guilt, and

Book 1.indb 229 06/03/2012 13:48

 230 C L I N I C A L P S Y C H O L O G Y : A N I N T R O D U C T I O N

promote self-care among non-symptomatic family members (Falloon et

al., 1993; Kuipers et al., 2002; McFarlane, 2004).
Meta-analyses have shown that compared with medication alone,
multimodal programmes including psychoeducational family therapy
and medication lead to lower relapse and rehospitalization rates, and
improved medication adherence (Pfammatter et al., 2006). Effective
family therapy spans about 9 months, and longer, more intense
programmes are more effective.

Cognitive-behaviour therapy (CBT)

Beck has proposed an integrative model to explain the development of
symptoms in schizophrenia and then developed a cognitive-behavioural
approach to address these symptoms based on this model (Beck et al.,
2011). This is diagrammed in Figure 7.2. According to the model, when
people with a neurobiological vulnerability to schizophrenia are exposed
to stress, this increases their physiological arousal (HPA axis hyperac-
tivity). There is a consequent reduction in their available cognitive
resources, which increases their experience of psychotic symptoms.
In early life, exposure to stressful events and trauma contributes to
the development of schemas containing dysfunctional attitudes and
beliefs, as well as cognitive biases to make inaccurate inferences.

Figure 7.2 Beck’s integrated model of schizophrenia for use in CBT (adapted from Beck, A., Rector, N., Stolar, N. &
Grant, P. (2011). Schizophrenia: Cognitive theory, research and therapy. New York: Guilford)

Book 1.indb 230 06/03/2012 13:48

 7 • SCHIZOPHRENIA 231

These are activated by exposure to stress in later life and inform the
content of hallucinations and delusions. Exposure to stress and related
hyperarousal in adulthood sets the scene for the development of
positive symptoms, negative symptoms and disorganization. This is
because at these times negative schemas and related cognitive biases
are reactivated. Also, limited cognitive resources are available to check
out the validity of inferences made about the environment and to
manage day-to-day problem-solving.
Within CBT, the symptoms of schizophrenia are viewed as being on
a continuum with normal experience. This view is consistent with the
finding that normal population surveys show that up to 25% of people
have auditory hallucinations, many hold strange, unfounded beliefs (for
example about horoscopes and faith healing), and under sufficient
stress or exhaustion disorganized thinking and inactivity may occur.
Patients are helped to view all of their symptoms as on a continuum with
normal experience, as arising within the context of a stress-vulnerability
model, and as being controllable through the use of cognitive-
behavioural strategies and medication. A fundamental premise of CBT
is that activating events give rise to negative automatic thoughts
(informed by beliefs in negative schemas), which in turn affect mood,
behaviour and the strength of beliefs within negative schemas.
From a CBT perspective, hallucinations are similar to negative auto-
matic thoughts in depression or intrusive thoughts typical of obsessive
compulsive disorder. However, they are experienced as loud, external,
‘real’ and true because people with schizophrenia have a propensity for
auditory imagery, a tendency to attribute unusual experiences to exter-
nal factors (an external bias), and a tendency towards premature clo-
sure and deficient reality testing. That is, they hear their negative
automatic thoughts as loud, attribute them to an external source, and do
not check out the validity of their beliefs against alternatives, for exam-
ple that these are their own loud thoughts, the content of which may not
be valid.
Auditory hallucinations are often incorporated into delusional systems
that may maintain them. For example, a patient who hears a critical,
omniscient controlling voice may develop paranoid delusions about
being persecuted by the owner of the voice, which in turn may raise
their arousal level and so make further hallucinations more likely.
Patients may try to control voices by engaging in safety behaviours
such as isolating themselves. These safety behaviours may reduce
hallucinations in the short term, but in the long term may lead to stressful
loneliness and this may cause further hallucinations. In CBT patients
learn to identify and control stresses that trigger auditory hallucinations,
to give up safety behaviours that maintain hallucinations and to
reappraise the source of their ‘voices’ and the content of what they say.
From a CBT perspective, delusions are beliefs or inferences about
events or experiences (including hallucinations) that in turn affect mood
and behaviour, in the same way that negative automatic thoughts and
dysfunctional beliefs affect mood and behaviour in depression and
anxiety disorders. However, in schizophrenia, delusions develop within

Book 1.indb 231 06/03/2012 13:48

 232 C L I N I C A L P S Y C H O L O G Y : A N I N T R O D U C T I O N

the context of markedly reduced cognitive resources which limit patients’

capacity to modify them. The content of delusions is influenced by
dysfunctional attitudes and assumptions contained in negative schemas,
by hallucinations and by cognitive biases. These include a strong
egocentric or self-referential bias, a bias towards external causation of
subjective experiences, and a bias towards indiscriminate attribution of
extreme positive or negative intentions to others. Thus, a patient who
experiences an unusual sensation on the skin may interpret this as
due to aliens activating subcutaneous microchips to try to control
their behaviour. Delusions are maintained by the belief that they
accurately represent reality rather than being testable inferences; by a
bias towards focusing on information that confirms the reality of
delusions and ignoring disconfirmatory evidence; by engaging in safety-
seeking behaviours that prevent the truth of delusions from being tested;
and by cognitive resource-sparing strategies such as jumping to
conclusions.
In CBT patients are helped to collect evidence to test out the validity
of their delusions, starting with the least strongly held ones, and then to
test out the validity of the non-delusional schemas that underpin these.
In order to test out delusional beliefs, patients are also helped to give up
safety behaviours, such as locking the door and disconnecting the
phone when strangers are outside their houses, in the case of people
with persecutory delusions.
Within CBT, formal thought disorder (characterized by derailment,
thought blocking, etc.) is conceptualized as a problematic thinking and
speaking pattern that occurs due to limited cognitive capacity arising
from stress within the context of a genetic vulnerability to schizophrenia.
It is analogous to stuttering. The primary CBT intervention is to help
patients recognize thought disorder when it occurs, the stressful situ-
ations in which it occurs, and the negative automatic thoughts that give
rise to it. They are then helped to challenge these negative automatic
thoughts and so reduce the stress associated with thought disorder.
Within CBT, negative symptoms (blunting of affect, alogia and
avolition) are conceptualized as ways of coping with the experience of
having limited cognitive resources and so limited expectations for
success or pleasure, and problematic delusional beliefs or hallucinations.
If a patient finds it difficult to think clearly, expects little success or
pleasure, believes that his actions are being controlled by others and
hears voices telling him that he is useless, then it is understandable that
he will be relatively inactive. In CBT behavioural experiments are set up
in which patients set goals, engage in activities and monitor their
experience of pleasure, success and self-control as they achieve goals.
Controlled trials and meta-analyses show that CBT has a moderate
effect, particularly on delusions and hallucinations, in medicated
patients whose positive symptoms are not fully controlled by anti-
psychotic medication (Pfammatter et al., 2006; Tai & Turkington, 2009;
Tandon et al., 2010). Effective CBT spans about 9 months, and longer,
more intense programmes are more effective.

Book 1.indb 232 06/03/2012 13:48

 7 • SCHIZOPHRENIA 233

Cognitive remediation
Neuropsychological investigations have shown that about three-
quarters of people with schizophrenia show significant cognitive deficits
(Palmer et al., 2009; Savla et al., 2008). On average the overall IQ of
people with schizophrenia is about one standard deviation below the
normative mean, although there is considerable heterogeneity between
persons and within cases over time.
In schizophrenia most cognitive functions are affected, including
attention, memory, processing speed, cognitive flexibility, social cogni-
tion and executive function. Episodic memory and processing speed
are the areas where greatest deficits occur. While about a quarter of
people with schizophrenia show no cognitive deficits, a distinct subgroup
show very severe general cognitive deficits (similar to Crow’s (1985)
type II schizophrenia or Kraepelin’s (1899) dementia praecox), and the
remainder show variable patterns of specific cognitive deficits (more in
keeping with Bleuler’s (1911) views on ‘loosening of associations’ and
other specific deficits in schizophrenia).
Many people with schizophrenia show mild premorbid cognitive defi-
cits, followed by a steep decline in cognitive functioning during psychotic
episodes, with some amelioration of cognitive deficits during remission
and relative stability over the long term. In many cases cognitive deficits
have a significant impact on social and occupational adjustment and ill-
ness management, and response to psychosocial interventions such as
social skills training and supported employment (Kurtz, 2011).
In schizophrenia, cognitive deficits are subserved by the many
structural and functional neurobiological abnormalities mentioned in
earlier sections. Cognitive rehabilitation therapy is a set of cognitive
drills that aim to help patients in remission enhance their attention,
memory and executive functions or develop strategies for compensating
for their cognitive deficits so that they can better achieve their recovery
goals (Tomás et al., 2010). In this type of treatment patients engage in
regular computer-based or paper-and-pencil-based training tasks and
puzzles a number of times each week over a period of months. Specific
tasks are designed to improve specific targeted deficits such as memory.
Task difficulty is pitched so that high success rates are achieved or
errorless learning occurs. Over time patients build up their cognitive
skills or develop strategies for compensating for them.
With compensatory approaches, patients learn strategies or use
memory prompts and other devices to make up for their cognitive defi-
cits. Meta-analytic studies of the effectiveness of cognitive remediation
report moderate effect sizes on cognitive test performance and indices
of daily functioning (Medalia & Choi, 2009; Pfammatter et al., 2006;
Tandon et al., 2010).

Social skills training

People with schizophrenia typically show deficits in accurately perceiving
social situations, understanding and planning what to do in them, and

Book 1.indb 233 06/03/2012 13:48

 234 C L I N I C A L P S Y C H O L O G Y : A N I N T R O D U C T I O N

then responding in a socially appropriate way. This renders them

vulnerable to engaging in stressful social interactions, to rejection, to
avoidance of further social interaction, and to social isolation (Fett et al.,
2011; Walker et al., 2004). The aim of social skills training is to enhance
social competence and so prevent social isolation.
Social skills training is usually offered within a group therapy context,
and involves the development of communication, conversation, assert-
iveness, medication management and social problem-solving skills.
Modelling, rehearsal, shaping and reinforcement are used during the
training process. The main emphasis is on practising skills rather than
talking about them (Bellack et al., 2004; Tenhula & Bellack, 2008).
Meta-analyses show that compared with medication alone, multimodal
programmes that include social skills training and medication lead to
significant improvements in social skills in service users with schizo-
phrenia (Kurtz & Mueser, 2008; Pfammatter et al., 2006).

Vocational rehabilitation
Unemployment is a highly prevalent problem in schizophrenia which
vocational rehabilitation aims to address (Becker, 2008). Effective
vocational rehabilitation involves assessment, job searching, matching
available jobs to client preferences, rapid placement in competitive
employment (rather than sheltered workshops), and the provision of
individualized vocational support and training while service users are in
employment (rather than beforehand). Systematic reviews and meta-
analyses consistently show that compared with traditional approaches,
such as sheltered workshop placement, supported employment doubles
the chances of engaging in long-term, paid, competitive employment
(Becker, 2008; Cook & Razzano, 2005). Employed service users
typically show improved self-esteem and better symptom control.

The recovery model

The recovery movement is being adopted as an overarching framework
for mental health services internationally (Roe & Davidson, 2008; Slade,
2009). Kraepelin’s (1899) conceptualization of schizophrenia as a neu-
rological disorder with a chronic declining course led to the develop-
ment of long-term institutional care and a reliance on physical treatments,
including medication, as the main interventions for schizophrenia during
much of the 20th century. This in turn led to the institutionalization of
‘psychiatric patients’ and the gradual erosion of their civil rights within
institutions. It also led to their stigmatization and marginalization within
society. A further consequence of Kraepelin’s position was a reduced
emphasis on the role of trauma and stress in the aetiology of schizo-
phrenia and the value of psychosocial interventions in its treatment. It
was in response to this position that the recovery model emerged at the
end of the 20th century and the dawn of the new millennium.
The recovery movement initially arose from service user-groups and
mental health professionals involved in rehabilitation, but more recently

Book 1.indb 234 06/03/2012 13:48

 7 • SCHIZOPHRENIA 235

has become adopted internationally as a best practice framework for

service delivery. The model conceptualizes the recovery process as a
personal journey, and privileges the concepts of optimism, well-being,
personal strengths, supportive relationships, collaboration, personal
choice, adaptive coping, developing a meaningful life, civil rights,
empowerment and inclusion.
The recovery model has been inspired by longitudinal research
which showed that chronic decline in schizophrenia was not inevitable
(Häfner & an der Heiden, 2008), that trauma and stress play a role in
the aetiology of schizophrenia (Bebbington & Kuipers, 2008), and that
psychosocial interventions have an important place in facilitating
recovery from psychosis (Mojtabai et al., 1998). The recovery movement
embraced these research findings, placing a strong emphasis on
professionals working collaboratively with service users to help them
achieve their preferred goals. There was a shift in emphasis from
institutional to community care, and from remediating patient deficits to
fostering service-user strengths. There was also an emphasis on the
civil rights of patients to make choices about their preferred treatments
and to have an inclusive place in society. The recovery movement has
created a context for the development of innovative community-based
approaches to mental health service delivery, such as the strengths-
based case management model and assertive community treatment.

Strengths-based case management

The strengths-based case management model was developed by
Charles Rapp in the Kansas School of Social Welfare (Rapp & Goscha,
2006, 2008). With this model professionals work in partnership with
clients to help them recover. Thus, the strengths model falls within the
overall framework of the recovery model.
The model is guided by six principles. First, people with schizophrenia
can recover and transform their lives. Second, the primary focus of
clinical work is on strengths rather than deficits. Third, the community is
a source of resources that may facilitate recovery. Fourth, case
managers are guided by service users’ preferences, and implement
plans only with their approval. Fifth, the community is the primary setting
for case management. Sixth, a strong therapeutic relationship between
the case manager and service user is essential for recovery.
There are four stages in the model: the engagement phase, strengths
assessment, creating personal plans and resource acquisition, and
disengagement. In the engagement phase the therapist forms a strong
and respectful, collaborative therapeutic alliance with the client.
Assessment focuses predominantly on evaluating clients’ personal
strengths, and strengths they can access in their environments.
Strengths are identified in domains of the daily living situation, finances,
education or work, social support, health, leisure, recreational activities
and spiritual or cultural activities. Strengths assessment forms the basis
for the client and case manager to set goals and plan an agenda of
things clients wish to achieve. To address this agenda, clients are
helped to acquire the necessary community resources and supports for

Book 1.indb 235 06/03/2012 13:48

 236 C L I N I C A L P S Y C H O L O G Y : A N I N T R O D U C T I O N

implementing their recovery plans which will increase their reintegration

into community life. As clients’ autonomy increases and is sustained,
and as clients come to live more independently in the community, the
process of gradual disengagement is negotiated.
A series of empirical evaluations has shown that this strengths
model, when implemented with adequate fidelity, is more effective than
routine psychiatric services in promoting recovery from schizophrenia
(Rapp & Goscha, 2008).

Assertive community treatment

Assertive community treatment was developed by Leonard Stein and
Mary Ann Test at the Mendota Mental Health Institute in Madison,
Wisconsin to address the challenges of deinstitutionalization. It is an
integrated community mental health service delivery model in which
hard-to-reach people with schizophrenia receive intensive, continuous
individualized treatment, rehabilitation, and support services from
community-based multidisciplinary teams in which team members carry
small case loads (DeLuca et al., 2008). Assertive community treatment
aims to promote rehabilitation and recovery, and to prevent homeless-
ness and unnecessary hospitalization. There is a major focus on helping
service users develop the skills to manage everyday problems of living.
All therapies and services are provided by team members and are not
‘farmed out’ to other professionals.
Multimodal treatment in which evidence-based pharmacological and
psychosocial therapies are provided in an integrated way is central to
this service-delivery model. Thus, evidence-based medication algo-
rithms, adherence programmes, psychoeducational family therapy,
cognitive behaviour therapy, supported employment and so forth can
be offered within the context of assertive community treatment pro-
grammes. Teams help service users to avoid crisis situations, and
where necessary provide rapid response crisis intervention on a 24/7
basis to prevent unnecessary hospitalizations. Services are provided to
clients in their homes or elsewhere in the community, on a time-
unlimited basis. Team composition, training, adherence to assertive
community treatment programme fidelity guidelines and ongoing super-
vision are essential for the effectiveness of this approach to service
delivery.
In a meta-analysis of six randomized controlled trials, Coldwell and
Bender (2007) found that assertive community treatment led to a 37%
reduction in homelessness and a 26% improvement in psychiatric
symptom severity compared with standard case management. In a
systematic review of 25 randomized controlled trials, Bond et al. (2001)
concluded that assertive community treatment substantially reduces
psychiatric hospital use, increases housing stability, and moderately
improves symptoms and subjective quality of life. It is highly successful
in engaging service users in treatment.
Bond et al. (2001) found that the more closely case management
programs followed assertive community treatment principles, the better
were the outcomes. While assertive community treatment services are

Book 1.indb 236 06/03/2012 13:48

 7 • SCHIZOPHRENIA 237

costly, these costs are offset by a reduction in hospital use by service

users with a history of extensive hospital use. In meta-analysis of 44
studies involving over 6,000 service users, Ziguras and Stuart (2000)
found that assertive community treatment was more effective than
treatment as usual in reducing care costs and family burden, and in
improving family satisfaction with services.

Assessment
The assessment and treatment of schizophrenia is ideally conducted by
multidisciplinary teams. The early detection and treatment of psychosis
is critical because better outcomes occur in cases where duration of
untreated psychosis is brief (Tandon et al., 2008a). For hard-to-reach
cases, the adoption of an assertive outreach approach is optimal
(DeLuca et al., 2008).
Typically, the preliminary assessment and management of acute
psychotic episodes is managed by psychiatrists and psychiatric nurses.
Once positive symptoms have been managed with antipsychotic
medication, a broader-based assessment is conducted to guide long-
term case management. Through careful clinical interviewing of patients
and members of their families, the symptoms of schizophrenia and
relevant history are obtained. A diagnosis is given in accordance with
the criteria outlined in ICD-10 and DSM-IV-TR, given in Table 7.1, and
a formulation explaining the symptoms entailed by the diagnosis is
developed in which the relevant predisposing, precipitating, maintaining
and protective factors are outlined. A general clinical formulation model
is given in Figure 7.3.
From Table 7.1 it may be seen that there are differences between
DSM and ICD criteria. For a DSM diagnosis, impairment in functioning
must have been present for 6 months, whereas for an ICD diagnosis
symptoms must have been present for at least a month. The psychotic
disorders module of the Structured Clinical Interview for DSM-IV Axis I
Disorders is a widely used and well-validated structured interview for
diagnosing schizophrenia (SCID, First et al., 1996). Psychotic symptom
severity may be initially rated and regularly monitored with the Brief
Psychiatric Rating Scale (BPRS, Lukoff et al., 1986) or the Positive and
Negative Symptom Scale (PANSS, Kay et al., 1987). With the BPRS
and PANSS, the severity of symptoms such as delusions and
hallucinations are rated on Likert scales on the basis of observations of
patients’ behaviour and their responses to questions.
Overall functioning may be monitored periodically with the clinician-
rated Global Assessment of Functioning scale (GAF, Luborsky, 1962).
On the GAF the patients’ overall functioning is rated on a single 100-
point rating scale. The social needs of service users indicating the
resources required to help them adjust within the community may be
assessed with the short version of the Camberwell Assessment of Need
(CAN, Slade et al., 1999; Trauer et al., 2008). This covers issues such
as mental and physical health, drug use, social relationships,
accommodation, transport, budgeting, and activities of daily living. The

Book 1.indb 237 06/03/2012 13:48

 238 C L I N I C A L P S Y C H O L O G Y : A N I N T R O D U C T I O N

Figure 7.3 General formulation model for schizophrenia

scale also offers a framework for identifying needs that have and have
not been met.
The use of the CAN as a central part of assessment is consistent
with Rapp’s strengths-based model of case management mentioned
earlier (Rapp & Goscha, 2006). In research studies, expressed emotion
of family members towards patients, which has an impact on their
relapse rates, is assessed by the Camberwell Family Interview (CFI,
Leff & Vaughn, 1985). Because this instrument is too cumbersome for
use in routine clinical practice, Hooley and Parker (2006) recommend
asking patients to rate how critical family members are of them on a
10-point scale, an assessment procedure that correlates highly with
expressed emotion assessed by the CFI.
Service users’ assessments of their recovery journey may be regu-
larly monitored with the Recovery Assessment Scale (RAS, Corrigan et
al., 2004). This self-report instrument assesses hope, meaning of life,
quality of life, symptoms and empowerment. During the process of
assessment and treatment, patients and family members may be invited
to keep daily records of medication adherence, fluctuations in symp-
toms, distress, beliefs, and the circumstances preceding and following
these fluctuations. These idiographic ratings are useful for fine-tuning
ongoing family therapy, CBT and other psychosocial interventions.

Book 1.indb 238 06/03/2012 13:48

 7 • SCHIZOPHRENIA 239

Treatment
The optimal treatment for schizophrenia is multimodal and includes
both antipsychotic medication and psychological therapies (Tandon et
al., 2010). Currently second-generation antipsychotic medications are
the pharmacological treatments of choice, for reasons stated earlier in
this chapter. Evidence-based psychological therapies include family
therapy, cognitive-behaviour therapy, cognitive remediation therapy,
social skills training and vocational rehabilitation, all of which have been
described above.
Treatment programmes should be offered in a carefully planned and
co-ordinated way by multidisciplinary teams with adequate training in
these evidence-based pharmacological and psychological interventions.
Treatment packages should be individually tailored to take account of
service users’ clinical needs as identified in the case formulation and
personal preferences as expressed during assessment, in line with the
recovery model orientation. In all cases psychoeducational family ther-
apy to help service users and their families understand schizophrenia
and to promote medication adherence is essential, but more intensive
family therapy is warranted where family members show high levels of
criticism, hostility or emotional overinvolvement. CBT is particularly use-
ful for the management of residual positive symptoms that are not con-
trolled by medication, or to facilitate a reduction in the medication dosage
required to control positive symptoms. To be optimally effective, both
family therapy and CBT should be offered for about 9 months.
Cognitive remediation therapy and social skills training are appropri-
ate where it is clear that significant cognitive and social skills deficits are
present. Vocational rehabilitation is appropriate where service users
require employment. Where there is comorbid alcohol or drug misuse or
obesity (a side-effect of some antipsychotic medications), evidence-
based treatment for these problems should be integrated into the over-
all treatment package (Kavanagh, 2008).
The development of a strong therapeutic alliance and the adoption of
an approach that modifies intrapsychic and interpersonal maintaining
factors underpins effective psychosocial interventions for schizophre-
nia. This overall approach to the management of schizophrenia is
broadly consistent with international best practice guidelines (American
Psychiatric Association, 2004b; Buchanan et al., 2010; Dixon et al.,
2010; NICE, 2009b).

Controversies
There are many controversies surrounding schizophrenia. These cen-
tre on issues such as the validity of the schizophrenia construct, the
validity of the schizotypy dimensional conceptualization of psychosis,
the idea that schizophrenia reflects a split personality, the view that
diagnosing schizophrenia is an act of oppression, the role of the family
in the aetiology of schizophrenia, and the psychoanalytic treatment of
psychosis. These issues will be briefly considered below.

Book 1.indb 239 06/03/2012 13:48

 240 C L I N I C A L P S Y C H O L O G Y : A N I N T R O D U C T I O N

Validity of the schizophrenia construct

There is ongoing controversy about the validity of the construct of
schizophrenia. At one extreme schizophrenia is conceptualized as a
discrete biomedical disease-like entity – a ‘mental illness’ – with clearly
defined symptoms, arising primarily from genetic and neurobiological
factors, and requiring treatment mainly with antipsychotic medication.
This is the prevailing position within mainstream psychiatry following
the tradition founded by Emil Kraepelin (1899) and currently expressed
most authoritatively in works such as the DSM-IV-TR and mainstream
psychiatry textbooks.
In the UK, critics of this position include Mary Boyle (2002) and
Richard Bentall (2003). They point out that there is scant evidence to
support the view that schizophrenia is a biomedical ‘mental illness’, and
marshal many different arguments to support this position. The
symptoms that define the illness are not distributed within the population
in the way that symptoms of diseases such as cancer or heart disease
are. They are distributed as dimensions, not categories. Many so-called
normal people have delusions and hallucinations. The supposed
biological causes of schizophrenia (genetic vulnerability, structural and
functional brain abnormalities, etc.) are not present in all cases or
absent in all non-cases. Not all cases of schizophrenia follow a distinct
uniform course. Not all cases of schizophrenia respond to biomedical
treatment. Some people with psychotic symptoms recover without
biomedical intervention either spontaneously or through engaging in
psychological therapy. Bentall (2003) and Boyle (2002) support all of
these arguments with research evidence (some of which has been
covered in this chapter) and conclude that the construct of schizophrenia
as a ‘mental illness’ has no validity.

Schizotypy
There is ongoing controversy about the validity of categorical and
dimensional models of psychotic processes (Linscott & van Os, 2010).
The schizotypy construct has been proposed by researchers such as
Gordon Claridge in the UK and Mark Lenzenweger in the US as a
dimensional alternative to the prevailing categorical conceptualization
of schizophrenia (Lenzenweger, 2010).
According to the categorical view, which derives from Kraepelin’s
(1899) work and is enshrined in the ICD and DSM classification systems,
schizophrenia is a discrete diagnostic category. Within a population, a
proportion of people have schizophrenia and the rest do not. In contrast
to this prevailing categorical view is the schizotypy hypothesis. This
proposes that anomalous sensory experiences, peculiar beliefs and
disorganized thinking are present in an extreme form in schizophrenia
as hallucinations, delusions and thought disorder, but these processes
are on a continuum with normal experience – a position originally
advocated by Bleuler (1911).
A variety of measures of schizotypy have been developed which
assess this continuum, and research programmes involving these

Book 1.indb 240 06/03/2012 13:48

 7 • SCHIZOPHRENIA 241

measures have provided support for the construct (Lenzenweger,

2010). For example, research on schizotypy shows that the continuum
may be composed of subdimensions; the continuum extends from
normal to psychotic experiences; schizotypy is heritable; and people
with high schizotypy scores but who are not psychotic show attentional,
eye-movement and other neuropsychological abnormalities associated
with schizophrenia.

Schizophrenia and split personality

In popular culture schizophrenia is often used to refer to split personality.
For example, in a UK survey of a national random sample Luty et al.
(2006) found that 40% of respondents equated split or multiple
personality with schizophrenia. However, in psychology, it is clear from
this chapter that schizophrenia does not refer to such a condition. The
closest scientific equivalent to split personality is a condition referred to
as multiple personality disorder (MPD) in ICD-10 and dissociative
identity disorder (DID) in DSM-IV-TR. The central feature of MPD or
DID is the apparent existence of two or more distinct personalities within
the individual, with only one being evident at a time. Each personality
(or alter) is distinct, with its own memories, behaviour patterns and
interpersonal style. Commonly, the host personality is unaware of the
existence of the alters and these vary in their knowledge of each other.
A developmental diathesis–stress model of dissociative identity
disorder is now widely accepted (International Society for the Study of
Trauma and Dissociation, 2011). Available evidence suggests that the
capacity to dissociate is normally distributed within the population.
People who have a high degree of this trait, when exposed to extreme
trauma (such as repeated severe child abuse) during early childhood
may cope by dissociating their consciousness from the experience of
trauma. They achieve dissociation by entering a trance-like state.
Where repeated trauma occurs in early childhood, and dissociation
is repeatedly used as an effective distress-reducing coping strategy, the
process of dissociation is negatively reinforced. That is, the habit of
dissociation is strengthened because it brings relief from distress during
trauma exposure. Furthermore, the process of dissociation allows the
child to preserve relationships with abusive or inadequate caregivers
during the periods when traumatic abuse is not occurring. Eventually,
sufficient experiences become dissociated to constitute a separate
personality. These may be activated in later life at times of stress or
trauma or through suggestion in hypnotic psychotherapeutic situations.
Psychological treatment commonly involves helping clients integrate
the multiple personalities into a single personality and develop non-
dissociative strategies for dealing with stress. Unlike schizophrenia,
psychotropic medication is of little value in treating the core symptoms
of multiple personality disorder.
In the ICD and DSM, MPD and DID are classified with other disso-
ciative conditions including dissociative amnesia (inability to recall
events following a trauma); dissociative fugue (sudden unexpected

Book 1.indb 241 06/03/2012 13:48

 242 C L I N I C A L P S Y C H O L O G Y : A N I N T R O D U C T I O N

travel away from the customary place of activities coupled with confu-
sion or amnesia for aspects of one’s identity following a trauma); and
depersonalization disorder (a sense of being out of one’s body following
trauma). People who have a strong capacity to dissociate may develop
one of the dissociative disorders rather than PTSD following trauma.
Dissociative phenomena fall on a continuum, with tip-of-the-tongue
experiences being a mild dissociative phenomenon, hypnotic trance
states being a more pronounced dissociative condition; depersonaliza-
tion disorder and dissociative amnesia and fugue being more extreme
forms of dissociation; and MPD or DID being the most extreme form of
dissociation. More extreme dissociative conditions develop when the
person has a strong capacity to dissociate and is exposed repeatedly to
severe trauma.

Diagnosis as oppression
The prevailing professional view within the field of mental health is that
a diagnosis of schizophrenia reflects the assignment of a person with
an objectively verifiable condition to a valid diagnostic category based
on careful and unbiased observation, and that this process is conducted
in the patient’s best interests. However, an alternative viewpoint most
strongly presented by Thomas Szasz (2010) since the early 1960s is
that diagnosis is an act of oppression, because it paves the way for
involuntary hospitalization and involuntary treatment.
Szasz, a US psychiatrist, argues that the process of diagnosing a
person with schizophrenia is a covert, politically oppressive transaction
in which a deviant or disadvantaged person is subjected to a process of
social control. This is offered as one explanation for the greater rates of
schizophrenia among ethnic minorities (particularly African Americans)
and people from low socio-economic groups. Furthermore, exponents
of this position argue that schizophrenia is not a valid diagnostic
category, but an invalid fabrication constructed to exert social control
over deviant people who do not conform to societal norms.

Schizophrenia as a sane reaction to an insane situation

R. D. Laing (2009), a Scottish psychiatrist and psychoanalyst, in the
1960s and 1970s strongly opposed the view that schizophrenia was a
genetically based medical condition requiring treatment with anti-
psychotic medication. He also opposed the prevailing orthodoxy that
the contents of delusions and hallucinations were incoherent. Laing
proposed that the contents of psychotic symptoms were understand-
able as psychological responses to complex, confusing, conflicting and
powerful parental injunctions that left no scope for more rational and
adaptive attempts at communication. That is, he viewed schizophre-
nia as ‘a sane reaction to an insane situation’.
For Laing, effective treatment involved creating a context within
which insight into the complex family process and the psychotic
response to this could be facilitated. The role of the therapist was to

Book 1.indb 242 06/03/2012 13:48

 7 • SCHIZOPHRENIA 243

understand the content of patients’ delusions and hallucinations, and

interpret these for the patient as responses to conflicting parental
injunctions. The experience of psychosis and recovery was a difficult
journey from which the person could emerge with new and valuable
insights. Laing advocated drug-free psychotherapeutic treatment for
psychosis within the context of a therapeutic community. He founded
the Philadelphia Association in the UK, which continues to run
therapeutic communities influenced by Laing’s ideas.
Laing’s view on the exclusive role of the family in the aetiology of
schizophrenia and the exclusive use of psychotherapy in its treatment
has not been supported by subsequent research. Genetic factors play a
major role in the aetiology of schizophrenia, and antipsychotic medi-
cation reduces positive symptoms in two-thirds of cases (Ritsner &
Gottesman, 2011; Tandon et al., 2010). However, research findings
have supported the hypothesis that the family does affect the psychotic
process and psychotherapy has a place in the management of
psychosis. Personal trauma, including child abuse increases the risk of
psychosis, stressful life events including those within the family can
precipitate an episode of psychosis, and high levels of family criticism,
hostility and emotional overinvolvement increase the risk of relapse
(Bebbington & Kuipers, 2008; Hooley, 2007; Shelvin et al., 2008).
Family therapy delays relapse in families characterized by high levels of
expressed emotion and cognitive behaviour therapy which stresses the
idea that psychotic symptoms are understandable and on a continuum
with normal experience can help patients control these symptoms
(Tandon et al., 2010).

Psychoanalysis and psychosis

There is controversy over the value of psychoanalysis in understanding
and treating psychosis. The developers of the influential PORT (Patient
Outcomes Research Team) guidelines, on the basis of a literature
review, concluded that psychoanalytically based psychotherapy has no
place in the treatment of schizophrenia (Lehman & Steinwachs, 1998).
In contrast, Gottdiener (2006), in a review of results of controlled trials
and meta-analytic results, concluded that psychodynamic psychotherapy
was as effective as CBT in the treatment of medicated patients with
schizophrenia.
Freud and later psychoanalysts attributed the development of
schizophrenia to adverse early family experiences, and many analysts,
like Freud, acknowledged that treatment of psychosis with psychoanalytic
methods was problematic because psychotic patients did not develop
transference to the analyst in the same way that neurotic patients did
(Lucas, 2009). Freud never treated a psychotic patient and was
pessimistic about the relevance of psychoanalysis to psychosis; this
attitude deterred many analysts from attempting to treat schizophrenia.
However, there were exceptions. Frieda Fromm-Reichman in the US
and Wilfred Bion in the UK developed supportive psychodynamic psy-
chotherapy approaches to treating psychosis (Lucas, 2009). Currently,

Book 1.indb 243 06/03/2012 13:48

 244 C L I N I C A L P S Y C H O L O G Y : A N I N T R O D U C T I O N

despite Gottdiener’s (2006) supportive review of psychodynamic treat-

ment outcome studies, psychoanalytically informed interventions are
rarely used to treat schizophrenia.

Summary
Schizophrenia refers to a complex group of psychotic disorders
that affects about 1% of the population. The condition is marked
by positive symptoms such as delusions and hallucinations,
negative symptoms such as flattened affect, alogia and avoli-
tion, and disorganized speech and behaviour. In the past, a
broad definition of schizophrenia was used in North America
and a narrow definition used in Europe, but there is now consid-
erable international agreement on a narrow-band definition of
schizophrenia. In the DSM and ICD classification systems dis-
tinctions are made between four main subtypes of schizophre-
nia: paranoid, catatonic, hebephrenic or disorganized, and
undifferentiated. Schizophrenia, schizophreniform disorder,
schizoaffective disorder and schizotypal, schizoid and paranoid
personality disorders constitute the schizophrenia spectrum
disorders which share a similar genetic aetiology and treatment
response.
Schizophrenia typically has its onset in late adolescence or
early adulthood and follows a chronic relapsing course,
although up to 20% of patients show complete remission. A
favourable outcome is associated with good premorbid adjust-
ment, and a brief duration of untreated psychosis character-
ized by an acute onset in response to precipitating stressful life
events, a family history of affective disorder and a favourable
life situation to return to following discharge from hospital.
The greatest risk factor for schizophrenia is a family history of
psychosis.
Currently there is wide acceptance of a stress-vulnerability
model of schizophrenia whereby the condition is proposed to
arise when a genetically vulnerable individual is exposed to
significant life stress. Life stresses include predisposing
trauma, precipitating acute stressful life events and maintaining
chronic stressful family interactions.
Neurobiological research has identified a number of candi-
date genes and structural and functional brain abnormalities
associated with schizophrenia. The two-syndrome hypothesis
offers a simplified way to integrate relevant findings on research
into the biological origins of schizophrenia. This hypothesis
entails the view that a distinction may be made between type 1
schizophrenia, which is a genetically inherited disease marked
by a dysregulation of the dopaminergic system and character-
ized by positive symptoms, and type 2 schizophrenia, which is

Book 1.indb 244 06/03/2012 13:48

 7 • SCHIZOPHRENIA 245

a neurodevelopmental disorder arising from prenatal or perina-

tal insults resulting in neuroanatomical abnormalities marked
by chronic negative symptoms.
Comprehensive multidisciplinary assessment and treatment
with multimodal evidence-based interventions is internationally
accepted as best practice in cases of schizophrenia. Individually
tailored multimodal treatment programmes based on the
stress-vulnerability model should include both antipsychotic
medication and evidence-based psychological therapies such
as family therapy, CBT, cognitive rehabilitation, social skills
training, and vocational rehabilitation.
Controversies about schizophrenia concern issues such as
the validity of the schizophrenia and schizotypy constructs,
confusion of schizophrenia with MPD/DID, diagnosis as an
oppressive process, family process in the aetiology of schizo-
phrenia, and the psychoanalytic treatment of psychosis.

Questions
● What are the main clinical features of schizophrenia and how is it
different from the popular conception of a ‘split personality’?
● What are the differences between paranoid, hebephrenic, catatonic
and undifferentiated schizophrenia?
● How prevalent is schizophrenia?
● What are the risk factors for schizophrenia?
● What are biological and diathesis–stress theories of schizophrenia,
and the main research findings relevant to these theories?
● What are the main evidence-based approaches to assessment and
treatment of schizophrenia?
● Which controversial issues concerning schizophrenia interest you
most, and why?

FURTHER READING
Professional
● Mueser, K. & Jeste, D. (2008). Clinical handbook of schizophrenia. New
York: Guilford.
● Rubin, A., Springer, D. & Trawver, K. (2010). Clinician’s guide to evidence-
based practice: Psychosocial treatment of schizophrenia. Hoboken, NJ:
Wiley.

Self-help
● Healy, C. (2007). Understanding your schizophrenia illness: A work-
book. Chichester, UK: Wiley

Book 1.indb 245 06/03/2012 13:48

 246 C L I N I C A L P S Y C H O L O G Y : A N I N T R O D U C T I O N

● Kuipers, E. & Bebbington, P. E. (2005). Living with mental illness (third

edition). London: Souvenir Press.
● Mueser, K. & Gingerich, S. (2006). The complete family guide to schizo-
phrenia. New York: Guilford.

WEBSITES
● American Psychiatric Association’s practice guidelines for treating schiz-
ophrenia:
http://psychiatryonline.org/guidelines.aspx
● National Institute for Clinical Excellence guidelines for treating
schizophrenia:
http://guidance.nice.org.uk/topic/mentalhealthbehavioural
● Schizophrenia Patient Outcomes Research Team (PORT) updated
treatment recommendations 2009:
http://schizophreniabulletin.oxfordjournals.org/content/36/1/94.full.
pdf+html
● Schizophrenia Research Forum:
www.schizophreniaforum.org

Book 1.indb 246 06/03/2012 13:48

 Personality disorders 8
Learning objectives
After studying this chapter you will be able to:
● define the concept of personality disorder
● list the main personality disorders in the DSM and
ICD classification systems
● distinguish between Cluster A, B and C personality
disorders in terms of their main clinical features
● summarize the epidemiology of personality disorders
● outline the diathesis–stress, psychodynamic and
cognitive-behavioural theories of personality
disorders
● name the main evidence-based approaches to
assessment and treatment of personality disorders
● describe some of the controversial issues concerning
personality disorders.

Introduction
Often episodes of psychological problems such as anxiety and depres-
sion occur against a backdrop of more pervasive and long-standing
personality-based difficulties. To address this, distinctions are made in
ICD-10 (World Health Organization, 1992) and DSM-IV-TR (American
Psychiatric Association, 2000) between episodic psychological disorders

Book 1.indb 247 06/03/2012 13:48

 248 C L I N I C A L P S Y C H O L O G Y : A N I N T R O D U C T I O N

on one hand and persistent personality disorders on the other. In

DSM-IV-TR a multiaxial system is used for summarizing diagnostic
assessments. The main diagnosis is given on Axis I, and personality dis-
orders are recorded on Axis II. (Comorbid medical conditions are coded
on Axis III, psychosocial stressors on Axis IV and current level of function-
ing on Axis V, although these other axes do not concern us at this point.)
Axis I disorders are characterized by atypical episodes of psycho-
logical functioning that deviate from an individual’s normal pattern of
experience and behaviour. In contrast, Axis II personality disorders are
pervasive, enduring, inflexible patterns of behaviour, cognition and
affect that differ markedly from prevailing cultural expectations and that
lead to distress or impairment.
In clinical practice about 40% of patients present with both classes of
disorder (Zimmerman et al., 2008). Personality disorders run a chronic
course and are associated with a poor outcome. In the Collaborative
Longitudinal Personality Disorders Study, Skodol et al. (2005) found
that personality disorders were characterized by functional impairment
in personal, social, educational and occupational domains; a poor
response to treatment for comorbid depression; a high risk of suicide;
and extensive health service usage. Individuals with comorbid Axis I
and II disorders have greater service needs than those with Axis I dis-
orders only (Hörz et al., 2010). The economic cost of meeting the treat-
ment needs of patients with personality disorders is therefore significant.
In a Dutch study of 1740 people with comorbid Axis I and II diagnoses
treated at six specialist mental health services, Soeteman et al. (2008)
found that the average cost in the 12 months prior to attending specialist
mental health services was €11,126 per patient. Two-thirds of this was
direct medical costs and the remainder was due to productivity losses.
The assessment and treatment of personality disorders are an important
concern for clinical psychology on both humanitarian and economic
grounds.
In this chapter, after considering the clinical features and epidemiology
of personality disorders, a number of specific theoretical explanations
for personality disorders will be considered, and an outline of their
assessment and treatment will be given.

Clinical features and case examples

The defining features of personality disorders described in DSM-IV-TR
and ICD-10 include the following:
● an enduring dysfunctional pattern of behaviour and experience
● the pattern begins in adolescence and is consistent across situations
● there are difficulties with cognition, affect, impulse control, behaviour
and interpersonal functioning
● recurrent relationship and occupational problems are present
● difficulties in learning from experience or benefiting from psycho-
therapy occur
● there is usually a history of other psychological disorders and/or
criminality.

Book 1.indb 248 06/03/2012 13:48

 8 • PERSONALITY DISORDERS 249

Personality disorders are characterized by an enduring pattern of

behaviour and experience that deviates markedly from cultural expecta-
tions. This pattern leads to significant personal distress or significant
impairment in social functioning. With personality disorders there are
marked difficulties in two or more of the following domains: cognition,
affect, impulse control, behaviour, and interpersonal functioning.
With cognition, there may be peculiarities or difficulties in the way
self, others and events are interpreted. At an affective level the range,
intensity, lability and appropriateness of emotional responses may be
out of keeping with cultural expectations. There may be serious
difficulties with impulse control leading to highly erratic or impulsive
behaviour, markedly inhibited behaviour, or peculiar behaviour. With
respect to interpersonal behaviour there are typically serious difficulties
in making and maintaining stable and fulfilling interpersonal relation-
ships. Most people find the rigid behavioural patterns of people with
personality disorders aversive and so avoid them. In the long term, the
social isolation or negative responses of others to people with personality
disorders causes them personal distress.
A hallmark of personality disorders is the fact that the cognitive,
affective, behavioural and interpersonal difficulties constitute a long-
standing and rigid pattern of psychological functioning. Usually person-
ality disorders can be traced back to adolescence or early adulthood.
Furthermore, individuals with personality disorders have great difficulty
learning from life experiences or therapeutic interventions how to alter
their rigid behaviour patterns. They repeatedly make the same mistakes
and find it very challenging to learn from their errors. Often they are
unaware of the impact of their behaviour on others, and wish to conceal
their history of social and psychological difficulties. It is therefore clini-
cally useful to include collateral information from family members when
assessing personality disorders.
For some personality disorders, such as antisocial personality disor-
der, diagnosis is made by reputation rather than presentation. Person-
ality disorders commonly occur in conjunction with other psychological
difficulties or criminality. In clinical settings personality disordered
patients usually create significant problems for staff and other patients.
Staff often describe them as manipulative and as playing one staff mem-
ber off against another, or as refusing to co-operate with treatment.
In DSM-IV-TR the 10 main personality disorders are subdivided into
three clusters on the basis of their cardinal clinical features. The first
cluster includes the paranoid, schizoid and schizotypal personality
disorders. These are grouped together because they are characterized
by odd or eccentric behaviour. It was noted in Chapter 7 that these
conditions are schizophrenia spectrum disorders. Their clinical features
resemble subclinical psychotic symptoms and they share the same
genetic aetiology as schizophrenia.
The second cluster includes the antisocial, borderline, histrionic and
narcissistic personality disorders. These are characterized
by dramatic, emotional or erratic impulsive behaviour. The third
cluster includes the avoidant, dependent and obsessive-compulsive

Book 1.indb 249 06/03/2012 13:48

 250 C L I N I C A L P S Y C H O L O G Y : A N I N T R O D U C T I O N

personality disorders, all of which are characterized by anxiety and fear-

fulness. A very similar classification system is used in ICD-10. There
are, however, some minor differences. The schizotypal syndrome is
listed as a psychotic condition along with schizophrenia in ICD-10, and
narcissistic personality disorder is omitted. Also, obsessive compulsive
personality disorder is referred to as anakastic personality disorder;
antisocial personality disorder is referred to as dissocial personality dis-
order; and avoidant personality disorder is referred to as anxious avoid-
ant personality disorder.
The clinical features of the 10 personality disorders are set out in
Table 8.1. The current classification of personality disorders has its
roots in the work of the German psychiatrist Kurt Schneider (1923).
Multiple personality disorder (MPD), which was discussed in the
closing section of Chapter 7, is not classified with other personality
disorders in ICD-10. Nor is dissociative identity disorder (the DSM-
IV-TR term for MPD) classified with personality disorders in DSM-IV-TR.
Rather, in both classification systems this condition is classified with
other disorders where dissociation is the core feature.

Cluster A: The odd, eccentric group

The odd, eccentric group of personality disorders includes:
● paranoid personality disorder
● schizoid personality disorder
● schizotypal personality disorder.

Paranoid personality disorder

Clinical features
People with paranoid personality disorder have a pervasive distrust of
others. At a cognitive level, they interpret the motives of others in nega-
tive, malevolent, conspiratorial or exploitative terms. They assume, on
the basis of minimal or ambiguous evidence, that others intend to harm
them, be disloyal to them, exploit them, or use personal information to
discredit them. At an affective level they are angry, combative and
unforgiving of those whom they view as having harmed them. At a
behavioural and interpersonal level, they constantly question the loyalty
of close friends, partners or spouses. They may refuse to confide in
others in case their confidences are used against them. They may con-
stantly check on their spouses’ or sexual partners’ whereabouts and
question their fidelity. They may hold grudges indefinitely if they believe
that their friends or partners have harmed, insulted, injured or betrayed
them. Kraepelin (1921) and Freud (1911) both gave early accounts of
paranoia as a distinct condition.

Case example
Margaret, age 35, had a paranoid personality disorder. She and Brian
came for therapy because of extreme marital distress. Brian complained

Book 1.indb 250 06/03/2012 13:48

Book 1.indb 251
TABLE 8.1
Main clinical features of major personality disorders
Cluster Personality Main clinical Cognition Affect Behaviour Relationships
disorder feature
Cluster A Paranoid Mistrust Paranoid ideas Aggressive Secretive Mistrustful
Odd,
Schizoid Detachment Odd ideas Constricted affect Eccentric Loner
eccentric
group Schizotypal* Eccentricity Bizarre thoughts Constricted affect Eccentric Loner
Ideas of reference Socially anxious
Superstitious
Strange speech
Cluster B Antisocial Moral immaturity No internalized set of moral Aggressive Violates rights of others Multiple exploitative
Dramatic, standards Criminality relationships
emotional,
Borderline Impulsivity Expectation of abandonment Impulsive Fights with others Multiple relationships
erratic group
Shifts between overvalued and Aggressive Self-harms with frantic
undervalued view of self and Depressed unsuccessful attempts
others to avoid abandonment
Histrionic Seductive Belief in entitlement to attention Shallow Theatrical, seductive Multiple shallow
Attention seeking no matter the cost to others attention seeking relationships
Narcissistic** Self-importance Belief in entitlement to VIP Craves admiration Admiration seeking Multiple relationships
and grandiosity treatment because they are and becomes angry that fail to meet their
better than others or depressed if this high expectations
need is frustrated
Cluster C Avoidant Shyness Belief that they will be rejected Fear of rejection Social withdrawal Loners
Anxious, by others
fearful group
Dependent Lack of Belief that they cannot function Fear of autonomy Refusal to take Multiple relationships
autonomy autonomously responsibility for in which they are
decision making completely dependent
Clinginess on their partners
Obsessive- Perfectionism Belief that safety and security Fear imperfection Detailed rule following Multiple relationships
compulsive can be sustained through without regard for in which their
orderliness deadlines or overall coldness and need for
8 • PERSONALITY DISORDERS

goals control cause conflict

Note: *Schizotypal syndrome is listed as a psychotic condition with schizophrenia in ICD-10. **Narcissistic personality disorder is not listed in ICD-10.
251

06/03/2012 13:48
 252 C L I N I C A L P S Y C H O L O G Y : A N I N T R O D U C T I O N

that he felt like a prisoner in the marriage. Before leaving each morning,
Margaret interrogated him about his daily schedule. She phoned him
frequently at work and would sometimes visit his office unexpectedly to
check up on him. One night he found her checking through his wallet
and the memory of his mobile phone to find clues about him having
contact with another woman. Margaret complained that Brian had been
unfaithful to her recently. He denied this but said that her suspiciousness
was making infidelity an attractive option.
Margaret’s suspiciousness was a longstanding characteristic. She
had a very small circle of friends, whom she had known since childhood,
She would not make new friends because she found it hard to trust and
confide in others. She also thought that new friends would ridicule her.
She had lost one of her closest female friends, Estelle, over an argu-
ment about loyalty. Estelle was ill on an occasion when Margaret had
made arrangements for the two of them to go to a James Taylor con-
cert. Margaret believed that she had gone to a party elsewhere on that
evening. There was no evidence for this, but Margaret believed that she
had been betrayed. She would not forgive Estelle despite the latter’s
attempts to put the incident to one side and continue the friendship.
There were many incidents like this in Margaret’s life, dating back to her
childhood.
Margaret had grown up in a family where her parents had separated
when she was 8 years old. In the time before the parents’ separation
she often heard them argue about her father’s whereabouts. These
arguments would often end with her father storming out of the house
and her mother shouting and crying. On some of these occasions she
would say to Margaret ‘You can’t trust anyone in this world’.
Margaret was attracted to Brian because of his openness and hon-
esty and his willingness to spend a great deal of time with her. Brian
found that after they were married the demands of work prevented him-
self and Margaret from spending as much time together. As a result of
this, Margaret began to accuse him of infidelity. He believed that if she
continued to accuse him, despite his innocence, he would seriously con-
sider separation. Margaret interpreted this as evidence of his infidelity.

Schizoid personality disorder

Clinical features
People with schizoid personality disorder show a pervasive pattern of
detachment from social relationships. They are loners. At a cognitive
level they have a preference for solitary activities and introspection.
They have no desire for intimacy and do not wish to have close,
confiding relationships with their families, friends or sexual partners.
They are indifferent to praise or criticism. At an affective level they have
a restricted range of emotions. They are neither depressed, nor do they
find that relationships or activities bring them great pleasure, nor are
they roused to anger even in extreme circumstances.
At an interpersonal level they have few relationships and others find
them cold and indifferent. They have little regard for social conventions,

Book 1.indb 252 06/03/2012 13:48

 8 • PERSONALITY DISORDERS 253

and so are not concerned about being seen to ‘do the right thing’. An early
account of the schizoid personality was given by Eugen Bleuler (1924).

Case example
Norman, aged 20, had a schizoid personality disorder. He was a math-
ematics student who came for counselling because he was concerned
that his addiction to an international multi-site computer game was
interfering with his work. He stayed in a college hall of residence but
lived an isolated life. This was the way he had always lived. As a child
he was ridiculed for being ‘too brainy’ and so became immersed in rec-
reational mathematics. At the counselling service he refused to join a
social skills group because he said he did not want to form relationships
with other students.

Schizotypal personality disorder

Clinical features
People with schizotypal personality disorder have unusual perceptual
experiences, eccentric thoughts and speech, inappropriate or con-
stricted affect, peculiar or eccentric behaviour, and a lack of close rela-
tionships. At a perceptual level, they may have unusual experiences.
For example, they may report sensing the presence of ghosts or spirits,
mystical forces or vibrations. They may experience depersonalization
and report that sometimes they become an outside observer of them-
selves in a dream-like state. They may also experience derealization
and report that sometimes they perceive the world as dream-like.
At a cognitive level they may have ideas of reference, and believe
that routine events have a unique personal significance; for example,
that the shape of a cloud means that they must carry out a particular
activity. They may also hold paranormal convictions about magic forces,
telepathy, aliens and so forth, which are outside the norms of their
subculture. They may also hold paranoid ideas and be suspicious of
others. Their speech may be unusual, vague, eccentric or peculiar.
At an affective level, people with schizotypal personality disorder
show a constricted range of emotions and social anxiety, usually based
on paranoid fears. At a behavioural level, people with schizotypal per-
sonality disorder are odd, eccentric and peculiar. For example, they
may dress in an unfashionable and unkempt way and have unusual
mannerisms. At an interpersonal level, people with schizotypal person-
ality disorder are typically socially isolated and find making and main-
taining friendships anxiety-provoking, so they avoid others.
Ernst Kretchmer (1936), a German psychiatrist, was among the first
to use the term schizotype to describe a character type associated with
a constitutional vulnerability to schizophrenia.

Case example
Silver, a man in his late forties, had a schizotypal personality disorder.
He was a periodic outpatient at a psychiatric hospital. His appearance

Book 1.indb 253 06/03/2012 13:48

 254 C L I N I C A L P S Y C H O L O G Y : A N I N T R O D U C T I O N

was distinctive. His long silver-grey hair and beard accounted for his
unusual name. He wore a black overcoat, the hem of which trailed on
the ground. He rarely washed and lived alone in a house that had
belonged to his parents before they died.
Silver had been referred to the psychiatric hospital by his family
doctor years before I met him, for participation in a group programme for
people with schizophrenia. He refused to participate in the programme
because he was suspicious of other people, but requested periodic indi-
vidual appointments with the psychologist who directed the group pro-
gramme. In these outpatient individual sessions he insisted on discussing
hypnosis and telepathy. He believed that he could hypnotize others from
a distance, that he could see into the future and that he could read
minds. He had held these beliefs since adolescence, when he had
numerous out-of-body experiences (depersonalization). Otherwise he
was in contact with reality and was on no medication.

Cluster B: The dramatic, emotional, erratic group

The dramatic, emotional, erratic group of personality disorders includes:
● antisocial personality disorder
● borderline personality disorder
● histrionic personality disorder
● narcissistic personality disorder.

Antisocial personality disorder

Clinical features
People with antisocial personality disorder show a pervasive disregard
for the rights of others and consistently violate these rights. Extreme
versions of this pattern are referred to as psychopathy, sociopathy, and
dissocial personality disorder.
At a behavioural level, people with antisocial personality disorder
are consistently aggressive, destructive and deceitful, and engage in
theft and lying. Commonly in clinical practice, antisocial personality
disorder is associated with a history of multiple arrests, multiple con-
victions and imprisonment. At a cognitive level, people with this
personality disorder have not internalized rules for moral and ethical
behaviour and are motivated by personal profit and pleasure seeking.
They believe that aggressiveness, destructiveness, theft, deceit, and
lying to achieve personal goals are justified. They develop elaborate
rationalizations and cognitive distortions to justify their violations of
others’ rights.
At an affective level, they are impulsive and reckless, displaying little
planning and showing no anxiety even in the most dangerous situations.
Their impulsivity and recklessness may find expression in an erratic
occupational history, poor financial planning, speeding while driving,
substance abuse and other forms of risk-taking which may lead to injury
or death in some cases.

Book 1.indb 254 06/03/2012 13:48

 8 • PERSONALITY DISORDERS 255

People with antisocial personality disorder are aggressive and

irritable and frequently become involved in fights. At an interpersonal
level they have difficulty maintaining intimate relationships with friends
or sexual partners. Commonly they charm people into believing that
they wish to pursue a close relationship and then violate the trust the
other person has placed in them through irresponsibility, disloyalty,
aggression, destruction, theft or deceit. They show little remorse for
violating trust in close relationships, and consequently have few if any
close friends and typically a history of multiple sexual partners. The
diagnosis of antisocial personality disorder is not given until after a
person is 18, and commonly it is preceded by conduct disorder.
Antisocial personality was first described in detail by Hervey Cleckley
(1941) in his book The Mask of Sanity and referred to as psychopathy,
although Cleckley’s criteria for the condition defined a narrower
construct than that in the current DSM classification system. Cleckley
emphasized the importance of callousness; lack of empathy, shame,
guilt or remorse; and the use of superficial charm, manipulation and
violence in violating others’ rights to satisfy their needs.

Case example
Tony, who had an antisocial personality disorder, was referred to a psy-
chiatric hospital from a prison for psychological assessment. He
was referred because he complained of depression to the visiting psy-
chiatrist at the prison. He had a history of theft and occasional drug
abuse.
A thorough clinical interview and a full psychometric evaluation
revealed no evidence of a mood disorder or, indeed, any other Axis I
psychopathology. During the feedback session when the results of the
assessment were presented to him, Tony said he had feigned depression
because he wanted to be referred to the psychiatric hospital from the
prison for a change of scene. He joked about the fact that he preferred
the conditions in the hospital to the prison.
During the psychological assessment he gave a history that drew a
picture of himself as a stable, caring man who had fallen on hard times
and so had stolen from time to time and unluckily been apprehended for
occasional drug abuse. I interviewed his sister and wife to corroborate
this essentially normal profile. They offered accounts that were at
variance with Tony’s. They drew a picture of a man who had grown up
in a disorganized family, which his father left when Tony was a baby.
His mother had a series of unreliable partners after that.
Tony began rule-breaking and stealing as a child and had continued
to do so right up to the present. He also truanted from school and began
drinking and drug taking in his teens. He had been married on four
occasions and in each marriage had been violent towards his wife for
trivial reasons. He had been involved in episodes of serious drug misuse
and alcohol binges. Tony had been imprisoned on numerous occasions
and participated in a wide range of treatment programmes to help him
alter his antisocial and drug-using behaviour patterns. All had been
ineffective. He had no close friends, just transient acquaintances. His

Book 1.indb 255 06/03/2012 13:48

 256 C L I N I C A L P S Y C H O L O G Y : A N I N T R O D U C T I O N

sister rarely saw him and his present wife (of a year’s standing) was
considering divorce.

Borderline personality disorder

Clinical features
People with borderline personality disorder are highly impulsive and
show a pattern of pervasive instability in interpersonal relationships,
self-image and mood. At a cognitive level they have a core belief that
within the context of friendships and relationships they will be aban-
doned. At an affective level, they experience an intense fear of aban-
donment. They also have a propensity to experience intense uncontrolled
aggression towards those whom they perceive as abandoning them.
Their fear of abandonment leads to frantic yet ineffective attempts to
make and maintain relationships, particularly with sexual partners.
Once in a relationship, their fear of abandonment may lead them to
demand continued contact with their partner and continued caregiving
and attention. When their partners cannot allay their fear of abandon-
ment or fail to meet their needs for continued caregiving and attention,
the person with borderline personality disorder may attempt to reduce
the interpersonal distance by either becoming aggressive to their part-
ner or engaging in self-harm. They may rage at their partner for frustrat-
ing their need for care and attention. They may then feel shame and
guilt and engage in self-harm or self-mutilation to elicit continued care-
giving from their partner, or to distract themselves from their internal
psychological distress. Their self-harm may involve overdosing, cutting
or burning. Sometimes self-mutilation is carried out while in a dissoci-
ated state. There may be a link between dissociative disorders such as
multiple personality disorder, discussed at the close of Chapter 7, and
borderline personality disorder.
Within close personal relationships and therapeutic relationships,
beliefs that people with borderline personality disorder hold about them-
selves and others alternate between extremes of idealization and
devaluation. Thus, they may on occasion view themselves or their part-
ners as perfect, kind, caring and highly valued, but on other occasions
when their needs to receive care and attention from their partners are
frustrated, they may view themselves or their partner as cruel, uncaring
and despicable. This alternation between overvalued and undervalued
views of the self and others and related changes in affect and behav-
iour may occur suddenly and unpredictably.
Underlying the belief in the inevitability of abandonment and the
related fear and anger is a pervasive sense of emptiness. People with
borderline personality disorder may cope with this through impulsive
spending, sexual activity, bingeing, drug use, reckless driving or other
risk-taking activities. Commonly borderline personality disorder occurs
following a history of physical or sexual child abuse, neglect or early
parental loss or death. A history of multiple partners and educational
and occupational instability is common in cases of borderline personality
disorder. The term ‘borderline’ was first used by the psychoanalyst

Book 1.indb 256 06/03/2012 13:48

 8 • PERSONALITY DISORDERS 257

Adolf Stern (1938) to describe this personality disorder, which he

believed was on the borderline between the neuroses (such as
depression and anxiety) and psychoses (such as schizophrenia).

Case example
Mary, aged 24, had a borderline personality disorder. She was referred
for a parenting assessment to a child and family psychology service
after her child was taken into foster care following a non-accidental
injury. Mary had become frustrated with her 10-month-old daughter’s
continuous crying and bruised her badly by squeezing and shaking her.
The parenting assessment showed that Mary had a good knowledge of
how to care for her child but little sensitivity to the infant’s signals; little
understanding that the baby could not intentionally try to annoy her; and
little tolerance for managing the routine daily demands of parenting.
She also had a very limited social support network and difficulties
making and maintaining friendships.
Mary had been involved in several heterosexual relationships. All
had ended in violent rows. When these relationships ended she felt
deep regret and a sense of being abandoned. Her attempts to rekindle
some of these relationships had been unsuccessful and led to further
violent or abusive rows. She had a history of episodes of major
depression and had frequently engaged in non-suicidal self-harm. She
had overdosed on a few occasions and cut her arms. A general feeling
of emptiness was occasionally broken by feelings of extreme joy (for
example, at the start of a new relationship) and anger. She lacked any
coherent life plan.
Mary herself had been in care as a child on two occasions when her
parents were unable to cope. She had also been regularly slapped and
punched as a child by her father when he came home drunk. In school,
she had never fitted in. She had left school at 14 and worked in a variety
of casual jobs. She had hoped when she met the baby’s father, Kevin,
that things would work out. But Kevin left her once she mentioned that
she was pregnant. She hoped that her child and her role as a parent
would give her happiness and a sense of direction. She was distraught
when she found that they had brought her further misery.

Histrionic personality disorder

Clinical features
People with histrionic personality disorder are characterized by a perva-
sive pattern of dramatic and excessively emotional attention seeking. At
a cognitive level there is the underlying belief that they are entitled to be
the centre of attention and to have their needs for attention and admira-
tion met, regardless of the cost to others. At an affective level they may
feel a hunger for attention that they fear will not be fulfilled. At a behav-
ioural level they routinely create situations in which they are the centre
of attention. To do this they may express their views in dramatic and
theatrical ways using excessive displays of emotion. However, when
questioned in detail about why they hold particular views, typically they

Book 1.indb 257 06/03/2012 13:48

 258 C L I N I C A L P S Y C H O L O G Y : A N I N T R O D U C T I O N

have little in the way of well-reasoned arguments or in-depth knowledge

to back their assertions. They are highly suggestible and may change
their views in response to changes in fads and fashions.
This shallowness that characterizes their views and opinions also
characterizes their relationships. They commonly consider their rela-
tionships with others (including health professionals) to be far more inti-
mate and deeper than they are. So they may call doctors that they have
seen infrequently by their first names and refer to acquaintances as
their old friends.
People with this personality disorder may dress and groom
themselves so that they become the centre of attention. Often their self-
presentation is deliberately seductive. Women with histrionic personality
disorder may dress, make themselves up and behave in a way that is
erotic, seductive and provocative. Men may dress and behave in a
macho manner, drawing attention to their physical appearance, strength,
athleticism and sexuality. One of the earliest descriptions of histrionic
personality disorder was given by Emil Kraepelin (1913).

Case example
Sarah, aged 18, had a histrionic personality disorder. She was originally
referred to a child and family clinic in her final year at secondary school.
She was to be excluded from school for instigating fights and disruption.
She typically dressed like a film star, spoke like a soap opera character,
and demanded everyone’s attention. If she didn’t get the attention she
craved, she threw a tantrum.
She divided her favours between a number of boys at her school and
incited them to compete with each other for her affections, promising
each an exclusive relationship with her if they defeated the other boys.
She was an only child and grew up in a family where her parents, who
were involved in the arts, had little time for her. She spent much of her
childhood alone and coped with the isolation by watching endless soap
operas. She was intelligent but could not apply herself at school or later
at college. She changed courses frequently and was led more by her
attraction to partners and excitement than by vocational interests.

Narcissistic personality disorder

Clinical features
People with narcissistic personality disorder have a pervasive pattern of
grandiosity, a need for admiration, and a lack of empathy for others. At
a cognitive level they believe that they are special or better than others
and so are entitled to be treated differently. They have an over-inflated
view of their own accomplishments and believe that they are entitled to
the best of everything and to associate only with people whom they
perceive to be special or outstanding like themselves. They are pre-
occupied with fantasies of success, power and romantic love.
At an affective level, they crave admiration, attention and deferential
treatment from others. To confirm this view of themselves, at a behaviour
level, they use their charm in social situations or their power in work

Book 1.indb 258 06/03/2012 13:48

 8 • PERSONALITY DISORDERS 259

situations to extract compliments and special treatment from others.

Thus they may ‘fish for compliments’ in social situations and overload
their employees in work situations to achieve their own personal goals.
At an interpersonal level they have difficulty sustaining long-term
relationships because they have a limited capacity for empathy and so
do not appreciate the negative effect that their grandiosity and need for
admiration have on others. They also leave many relationships because
they fail to meet their high expectations of ‘perfect love’. They have
difficulties maintaining peer friendships because they are arrogant,
patronizing and envious of others’ accomplishments and possessions,
and expect others to be envious of them.
Occupationally, they may excel at their work or may avoid trying to
excel for fear of failure. Furthermore, they are extremely sensitive to
criticism and when their partners or others frustrate their need for
admiration or are the least bit critical, their self-esteem drops. They feel
degraded, humiliated, hollow and empty. This may find expression as
range and anger or depression. Detailed psychoanalytic accounts of
narcissistic personality disorder and its treatment were first given by
Otto Kernberg (1975) and Heinz Kohut (1968).
Case example
Frank, aged 34, had a narcissistic personality disorder. He came for
therapy at the insistence of his partner, Maria. She complained that he
had become impossible to live with. Since they had met Frank had
always depended on her for emotional support and admiration. While
she felt that this was appropriate when they were young lovers, she now
felt that his demands were immature and excessive.
For example, when he arrived home from work he expected all
household routines to cease and Maria and the three children to devote
their attention to his accounts of his day’s achievements. If they did not
meet his expectations he would fly into a rage and verbally abuse them.
Later he would be remorseful and if he was not forgiven by Maria he
would sink into a cold, detached, depressed state.
The problem had become particularly bad recently when his business
partner, Martin, had questioned his judgement in a major deal that went
badly wrong and the company made a significant loss. Frank had relied
on continued support and admiration from Martin (whom he considered
to be a lesser person than himself) and was devastated at his criticism.
He had oscillated between threatening to take legal action against
Martin for defamation of character and withdrawing completely from
frontline business transactions with the company’s clients because of
his incompetence.

Cluster C: The anxious, fearful group

The anxious, fearful group of personality disorders includes:
● avoidant personality disorder
● dependent personality disorder
● obsessive-compulsive personality disorder.

Book 1.indb 259 06/03/2012 13:48

 260 C L I N I C A L P S Y C H O L O G Y : A N I N T R O D U C T I O N

Avoidant personality disorder

Clinical features
People with avoidant personality disorder show a pervasive pattern of
social inhibition and shyness beginning in adolescence or early
adulthood. At a cognitive level people with avoidant personality disorder
believe that they are inferior to others, unlikable and socially unskilled.
They also believe that when they meet new people, there is a high risk
that they will be criticized, rejected, ridiculed, shamed or humiliated.
At an affective level they experience intense anxiety in social situ-
ations. At a behavioural level they avoid situations, occupations, job
promotions and pastimes that involve significant interpersonal contact
with unfamiliar people. At an interpersonal level they live a constricted
social lifestyle and avoid, or show extreme restraint in, intimate relation-
ships, to avoid humiliation and embarrassment.
Cases with the symptoms of avoidant personality disorder were
described by Bleuler (1911) as a variant of schizoid conditions in his
work on the schizophrenias.

Case example
Seamus, aged 45, was a bank official with avoidant personality dis-
order. He was referred to a communications consultancy centre for
job interview preparation training. The process involved role-playing,
videoing and reviewing the type of job interview in which he was
due to participate to achieve promotion. While he was thoughtful and
quite coherent during a conversation that preceded the role-play, during
it he was virtually incoherent.
In the small rural branch of the bank where he worked he was just
about able to tolerate the social anxiety he experienced when dealing
with regular customers. He was shy and avoided all social contact
outside work. He didn’t want to attend our communications consultancy
for interview skills training, but the regional personnel manager of his
bank said he needed to develop his job interview skills so he could be
promoted to Assistant Manager level. He had attended our consultancy
so as not to disappoint the personnel manager. However, he would
happily have avoided promotion because it would involve increased
contact with unfamiliar people.

Dependent personality disorder

Clinical features
People with dependent personality disorder show a pervasive pattern
of submissiveness and clinginess. At a cognitive level, they have a
belief that they must be taken care of by others (such as parents
and partners) and that if separated from others their safety will be
jeopardized.
At an affective level, they experience extreme anxiety when separated
from parents or partners, whom they view as essential for their safety
and security. At a behavioural level, they have difficulty making decisions

Book 1.indb 260 06/03/2012 13:48

 8 • PERSONALITY DISORDERS 261

without asking for and receiving advice and reassurance from others.
They have difficulty disagreeing with others, particularly parents or
partners, lest this lead to loss of support. They arrange for others to take
responsibility for major areas of their lives and rarely initiate projects on
their own. They go to great lengths to receive reassurance from others,
even when this involves doing very unpleasant tasks. At an interpersonal
level, when one intimate relationship ends they quickly seek another,
lest they be left to cope and make decisions alone.
One of the first detailed descriptions of dependent personality disor-
der was given by the psychoanalyst Karl Abraham (1924) and referred
to this condition as the oral character type, due to his hypothesis
that the seeds of this personality disorder were sown during the oral
stage of psychosexual development. This is the earliest stage of devel-
opment, during which pleasure comes mainly from the process of feed-
ing, hence the term ‘oral’ and the primary characteristic of dependency.

Case example
Tracy, aged 32, had a dependent personality disorder. She was the wife
of a man who phoned a child and family psychology service requesting
help with a sexual problem. He initially said that he was attracted to his
15-year-old daughter. It was suspected that sexual abuse had occurred
in this case and so a full family assessment was offered. The family
assessment revealed that he had had sexual intercourse with the
daughter repeatedly for over a year.
We advised that the father leave the home and live separately while
a programme of rehabilitation occurred. The programme would involve
the mother and daughter strengthening their relationship; the daughter
learning self-protection skills; and the father attending group therapy for
sex-offenders. Tracy refused to co-operate because she felt unable to
make decisions and function without her husband. Thus Tracy was pre-
pared to jeopardize her daughter’s safety for her own dependency
needs.

Obsessive compulsive personality disorder

Clinical features
People with obsessive compulsive personality disorder show a perva-
sive pattern of preoccupation with orderliness, perfectionism, ethics,
interpersonal control and fiscal economy. At a cognitive level, there is a
central belief that for safety and security to be maintained in all areas of
life a carefully constructed set of organizational rules must be followed
to perfectionistic standards. This belief covers the execution of routine
activities of daily living, all areas of occupational responsibility, fairness
in dealings with others, co-operating with others in jointly completing
tasks, and managing money.
At an emotional level, people with this personality disorder experience
anxiety when their set of perfectionistic rules covering all areas of
activity is not followed. At a behavioural level, a wide range of problems
occur. There is extreme difficulty in finishing tasks on time and meeting

Book 1.indb 261 06/03/2012 13:48

 262 C L I N I C A L P S Y C H O L O G Y : A N I N T R O D U C T I O N

deadlines, and in some instances tasks are never finished because

perfectionistic standards are never reached. Flexible problem-solving
also suffers, because a person with this personality disorder will become
so fixed on following the original plan that even when unforeseen
obstacles are encountered, the original plan is still followed.
Leisure pursuits and family relationships receive little attention
because of devotion to work-related tasks, and this is not accounted for
by economic necessity. If a person with obsessive compulsive person-
ality disorder does involve themselves or their children in sports, their
dedication to perfectionism makes sporting events unhappy affairs
marked by conflict. Practical solutions to problems at work or at home
are difficult to find because of ethical scruples, beyond those accounted
for by religious or cultural standards.
In work, leisure and family situations, tasks are not delegated
because of concerns that others will not do them to a perfectionistic
standard. Conflict and eventually social isolation may arise as a result
of this. In economic matters, people with obsessive compulsive person-
ality disorder are miserly and hoard money (however abundant) and
possessions (however worthless) against possible future times of eco-
nomic hardship.
At an interpersonal level people with obsessive compulsive person-
ality disorder may become isolated because they place such harsh
demands on others to reach high standards and because they have dif-
ficulty expressing tender feelings. This is because they can rarely find
the perfect way to express their positive feelings for others, and they
find it imperative to express their feelings of disappointment when
others fail to meet their standards.
Freud (1908) offered a detailed description of the obsessive compul-
sive personality disorder and referred to it as the ‘anal character’. He
used this term because his hypothesis was that its seeds were sown
during the anal stage of psychosexual development. During this stage
there is a psychological focus on the anus as a source of pleasure, and
on the capacity to control the sphincter in the process of toilet training.
The term ‘anal’ is now commonly used to describe fussy, perfectionistic,
control-oriented people.

Case example
Hank, aged 50, had an obsessive compulsive personality disorder. He
was a divorced professor of experimental psychology. He came for
therapy because of depression. This was related to the fact that his
children and students had refused to have contact with him.
In his home life he had always been meticulous and set the highest
standards for family relationships and household routines. It was his
anger when these standards were not reached that led to his divorce.
However, he continued to have contact with his children. His insistence
on punctuality and the critical attitude he took to his children’s behaviour
had led them to reduce the frequency of their visits with him, and
eventually to his wife suggesting that he have very infrequent access to
the children.

Book 1.indb 262 06/03/2012 13:48

 8 • PERSONALITY DISORDERS 263

He was meticulous in his work. He wrote all his own computer

programs for conducting his experiments and analysing his data. He
insisted that his research students receive daily supervision and follow
his guidance to the letter. If they did not meet his standards, he vilified
them. His work was internationally known and all of his students had
their work published or presented at major conferences. However,
students who worked with him found his criticism of tiny errors in their
work, his insistence that they follow his guidelines to the letter and his
excessive devotion to work to the exclusion of leisure difficult to take.
They had complained to the dean about his criticism of them. He took
the dean’s suggestion that he take a more flexible approach and be less
critical with his students very hard. He felt misunderstood and saw it as
a personal attack.

Epidemiology and course

Prevalence rates for personality disorders are given in Table 8.2. In the
general population the prevalence of personality disorders is about
10%, whereas in samples of mental health service users, the rate is four
times that at about 40% (Torgersen, 2009; Zimmerman et al.’s, 2008).
The results of the US National Comorbidity Survey Replication showed

TABLE 8.2
Epidemiology of major personality disorders
Cluster Personality Prevalence (%) in Prevalence (%) in Gender differences
disorder the community clinical samples in community studies
Any personality 10.3 40.5 No differences
disorder
Cluster A 5.7 – Higher in males
Cluster B 1.5 –
Cluster C 6.0 –
Cluster A Paranoid 1.7 4.1
Odd, eccentric group
Schizoid 0.9 1.1
Schizotypal 0.9 4.6
Cluster B Antisocial 1.1 4.3 Higher in males
Dramatic, emotional,
Borderline 1.6 15.8
erratic group
Histrionic 1.5 9.5
Narcissistic 0.5 4.5
Cluster C Avoidant 1.7 11.4
Anxious, fearful
Dependent 0.7 8.0 Higher in females
group
Obsessive- 2.1 5.3
compulsive

Note: Community prevalence rates for any personality disorder and individual personality disorders are median rates from
12 community studies summarized in Torgersen (2009). Community prevalence rates for Clusters A, B and C are from
Lenzenweger et al.’s (2007) US National Comorbidity Survey Replication. Clinical prevalence rates are median rates from
Zimmerman et al.’s (2008) review of 16 clinical studies. Gender differences are from Torgersen (2009).

Book 1.indb 263 06/03/2012 13:48

 264 C L I N I C A L P S Y C H O L O G Y : A N I N T R O D U C T I O N

that in rank order, Cluster C personality disorders were the most

prevalent (6.0%); Cluster A were the next most prevalent (5.7%); and
Cluster B, the least prevalent (1.5%) types of personality disorders in
the general population (Lenzenweger et al., 2007).
For individual types of personality disorder, prevalence rates vary
from 0.5% to 2.1% in the general population, with obsessive compulsive
personality disorder being the most prevalent. In samples of service
users, prevalence rates vary from 1.1% to 15.8%, with borderline per-
sonality disorder being far more prevalent than other types. Within the
general population the overall rates of personality disorders are similar
for males and females. However, Cluster A disorders and antisocial per-
sonality disorder have consistently been found to be more prevalent
among males, whereas dependent personality disorder has consistently
been found to be more prevalent among females (Torgersen, 2009).
The high prevalence of borderline personality disorders in females
found in clinical practice is not found in general population surveys.
There is considerable comorbidity among personality disorders.
Many people who have one personality disorder meet the criteria for a
number of others (Lenzenweger et al., 2007). There is also considerable
comorbidity of Axis I disorders with Axis II disorders. For example, in a
review of 20 large studies, Guzzetta and di Girolamo (2009) found that
57% of people with substance abuse disorders, 49% of people with
mood disorders and 40% of people with anxiety disorders also had
comorbid personality disorders.
The results of longitudinal studies where the same group of patients
is followed up over time and cross-sectional studies where the
prevalence of personality disorders in different age groups is examined
are fairly consistent. Personality disorders are fairly stable over time,
although some improvement does occur, especially among those with
Cluster B personality disorders (Grilo & McGlashan, 2009). In midlife
people with antisocial and borderline personality disorder begin to
mature out of their dysfunctional behaviour patterns. Borderline patients
become less impulsive and self-harming and antisocial patients reduce
their involvement in criminality. However, for both conditions only a
minority establish successful relationships.
People with personality disorders show significant impairment in
functioning. They tend to remain single, to have educational, occupa-
tional and financial problems that lead them to be of lower SES, and
have a lower quality of life (Torgersen, 2009). Between a half and three-
quarters of people with personality disorders attempt suicide; attempted
and completed suicide rates are highest for borderline and antisocial
personality disorder; and about 10% of borderline patients actually
commit suicide (Links & Kolla, 2009).
Personality disorders affect the extent to which Axis I disorders
respond to treatment. People with mood, anxiety and substance use
disorders who also have comorbid personality disorders show less
improvement in response to psychotherapy compared with people who
have no comorbid personality disorders (Haaga et al., 2006; Newton-
Howes et al., 2006; Newman et al., 2006a).

Book 1.indb 264 06/03/2012 13:48

 8 • PERSONALITY DISORDERS 265

Theories
Diathesis–stress, psychodynamic and cognitive-behavioural theories of
personality disorders have been developed and summaries of these are
outlined below.

Diathesis–stress theories
Diathesis–stress theories of personality disorders propose that both
biological factors and stressful environmental factors, particularly those
within the individual’s family of origin, contribute to the development of
personality disorders. These theories entail the view that people with
certain genetically determined temperamental characteristics develop
particular personality traits, and that personality disorders emerge when
such people are exposed to certain types of psychosocial risk factors
within their families or wider social systems (Clark & Watson, 2008;
Lenzenweger & Clarkin, 2005; Paris, 1996).

Genetics, temperament and personality traits

The weight of evidence shows that 50% of the variance in major per-
sonality traits such as neuroticism, extraversion, openness to experi-
ence and conscientiousness may be accounted for by genetic factors
(Krueger & Johnson, 2008; Paris, 1996). The mechanisms by which
genetic factors influence personality traits are complex. Probably multi-
ple genes determine temperamental characteristics, and these interact
with environmental influences in the development of personality traits.
There is considerable evidence from longitudinal studies for the link
between temperament and personality traits (Clark & Watson, 2008;
Rothbart & Bates, 2006).
Children with temperaments characterized by irritability and fearful-
ness develop high levels of neuroticism in later life. Children with tem-
peraments characterized by high activity levels and positive affect
become extraverted as they mature. Children who temperamentally
show attentional persistence later develop high levels of conscientious-
ness. Children with extreme maladaptive temperamental characteristics
may be more vulnerable to environmental stressors or they may elicit
reactions from parents and others that exacerbate their extreme
temperamental characteristics. This in turn may lead them to develop
maladaptive personality traits, placing them at risk of developing per-
sonality disorders (DePauw & Mervielde, 2010).

Genetics and personality disorders

Genetic studies indicate that personality disorders are moderately herit-
able, with heritability estimates ranging from about 20% to 70%, and
that the extensive comorbidity between personality disorders can be
explained by four main genetic factors and three environmental factors
(Reichborn-Kjennerud, 2010). The genetic factors include neuroticism
(common to most personality disorders), introversion (which mainly

Book 1.indb 265 06/03/2012 13:48

 266 C L I N I C A L P S Y C H O L O G Y : A N I N T R O D U C T I O N

affects schizoid and avoidant personality disorder), disagreeableness

and impulsivity (which mainly affects antisocial and borderline personal-
ity disorder) and conscientiousness or compulsivity, which uniquely
affects obsessive compulsive personality disorder. On the other hand,
comorbidity within Clusters A, B and C is best explained by three dis-
tinct environmental factors. For each of the clusters of personality disor-
ders, research has thrown light on the role neurobiological factors in the
aetiology of some specific personality disorders. This will be briefly
summarized below.

Neurobiology of schizotypal personality disorder

There is some evidence that neurobiological factors may play a role in
the development of schizotypal personality disorder. This disorder
forms part of a spectrum of psychotic or psychotic-like disorders that
includes schizophrenia. People with schizotypal personality disorder
have symptoms similar to those of schizophrenia; they share many of
the attentional and information-processing deficits found in people
with schizophrenia; and many have been found to have a positive
family history for schizophrenia (Mamah & Barch, 2011; Siever & Davis,
1991).
Neurobiological studies have shown that schizotypal personality dis-
order shares candidate genes, and certain structural and functional
brain abnormalities, with schizophrenia (Coccaro & Siever, 2009;
Reichborn-Kjennerud, 2010). Candidate genes implicated in the aetiol-
ogy of schizotypal personality disorder include catechol-O-methyltrans-
ferase (COMT), which regulates dopamine signalling in the frontal
cortex, and D-amino acid oxidase activator (DAOA) and dysbindin
(DTNBP1), which affect glutamate signalling.
Schizotypal personality disorder is associated with less dysregula-
tion of the dopamine neurotransmitter system than that found in schizo-
phrenia, and reduced temporal lobe volumes similar to that present
in schizophrenia; but unlike schizophrenia, intact frontal lobes charac-
terize people with schizotypal personality disorder. It is probable
that the dopamine system and temporal lobe abnormalities subserve
the eccentricities that characterize people with schizotypal personality
disorder, but that the less extreme dysregulation of the dopamine
system and the normal frontal lobes prevent the emergence of frank
psychosis.

Neurobiology of borderline personality disorder

Neurobiological studies have identified candidate genes and structural
and functional brain abnormalities associated with borderline personal-
ity disorder (Coccaro & Siever, 2009; Reichborn-Kjennerud, 2010). The
main candidate gene associated with borderline personality disorder is
SLC6A4 or 5-HTT, which affects the efficiency of the serotonin neuro-
transmitter system. The short allele variant of the 5-HTTLPR polymor-
phism, which regulates expression of the serotonin transporter gene

Book 1.indb 266 06/03/2012 13:48

 8 • PERSONALITY DISORDERS 267

(SLC6A4 or 5-HTT), is a risk factor for borderline personality disorder

(and is also associated with vulnerability to depression and PTSD, as
mentioned in Chapters 5 and 6).
While there is evidence for dysregulation of a range of neurotrans-
mitters in borderline personality disorder, the most robust support is for
hypoactivity of the serotonin neurotransmitter system (Coccaro &
Siever, 2009). This system affects mood and impulsivity. Neuroimaging
studies show that a dysfunction of the frontal and limbic circuitry under-
pins borderline personality disorder (Schmahl & Bremner, 2006). This
network includes the orbitofrontal and dorsolateral prefrontal cortex, the
anterior cingulate cortex, the hippocampus and the amygdala. A meta-
analysis has shown that people with borderline personality disorder
have bilateral decreases in hippocampal and amygdala volumes (Hall
et al., 2010). Structural changes and overactivity of the amygdala may
underpin enhanced threat perception and the tendency to repeat emo-
tionally charged relationship patterns in borderline personality disorder,
while frontal lobe deficits may subserve difficulties in evaluating height-
ened threat reactions and regulating emotional responses to perceived
threats. Reduced hippocampal volume may compromise the capacity
for developing coherent adaptive autobiographical narratives as an
alternative to repeating destructive, emotionally charged relationship
patterns.
It has consistently been found that people with borderline person-
ality disorder have a history of severe trauma including child abuse,
particularly child sexual abuse (Johnson et al., 2009). In the emer-
gence of borderline personality disorder, this life stress may both
interact with neurobiological vulnerabilities and contribute to their
development.

Neurobiology of antisocial personality disorder

Candidate genes for antisocial personality disorder and psychopathy
for which there is some support include monoamine oxidase A (MAOA)
and the serotonin transporter gene (5-HTT) (Ferguson, 2010; Gunter
et al., 2010). Both of these affect the efficiency of the serotonin neuro-
transmitter system, which in turn affects mood, impulsivity and aggres-
sion. Retz et al. (2004) found that a deletion/insertion polymorphism on
the 5-HTT gene was a risk factor for violence in male criminals. The
MAOA gene has earned the nickname ‘warrior gene’ because people
with low MAOA activity show greater aggression in challenging situ-
ations (McDermott et al., 2009). Caspi et al. (2002) found that males
with both a low MAOA activity genotype and a history of child abuse
were more likely have antisocial behaviour in adulthood than were high
MAOA activity genotype males who had been similarly abused.
Neurobiological studies of antisocial personality disorder have led to
a distinction between reactive–impulsive aggression (typical of most
criminals who engage in opportunistic violence) and proactive–instru-
mental aggression (which is characteristic of psychopaths who engage
in predatory, planned aggression to achieve goals such as money,

Book 1.indb 267 06/03/2012 13:48

 268 C L I N I C A L P S Y C H O L O G Y : A N I N T R O D U C T I O N

status and power) (Roth & Buchheim, 2010). With reactive–impulsive

aggression, there is hyperarousal to threatening stimuli (subserving
increased anger and fear) associated with increased activity in the
amygdala and decreased volume and activity in the frontal cortex,
notably the orbitofrontal and ventro-medial prefrontal cortex. The
increased amygdala activity subserves increased threat perception,
while the reduced frontal activity subserves a lack of impulse control. In
contrast, with proactive-instrumental aggression, there is hypoarousal
to threatening stimuli shown by low heart rate and electrodermal activity
(Edens et al., 2007). In some, but not all studies this is associated with
decreased activity in the amygdala.
These neurobiological processes subserve low levels of anger or
fear. Thus, people with antisocial personality disorders have very low
levels of physiological arousal, fail to develop conditioned responses to
fear-related stimuli, and are unable to learn from negative experiences.
This lack of conditionability reflects a neuropsychological vulnerability
to developing antisocial behaviour. However, this vulnerability only
leads to antisocial personality disorder when combined with psychosocial
risk factors, particularly family disorganization, paternal criminality,
maternal psychological difficulties, parental alcoholism, and inconsistent
discipline (Kazdin, 1995).

Cluster C personality disorders

Relatively little research has been conducted on the neurobiology of
Cluster C personality disorders. An anxious temperament and the per-
sonality trait neuroticism (both of which are approximately 50% herit-
able) probably predispose individuals to developing avoidant and
dependent personality disorders (Meyer et al., 2005). However, people
with these attributes require exposure to a highly enmeshed family cul-
ture in which there is a high degree of parental control and little encour-
agement for the development of autonomy for the development of
avoidant and dependent personality disorders (Paris, 1996). Obsessive
compulsive personality disorder has a unique genetic diathesis, which
is not shared with other personality disorders (Kendler et al., 2008).
There is no evidence to support the link between toilet training (as sug-
gested by Freud’s (1908) ‘anal character hypothesis’) and obsessive
compulsive personality disorder (Emmelkamp, 1982).

Stress and personality disorders

In prospective and retrospective studies a wide variety of family-based
risk factors have been found to contribute to the development of
personality disorders (Bakermans-Kranenburg & van IJzendoorn, 2009;
Johnson et al., 2009; Paris, 1996). These include trauma, physical and
sexual abuse, neglect, separation from or loss of a parent, parental
psychopathology and related impaired parenting, insecure attachment,
problematic parent–child relationships, extremely low or high levels of
family cohesion, and the absence of social support.

Book 1.indb 268 06/03/2012 13:48

 8 • PERSONALITY DISORDERS 269

The effectiveness of psychotherapy

and medication
Duggan et al. (2007, 2008) reviewed 35 randomized controlled trials
(RCTs) of pharmacological studies and 27 RCTs of psychological treat-
ments for personality disorders. They concluded that there was evi-
dence for the effectiveness of specific psychological treatments for
certain personality disorders, and for the effectiveness of some phar-
macological interventions in managing specific symptoms associated
with some Axis II disorders. There was evidence for the effectiveness of
cognitive-behaviour therapy and psychodynamic psychotherapy, either
alone or in combination with pharmacotherapy. Most studies focused
on borderline personality disorder, or heterogeneous groups of patients
with various personality disorders. With regard to pharmacological
treatments there was evidence for the effectiveness of antipsychotics in
reducing cognitive, perceptual and psychotic-like symptoms; mood
stabilizers in reducing aggression; and antidepressants in regulating
mood.

Psychodynamic approaches
Meta-analyses show that psychodynamic psychotherapy leads to an
improvement in the adjustment of people with personality disorders,
notably those that fall within Clusters B and C (Leichsenring, 2010).
Evidence-based psychodynamic approaches to psychotherapy include
transference-focused psychotherapy and mentalization-based treat-
ment for borderline personality disorder (Bateman & Fonagy, 2010a,
2010b; Yeomans and Diamond, 2010) and short-term dynamic psycho-
therapy for Cluster C personality disorders (Svartberg & McCullough,
2010).

Transference-focused psychotherapy for borderline

personality disorder
In modern psychoanalytic practice, Kernberg’s approach to understand-
ing borderline personality disorder and an evidence-based practice
model derived from it – transference-focused psychotherapy – have
been particularly influential (Caligor, 2010; Kernberg & Caligor, 2005;
Yeomans & Diamond, 2010). Kernberg’s psychoanalytic object rela-
tions theory assumes that during the course of early development, indi-
viduals evolve through a series of stages. As they mature through these,
their internal representations of self and others become increasingly
sophisticated. In object relations theory, it is assumed that the children
learn about others through their relationships with their mothers or
caregivers. ‘Object’ is the technical term used in object relations theory
to refer to others (as distinct from the self) and particularly to the mother
during early development.
At a very early stage of development, the infant does not distinguish
between representations of the self and the mother. The main distinction
that is made is between experiences that make the child feel good or

Book 1.indb 269 06/03/2012 13:48

 270 C L I N I C A L P S Y C H O L O G Y : A N I N T R O D U C T I O N

bad. So at the earliest stage the child develops symbiotic fused self–
object representations that are ‘all good’ or ‘all bad’. At a second stage
of development, the child learns that the self and the mother (or object)
are separate. At this stage the child develops representations for an ‘all-
good self’ and an ‘all-bad self’; an ‘all-good object’ and an ‘all-bad
object’. As the child matures into the third stage of development the ‘all-
good’ and ‘all-bad’ self-representations are integrated. The child
develops a more complete view of the self as having both positive and
negative impulses and wishes. Concurrently the ‘all-good’ and ‘all-bad’
representations of others (parents, siblings, friends) are integrated. The
child develops representations of others as having both positive and
negative attributes. When this happens the child becomes capable of
having realistic relationships in which ambivalent feelings towards
others can be tolerated. So children may feel that they love their parents
who are good a lot of the time and a bit annoying some of the time.
In adulthood the way people behave within intimate relationships is
predominantly informed and organized by their internal object relations
that they learned in childhood; that is, by mental images of how the self
and others will function in relationships, and the strong emotions
associated with these types of relationship. An image of a bad child-like
self, interacting with a threatening, powerful authority figure associated
with a strong feeling of fear; or the image of a good child-like self
interacting with a good protective authority figure associated with a
strong feeling of security, are examples of internal object relations.
Where parents are over-indulgent or overly neglectful, violent or
controlling, the child fails to develop mature self–other internal object
relations. In their relationships with others, splitting occurs. They view
others as ‘all-good’ idealized rescuers who will meet all their needs or
‘all-bad’ persecutors who are out to harm them. They also oscillate
between viewing the self as ‘all-good’ or ‘all-bad’. These difficulties are
the hallmark of all personality disorders. Different types of personality
disorder develop depending on the person’s temperament, whether the
child was over-indulged, neglected or traumatized, the degree to which
this occurred, and the specific defence mechanisms that they used to
cope with forbidden sexual and aggressive impulses. Cluster A and B
personality disorders arise from neglect, rejection or abuse, whereas
excessive parental control or over-protection lead to the development of
Cluster C personality disorders.
Defences are psychological strategies used to cope with conflict
between unacceptable impulses (often unconscious sexual or aggres-
sive urges from the id) and the prohibitions of the conscience (or super-
ego). Thus, if a person experiences an unacceptable impulse, anxiety
about the consequences of acting on this impulse will be experienced.
Defences are used to reduce anxiety. Defences are essential, but some
are more adaptive than others. From Table 8.3 it may be seen that the
defences of splitting and projection, which typify many personality dis-
orders, particularly borderline personality disorder, are at the most prim-
itive level. Splitting involves reverting to viewing the self and others in
‘all-good’ or all-bad’ terms. Projection involves attributing negative

Book 1.indb 270 06/03/2012 13:48

 8 • PERSONALITY DISORDERS 271

TABLE 8.3
Defence mechanisms at different levels of maturity
Level Features of Defence The individual regulates emotional discomfort
defences associated with conflicting wishes and impulses
or external stress by …
High-adaptive Promote an Anticipation considering emotional reactions and
level optimal balance consequences of these before the conflict or
among stress occurs and exploring the pros and cons of
unacceptable various solutions to these problematic emotional
impulses and states
prosocial wishes
Affiliation seeking social support from others, sharing
to maximize
problems with them without making them
gratification and
responsible for them or for relieving the distress
permit conscious
they entail
awareness of
conflicting Altruism dedication to meeting the needs of others and
impulses and receiving gratification from this (without excessive
wishes self-sacrificing)
Humour reframing the situation that gives rise to conflict or
stress in an ironic or amusing way
Self-assertion expressing conflict-related thoughts or feelings in
a direct yet non-coercive way
Self-observation monitoring how situations lead to conflict or stress
and using this new understanding to modify
negative affect
Sublimation channelling negative emotions arising from conflict
or stress into socially acceptable activities such as
work or sports
Suppression intentionally avoiding thinking about conflict or
stress
Mental Keep Displacement transferring negative feelings about one person
inhibitions unacceptable onto another less threatening person
compromise impulses out of
Dissociation experiencing a breakdown in the integrated
formation awareness
functions of consciousness, memory, perception,
level
or motor behaviour
Intellectualization the excessive use of abstract thinking or
generalizations to minimize disturbing feelings
arising from conflict
Isolation of affect losing touch with the feelings associated with
descriptive details of the conflict, trauma or stress
Reaction substituting acceptable behaviours, thoughts or
formation feelings that are the opposite of unacceptable or
unwanted behaviours, thoughts or feelings that
arise from a conflict
Repression expelling unwanted thoughts, emotions or wishes
from awareness
Undoing using ritualistic or magical words or behaviour to
symbolically negate or make amends for
unacceptable impulses
(Continued)

Book 1.indb 271 06/03/2012 13:48

 272 C L I N I C A L P S Y C H O L O G Y : A N I N T R O D U C T I O N

TABLE 8.3
(Continued)
Level Features of Defence The individual regulates emotional discomfort
defences associated with conflicting wishes and impulses
or external stress by …
Minor image Distort image of Devaluation attributing exaggerated negative characteristic to
distorting level self and others to the self or others
regulate self-
Idealization attributing exaggerated positive characteristics to
esteem
others
Omnipotence attributing exaggerated positive characteristics or
special abilities and powers to the self which make
oneself superior to others
Disavowal Keep Denial refusing to acknowledge the painful features of
level unacceptable the situation or experiences which are apparent to
impulses and others
ideas out of
Projection attributing to others one’s own unacceptable
consciousness
thoughts, feelings and wishes
with or without
misattribution of Rationalization providing an elaborate self-serving or self-
these to external justifying explanation to conceal unacceptable
causes thoughts, actions or impulses
Major image Gross distortion Autistic fantasy engaging in excessive daydreaming or wishful
distorting level or misattribution thinking as a substitute for using problem-solving
of aspects of the or social support to deal with emotional distress
self or others
Projective attributing to others one’s own unacceptable
identification aggressive impulses. Then inducing others to feel
these by reacting aggressively to them. Then
using the other person’s aggressive reactions as
justification for acting out unacceptable aggressive
impulses
Splitting of self- failing to integrate the positive and negative
image or image qualities of self and others and viewing self and
of others others as either all good or all bad
Action level Action or Acting out acting unacceptably to give expression to the
withdrawal from experience of emotional distress associated with
action conflict or stress
Apathetic not engaging with others
withdrawal
Help-rejecting making repeated requests for help and then
complaining rejecting help when offered as a way of
expressing unacceptable aggressive impulses
Passive unassertively expressing unacceptable aggression
aggression towards others in authority by overtly complying
with their wishes while covertly resisting these
Level of Failure of Delusional attributing to others one’s own unacceptable
defensive defences to projection thoughts, feelings and wishes to an extreme
dysregulation regulate conflict- degree
related feelings
Psychotic denial refusing to acknowledge the painful features of
leading to a
the situation or experiences which are apparent to
breakdown in
others to an extreme degree
reality testing
Psychotic viewing reality in an extremely distorted way
distortion

Note: Based on American Psychiatric Association (2000) Diagnostic and statistical manual of mental disorders (fourth edition,
text revision, DSM-IV-TR). Defensive Functioning Scale (pp. 807–809). Washington, DC: American Psychiatric Association.

Book 1.indb 272 06/03/2012 13:48

 8 • PERSONALITY DISORDERS 273

aspects of the self to others: for example, attributing extreme anger or

spite to another person, and then feeling justified in being hurt and dis-
appointed, because feelings of anger and spite are unacceptable to the
self.
Transference-focused psychodynamic psychotherapy for borderline
personality disorder is based on Kernberg’s model of the development
of object relations (Kernberg & Caligor, 2005; Yeomans & Diamond,
2010). With this form of therapy, the therapist initially forms a contact
with the patient for twice weekly sessions over a year-long period. In
these sessions the therapist creates a safe and secure context within
which patients can describe challenging episodes in their lives and
express strong emotions, without physically acting these out through
violence, self-harm or leaving therapy. For borderline patients these
strong emotions typically involve primitive internal object relations dyads
where patients experience the self and significant others in their lives
(including the therapist) as ‘all good’ or ‘all bad’. The therapist carefully
observes the patients’ expression of strong affects, the primitive object
relations and defences of splitting and projection associated with them,
and talks with the patient about these observations in a non-judgemental
way.
The main therapeutic interventions are clarification, confrontation
and interpretation. With clarification, the therapist invites patients to
elaborate on the thoughts, actions and emotions of the self and others
(including the therapist) in problematic situations. With confrontation,
the therapist points out inconsistencies and contradictions between
patients’ differing accounts of the self and others at different times, or
between patients’ accounts, affects and behaviours in a single episode.
For example, the therapist may point out that in one instance the
therapist–client transference relationship resembles that of a persecuting
parent to a frightened and needy child with the client in the role of the
child; that at another time the relationship is the same but the roles are
reversed, with the client adopting the role of the persecuting parent;
while on other occasions the relationship resembles that of a satisfied
child and an all-giving mother. With interpretation, the therapist may
offer explanations for such inconsistencies by suggesting links between
the use of splitting, primitive idealization and projection as defences to
reduce anxiety associated with attempting to integrate the all-good and
all-bad primitive object relations. For example, the therapist may point
out that one reason for viewing people as all-good or all-bad is that it
preserves the possibility of having one’s needs met by an all-gratifying
mother. However, the down-side of using splitting and projection is that
it prevents the development of sustainable intimate relationships
because it requires denying the existence of frustrating characteristics
in people defined as all-good, and positive characteristics of people
defined as all-bad. This in turn may involve patients accepting that they
have strong unacceptable sexual and aggressive feelings.
As patients repeatedly engage in therapeutic conversations involving
clarification, confrontation and interpretation, their capacity for reflec-
tion on their own and others’ roles in emotionally intense interaction

Book 1.indb 273 06/03/2012 13:48

 274 C L I N I C A L P S Y C H O L O G Y : A N I N T R O D U C T I O N

increases. That is, they show increased reflective functioning, which is

the capacity to understand the psychological states, motives and inten-
tions of the self and others. They become better able to tolerate painful
emotions without resorting to seeing the self and others as ‘all-good’ or
‘all-bad’ and acting out their intense emotions in destructive ways.
A series of trials support the effectiveness of transference-focused
psychotherapy in improving the functioning of patients with borderline
personality disorder on a number of parameters including reflective
functioning, mood, self-harm and hospitalization (Yeomans & Diamond,
2010).

Mentalization-based treatment for borderline

personality disorder
Mentalization-based treatment is an evidence-based psychodynamic
therapy developed by Anthony Bateman and Peter Fonagy in the UK
(Bateman & Fonagy, 2010a, 2010b). It aims to improve adjustment in
borderline personality disorder by enhancing mentalization skills.
Mentalization or mentalizing is the capacity to understand mental states
of the self and others, and to conceptualize these states as being
separate from behaviour. Mentalizing involves being able to think about
thoughts, emotions, wishes, desires, and needs in the self and others;
to understand that these internal events may have an impact on actions;
but to recognize that they are distinct from those actions. The impulsivity,
emotional regulation problems and consequent relationship difficulties
that occur in borderline personality disorder arise from a limited capacity
to mentalize.
Mentalization develops in early life in the context of caregiver–child
attachment relationships within which the child’s mental states are
understood and ‘mirrored’ by their caregivers and appropriately
responded to. The development of mentalization is compromised where
such understanding, mirroring and responsive parenting are absent.
Thus, neglectful or abusive parenting and the insecure, and often disor-
ganized, attachment that develops as a consequence inhibits the devel-
opment of a robust capacity to mentalize within attachment relationships.
These processes in combination with the predisposing factors of child-
hood trauma or abuse and constitutional vulnerability (for example, dif-
ficult temperament) lead to the development of borderline personality
disorder. In borderline personality disorder a hypersensitive attachment
system develops in which there is extreme sensitivity to loss. In situ-
ations where loss occurs or is anticipated, the person experiences
hyper-arousal. Hyper-arousal radically reduces the capacity to men-
talize in such situations. This may occur because hyper-arousal directly
reduces the capacity to mentalize, or in cases of child abuse children
may defensively inhibit the mentalization process to avoid having to
recognize that their attachment figures have intentionally hurt them.
Mentalization-based treatment focuses on facilitating an optimal
level of arousal in the context of a secure attachment relationship
between patient and therapist which is not too intense or too detached.

Book 1.indb 274 06/03/2012 13:48

 8 • PERSONALITY DISORDERS 275

Initially the therapist facilitates this optimal level of arousal with

techniques such as empathy, support and clarification. These techniques
soothe the patient, reduce arousal and create a context that supports
mentalization. When patients engage in transference reactions, rather
than interpreting these to provide insight, the therapist collaborates with
the patient and helps them to mentalize the transference. This involves
encouraging patients to think about the current client–therapist
relationship with the aim of focusing their attention on another mind –
the mind of a therapist – and assisting them to contrast their own
perception of themselves with how they are perceived by the therapist.
In this form of treatment, therapists adopt a mentalizing therapeutic
stance. This is characterized by humility, curiosity, patience and respect.
The therapist humbly adopts a ‘not-knowing’ position; curiously asks
patients in detail about their experiences; patiently takes time to
understand these; and legitimizes in a respectful way the differing
perspectives of the patient and the therapist. If similarities in patterns of
relationships in the therapy and in childhood or currently outside of the
therapy are pointed out (following the triangle of person in Figure 5.5),
the aim of this is not to provide patients with insight so that they can
control this behaviour pattern in future, but to draw attention to other
situations that require mentalization. Therapists actively avoid offering
transference interpretations in a way that involves them ‘thinking for’
patients. Rather they stimulate patients to ‘mentalize’ about transference
reactions and reach their own conclusions.
Evidence from trials in which mentalization-based treatment was
offered to partially hospitalized patients and to outpatients over periods of
12–18 months shows that it is effective in the short and long terms
(Bateman & Fonagy, 2010a, 2010b). In a number of trials it led to improved
adjustment of patients with borderline personality disorder, as shown by
reduced self-harm and rehospitalization and increased employment.

Short-term psychodynamic psychotherapy for

Cluster C personality disorders
Short-term psychodynamic psychotherapy is an evidence-based treat-
ment developed by Leigh McCullough in the US and has been shown in
a controlled trail to be effective for Cluster C personality disorders
(Svartberg & McCullough, 2010). Within this model (which is dia-
grammed in Figure 5.5), Cluster C personality disorders are assumed to
arise from a dynamic conflict between prohibited adaptive feelings (F)
such as anger, grief, attachment or sexual excitement one hand, and
inhibiting feelings (A) such as anxiety, guilt and shame on the other.
Defences (D) such as social withdrawal, dependency or an excessive
concern with order emerge as compromise responses to these con-
flicts, and as the symptoms of Cluster C personality disorders. For
example, a person who is angry (F) may become anxious about repris-
als (A) and so may become withdrawn and deferential (D); a person
who feels grief due to loss (F) may fear further pain due to loss (A) and
so may avoid intimacy by becoming dutiful and orderly (D).

Book 1.indb 275 06/03/2012 13:48

 276 C L I N I C A L P S Y C H O L O G Y : A N I N T R O D U C T I O N

McCullough refers to this process as ‘affect phobia’ which is a social

learning theory way of describing psychodynamic conflict. F–A–D pat-
terns, referred to as the triangle of conflict, are learned in childhood with
parents and caregivers (P), and are repeated in adult patients’ current
lives with partners, friends and colleagues (C) and also in transference
relationships with therapists (T). These three contexts, T–C–P, within
which the triangle of conflict is replicated are referred to as the triangle
of person. In short-term dynamic psychotherapy, through interpretation
therapists help patients understand how they repeatedly enact the
triangle of conflict in multiple contexts represented by the triangle of
person. They then help patients desensitize themselves to their unac-
ceptable feelings (F) by encouraging them to repeatedly experience
these hidden feelings in an intense way within therapy sessions, with-
out resorting to the use of defences. This treatment typically involves
a year of weekly sessions.

Cognitive-behavioural approaches
Results from a meta-analysis show that cognitive-behavioural ap-
proaches and psychodynamic approaches to the treatment of person-
ality disorders are equally effective (Leichsenring & Leibing, 2003).
Within the cognitive-behavioural tradition Marsha Linehan’s dialectical
behaviour therapy for borderline personality disorder is the best vali-
dated approach (Stanley & Brodsky, 2009). Aaron T. Beck’s cognitive-
behavioural conceptualization of personality disorders has also been
influential (Beck et al., 2003).

Dialectical behaviour therapy

Dialectical behaviour therapy was developed by Marsha Linehan in the
US. Marsha is both an eminent clinical psychologist and a survivor of
borderline personality disorder. Dialectical behaviour therapy is based
on a biosocial diathesis–stress conceptualization of the aetiology of
borderline personality disorder (Stanley & Brodsky, 2009). The theory
proposes that the condition arises when individuals with a constitutional
vulnerability that compromises their capacity for emotion regulation are
chronically exposed to invalidating environments. In such environ-
ments, individuals’ communications about their inner challenging expe-
riences are repeatedly invalidated, so that eventually they become
self-invalidating, which is a central feature of borderline personality dis-
order. Their moderate displays of emotion are regularly punished, but
extreme emotional displays are inadvertently reinforced by family mem-
bers’ expressions of concern or medical care. This results in ongoing
emotional inhibition with periodic intense emotional displays character-
istic of borderline personality disorder.
Dialectic behaviour therapy aims to decrease suicidal behaviour,
posttraumatic symptomatology, behaviours that interfere with engaging
in therapy, and behaviours that interfere with quality of life. It also aims
to increase behavioural skills for emotion regulation and enhance self-

Book 1.indb 276 06/03/2012 13:48

 8 • PERSONALITY DISORDERS 277

respect. Dialectic behaviour therapy begins with the formation of a

therapeutic contract which is typically between 6 months and a year.
The cornerstone is a dialectical worldview where polar opposites, or
thesis and antithesis, are integrated through synthesis. Clients are
helped to acknowledge polarizations in their experiences and work
towards a synthesis of these extremes.
For therapists and clients, the overriding dialectic within therapy in
between acceptance and change. Dialectical behaviour therapy inte-
grates cognitive-behavioural, change-based interventions with accept-
ance-based approaches, notably mindfulness meditation derived from
Zen practice. It is a multimodal programme that incorporates individual
psychotherapy, telephone consultation, group-based skills training,
therapists’ consultation meetings and ancillary treatments such as med-
ication and acute–inpatient psychiatric services. In group sessions
mindfulness meditation, skills for tolerating distress and regulating emo-
tions, and interpersonal effectiveness skills such as assertiveness are
acquired. In individual therapy, clients are helped to become motivated
to use these skills, and to increase adaptive and decrease maladaptive
behaviours by altering the factors that reinforce these behaviours in
their day-to-day lives. There is a strong emphasis on validation of cli-
ents’ experiences and using behavioural analysis to understand factors
that promote and inhibit therapeutic progress. In telephone consulta-
tions between sessions clients are helped to generalize the skills they
have learned to multiple real-life settings and to manage crises. In con-
sultation meetings, liaison with family members and other involved pro-
fessionals and agencies occurs.
A meta-analysis has shown that dialectical behaviour therapy
reduces suicidal and self-injurious behaviour in patients with borderline
personality disorder and improves their overall adjustment (Kliem et al.,
2010).

Cognitive-behavioural theories
In Aaron T. Beck’s cognitive behavioural conceptualization of personal-
ity disorders he proposes that people with personality disorders have
developed pervasive, self-perpetuating cognitive–interpersonal cycles
that are severely dysfunctional (Beck et al., 2003). Early life experi-
ences, including family routines and relationships as well as traumatic
events, lead to the formation of assumptions about the world and in
particular about interpersonal relationships: for example, ‘people are
not trustworthy’. In day-to-day interactions, these underlying assump-
tions lead to automatic thoughts such as ‘He’s trying to con me’. These
in turn lead to emotional reactions such as anger and behavioural reac-
tions such as oppositional and confrontative conversation. This in turn
elicits behaviour from others such as secretiveness and avoidance,
which reinforces the basic assumption that ‘people are not trustworthy’.
For each personality disorder there are predominant mood states
and predominant behavioural strategies used to deal with interpersonal
situations. Collections of basic assumptions, learned in early life, may

Book 1.indb 277 06/03/2012 13:48

 278 C L I N I C A L P S Y C H O L O G Y : A N I N T R O D U C T I O N

be formed into schemas that inform those aspects of the world to which
the person attends and how they are apt to interpret most situations.
For example, an abuse–mistrust schema may contain a collection of
beliefs about the untrustworthiness of others and their potential for
abusing or harming the person. In addition to schemas, cognitive
distortions such as mind-reading (I just know he’s trying to get at me
with that remark) or emotional reasoning (I feel angry, so he must be
persecuting me) contribute to the way a person reacts to interpersonal
situations. Also, predominant mood states may predispose people to
attend to particular types of information or to evaluate situations in
particular ways. For example, anger may predispose a person to attend
to potential threats and to evaluate situations as opportunities for
confrontation.
Cognitive therapy aims to break the dysfunctional cognitive–interper-
sonal cycles that constitute the person’s personality disorder using a
variety of cognitive and behavioural strategies. These include helping
people learn to identify and challenge their automatic thoughts and core
assumptions; helping people develop different interpersonal strategies
and skills that are less likely to elicit from others behaviour that rein-
forces dysfunctional beliefs; and helping people engage in activities that
will directly alter their mood states. There is some evidence from meta-
analyses for the effectiveness of CBT with a range of personality disor-
ders (Leichsenring & Leibing, 2003).

Marital and family therapy

Marital and family therapy interventions for personality disorders focus
on helping couples and families recognize and alter current family-
based patterns of interaction that maintain the personality disorder.
They also help family members identify and challenge the belief systems
and narratives that underpin these rigid interaction patters. Finally, in
marital and family therapy, family members may be invited to understand
how particular personal characteristics or traits and particular family of
origin experiences have predisposed them to developing family belief
systems and behaviour patterns that maintain personality disorders.
Controlled trials of marital and family therapy for personality disorder
have not been reported in the literature, but guidelines on current best
practice have been published (e.g., Lebow & Uliaszek, 2010).

Risk of violence
The assessment and management of risk of violence is essential in
cases of antisocial personality disorder, because of the association
between this condition and aggression. In clinical interviews, patients
with antisocial personality disorder may not give true accounts of their
aggressive impulses. Because of this, the use of validated structured
clinical instruments and information from collateral sources such as
relatives or other agencies that have had contact with the patient to

Book 1.indb 278 06/03/2012 13:48

 8 • PERSONALITY DISORDERS 279

assess risk violence is important (Scott & Resnick, 2006). Thus, risk
management typically involves interviews with the patient and members
of their families as well as multidisciplinary and multiagency meetings.
Multiagency meetings may involve staff from probation services, since
many patients with antisocial personality disorder are on probation.
The Psychopathy Checklist (PCL-R, Hare, 2003) and Historical,
Clinical, Risk Management–20 (HCR-20, Douglas et al., 2001) are
examples of well-validated and widely used instruments for assessing
risk of violence. The HCR-20 consists of 20 items on historical, clinical
and risk management issues. The historical items cover previous
violence, substance misuse problems, major mental illness, psychopathy
and personality disorder. The clinical items are concerned with lack of
insight, negative attitudes, active symptoms of mental illness, impulsivity
and unresponsiveness to treatment. The risk management items
include feasibility of plans, exposure to destabilizing influences, lack of
personal support, non-compliance with treatment and stress.
In light of the assessment a formulation of the risk of violence is
developed, identifying factors likely to increase or decrease the risk and
a plan for managing these. Risk management plans should be directed
at crisis resolution, decreasing risk factors and increasing protective
factors. Members of the patient’s family and other involved profes-
sionals such as probation officers and social workers may play a role
in risk management plans. Unfortunately, there are no well-validated
treatments for antisocial personality disorder, so risk management
strategies must focus on using available evidence-based practices to
address specific problems such as motivational interviewing for comor-
bid substance use or training in anger management skills.

Assessment
The assessment of personality disorder occurs within the context of the
assessment of the whole person. When assessing patients with person-
ality disorder, typically Axis I disorders such as mood, anxiety, sub-
stance use or eating disorders are present, and these are assessed in
ways described in Chapters 3–6. In a significant proportion of cases,
risky behaviours such as self-harm or violence may also be present.
The assessment and management of risk of harm to the patient or
others is always prioritized. (Suicide risk assessment has been discussed
in Chapter 6.)
Ideally the assessment and treatment of personality disorders is
conducted by multidisciplinary teams. Initial screening for personality
disorders may be conducted with self-report inventories such as the
Millon Clinical Multiaxial Inventory–III (MCMI-III, Millon, 2009), the
Schedule for Nonadaptive and Adaptive Personality–II (SNAP-2, Clark
et al., 2008) or the personality disorder scales of the Minnesota
Multiphasic Personality Inventory–2 (MMPI-2, Colligan et al., 1994).
Where self-report instruments suggest the presence of a personality
disorder, a diagnosis may be confirmed through clinical interviewing. A

Book 1.indb 279 06/03/2012 13:48

 280 C L I N I C A L P S Y C H O L O G Y : A N I N T R O D U C T I O N

number of structured interviews for the diagnosis of personality disorders

are available, such as the Structured Clinical Interview for DSM-IV
Personality Disorders (SCID-II, First et al., 1997) and the International
Personality Disorder Examination (IPDE, Loranger, 1999). The Revised
NEO Personality Inventory (NEO-PI-R, Costa & McCrae, 1992) is the
best available instrument for assessing the Big 5 personality factors and
their 30 facets, and this may provide a useful profile of personality traits
and facets to take into account in formulating the case. (The trait
approach to personality disorders is discussed below in the section on
controversies.)
The personality disorder diagnosis, along with information from an
assessment of personality traits and facets and the clinical history, is
used to construct a formulation. The formulation explains the main
clinical problems entailed by the personality disorder with reference to
predisposing, maintaining and protective factors. Precipitating factors
may be included in formulations of personality disorders, to identify
events that precipitated referral for treatment or a recent crisis. However,
since personality disorders are by definition longstanding patterns of
adjustment, factors that precipitated their onset usually are not
meaningfully identifiable. During the process of assessment and
treatment patients with personality disorders and family members may
be invited to keep daily records of fluctuations in symptoms, distress,
and beliefs and the circumstances preceding and following these
fluctuations. These idiographic ratings are useful for fine-tuning ongoing
therapy. Comprehensive reviews of personality disorder assessment
instruments are given in Strack (2010) and Widiger (2008).

Treatment
In extensive narrative reviews of the design and delivery of psychotherapy
programmes for service users with personality disorders, Bateman and
Fonagy (2000) and Linehan et al. (2006) concluded that effective
programmes – whether cognitive behavioural or psychodynamic –
share a number of common features. They are theoretically coherent
(not eclectic), offering an explanation for problematic behaviours and
interpersonal styles, and for the role of psychotherapy in offering a
solution to these problems. They are well structured and of long duration,
usually extending beyond a year. They include procedures for helping
clients engage in treatment, maintain therapeutic contact and adhere to
therapeutic regimes.
Effective psychotherapy programmes may include sequential or con-
current individual, group and family sessions, following a pre-established
coherent pattern. Effective outpatient psychotherapy programmes are
offered within the context of broader multimodal, multidisciplinary ser-
vices in which there are clear policies and practices for inpatient care,
use of medication, and crisis management where high-risk behaviour in-
cluding self-harming, aggression or other crises occurs. Effective pro-
grammes have a clear focus on key problem areas such as self-harm,
aggression and difficult interpersonal relationships. Effective therapeutic

Book 1.indb 280 06/03/2012 13:48

 8 • PERSONALITY DISORDERS 281

techniques strike a balance between a focus on acceptance of clients’

constraints and limitations on one hand, and a focus on behavioural
change and developing less problematic ways of living on the other.
Psychotherapists offering effective treatment programmes for per-
sonality disorders receive sustained intensive supervision, in which
intense countertransference reactions elicited by psychotherapy with
these clients are addressed. Positive outcomes are more probable
where therapists are patient, flexible and creative in their approach to
therapy; are comfortable with long-term, intense therapeutic relation-
ships; are tolerant of their own negative feelings about patients and the
therapy process; and have specific training in treating personality disor-
ders (Fernandez-Alderez et al., 2006).
For borderline personality disorder, dialectical behaviour therapy,
mentalization-based treatment and transference-focused psychother-
apy are well-developed evidence-based treatments. For other person-
ality disorders, either psychodynamic or cognitive behaviour therapy of
at least a year’s duration may be effective in a proportion of cases.
Adjunctive psychopharmacological interventions for symptom manage-
ment may be integrated into psychological treatment programmes for
personality disorders. The central role of psychotherapy in the treat-
ment of personality disorders is consistent with international guidelines
for best practice (Alwin et al., 2006; American Psychiatric Association,
2001b; National Institute of Mental Health in England, 2003; NICE,
2009c, 2009d).

Controversies
In the field of personality disorders the main controversies centre on the
categorical or dimensional conceptualization of abnormal personality
functioning, the validity of the distinction between Axis I and Axis II
disorders, and therapeutic communities as an alternative to hospital or
outpatient treatment.

Trait theory as an alternative to categorical diagnoses

Within DSM-IV-TR and ICD-10, personality disorders are conceptual-
ized in categorical terms. That is, it is assumed that within a population
some people have personality disorders and some do not, and that
there are qualitative differences between those that do and do not meet
the diagnostic criteria for personality disorders. Trait theories, in con-
trast, propose that a limited number of dimensions may be used to char-
acterize important aspects of behaviour and experience. Traits are
normally distributed within the population. So for any given trait (for
example, introversion–extraversion), most people show a moderate
level of the trait, but a few people show extremely low or extremely high
levels. Within a population, people who fall at the extreme ends of these
dimensions may have the sorts of difficulties attributed in DSM-IV-TR
and ICD-10 to people with personality disorders. However, these people
differ from others only in the degree to which they show particular traits.

Book 1.indb 281 06/03/2012 13:48

 282 C L I N I C A L P S Y C H O L O G Y : A N I N T R O D U C T I O N

Traits are identified by factor-analysing responses of large samples of

people to extensive personality questionnaires and rating scales. Factor
analysis is a procedure for mathematically clustering questionnaire or
rating scale items that correlate with each other into a small set of
dimensions.
In recent years trait theory has come to be dominated by the five-factor
model of personality (McCrae & Costa, 2008). This model includes the
following dimensions: neuroticism, extraversion, openness to experience,
agreeableness, and conscientiousness. Neuroticism reflects differences
in emotional lability and varies from emotionally stable to unstable.
Extraversion reflects differences in sociability and varies from introverted
to extraverted. Openness to experience reflects willingness to accept new
ideas, feelings and actions and extends from imaginative creativeness to
constriction. Agreeableness refers to interpersonal warmth or coldness.
Conscientiousness varies from highly dutiful and self-disciplined to irre-
sponsible and undisciplined. Each of the factors within the five-factor
model contains six facets, which are listed in Table 8.4. There is evidence

TABLE 8.4
Factors and facets of the five-factor model of personality
Factor Facet
Neuroticism Anxiety
Angry hostility
Depression
Self-consciousness
Impulsiveness
Vulnerability
Extraversion Warmth
Gregariousness
Assertiveness
Activity
Excitement seeking
Positive emotions
Openness to experience Fantasy
Aesthetics
Feelings
Actions
Ideas
Values
Agreeableness Trust
Straightforwardness
Altruism
Compliance
Modesty
Tender-mindedness
Conscientiousness Competence
Order
Dutifulness
Achievement striving
Self-discipline
Deliberation

Book 1.indb 282 06/03/2012 13:48

 8 • PERSONALITY DISORDERS 283

for the heritability of all of factors within the Five Factor Model except
agreeableness which seems to be predominantly environmentally
determined (Costa & Widiger, 1994).
Thomas Widiger has proposed that the five-factor model may be used
as an alternative system for describing personality disorders (Widiger &
Mullins-Sweatt, 2010). The profiles of major personality disorders on the
dimensions of the five-factor model of personality are presented in Table
8.5. These profiles are based on Samuel and Widiger’s (2008) meta-
analysis of data from 16 studies of 30 facets of the five-factor model of
personality in groups of patients with personality disorders.
Widiger argues that trait theory offers a more scientifically useful
approach to assessment. Personality questionnaires that have been
developed to measure the Big Five personality traits have good psycho-
metric properties (De Raad & Perugini, 2002). They are reliable and
valid, and have population norms. The five-factor personality trait theory
and related measures assume a demonstrated continuity between nor-
mal and abnormal personality. Research on the Big Five personality
traits has led to a significant body of knowledge on the genetic and
childhood antecedents of normal adult personality, neurobiological cor-
relates of personality traits, and the stability and change in personality
traits over the life course. This body of research may inform our under-
standing of personality disorders, if we base our assessment on the
five-factor model. Compared with categorical classification systems,
trait models offer a more parsimonious way of describing people with
rigid dysfunctional behaviour patterns. This in turn offers a more parsi-
monious way to conceptualize the development of effective treatments.

Continuity between Axis I and Axis II disorders

A second controversy concerns the validity of the distinction between
Axis I and Axis II disorders. There are significant similarities between
each of the personality disorders and certain Axis I disorders. However,
there are also distinct differences. These are listed in Table 8.6.
Paranoid, schizoid and schizotypal personality disorders each bear a
marked resemblance to aspects of schizophrenia. However, people
with these three personality disorders do not show frank delusions,
hallucinations, thought disorder or negative symptoms. There are clear
parallels between antisocial personality disorder and conduct disorder,
since both involve moral immaturity and violation of others’ rights. About
a third of youngsters with conduct disorder, when they reach adulthood,
meet the diagnostic criteria for antisocial personality disorder (Kazdin,
1995). Borderline personality disorder resembles depression, insofar as
loss and abandonment are central themes and negative affect is a core
feature of both conditions.
Hysterical personality disorder and conversion hysteria are similar
insofar as in both conditions a caricature of a role is adopted and this is
associated with attention seeking and secondary gain. However, with
hysterical personality disorder, the role is that of a stereotypically
seductive woman or macho male, whereas in conversion hysteria a

Book 1.indb 283 06/03/2012 13:48

Book 1.indb 284
TABLE 8.5
Profiles of DSM-IV personality disorders from a meta-analysis of 30 facets of the five-factor model of personality
Cluster Personality Neuroticism Extraversion Agreeableness Conscientiousness Openness Top three facets
disorder
Cluster A Paranoid Angry Cold Mistrustful Mistrustful
Odd, eccentric group Depressed Joyless Conflictual Angry
Self-conscious Aloof Guarded Depressed
Anxious Selfish
Schizoid Depressed Cold Mistrustful Aloof
Self-conscious Joyless Cold
Aloof Joyless
Inactive
Submissive
Avoids excitement
Schizotypal Depressed Cold Mistrustful Depressed
Self-conscious Aloof Self-conscious
Angry Mistrustful
Anxious
Cluster B Antisocial Angry Seeks excitement Guarded Careless Careless
Dramatic, emotional, Impulsive Conflictual Not dutiful Guarded
erratic group Selfish Undisciplined Conflictual
Mistrustful Lacks self-belief
Borderline Depressed Joyless Mistrustful Undisciplined Depressed
Angry Cold Conflictual Lacks self-belief Angry
Vulnerable Guarded Careless Anxious
284 C L I N I C A L P S Y C H O L O G Y : A N I N T R O D U C T I O N

Anxious Not dutiful

Self-conscious
Impulsive
Histrionic Gregarious Gregarious
Assertive Assertive
Excitement Excitement
seeking seeking
Warm
Active
Joyful

06/03/2012 13:48
Book 1.indb 285
Narcissistic Angry Boastful Boastful
Guarded Guarded
Conflictual Conflictual
Selfish
Mistrustful
Cluster C Avoidant Self-conscious Aloof Mistrustful Lacks self-belief Avoids new Self-conscious
Anxious, fearful Depressed Submissive Modest Undisciplined experiences Depressed
group Anxious Joyless Aloof
Vulnerable Cold
Angry Inactive
Avoids excitement
Dependent Vulnerable Submissive Lacks self-belief Vulnerable
Self-conscious Undisciplined Self-conscious
Depressed Depressed
Angry
Obsessive- Orderly Orderly
compulsive Dutiful Dutiful
Achievement striving Achievement
Careful striving
Self-disciplined

Note: Based on Samuel and Widiger’s (2008) meta-analysis of data from 16 studies of 30 facets of the five-factor model of personality. For each personality disorder, facets within each
factor are listed in order of the size of their correlations with personality disorders. Only facets that had significant correlations (p < .05) greater than r = 0.2 are listed. In the final column,
for each personality disorder the top 3 facets (out of 30) are listed in order of the size of their correlations.
8 • PERSONALITY DISORDERS
285

06/03/2012 13:48
 286 C L I N I C A L P S Y C H O L O G Y : A N I N T R O D U C T I O N

TABLE 8.6
Comparison of personality disorders and Axis I disorders with similar features
Cluster Personality Similar Axis 1 Common clinical Differences in clinical features
disorder disorder features
Cluster A Paranoid Schizophrenia Mistrust and In PPD delusions, hallucinations,
Odd, (PPD) suspiciousness thought disorder, and negative
eccentric symptoms of schizophrenia are
group absent.
Schizoid Schizophrenia Attachment In SDPD delusions,
(SDPD) problems and hallucinations, thought disorder,
social isolation and negative symptoms of
schizophrenia are absent.
Schizotypal Schizophrenia Eccentric thoughts, In SLD delusions, hallucinations,
(SLPD) perceptual thought disorder, and negative
experiences and symptoms of schizophrenia are
speech absent.
Cluster B Antisocial Conduct Moral immaturity For a diagnosis of ALPD the
Dramatic, (ALPD) disorder person must be over 18. Conduct
emotional, disorder applies to children and
erratic group adolescents.
Borderline Depression Impulsivity In BPD, episodes of low mood
(BPD) are brief and the course of the
disorder is lifelong beginning in
childhood.
Histrionic Conversion Attention seeking In HPD attention is gained
(HPD) hysteria through adopting seductive or
macho role but with hysteria it is
gained by adopting a sick-role.
Narcissistic ?
(NPD)
Cluster C Avoidant Social phobia Shyness In ATPD people avoid
Anxious, (ATPD) relationships, but with social
fearful group phobia they avoid situations
Dependent Separation Lack of autonomy DPD continues into adulthood
(DPD) anxiety and affects all areas of
functioning
Separation anxiety is a childhood
disorder
Obsessive- Obsessive- Perfectionism In OCPD symptoms are accepted
compulsive compulsive but in OCD they are resisted
(OCPD) disorder

sick-role is adopted. The symptoms of conversion hysteria, which are

not feigned, include deficits in sensory or motor functioning in the
absence of an organic illness. Avoidant personality disorder and social
phobia are similar insofar as shyness typifies both conditions. However,
those with the personality disorder avoid relationships, whereas those
with the phobia avoid particular social situations.
Dependent personality disorder and separation anxiety both entail
problems with autonomy. Separation anxiety is a childhood disorder,

Book 1.indb 286 06/03/2012 13:48

 8 • PERSONALITY DISORDERS 287

but dependent personality disorder is the adult expression of the same

core issues. Obsessive compulsive personality disorder closely resem-
bles obsessive compulsive disorder. However, with the personality dis-
order the obsession with orderliness and rule-following is fully accepted
and embraced as a valued part of the person’s lifestyle, whereas with
OCD the obsessions and compulsions are resisted.
The similarities between Axis I and Axis II disorders described call
into question the validity of the distinctions made between these classes
of disorder. For example, it might be more parsimonious to amalgamate
diagnoses such as conduct disorder and antisocial personality disorder,
and express these difficulties in dimensional terms such as externalizing
behaviour problems. This approach is supported by results of genetic
studies which show that certain Axis I and Axis II disorders share genetic
risk factors (Reichborn-Kjennerud, 2010). These include schizophrenia
and Cluster A personality disorders, especially schizotypal personality
disorder; borderline personality disorder and depression; avoidant
personality disorder and social phobia; and antisocial personality
disorder, conduct disorder and substance use disorders.

Therapeutic communities
Therapeutic communities developed as an alternative approach to
treating personality disorders, addictions and other severe mental
health problems. Traditional inpatient mental health settings were hier-
archically organized, and run on authoritarian lines. They encouraged
patients to be passive recipients of treatment. Therapeutic communities
were run on more democratic lines and encouraged service users to
take an active role in their own rehabilitation. Responsibility for the daily
running of the community was shared among service users and staff.
In the UK, the radical psychiatrists Maxwell Jones (Jones, 1952) and
R. D. Laing (mentioned in Chapter 7 in the section on controversies)
were pioneers in the development therapeutic communities. In the US,
therapeutic communities were developed mainly for people with
addiction problems. Therapeutic communities for people with personality
disorders have been run in prisons, hospitals and day hospitals. In
these communities there are usually daily meetings of service users
and staff, and a predominance of group activities.
The hallmark of therapeutic communities is their democratic,
participative approach to decision-making. This creates a context within
which service users significantly influence the way their therapeutic
communities are run. Complex, participative community processes are
the central therapeutic factors of therapeutic communities (Jones, 1952).
In a systematic review of 52 outcome studies of the effects of therapeutic
communities on people with personality disorders and a meta-analysis
of 29 of these, Lees et al. (1999) found that a significant positive effect
occurred in 19 of the 29 studies in their meta-analysis. Participants in
these trials were young offenders or psychiatric service users with a
range of personality disorders. In their narrative review, Lees et al.
concluded that for people with personality disorder, long-term treatment

Book 1.indb 287 06/03/2012 13:48

 288 C L I N I C A L P S Y C H O L O G Y : A N I N T R O D U C T I O N

in therapeutic communities may lead to improvements in mental health

and interpersonal functioning, and that the longer a service user stays in
treatment, the better the outcome. They also found that secure
therapeutic communities were effective in managing difficult prisoners,
and significantly reducing serious prison discipline incidents including
fire-setting, violence, self-harm and absconding.

Summary
Personality disorders are characterized by enduring dysfunc-
tional patterns of behaviour and experience that begin in ado-
lescence and are consistent across situations. There are
difficulties with cognition, affect, impulse control, behaviour
and interpersonal functioning. There are also recurrent rela-
tionship problems or occupational problems with a history of
other psychological disorders or criminality. People with per-
sonality disorders have difficulty learning from experience or
benefiting from psychotherapy for their personality disorders or
other comorbid Axis I disorders.
In DSM-IV-TR, 10 main personality disorders are subdi-
vided into three clusters on the basis of their cardinal clinical
features. The odd, eccentric cluster includes the paranoid,
schizoid and schizotypal personality disorders. The dramatic,
emotional, erratic cluster includes the antisocial, borderline,
histrionic and narcissistic personality disorders. The third
cluster includes the avoidant, dependent and obsessive-
compulsive personality disorders, all of which are character-
ized by anxiety and fearfulness. A very similar classification
system is used in ICD-10.
The prevalence of personality disorders is approximately
10% in the general population, whereas in samples of mental
health service users the rate is about 40%. Many people who
have one personality disorder meet the criteria for a number of
others. Personality disorders are fairly stable over time,
although some improvement does occur, especially among
those with Cluster B personality disorders.
Diathesis–stress theories argue that personality disorders
emerge when genetically or constitutionally vulnerable individ-
uals are exposed to particular types of environmental stress.
Heritability estimates for personality disorders range from 20%
to 70% and recent research has begun to discover the neuro-
biological basis for some personality disorders, especially
schizotypal, borderline and antisocial personality disorder.
There is evidence for early adversity, problematic parenting,
trauma and child abuse in the aetiology of many personality

Book 1.indb 288 06/03/2012 13:48

 8 • PERSONALITY DISORDERS 289

disorders. Psychodynamic and cognitive behavioural theories

of personality disorders explain the emergence of person-
ality disorders in diathesis–stress terms, but propose detailed
psychological processes to account for symptom aetiology
and maintenance. Controlled trials of treatment programmes
based on these conceptualizations have been shown them
to be effective for some personality disorders, with the stron-
gest evidence base being for dialectical behaviour therapy,
transference-focused therapy and mentalization therapy for
borderline personality disorder.
With regard to pharmacological treatments there was
evidence for the effectiveness of antipsychotics in reducing
psychotic-like symptoms, mood stabilizers in reducing aggres-
sion, and antidepressants in regulating mood. Patients with
personality disorders usually have other Axis I disorders and
frequently are at risk of self-harm or violence. The assessment
and management of such patients is ideally conducted by
multidisciplinary teams and often involves multiagency liaison.
The main controversies in the field centre on the categorical or
dimensional conceptualization of abnormal personality func-
tioning, the validity of the distinction between Axis I and Axis II
disorders and the value of democratic therapeutic communities
as an alternative to traditional authoritarian inpatient treatment
settings.

Questions
● What is a personality disorder and how does it differ from an Axis I
disorder?
● What are the main personality disorders included in the DSM and
ICD classification systems?
● What is the main clinical feature of each of the personality disorders?
● How prevalent are personality disorders?
● What are the diathesis–stress, psychodynamic, and cognitive-
behavioural theories of personality disorders and the key research
findings relevant to these theories?
● What evidence-based approaches have been developed for the
assessment and treatment of personality disorders?
● What are the pros and cons of adopting a ‘Big 5’ dimensional
approach to personality disorders as an alternative to the DSM and
ICD categorical systems?

Book 1.indb 289 06/03/2012 13:48

 290 C L I N I C A L P S Y C H O L O G Y : A N I N T R O D U C T I O N

FURTHER READING
Professional
● Clarkin, J. & Lenzenweger, M. (2005). Major theories of personality dis-
order (second edition). New York: Guilford.
● Magnavita, J. J. (2010). Evidence-based treatment of personality dys-
function: Principles, methods, and processes. Washington, DC: American
Psychological Association.
● Oldham, J., Skodol, A. & Bender, D. (2009). Essentials of personality
disorders. Arlington, VA: American Psychiatric Publishing.

Self-help
● Fusco, G. & Freeman, A. (2004). Borderline personality disorder: A pa-
tient’s guide to taking control. New York: Norton.
● Mason, P. T. & Kreger, R. (1998). Stop walking on eggshells: Taking
your life back when someone you care about has borderline personality
disorder. Oakland, CA: New Harbinger.

WEBSITES
● American Psychiatric Association’s practice guidelines for treating border-
line personality disorder:
http://psychiatryonline.org/guidelines.aspx
● National Educational Alliance for Borderline Personality Disorder in the
US:
www.borderlinepersonalitydisorder.com
● National Institute for Clinical Excellence guidelines for treating antisocial
and borderline personality disorders:
http://guidance.nice.org.uk/topic/mentalhealthbehavioural
● PsychNet – Personality Disorders page:
www.psychnet-uk.com/x_new_site/personality_psychology/a_index_
personality_psychology.html
● UK Department of Health Personality Disorder policy documents:
www.dh.gov.uk/en/publicationsandstatistics/publications/publications
policyandguidance/dh_4009546
● UK Personality Disorder site:
www.personalitydisorder.org.uk

Book 1.indb 290 06/03/2012 13:48

 Models that influence
the practice of clinical
psychology 9
Learning objectives
After studying this chapter you will be able to:
● list the key assumptions of biological,
psychodynamic, cognitive-behavioural and family
systems models that influence the practice of clinical
psychology
● outline the main achievements of the biological,
psychodynamic, cognitive-behavioural and family
systems models
● critically evaluate the limitations of the biological,
psychodynamic, cognitive-behavioural and family
systems models
● describe the contributions of the humanistic client-
centred tradition, personal construct psychology
and positive psychology to the practice of clinical
psychology.

Introduction
Explanations and interventions for the various clinical problems des-
cribed in Chapters 2–8 have arisen from four main models:
● the biological model
● the psychodynamic model
● the cognitive-behavioural model
● the family systems model.

Book 1.indb 291 06/03/2012 13:48

 292 C L I N I C A L P S Y C H O L O G Y : A N I N T R O D U C T I O N

In this chapter the main assumptions of each of these models will

be outlined, along with an account of their achievements or strengths
and shortcomings or limitations. A summary of these issues is given in
Table 9.1. The contribution of a number of other influential approaches
to practice will be briefly considered in this chapter, including those
based on client-centred humanistic psychology, personal construct
psychology and the positive psychology.

Biological model
Assumptions
The biological model of psychological problems is also referred to
as the neurobiological, organic, medical or disease model. In this
framework it is assumed that the various psychological difficulties that
people with a particular syndrome display are symptoms of a specific
disease with a discrete neurobiological cause, a unique course and
prognosis, and for which a specific physical treatment will ultimately be
identified (Nestler & Charney, 2008). This model evolved within the
medical tradition where there were numerous examples of physical
conditions involving a syndrome of signs and symptoms that could
be explained by a discrete cause, such as an infection or metabolic
dysfunction.
Syphilis is a good example of a condition where a discrete physical
cause (syphilitic infection) leads to a psychological syndrome (general
paresis of the insane) and can be treated by a specific physical inter-
vention (inoculation). In 1897 Richard von Krafft-Ebing, a German neu-
rologist, following the work of Louis Pasteur, inoculated patients who
had general paresis with pus from syphilitic sores, and this halted the
development of the degenerative condition, which typically culminated
in insanity. The success of this work gave impetus to the biological
model of mental health problems. The model has been championed by
psychiatry more than other mental health professions.
Diathesis–stress or stress-vulnerability models are modern variants
of the biological model. In these types of model it is assumed that psy-
chological problems or ‘psychiatric illnesses’ occur when people who
are neurobiologically vulnerable to such difficulties are exposed to par-
ticular stresses. For example, a diathesis–stress model of schizophre-
nia was described in Chapter 7 (Walker et al., 2008; Zubin & Spring,
1977).

Achievements
The biological or medical model has led to a number of important
achievements. The first of these has been the development of mental
health legislation (Bartlett & Sandland, 2007; Gunn & Wheat, 2009).
This legislation makes provision for the involuntary detention and treat-
ment of people with psychological disorders whose judgement is
severely impaired, especially if they are a danger to themselves or other

Book 1.indb 292 06/03/2012 13:48

Book 1.indb 293
TABLE 9.1
Model of abnormal behaviour
Biological model Psychoanalytic model Cognitive behavioural model Family systems model
Cause of Central nervous system abnormality Unconscious psychopathology Learned habits Dysfunctional family system
abnormal
behaviour
Therapy goal • Rectify CNS abnormality • Resolve unconscious • Learn more adaptive • Alter problem-maintaining family
conflicts habits interaction patterns and beliefs
Therapy • Pharmacological • Long-term one-to-one • Short-term cognitive • Short-term marital or family
process • ECT psychoanalysis behaviour therapy therapy
• Psychosurgery
Achievements • Liberation of insane • Discovery of unconscious • Brief and effective • Highlighted social context of
• Mental health legislation • Makes madness meaningful • Permits evidence-based abnormal behaviour
• Classification • Discovery of transference practice • Brief and cost-effective
• Scientific method • Legitimized talking cure • Has specific interventions • Permits evidence-based practice
• Medical technology • Inspired other models of for specific problems • Permits integration of biological,
• Pharmacological and physical personality and therapy • Scientifically rigorous psychological and social factors
treatments • Gives framework for managing
complex multi-problem families
Limitations • Discounts environmental influences • Contains untestable • Danger of trivializing • Danger of vagueness
• Discounts dimensional models hypotheses problems • Danger of discounting organic
• Side-effects of medications • Inaccurate account of • Danger of discounting factors
• Discounts socio-political factors infantile sexuality organic factors • Danger of discounting intrapsychic
• Promotes exclusion • Not cost-effective • Danger of discounting factors
• Mental health legislation is abused social system factors
• Marginalizes non-medics
9 • INFLUENTIAL MODELS
293

06/03/2012 13:48
 294 C L I N I C A L P S Y C H O L O G Y : A N I N T R O D U C T I O N

people. Suicidal behaviour and extremely violent behaviour are recog-

nized within mental health legislation in most countries as possible
reflections of impaired judgement and possible grounds for involuntary
detention or treatment in a psychiatric treatment centre.
A second important achievement of the biological model has been
the development of widely used classification systems. This began with
the painstaking work of Kraepelin (1899), who catalogued symptoms
characteristic of different groups of patients. Psychological problems
are currently classified in the fifth chapter of the World Health
Organization’s (1992) International Classification of Diseases (now in
its 10th edition) and in the American Psychiatric Association’s (2000)
Diagnostic and Statistical Manual of Mental Disorders (now in its text-
revised fourth edition). These two systems – ICD-10 and DSM-IV-TR –
are now used widely throughout the world and provide a way for
clinicians and researchers to communicate with each other in a rela-
tively unambiguous manner. This was not always the case. In the past
there has been wide variation in diagnostic criteria used in different
countries. For example, in the US a very broad definition of schizophre-
nia was typically used until the development of DSM-III in 1980. The
extraordinary differences in rates of diagnoses are highlighted by the
results of the US–UK project presented in Table 9.2.
The use of scientific methods and quantitative techniques to study
psychological problems is a third achievement of the biological model.
Case–control studies, longitudinal studies, and randomized controlled
trials are three common research designs used in studies conducted
within the medical tradition. Case–control studies may be used to deter-
mine the unique characteristics associated with a particular psychologi-
cal disorder. In such studies a group of diagnostically homogeneous
cases about which the researcher is trying to find out more information
is compared to another group of patients with a known condition or with
a normal control group. This was the method Kolvin et al. (1971) used
to differentiate between childhood schizophrenia and autism. They
found that compared with childhood schizophrenia, autism was associ-
ated with an earlier onset, delayed language development, catastrophic
reactions to environmental changes, gross stereotypic behaviours, and
the absence of delusions and hallucinations.
Longitudinal studies may be used to determine the course of a psy-
chological disorder. In longitudinal studies the researcher obtains infor-
mation on a group of diagnostically homogeneous cases on a number

TABLE 9.2
Rates of diagnosis of schizophrenia in the US and the UK
Hospital diagnosis Project diagnosis
US 61% 29%
UK 34% 35%

Note: N = 192 in US; N = 174 in UK. Adapted from Cooper, J., Kendall, R., Gurland, B.,
Sharp, L. Copeland, J., & Simon, R. (1972). Psychiatric diagnosis in New York and London.
London: Oxford University Press.

Book 1.indb 294 06/03/2012 13:48

 9 • INFLUENTIAL MODELS 295

of occasions; for example, in childhood and adulthood. This was the

research design used by Robins (1966) to establish the course of child-
hood conduct disorder. He found that about a third of cases developed
antisocial personality disorder and a third adjusted well in adulthood.
The remaining third had a more variable course.
Randomized controlled trials are used to evaluate the effectiveness
of specific treatments. Diagnostically homogeneous cases are randomly
assigned to treatment or control conditions. All cases are assessed
immediately before and after treatment and then at follow-up some
months after treatment has been completed. Standard assessment
procedures are used for all cases at all three time points. If the group
that receives treatment shows greater improvement than the control
group, then the treatment may be said to be effective. This design is
typical of studies reviewed in books such as What Works with Children,
Adolescents and Adults? (Carr, 2009a), What Works for Whom? (Roth
& Fonagy, 2005) and A Guide to Treatments That Work (Nathan &
Gorman, 2007).
The development of sophisticated methods for monitoring activity
within the central nervous system is a fourth achievement of the bio-
logical model. These include brain imaging systems such as the CAT
(computerized axial tomography) scan; the PET (positron emission
tomography) scan; the SPECT (single photon emission tomography)
scan; MRI (magnetic resonance imaging); and fMRI (functional mag-
netic resonance imaging) (Bremner, 2005). Imaging techniques have
thrown light on those areas of the brain associated with particular disor-
ders. For example, Thompson et al. (2001) using MRI scanning have
documented extensive grey matter loss in early onset schizophrenia, as
shown in Figure 9.1.
A fifth achievement of the biological model is the development of
physical treatments for psychological problems. These include psy-
chopharmacological advances such as antipsychotic medication for
psychoses; antidepressant medication for unipolar mood disorders; and
lithium carbonate for bipolar disorder (Nathan & Gorman, 2007). There
is some evidence for the effectiveness of electroconvulsive therapy for
major depression that does not respond to medication and psychother-
apy (Royal College of Psychiatrists, 2005), although, as was mentioned
in Chapter 6, there is considerable controversy about this (Read &
Bentall, 2010). Psychosurgery has been found to be effective in extreme
cases of OCD (Matthews & Christmas, 2009; Mindus et al., 2001). The
development of the physical treatments, particularly psychopharmaco-
logical treatments, has depended on hypotheses in which dysregulation
of neurotransmitter systems has played a central part; for example, the
dopamine theory of schizophrenia (Seeman, 2011).

Limitations
Despite these major achievements, the biological model is not without its
limitations. First, psychological problems are not caused exclusively by
organic factors. Rather, for conditions such as anxiety, depression and

Book 1.indb 295 06/03/2012 13:48

 296 C L I N I C A L P S Y C H O L O G Y : A N I N T R O D U C T I O N

Figure 9.1 MRI image of grey matter loss in very early onset schizophrenia. From Thompson,
P., Vidal, C., Giedd, J., Gochman, P. Blumenthal, J., Nicolson, R., Toga, A., & Rapoport, J.
(2001). Mapping adolescent brain change reveals dynamic wave of accelerated grey matter
loss in very early-onset schizophrenia. Proceedings of the National Academy of Sciences of the
United States of America, 98, 11650–11655. Copyright (2010) National Academy of Sciences,
USA.

schizophrenia, people with a genetic vulnerability to a particular condi-

tion develop psychological problems if they are exposed to particular
stresses within their environment (Hankin & Abele, 2005). This observa-
tion has led people working within the ‘medical model’ tradition to a move
away from a purely biological model to a diathesis–stress conceptualiza-
tion of psychological problems. Such models acknowledge the impor-
tance of psychosocial factors such as family environment, gender, social
class and culture in the development of psychological problems. For
example, confusing and unsupportive family environments, the societal
inequalities that favour men over women, membership of disadvantaged
ethnic minorities, or membership of low socio-economic groups may all
contribute to the stress experienced by individuals who are biologically
vulnerable to psychopathology and who, as a result, develop psycho-
logical problems.
Second, many psychological problems are not distributed within the
population as a set of discrete syndromes with an underlying biological
cause. Boyle (2002) has shown, for example, that schizophrenia does
not meet the criteria for a medical syndrome. Furthermore, many psy-
chological problems are normally distributed within the population.
Thus, dimensional rather than categorical conceptualizations of specific
conditions are probably more valid for many psychological problems

Book 1.indb 296 06/03/2012 13:48

 9 • INFLUENTIAL MODELS 297

(Helzer et al., 2008). For example, conduct disorder may probably be

most validly conceptualized as cases characterized by extreme levels
of externalizing behaviour problems, which fall on a continuum, with
most children showing moderate levels of these types of difficulty
(Walton et al., 2011). This was discussed in Chapter 2. Also, trait con-
ceptualizations of personality disorders are probably more valid than
categorical conceptualization (Widiger & Mullins-Sweatt, 2010). This
was discussed in Chapter 8.
Third, many psychopharmacological and physical treatments for psy-
chological problems have harmful or unknown side-effects (Breggin,
1991). For example, many widely used antipsychotic medications lead to
an irreversible neurological movement disorder known as tardive dys-
kinesia (Tammenmaa et al., 2004). Electroconvulsive therapy (ECT),
which is commonly used to treat major depression that is unresponsive
to antidepressant medication, invariably leads to relatively long-term
memory loss and confusion, while its therapeutic effects are short-lived
(Read & Bentall, 2010). Stimulant therapy with drugs such as Ritalin
(methylphenidate), which is widely used to treat ADHD, may adversely
affect growth and cardiovascular functioning and its long-term effects in
adulthood and old age are unknown (Paykina et al., 2007; Rapport &
Moffitt, 2002). Despite the shortcomings of psychoactive medications,
the pharmacological treatment of psychological problems has wide-
spread acceptance. This is partly because the development, marketing
and sale of psychopharmacological treatments is an influential, lucrative
global industry, supported by the medical profession and governments
as the mainstay of treatment for psychological problems.
Fourth, in some instances psychological problems are reactions to
stresses inherent in family structures such as oppressive, neglectful or
abusive patterns of family organization. In others, psychological prob-
lems are a reaction to stresses inherent in the structure of society at
large such as poverty, injustice, prejudice, racism, sexism, ageism and
intolerance for nonconformity. The biological model, with its exclusive
emphasis on organic factors in the aetiology of psychological problems
and its privileging of physical treatment, draws attention away from
important psychosocial and political changes that may be required to
alleviate psychological distress and to preserve civil liberties (Laing,
2009; Szasz, 2010). By insisting from the privileged position of a high-
status profession that psychological problems are a reflection of mental
illness requiring physical treatment, proponents of the biological model
prevent society from addressing injustices, stresses and intolerance for
nonconformity at a political level.
Fifth, the development of inpatient treatment facilities such as asy-
lums and psychiatric hospitals has led to the exclusion of people with
psychological problems from society. This in turn has promoted stigma-
tization and marginalization of large groups of people with psychologi-
cal problems, which may further reinforce the difficulties of people with
psychological problems and coping difficulties (Rosenhan, 1973).
Sixth, mental health legislation, which emerged within the biological
and medical tradition, has been abused so as to limit the freedom of

Book 1.indb 297 06/03/2012 13:48

 298 C L I N I C A L P S Y C H O L O G Y : A N I N T R O D U C T I O N

people with psychological problems. Szasz (2010) has argued that

imprisoned criminals have more liberty and fewer violations of personal
rights than people with psychological problems who are involuntarily
detained.
Seventh, because the biological model of psychological problems
and practices based on it are championed by biologically oriented
psychiatry, non-medical professions, including clinical psychology and
psychotherapy, have often been marginalized in the development of
mental health services.

Psychoanalytic model
Assumptions
The psychoanalytic or psychodynamic model assumes that psycho-
logical problems are symptoms of underlying unconscious conflict or
psychopathology (Skelton, 2006). As a child develops, according to
classical psychoanalytic theory, primitive sexual and aggressive urges
of the unconscious ‘id’ become gradually controlled by the rational ‘ego’.
The ego is guided by an internalization of society’s standards: the
‘superego’. However, intrapsychic conflict is inevitable. Conflict occurs
between the sexual and aggressive impulses of the id and societal
standards as reflected in the superego.
Such conflict is managed unconsciously by using various defence
mechanisms, the function of which is to keep forbidden sexual and
aggressive impulses from consciousness. For example, a man who is
angry at his boss in work may sing his superior’s praises, thereby using
the defence of reaction formation. A full list of defences is given in Table
8.3 in Chapter 8. However, defences are compromises between the
forces of the id and superego and often carry costly side-effects. For
example, the man who is angry at his boss may eventually develop
chest pains and anxiety, as a result of repressing rather than acknow-
ledging the anger felt.
Furthermore, the psychoanalytic model proposes that relationship
styles learned early in life are transferred in later life to other relation-
ships, notably relationships with authority figures, sexual partners and
psychotherapists. These relationship styles or ‘transference phenom-
ena’, as they are called in psychoanalysis, are coloured in part by feel-
ings aroused and partially resolved during the Oedipus complex phase
(for boys) or Electra complex phase (for girls). These developmental
phases refer to the psychoanalytic hypothesis that children in early life
desire their opposite-sex parent and harbour aggression towards the
parent of their own gender. However, these sexual and aggressive
impulses are repressed and the child eventually identifies with the par-
ent of the same gender for fear of the consequences of acting them
out. In later life patients, such as the man with chest pains referred to
earlier, experience feelings towards significant others and deal with
them in a manner similar to that which occurred during the Oedipal
phase of development. So the man with chest pains experienced
aggression towards his boss and later towards his psychotherapist in a

Book 1.indb 298 06/03/2012 13:48

 9 • INFLUENTIAL MODELS 299

similar fashion, and dealt with this using reaction formation in a manner
similar to that with which he handled the Oedipal triangle as a child.
Psychoanalysis and psychoanalytic psychotherapy provide a context
within which patients can experience transference towards a psycho-
therapist and then through interpretation gain insight into the transfer-
ence and related defences that underlie their psychopathology. The
analyst or therapist and client meet frequently according to a strict
schedule. The patient reports in an uncensored way his or her contents
of consciousness. Eventually the client develops transference and
the analyst interprets this repeatedly over time until the patient
has gained insight into the transference and related defences and
worked through related unresolved feelings. Concurrently, the patient’s
symptoms abate.
In order to be able to practise psychoanalysis, therapists must
undergo their own analysis so that they have a first-hand understanding
of the process and so that they will recognize transference feelings that
they have towards patients (countertransference). Traditionally strict
selection criteria are used for psychoanalysis, and typically YAVIS
(young, adult, verbal, intelligent and single) patients only have been
deemed suitable. However, this has changed in recent years with devel-
opments such as object relations approaches to conditions such as
borderline personality disorder (discussed in Chapter 8).

Achievements
First, the most outstanding achievement of the psychoanalytic model is
the discovery of the unconscious (Ellenberger, 1970). Freud drew
together a set of ideas from a wide range of sources and crystallized them
in the notion of the unconscious, not as a passive repository of irretriev-
able memories but as an active set of psychological processes. According
to the psychoanalytic model of the unconscious, people can make them-
selves forget things or keep them outside awareness. Repressed uncon-
scious aggressive and sexual impulses may motivate behaviour.
Second, psychoanalysis gave meaning to apparently meaningless
behaviour. For example, Freud (1909a) showed how in phobias, fears
of one stimulus (e.g. one’s father) could be displaced onto other stimuli
(e.g. horses). He also showed how unconscious processes that
explained psychological disorders could also explain peculiar everyday
behaviour. For example, in his book The Psychopathology of Everyday
Life, Freud showed how forgetting people’s names, slips of the tongue,
errors in writing and so forth in some cases are due to repression
(Freud, 1901). Such errors or parapraxes have come to be referred to
colloquially as ‘Freudian slips’. He also showed that apparently mean-
ingless dreams may be interpreted and made coherent to aid self-
understanding, a proposition that has been partially supported by
subsequent research (Freud, 1900; Siegel, 2010).
Third, psychoanalysis introduced the ideas of transference and
countertransference into the practice of psychotherapy. The idea that
people have a limited number of relationship-maps which they learn
early in life and transfer onto significant others in adulthood has been

Book 1.indb 299 06/03/2012 13:48

 300 C L I N I C A L P S Y C H O L O G Y : A N I N T R O D U C T I O N

supported by recent empirical work on continuity in patterns of attach-

ment from childhood to adulthood (Cassidy & Shaver, 2008; Rholes &
Simpson, 2004).
Fourth, psychoanalysis established the place of the ‘talking cure’ in
mainstream mental health practice. It also provided a model for the
development of both short-term and long-term outpatient treatment of
patients with a range of psychological difficulties. In the UK the compe-
tencies required for delivering psychodynamic psychotherapy have
been delineated by the British Psychological Society’s Centre for
Outcomes Research and Effectiveness (Lemma et al., 2008).
Fifth, empirical studies of long-term psychoanalysis and short-term
psychodynamic psychotherapy show that it is effective with a range of
problems including anxiety, mood and personality disorders and com-
plex comorbid presentations (Shedler, 2010; Leichsenring & Rabung,
2008, 2011; Leichsenring et al., 2004).
Finally, Freud provided a model for developing a theory of personality
and therapy which spawned a wide range of neo-Freudian derivatives
including those of Jung, Adler, Horney, Stack Sullivan, Reich, Fairburn,
Klein, Erikson and many others (Schultz & Schultz, 2008).

Limitations
Classical psychoanalysis has many limitations. First, many of its hypoth-
eses were untestable due to the imprecision of the constructs or the
imprecision of predictions entailed by psychoanalytic theory. Also, for a
considerable time there was little evidence for the effectiveness of psy-
choanalytic psychotherapy. Recent meta-analyses of treatment out-
come studies have addressed this limitation (Shedler, 2010; Leichsenring
& Rabung, 2008, 2011; Leichsenring et al., 2004).
Second, Freud’s speculations about infantile sexuality were not
borne out by subsequent developmental research and in particular by
research on child sexual abuse. It is quite likely that many of Freud’s
patients who reported sexual contact with a parent had in fact been
sexually abused and were not simply fantasizing about seducing their
parents in Oedipal dramas (Masson, 1984).
Third, as a model for practice, classical psychoanalysis is too time-
consuming and expensive. Classical psychoanalysis involves multiple
sessions each week for a number of years. It is therefore not sufficiently
cost-effective for routine use in a public mental health service where
resources are limited. However, in recent times attempts have been
made to use psychoanalytic ideas and practices as a basis for brief
psychodynamic therapy (Lemma et al., 2010; Leichsenring et al., 2004).

Cognitive-behavioural model
Assumptions
The cognitive-behavioural tradition incorporates a range of psychothera-
peutic theories and practices including behaviour therapy, behaviour
modification, cognitive therapy and cognitive-behaviour therapy, all
of which have their roots in learning theories, both behavioural and

Book 1.indb 300 06/03/2012 13:48

 9 • INFLUENTIAL MODELS 301

cognitive (Freeman et al., 2005). Within the cognitive-behavioural

tradition it is assumed that psychological problems are distressing habits
that are learned through the same processes as normal behaviour.
These processes include operant and classical conditioning, imitation
and insight.
Therapy involves helping clients to replace distressing habits of think-
ing and behaving with more adaptive ones. This process is based on the
principles of learning theory. Through careful interviewing and observa-
tion, the antecedents that trigger problematic behaviours, beliefs and
mood states, and the consequences that reinforce them, are identified.
Treatment programmes, based on this type of assessment, include inter-
ventions that alter antecedents which signal the onset of psychological
problems; interventions that challenge non-adaptive beliefs and styles of
information processing that accompany psychological problems; and
interventions that change the consequences of behaviour so that normal
alternatives to abnormal behaviour patterns are reinforced.
In the behavioural treatment of depression, antecedents of low mood
may be altered through inviting clients to schedule pleasant events reg-
ularly throughout their day (Lewinsohn & Gotlib, 1995). In the cognitive
therapy of depression, anxiety and personality disorders, clients are
coached in how to identify and challenge negative automatic thoughts
and to identify the use of cognitive distortions (Beck et al., 1979, 2003;
Clark & Beck, 2010a). With conduct disordered children, reward pro-
grammes are used so that prosocial behavioural targets are routinely
reinforced (Forgatch & Patterson, 2010). Modelling, rehearsal, shaping
and operant reinforcement procedures may be used to help individuals
with skills deficits learn self-regulation, social, communication and
problem-solving skills. Skills training is routinely used when working
with people who have skills deficits, for example people with schizo-
phrenia who have negative symptoms and limited social skills (Tenhula
& Bellack, 2008).
Treatment programmes also include procedures based on classical
conditioning. For example, with systematic desensitization for people
who have phobias, increasingly threatening stimuli are paired with the
experience of relaxation (Head & Gross, 2008). Another example of a
classical conditioning based intervention is the use of urine alarm
programmes for nocturnal enuresis in which bedwetting is paired with
the sound of an alarm (Houts, 2010). Through this procedure, the child
learns eventually to awaken when the bladder is full.
Within the cognitive-behavioural tradition, specific treatment pro-
grammes are developed for specific symptoms and detailed assess-
ments of the impact of treatment on psychological problems targeted in
treatment are routinely made. The tradition has been championed by
clinical psychologists.

Achievements
The cognitive-behavioural tradition has made a number of important
contributions to the understanding and treatment of psychological
difficulties.

Book 1.indb 301 06/03/2012 13:48

 302 C L I N I C A L P S Y C H O L O G Y : A N I N T R O D U C T I O N

First, this tradition has led to the development of brief effective

approaches to therapy which are applicable to a wide range of patients
(Freeman et al., 2005). Typically cognitive-behaviour therapy is brief,
ranging from one to 30 sessions, depending on the nature and severity
of the problems.
Second, the cognitive-behavioural tradition has shown empirically
that its treatment strategies are effective. It has led the evidence-based
practice movement in the mental health field. More than any other
approach to treating psychological difficulties, the cognitive-behavioural
tradition has generated an enormous volume of empirical research to
test the effectiveness of a wide variety of treatment programmes for a
broad range of problems in adults and children (Carr, 2009a; Nathan &
Gorman, 2007).
Third, the cognitive-behavioural model has led to the development of
specific psychological treatment packages for specific types of problem.
For example, exposure-based treatments have been developed for
anxiety disorders (described in Chapter 5), cognitive therapy has been
developed for mood disorders (described in Chapter 6), and cognitive-
behavioural approaches have been developed to treat the positive
symptoms of schizophrenia (outlined in Chapter 7).
Fourth, compared to other treatment approaches, CBT has been
more widely disseminated in books, training videos and brief training
programmes that are highly accessible to a range of mental health pro-
fessionals. In the UK the dissemination of CBT has been mainstreamed
within the National Health Service through the Improving Access to
Psychological Therapies programme (www.iapt.nhs.uk).
Fifth, methodological and scientific rigour has characterized cognitive-
behavioural research on psychological problems and their treatment.

Limitations
The main limitation of the cognitive-behavioural model is the risk it
entails of trivializing psychological problems. When people are suffering
profound psychological distress, it may seem to them that to construe
their difficulties as bad habits does not do justice to the gravity of their
distressing life situations.
Two other possible limitations of the cognitive-behavioural model
deserve mention. First, there is the danger of disregarding the possible
role of organic factors in the aetiology of psychological difficulties. This
is problematic because there is extensive evidence for the role of
genetic and neurobiological factors in the aetiology of many mental
health problems. Second there is the risk of not taking the role of the
patient’s wider social context into account. Poverty, unemployment, low
socio-economic status and stressful family environments may all
contribute to the development of psychological problems.
Having noted these two dangers, it should be mentioned that they
have been addressed by various members of the cognitive-behavioural
tradition at different times. For example, cognitive-behavioural approaches
to understanding conditions such as schizophrenia (outlined in Chapter 7)

Book 1.indb 302 06/03/2012 13:48

 9 • INFLUENTIAL MODELS 303

and borderline personality disorder (described Chapter 8) are based on

diathesis–stress conceptualizations of their aetiology, which take account
of the important role of genetic and neurobiological factors. Also, there is
increasing recognition within the cognitive-behavioural tradition for the
important role of life stress and immediate family environment in the main-
tenance and amelioration of psychological problems (Dattilio, 2009).

Family systems model

Assumptions
The family systems model assumes that psychological problems are
maintained by patterns of interaction and belief systems within the fam-
ily and the wider social system of the client. Historical, contextual and
constitutional factors may predispose family members to engage in
these interaction patterns and adopt these belief systems. The many
family therapy schools within this tradition may be classified in terms of
their central focus of therapeutic concern and in particular with respect
to their emphasis on (1) problem maintaining behaviour patterns; (2)
problematic and constraining belief systems; and (3) historical, contex-
tual and constitutional predisposing factors (Carr, 2006b).
With respect to the first theme, some family therapy schools highlight
the role of repetitive patterns of family interaction in the maintenance of
problem behaviour and advocate practices that aim to disrupt these
patterns of interaction. Schools that fall into this category include the
MRI brief therapy approach (Segal, 1991), strategic therapy (Robbins et
al., 2009), structural therapy (Colapinto, 1991) and functional family
therapy (Sexton, 2009).
With respect to the second theme, some schools of family therapy
point to the centrality of belief systems and narratives which subserve
repetitive interaction patterns that maintain presenting problems. Prac-
tices that facilitate the emergence of new belief systems and narratives
which liberate family members from problem-maintaining interaction
patterns are espoused by these schools. Schools that fall into this cat-
egory include social constructionist approaches (Anderson, 2003), the
Milan school (Campbell et al., 1991), solution-focused family therapy
(Cheung, 2009) and narrative therapy (Duvall & Béres, 2011).
With respect to the third theme, a number of family therapy traditions
highlight the role of historical, contextual and constitutional factors in pre-
disposing family members to adopt particular belief systems and engage
in particular problematic interaction patterns. Such schools advocate
using practices that specifically address these historical, contextual and
constitutional predisposing factors, including working with members of the
extended family and wider social network as well as coaching individuals
to manage historical, contextual and constitutional constraints. This
category contains transgenerational family therapy (Hargrove, 2009);
psychoanalytic family therapy traditions (Magnavita, 2009), attachment
theory-based approaches (Diamond, 2005; Johnson & Bradley, 2009),
experiential family therapy (Wetchler & Piercey, 1996), multisystemic

Book 1.indb 303 06/03/2012 13:48

 304 C L I N I C A L P S Y C H O L O G Y : A N I N T R O D U C T I O N

therapy which includes reference to the wider system (Henggeler et al.,

2009) and psychoeducational approaches (McFarlane, 2005).
Elsewhere I have argued that an integrative approach to family ther-
apy may be taken so that for any problem, a formulation may be con-
structed using ideas from many schools of family therapy in which the
pattern of family interaction that maintains the problem is specified, the
constraining beliefs and narratives that underpin each family member’s
role in this pattern are outlined, and the historical and contextual factors
that underpin these belief systems and narratives are specified (Carr,
2006b). In parallel with this, a similar formulation may be constructed to
explain why the problem does not occur in exceptional circumstances,
which, while similar to problematic situations, differ in important key
respects.
In light of these formulations, a range of interventions that address fac-
tors within each column of the formulations may be considered. Some
interventions aim primarily to disrupt problem-maintaining behaviour pat-
terns or amplify exceptional non-problematic patterns. Others aim to help
family members change the personal narratives that make them repeat
the same problematic behaviour patterns and develop more liberating
and flexible belief systems that underpin exceptions to the problem. Still
others aim to modify the negative impact of historical, contextual and
constitutional factors or to draw on family strengths in these domains.
In family systems therapy, assessment and treatment involves the
client and the family participating in multi-person meetings. Multiple per-
spectives on the problem and related interaction patterns, belief sys-
tems and predisposing factors are therefore available to the therapist.
Furthermore, there is the possibility of multiple people being involved in
therapeutic change. Because of this, it is a fundamental assumption of
family systems therapy that a small intervention may lead to a big
change. It is therefore not surprising that family therapy is usually brief,
with treatment rarely extending beyond 20 sessions. Furthermore, fam-
ily therapy is dominated neither by clinical psychology nor by psychia-
try. Many disciplines are involved, including social work and nursing.

Achievements
Family therapy has made an important contribution to the understand-
ing and treatment of psychological problems. First, in a field dominated
by essentially individualistic models of practice, it has highlighted the
role of the social context in the aetiology and treatment of psychological
difficulties. Second, family therapy is a brief, affordable form of treat-
ment well suited to public health services. It is highly cost-effective
(Crane, 2011). Where different family members have problems, they
may all be treated by the same therapist or team. Third, empirical
research shows that family therapy is effective with a wide range of
problems in children and adults (Carr, 2009b, 2009c). Thus, there is a
sound foundation for evidence-based practice. Fourth, systems theory
can offer an integrative framework for comprehending not just the role
of social factors but also those of biological and intrapsychic factors in
the understanding and treatment of psychological difficulties. Fifth, in

Book 1.indb 304 06/03/2012 13:48

 9 • INFLUENTIAL MODELS 305

clinical practice, an integrative approach to family therapy is particularly

useful in managing complex cases in which multiple family members
have multiple problems, since often these are interconnected – a point
missed by individualistic conceptualizations of psychological problems.

Limitations
The main limitations of the family systems model are a danger of vague-
ness, the risk of losing sight of the needs and rights of the individual,
and the danger of failing to take account of neurobiological factors.

Other influential models

The four models described above are the most influential in the field of
clinical psychology. However, there are many other frameworks that
influence the way clinical psychologists conduct their work. These
include the client-centred humanistic tradition, personal construct psy-
chology and positive psychology.

Client-centred humanistic psychology

Client-centred humanistic psychotherapy is an overarching term for a
tradition that includes a variety of specific approaches to therapy and
counselling; for example, Carl Rogers’ client-centred therapy, Fritz
Perls’ gestalt therapy and various experiential therapies (Cain &
Seeman, 2001). Within this tradition, it is assumed that avoidance or
denial of current feelings, emotions and desires, and deliberate or inad-
vertent failure to take responsibility for these aspects of experience,
prevent self-actualization and give rise to psychological symptoms.
A defining feature of client-centred humanistic psychotherapy is the
use of the therapeutic relationship between client and therapist as a
resource in promoting self-actualization and personal growth. A second
defining feature of this tradition is facilitating personal growth by helping
clients to become more aware of their disavowed emotions and desires
and to take responsibility for these. Within this tradition, personal growth
is the main goal of therapy. Resolving presenting problems is often sec-
ondary to this superordinate goal. The practice within clinical psychol-
ogy of establishing a strong therapeutic alliance with the client reflects
the influence of the client-centred humanistic tradition.

Constructivist psychotherapy
Constructivist psychotherapy is based on George Kelly’s personal con-
struct psychology (Winter & Viney, 2005). Personal construct psychol-
ogy holds that people’s problems are rooted in the way they construe or
interpret the world. Consequently a defining feature of personal con-
struct psychotherapy is the exploration and transformation of clients’
unique construct and belief systems. In the UK personal construct psy-
chology and constructivist psychotherapy have had an impact on the
practice of clinical psychology through influential clinical psychologists,
notably Don Bannister and Fay Francella.

Book 1.indb 305 06/03/2012 13:48

 306 C L I N I C A L P S Y C H O L O G Y : A N I N T R O D U C T I O N

Positive psychology
Remediating deficits and managing disabilities has been a central con-
cern for clinical psychology since its inception. Positive psychology, in
contrast, complements this aim by focusing instead on the enhance-
ment of happiness. Positive psychology was founded by Martin
Seligman in the US at the turn of the millennium.
While modern positive psychology is a new movement, it draws on a
rich intellectual heritage that includes the humanistic tradition. However,
the distinguishing features of the modern positive psychology movement
are its commitment to the scientific study of positive aspects of human
experience, the academic infrastructure that has been established to
support this research, and the intellectual leadership provided by the
founders of the movement.
Positive psychology focuses on understanding and facilitating
(1) happiness and well-being, (2) positive traits and engagement in
absorbing activities, and (3) the development of meaningful positive
relationships, social systems and institutions (Lopez & Snyder, 2009).
Common themes within positive psychology that influence the practice
of clinical psychology include resilience, optimism, hope, forgiveness,
curiosity, creativity, wisdom, emotional intelligence, self-efficacy, self-
determination, self-regulation, humour, mindfulness, therapeutic writ-
ing, posttraumatic growth, attachment, empathy and altruism.
The client-centred humanistic, personal construct and positive
psychology models, with their emphasis on the quality of the thera-
peutic alliance, the uniqueness of each client, client strengths and
optimism, are common themes in the practice of clinical psychology.

Summary
The biological, psychoanalytic, cognitive-behavioural and fam-
ily systems models are each based on a unique set of assump-
tions. Despite limitations, each model has given rise to a unique
set of achievements. With the biological model it is assumed
that psychological problems may be classified into syndromes.
Each syndrome is due to an underlying brain disease for which
a discrete cause and physical cure may be ultimately identified.
It is also assumed that each condition follows a distinctive
course and has a particular prognosis.
The biological model’s greatest achievement was the libera-
tion of people with psychological problems and the creation of
asylums where those in psychological distress received
humane treatment. Mental health legislation, widely used clas-
sification systems such as the DSM and ICD, a commitment to
scientific study of psychological problems, and the develop-
ment of psychopharmacological treatments are among the
major achievements of the biological model. Its limitations

Book 1.indb 306 06/03/2012 13:48

 9 • INFLUENTIAL MODELS 307

include the facts that many psychological problems are not

caused by organic factors, many psychopharmacological treat-
ments have harmful side-effects, asylums have led to social
exclusion and mental health legislation has been abused.
The psychoanalytic model assumes that psychological
problems are symptoms of underlying psychopathology.
Psychotherapy gives insight into the conflicts, defences and
transference phenomena that constitute this psychopathology.
Achievements of the psychoanalytic model include the discov-
ery of the unconscious, the demonstration of continuity between
normality and psychological problems and the establishment of
talking therapy as a valid method for treating psychological
problems. Classical psychoanalysis, however, is too expensive
to be a viable approach for routinely treating people in the pub-
lic health services. This and the fact that is diagnostically
vague, many of its propositions are untestable, and it patholo-
gizes everyone are its major limitations.
The cognitive-behavioural model assumes that symptoms
are learned through conditioning, imitation and insight and that
therapy involves changing patterns of learned behaviour using
specific treatments that have been developed for specific
symptoms. The development of brief evidence-based effective
approaches to therapy applicable to a wide range of patients is
the main achievement of the cognitive-behavioural model. The
risk of trivializing psychological problems and of paying insuf-
ficient attention to organic or social factors are its principal
limitations.
The systems model assumes that psychological problems
are maintained by patterns of interaction and belief systems
within the family and the wider social system of the patient.
Historical, contextual and constitutional factors may predispose
family members to engage in these interaction patterns and
adopt these belief systems. In family therapy, assessment and
treatment involves the client and the family. In terms of achieve-
ments, empirical research shows that family therapy is effective
with a wide range of problems and that systems theory offers a
framework for integrating biological, psychological and social
factors. The main limitations of this approach are a danger of
vagueness, a risk of losing sight of the individual, and a danger
of failing to take account of neurobiological factors.
The biological, psychoanalytic, cognitive-behavioural and
family systems models have been the most influential in the
field of clinical psychology. Other frameworks that have
influenced the practice of clinical psychology include the client-
centred humanistic tradition, personal construct psychology
and positive psychology.

Book 1.indb 307 06/03/2012 13:48

 308 C L I N I C A L P S Y C H O L O G Y : A N I N T R O D U C T I O N

Questions
● What are the key assumptions, general achievements and general
limitations of the biological, psychodynamic, cognitive-behavioural
and family systems models?
● Having read Chapters 2–8, what do you consider to be the top three
specific achievements of the biological, psychodynamic, cognitive-
behavioural and family systems models?
● Why are the client-centred humanistic tradition, personal construct
psychology and positive psychology important for the practice of
clinical psychology?

FURTHER READING
● Tyrer, P. & Sternberg, D. (2005). Models of mental disorder: Conceptual
models in psychiatry (fourth edition). Chichester, UK: Wiley.
● Watchel, P. & Messer, S. (1997). Theories of psychotherapy: Origins
and evolution. Washington, DC: APA. This text includes up-to-date
accounts of psychodynamic, cognitive-behavioural and family systems
approaches to psychotherapy.

WEBSITES
Psychiatric associations that privilege the
neurobiological model
● American Psychiatric Association:
www.psych.org
● Royal Australian & New Zealand College of Psychiatrists:
www.ranzcp.org
● Royal College of Psychiatrists:
www.rcpsych.ac.uk

Psychoanalytic associations
● American Psychoanalytical Association:
www.apsa.org
● Australian Psychoanalytical Society:
www.psychoanalysis.asn.au
● British Psychoanalytical Society:
www.psychoanalysis.org.uk
● International Psychoanalytical Association:
www.ipa.org.uk

Cognitive-behavioural associations
● Association for Behavioural and Cognitive Therapies (US):
www.abct.org
● Australian Association for Cognitive and Behaviour Therapy:
www.aacbtqld.org.au

Book 1.indb 308 06/03/2012 13:48

 9 • INFLUENTIAL MODELS 309

● British Association of Behavioural & Cognitive Psychotherapies:

www.babcp.com

Family therapy associations

● American Association for Marital and Family Therapy:
www.aamft.org
● Association for Family Therapy (UK):
www.aft.org.uk
● European Family Therapy Association:
www.europeanfamilytherapy.eu
● Family Therapy Association of Ireland:
www.familytherapyireland.com

Book 1.indb 309 06/03/2012 13:48

 10 Effectiveness of
psychological therapies

Learning objectives
After studying this chapter you will be able to:
● define evidence-based practice in clinical psychology
● explain the hierarchy of evidence that informs
evidence-based practice
● summarize the main findings from the evidence base
for the effectiveness of psychotherapy
● outline the medical cost offset associated with
psychotherapy
● describe the role of common and specific factors in
the effectiveness of psychotherapy.

Introduction
One of the main ways in which clinical psychologists help clients is
through psychotherapy. Psychotherapy is a contractual process in
which trained professionals with expert knowledge of their discipline
interact with clients to help them resolve psychological problems and
address mental health difficulties. Psychotherapy may be offered to
children and adults on an individual, couple, family or group basis.
Often clinical psychologists offer psychotherapy as one element of a
multimodal programme provided by a multidisciplinary team. For exam-
ple, a multidisciplinary adult mental health team may routinely offer a
multimodal programme of cognitive behaviour therapy combined with
antidepressants for depression, as described in Chapter 6. A

Book 1.indb 310 06/03/2012 13:48

 10 • EFFECTIVENESS OF PSYCHOLOGICAL THERAPIES 311

multidisciplinary child and adolescent mental health team may routinely

offer a multimodal programme for children with attention deficit hyper-
activity disorder which includes behavioural parent training, school-
based behavioural consultation, child-focused self-instructional and
social training and methylphenidate, as outlined in Chapter 2. In this
chapter the focus will be on the evidence base for the overall effective-
ness of psychotherapy and common factors that underpin effective
approaches.

Evidence-based practice
In clinical psychology there has been a gradual move from practice
guided exclusively by descriptions of clinical cases to evidence-based
practice guided by the results of scientific studies on the effectiveness
of psychological interventions. This evolution has occurred as part of
the broader movement of evidence-based medicine (Sackett et al.,
1996, 2000).
Evidence-based practice in medicine and clinical psychology involves
the judicious and compassionate use of the best available scientific evi-
dence to make decisions about patient or client care. In clinical psychol-
ogy, it involves taking account of available scientific evidence about
‘what works’ on one hand, and clients’ unique problems, needs, rights
and preferences on the other, and making balanced, compassionate
judgements (APA Presidential Task Force on Evidence Based Practice,
2006; Norcross et al., 2006).

Hierarchy of evidence
When considering scientific evidence for the effectiveness of psycho-
logical interventions, it is useful to organize categories of available sci-
entific evidence into a hierarchy, from the least to the most persuasive,
as illustrated in Figure 10.1. In this hierarchy, case studies are the least
persuasive form of evidence. The most persuasive evidence for the
effectiveness of psychotherapy and other psychological interventions
comes from meta-analyses of controlled trials.

Case studies and case series

In case studies descriptions and explanations are given of the way ther-
apy was conducted with individual cases and the impact of therapy on
clients’ problems or symptoms. Such studies offer important insights into
the details of how particular types of psychotherapy may be conducted
with specific cases. Some examples are sketched in Figure 10.2.
The main limitation of case study evidence is that any observed
improvements in clients’ problems may be due to the passage of time,
idiosyncratic responses of individual cases, or biased observation.
Studies of case series provide more convincing evidence for the effec-
tiveness of therapy. In such studies, groups of cases with similar sorts
of problem are assessed before and after treatment with a standard set

Book 1.indb 311 06/03/2012 13:48

 312 C L I N I C A L P S Y C H O L O G Y : A N I N T R O D U C T I O N

Figure 10.1 Hierarchy of evidence

Figure 10.2 Case studies

Book 1.indb 312 06/03/2012 13:48

 10 • EFFECTIVENESS OF PSYCHOLOGICAL THERAPIES 313

of assessment instruments. Because data are collected on more than

one case, case series studies rule out the possibility that improvements
reflect idiosyncratic responses of single cases.
The main shortcoming with evidence from case series studies is that
they leave open the possibility that improvements in clients’ functioning
may have been due to the passage of time, rather than the effects of
treatment.

Controlled trials
In controlled trials, to rule out the possibility that observed improvements
in clients’ problems following treatment were due to the passage of time,
gains made by treated cases are compared with gains made by a control
group (case–control studies). In psychotherapy studies, clients in control
groups usually receive routine clinical management of their problems. An
example of results from a controlled trial – The London Depression
Intervention Trial (Leff et al., 2000) – is given in Figure 10.3. The average
score of the group that received couples therapy for chronic depression
was lower after treatment than before therapy began, and this gain was
maintained at follow-up a year later. This pattern of improvement was
better than that for cases treated with antidepressants.
There are many variations of the basic controlled trial, but the gold
standard is the randomized controlled trial. In randomized controlled
trials, cases are randomly assigned to treatment and control groups, to
rule out the possibility that differences in improvement rates are due to
responsive and unresponsive cases having been systematically
assigned to treatment and control groups. There is a tradition in medical

Figure 10.3 Improvement in mean symptom scores on the Beck Depression Inventory for
adults with chronic depression receiving systemic couples therapy or antidepressants before
treatment, 1 year after treatment and 2 years after treatment. Based on Leff et al. (2000)

Book 1.indb 313 06/03/2012 13:48

 314 C L I N I C A L P S Y C H O L O G Y : A N I N T R O D U C T I O N

randomized controlled trials to use ‘sugar pills’ as placebos, so patients

in the control group do not receive the medicine that is being evaluated,
but believe that they are being helped since they are receiving what
looks like an active treatment (the placebo sugar pill).
In some psychotherapy treatment outcome studies, clients receive
placebo therapy. This usually involves having as much contact with a
therapist as those in the treatment group, but receiving some innocu-
ous, though credible, placebo psychotherapy, for example engaging in
‘intellectual discussions’ about plausible topics. When placebo control
groups are included in randomized controlled trials, they rule out the
possibility that treatment gains were due simply to therapist contact
rather than psychotherapeutic techniques and processes.

Narrative reviews
While an individual trial with positive results provides evidence that in
one context, a particular form of treatment was effective for a group of
clients with a specific type of problem, narrative reviews provide more
convincing evidence because they show the extent to which positive
results were replicated across a series of trials. However, the conclusions
drawn in narrative reviews are inevitably biased by the conscious and
unconscious prejudices of the reviewer.

Meta-analyses
Meta-analysis is a systematic, quantitative approach to reviewing
evidence from multiple trials. The impact of reviewer bias inherent in
narrative reviews is greatly reduced in meta-analyses because data
from many trials are synthesized using statistical methods.
In a meta-analysis effect sizes are calculated for each trial and then
averaged across all trials to provide a quantitative index of the effective-
ness of a particular form of treatment with a specified population. Effect
sizes calculated in meta-analyses express quantitatively the degree to
which treated groups improved more than control groups. A graphic
explanation of the calculation of an effect size is given in Figure 10.4.
Table 10.1 gives a system for interpreting effect sizes. Using this
table, it may be seen that an effect size of .8 is large. If such an effect
size were obtained in a meta-analysis it would mean that the average
treated case fared better than 79% of cases in the control group. It
would also indicate that 69% of cases in the treatment group had a suc-
cessful outcome compared with 31% of control group cases. Finally, a
large effect size of .8 would indicate that 14% of the variance in out-
come could validly be attributed to the effects of treatment, rather than
other factors.

How effective is psychotherapy?

Mary Smith and Gene Glass published the first major meta-analysis of
psychotherapy outcome studies in American Psychologist in 1977.

Book 1.indb 314 06/03/2012 13:48

 10 • EFFECTIVENESS OF PSYCHOLOGICAL THERAPIES 315

Figure 10.4 Graphic representation of an effect size of 1

They included 375 controlled trials of psychotherapy in their analysis

and found an average effect size of .68. They concluded that a typical
therapy client was better off than 75% of untreated individuals.
Since that seminal study many meta-analyses have been conducted.
In a synthesis of 68 separate meta-analyses of psychotherapy with chil-
dren, adolescents and adults with a wide range of different psychologi-
cal problems, Grissom (1996) found an aggregate effect size of .75,
indicating that the average treated case fared better than 77% of
untreated controls.

Book 1.indb 315 06/03/2012 13:48

 316 C L I N I C A L P S Y C H O L O G Y : A N I N T R O D U C T I O N

TABLE 10.1
Interpretation of effect size
Effect Cohen’s Percentage of Success Success rate Percentage of
size designation1 untreated cases that rate for for untreated outcome variance
d the average treated treated group3 group3 accounted for by
case fares better than2 treatment4
1.0 Large 84 72 28 20
.9 82 71 29 17
.8 79 69 31 14
.7 76 67 33 11
.6 73 64 36 8
.5 Medium 69 62 38 6
.4 66 60 40 4
.3 62 57 43 2
.2 Small 58 55 45 1
.1 54 53 47 0

Note: Adapted from Wampold (2001, p. 53). 1. From Cohen (1988). 2. From Glass (1976). 3. From Rosenthal and Rubin
(1982). Binomial effect size display, assuming overall success rate of .5, success rate for treated cases is .5 + correlation
with outcome/2, and success rate for untreated cases is .5 – correlation with outcome/2. 4. From Rosenthal (1994, p. 239),
percentage of variance = d2/(d2 + 4).

Effects of psychotherapy with adults

While Smith and Glass’s (1977) meta-analysis, mentioned above,
included mainly studies of psychotherapy with adults, it also included
many studies of therapy with children. With a view to determining the
effects of psychotherapy for adults with psychological problems, Shapiro
and Shapiro (1982) conducted a meta-analysis of 143 studies of psy-
chotherapy exclusively involving adult populations. They found an over-
all effect size of 1.03, indicating that after treatment the average adult
who participated in psychotherapy fared better than 84% of untreated
control group cases.

Effectiveness of psychotherapy with children and adolescents

The results of four broad meta-analyses of studies involving children
and adolescents under 18 years with a diverse range of psychological
problems receiving a variety of forms of psychotherapy provide evi-
dence for the overall effectiveness of psychotherapy with children
(Casey & Berman, 1985; Kazdin et al., 1990; Weisz et al., 1987, 1995).
These meta-analyses included more than 350 treatment outcome
studies. Effect sizes ranged from .71 to .88, with a mean effect size
of .77. This indicates that the average treated case fared better than
78% of control group cases.

Efficacy and effectiveness studies

A useful distinction is made between efficacy and effectiveness trials
(Cochrane, 1972). In efficacy studies clients with a specific type of

Book 1.indb 316 06/03/2012 13:48

 10 • EFFECTIVENESS OF PSYCHOLOGICAL THERAPIES 317

problem (and no comorbid difficulties) are randomly assigned to treat-

ment and control groups. The treatment group receives a pure and
potent form of a very specific type of psychotherapy from specialist psy-
chotherapists in practice centres of excellence.
Efficacy studies are typically conducted at university-affiliated
centres, with carefully selected clients who meet stringent inclusion and
exclusion criteria. For example, often patients with comorbid substance
abuse and personality disorders or self-harming behaviour are excluded
from efficacy studies of treatments for depression. Therapists are highly
trained, intensively supervised, have small case loads, and the fidelity
with which they offer treatment is scientifically checked by rating the
degree to which recordings of therapy sessions conform to treatment
protocols specified in therapy manuals.
Effectiveness studies, in contrast, are conducted in routine clinical
settings rather than centres of excellence, with typical therapists carry-
ing normal case loads, offering treatment to clients who are representa-
tive of typical referrals, and while therapy manuals and supervision are
often employed, there is a greater degree of flexibility about their use
than in efficacy studies. Efficacy studies tell us how well treatments
work under ideal conditions. Information about the impact of treatments
under routine conditions is provided by effectiveness studies. It is useful
to think of effectiveness and efficacy studies as representing the
extremes of a continuum along which a variety of trial designs fall.
One of the criticisms of broad meta-analyses of psychotherapy trials
is that many of the studies included in them are efficacy rather than effec-
tiveness trials, and so are not representative of clients who attend typical
services. To address this criticism, Shadish et al. (1997) conducted a
meta-analysis of 56 effectiveness trials. The studies were conducted in
non-university, community settings; included children, adolescents and
adults referred for treatment, not solicited by the researcher; and involved
experienced professional therapists with normal case loads. The aver-
age effect size from these 56 clinically representative studies was .68,
which is precisely the effect size found by Smith and Glass in their semi-
nal meta-analysis mentioned above. The results of this meta-analysis
show that psychotherapy is effective when conducted under clinically
representative conditions.

Psychodynamic psychotherapy
Within the psychodynamic tradition, a distinction is made between
short-term psychodynamic psychotherapy and intensive long-term psy-
choanalysis. The former involves weekly sessions for periods of 6–12
months, while the latter involves two or more sessions per week, usu-
ally for periods longer than a year.
Two important broad meta-analyses have been conducted to evalu-
ate the effectiveness of psychodynamic psychotherapy with adult men-
tal health problems (Leichsenring et al., 2004; Leichsenring & Rabung,
2011). In a meta-analysis of 17 studies, Leichsenring et al. (2004) found
that short-term psychodynamic psychotherapy yielded an effect size of

Book 1.indb 317 06/03/2012 13:48

 318 C L I N I C A L P S Y C H O L O G Y : A N I N T R O D U C T I O N

.7 for psychiatric symptoms in patients mainly diagnosed with anxiety

and mood disorders when therapy was compared with waiting list or
minimal intervention control groups. This indicates that after treatment
the average treated case fared better than 76% of controls. In this meta-
analysis, the outcome for psychodynamic psychotherapy did not differ
from that of other forms of psychotherapy in the 14 studies where such
comparisons were made.
In a further meta-analysis of 10 studies, Leichsenring and Rabung
(2011) found that long-term psychodynamic psychotherapy involving
more than 50 sessions over periods longer than a year yielded an effect
size of .54 for overall effectiveness for complex cases with severe
symptomatology, comorbid diagnoses, or personality disorders, when
long-term psychodynamic psychotherapy was compared with a range
of other therapies including CBT, dialectical behaviour therapy, family
therapy and short-term psychodynamic psychotherapy. This indicates
that after treatment the average case treated with long-term psycho-
dynamic psychotherapy fared better than 70% of cases treated with
other therapies. Gains made during treatment were sustained at 1–8
years’ follow-up.
The results of these two meta-analyses show that short-term psy-
chodynamic psychotherapy is as effective as other widely used forms of
psychotherapy, including CBT, for common psychological problems
such as anxiety and depression in adults; and that long-term psycho-
dynamic psychotherapy is more effective than some other forms of
therapy for adults with complex mental health difficulties.

Client-centred humanistic psychotherapy

Elliott et al. (2004) conducted a meta-analysis of trials of psycho-
therapy that fall broadly within the client-centred humanistic psycho-
therapy tradition. Over 90 trials of client-centred, experiential, gestalt
and emotionally-focused therapy were included in the analysis. Clients
in these studies had a wide variety of psychological problems including
anxiety, mood, eating and personality disorders and relationship
distress. The average duration of treatment was 22 sessions, reflecting
about 6 months of therapy. An effect size of .78 was obtained, indicating
that the average treated case fared better than 78% of cases in
control groups. These results indicate that client-centred humanistic
psychotherapy is an effective form of treatment for a range of common
psychological problems in adulthood.

Cognitive-behaviour therapy
In a review of 16 meta-analyses that included 332 studies of the effec-
tiveness of cognitive-behaviour therapy with 16 different disorders or
populations, Butler et al. (2006) obtained a mean weighted effect size
of .95 for depression and a range of anxiety disorders in children, ado-
lescents and adults. Thus, the average treated case with anxiety
and depression fared better than 83% of untreated controls. For marital

Book 1.indb 318 06/03/2012 13:48

 10 • EFFECTIVENESS OF PSYCHOLOGICAL THERAPIES 319

distress, anger control and chronic pain in adults, and childhood somatic
disorders, effect sizes were moderate, with a mean of .62. Thus, the
average treated case with these problems fared better than 73% of
untreated controls.
For sexual offending the average effect size of .35 was relatively
small. However, it was the most effective form of psychotherapy for
reducing recidivism in this population. Thus, the average treated sex
offender fared better than 64% of untreated controls. There was signifi-
cant evidence for the long-term effectiveness of cognitive-behaviour
therapy, with an average effect size of .79, indicating that the average
treated case fared better than 79% of untreated controls at follow-up at
least 6 months after therapy.

Systemic therapy
Shadish and Baldwin (2003) reviewed 20 meta-analyses of systemic
marital and family interventions for a wide range of child- and adult-
focused problems. These included child and adolescent conduct and
emotional disorders; drug and alcohol abuse in adolescents and adults;
adult anxiety, depression and psychosis; and marital distress. Sixteen
of the 20 meta-analyses were of therapy studies and four included
marital and family enrichment studies.
For marital and family therapy the average effect size was .65 after
therapy and .52 at follow-up 6 months to a year later. These results
show that, overall, the average treated couple or family with clinically
significant problems fared better after treatment than 75% of untreated
controls, and at follow-up fared better than about 71% of cases in control
groups. For marital and family enrichment, the effect sizes after therapy
and at follow-up were .48 and .32 respectively. These results show that,
overall, the average treated couple or family without clinically significant
problems fared better after enrichment programmes than 68% of
untreated controls, and at follow-up fared better than about 63% of
cases in control groups.
Shadish and Baldwin’s synthesis of the results of 20 meta-analyses
supports the efficacy of systemic therapy for couples and families
with a wide range of clinically significant problems, and for couples and
families without clinical problems but who want to develop family
strengths such as communication and problem-solving skills and
greater emotional cohesion.

Summary of the overall effects of psychotherapy

Figure 10.5 summarizes the results of meta-analyses, described above,
of the effectiveness of psychotherapy from a range of different traditions
with adults and children. In this figure, where appropriate, effect sizes
from multiple meta-analyses have been averaged, and graphed as
success rates based on the system given in Table 10.1.
From Figure 10.5 it may be seen that meta-analyses of psychother-
apy trials yield moderate to large effect sizes that range from .65 to

Book 1.indb 319 06/03/2012 13:48

 320 C L I N I C A L P S Y C H O L O G Y : A N I N T R O D U C T I O N

Figure 10.5 Success rates of psychotherapy with adults and children, and therapy from
different traditions based on effect sizes from meta-analyses

1.02. When expressed as success rates, the results of meta-analyses

indicate that 65–72% of people with psychological problems benefit
from psychotherapy. Thus approximately two-thirds to three-quarters of
people who engage in psychotherapy find that it leads to improvements
in their mental health.

Comparison of the relative effects of psychotherapy

and medical procedures
To place the evidence on the overall effectiveness of psychotherapy in
a broader context, it is useful to ask: Are the moderate to large effect
sizes associated with psychotherapy very different from those associ-
ated with the medical and surgical treatment of physical illnesses, dis-
eases and medical conditions?
In a synthesis of 91 meta-analyses of various medical and surgical
treatments for a range of medical conditions, Caspi (2004) found an
average effect size of .5. This falls in the moderate range of effect sizes
(.5–.8) and is not vastly dissimilar to the effect size of .75 from Grissom’s
(1996) synthesis of 68 meta-analyses of psychotherapy trials men-
tioned earlier. Thus it may be concluded that the moderate effect sizes
associated with psychotherapy are similar to those associated with the
treatment of medical conditions.

Book 1.indb 320 06/03/2012 13:48

 10 • EFFECTIVENESS OF PSYCHOLOGICAL THERAPIES 321

Deterioration and drop-out

A consistent finding within the psychotherapy research literature is that
up to 10% of clients deteriorate following treatment (Lambert and Ogles,
2004; Lilienfeld, 2007). In a review of 46 studies on negative outcome in
adult psychotherapy, Mohr (1995) found that deterioration was associ-
ated with particular client and therapist characteristics and particular
features of psychotherapy. Deterioration was more common among cli-
ents with borderline personality disorder, obsessive compulsive disor-
der, or severe interpersonal difficulties. Lack of motivation and the
expectation of benefiting from psychotherapy without personal effort
were also associated with deterioration. Deterioration was more com-
mon when unskilled therapists lacked empathy and did not collaborate
with clients in pursuing agreed goals. Failure to manage counter trans-
ference appropriately and frequent transference interpretations were
also associated with deterioration.
Dropping out of psychotherapy is a relatively common event. In a
meta-analysis of 125 studies, Wierzbicki and Pekarik (1993) found a
mean dropout rate of 47%. Dropout rates were higher for minority ethnic
groups, less educated clients, and those with lower incomes. Thus, we
can conclude that about 1 in 10 clients deteriorate following therapy and
that marginalized clients with particularly troublesome disorders and
negative attitudes to psychotherapy are vulnerable to dropping out of
psychotherapy and deterioration.

Medical cost offset

The evidence reviewed so far shows that psychotherapy is effective for
a range of problems and populations. However, an important concern is
the financial implications of providing such a psychotherapy service. In
this context, two questions are of interest. First: Do clients who avail of
psychotherapy services use fewer medical services and so incur
reduced medical costs? This saving is referred to as the medical cost
offset. The second question is: Is the medical cost offset associated
with psychotherapy greater than the cost of providing psychotherapy? If
so, we can conclude that psychotherapy has a total cost offset. Findings
of meta-analyses and narrative reviews of the cost-offset literature
throw light on both of these questions.
In a meta-analysis of 91 studies conducted between 1967 and 1997,
Chiles et al. (1999) found that psychotherapy and psychological inter-
ventions led to significant medical cost offsets. Participants in reviewed
studies included surgery inpatients, high health-service users, and
people with psychological and substance use disorders who received
psychotherapy or psychological interventions alone or as part of multi-
modal programmes. Chiles and his team concluded that medical cost
offsets occurred in 90% of studies and ranged from 20% to 30%. In 93%
of studies where data were provided, cost offsets exceeded the cost
of providing psychotherapy. Greater cost offsets occurred for older
inpatients who required surgery, oncology, and cardiac rehabilitation

Book 1.indb 321 06/03/2012 13:48

 322 C L I N I C A L P S Y C H O L O G Y : A N I N T R O D U C T I O N

than for outpatients who required care for minor injuries and illnesses.
Structured psychological interventions, tailored to patient needs associ-
ated with their medical conditions, led to greater medical cost offsets
than traditional psychotherapy.
In an earlier set of meta-analytic studies involving Blue Cross and
Blue Shield US Federal Employees Plan claim files and 58 controlled
studies, Mumford et al. (1984) found that in 85% of studies medical cost
offset for psychotherapy occurred. This was due to shorter periods of
hospitalization for surgery, cancer, heart disease and diabetes, particu-
larly in patients over 55. In a review of psychological interventions for
people with a variety of health-related difficulties, Groth-Marnat and
Edkins (1996) found that medical cost offsets occurred when such inter-
ventions targeted patients preparing for surgery and patients with diffi-
culty adhering to medical regimens. Medical cost offset also occurred
for smoking cessation programmes, rehabilitation programmes, and
programmes for patients with chronic pain disorders, cardiovascular
disorders and psychosomatic complaints.
Three other important reviews of the medical cost-offset literature,
which focused largely on mental health problems in adults rather than
adjustment to physical illness, deserve mention. In a review of 30 studies
of psychotherapy for psychological disorders and drug and alcohol
abuse, Jones and Vischi (1979) found that medical cost offsets occurred
in most cases. In a review of eight cost-effectiveness studies for sub-
stance abuse, Morgan and Crane (2010) concluded that family-based
treatments can be cost-effective and deserve inclusion in health-
care delivery systems. In a review of 18 studies of psychotherapy for
psychological disorders, Gabbard et al. (1997) found that in more than in
80% of studies, medical cost offsets exceeded the cost of providing psy-
chotherapy. Particularly significant cost offsets occurred for complex
problems, notably in studies of psychoeducational family therapy for
schizophrenia and dialectical behaviour therapy for personality disor-
ders, by reducing the need for inpatient care and improving occupational
adjustment.
From the evidence reviewed here, it is clear that psychotherapeutic
interventions have a significant medical cost offset. Those who partici-
pate in psychotherapy use fewer other medical services at primary, sec-
ondary and tertiary levels and are hospitalized less than those who do
not receive psychotherapy.

Common factors and specific psychotherapies

A striking feature of the evidence base for psychotherapy is the similarity
in outcomes of diverse approaches with a range of populations and
problems, as shown in Figure 10.5. All approaches to psychotherapy,
when averaged across different populations, problems and studies,
lead to moderate to large effect sizes, and benefits for two-thirds to
three-quarters of treated cases. When therapies are compared,
differences rarely exceed an effect size of .2, as shown in Figure 10.6,
which is based on Grissom’s (1996) synthesis of many meta-analyses.

Book 1.indb 322 06/03/2012 13:48

 10 • EFFECTIVENESS OF PSYCHOLOGICAL THERAPIES 323

Figure 10.6 The effects of psychotherapy compared with placebo control groups. Based on
Grissom (1996)

The hypothesis that different psychotherapies lead to similar

improvement rates was first referred to as the Dodo bird verdict by Saul
Rosenzweig in 1936. The reference is to a quotation from Lewis Carroll’s
Alice in Wonderland – At last the Dodo said ‘Everybody has won, and
all must have prizes’ – The Dodo’s remark was made after a caucus
race in which competitors started at different points and ran in different
directions for half an hour. This finding that most forms of psychotherapy
have similar outcomes has led to the hypothesis that a set of common
factors may underpin all effective psychotherapies.
One possibility is that the underlying common factor is the placebo
effect. That is, psychotherapy may be no more than a placebo, a psy-
chological sugar pill that gives clients hope and creates the expectation
of improvement. It was mentioned above that to evaluate this hypoth-
esis researchers have conducted studies in which a specific form of
psychotherapy is compared with a psychological or pharmacological
placebo condition. Common psychological placebo conditions involve
engaging in intellectual discussion groups, participating in recreational
activities, or receiving an inert procedure that is described as providing
subliminal treatment.
In Grissom’s (1996) synthesis of many meta-analyses summarized
in Figure 10.6, the effect size for psychotherapy compared with placebos
was .58. Thus, the average treated case fared better than 72% of cases
in control groups who received placebos. This shows that psychotherapy
is not just a placebo that generates hope, but a set of procedures that
actively influences the recovery process. From Figure 10.6 it may also
be seen that the effect size for therapy versus waiting list control groups
(.75) is larger than the effect size of placebo versus waiting list control
groups (.44). This shows that the effects of psychotherapy are nearly
double those of placebos.

Book 1.indb 323 06/03/2012 13:48

 324 C L I N I C A L P S Y C H O L O G Y : A N I N T R O D U C T I O N

The results of two important analyses of the relative contribution of

common and specific factors to psychotherapy outcome are summarized
in Figure 10.7. In a narrative review of over 100 psychotherapy studies
Michael Lambert (1992; Lambert & Barley, 2002) estimated that
common factors were about twice as important as specific factors in
contributing to the outcome of psychotherapy. From the left-hand panel
in Figure 10.7, it may be seen that Lambert estimated that about 30% of
psychotherapy outcome variance may be accounted for by common
factors, and 15% by specific factors; 15% of the remainder of the
variance in outcome, Lambert estimated, was due to placebo effects or
creating the expectation of recovery. The remaining 40% of variance in
outcome, according to Lambert’s analysis, was accounted for by factors
outside therapy such as social support from family and friends.
The results of an analysis conducted by Bruce Wampold (2001) are
presented in the right-hand panel in Figure 10.7. Wampold, like Lambert,
concluded that common factors are more important than specific factors
in determining the outcome of psychotherapy, but the results of his rigor-
ous analysis led to a far more extreme statement of this position. Wampold
(2001) conducted a quantitative review of more than a dozen meta-
analyses, and estimated that common factors are nine times more influ-
ential than specific factors in determining the outcome of psychotherapy.
He concluded that only 13% of the variance of outcome for psychother-
apy clients is due to psychotherapy (including common, specific and
other factors). This was based on his computation of an overall effect size
for psychotherapy of between .7 and .8. He also concluded that only 1%
of the variability in outcome for psychotherapy clients was due to specific
factors. This was based on an average between-treatment effect size
of .2, similar to that shown in Figure 10.6. He estimated that 3% of the
variance in outcome was due to unexplained therapy factors, probably
client characteristics. The remaining 9% of the variance in outcome, he
concluded, was accounted for by common factors.

Figure 10.7 Factors that affect the outcome of psychotherapy. Based on Lambert and Barley (2002) and Wampold (2001)

Book 1.indb 324 06/03/2012 13:48

 10 • EFFECTIVENESS OF PSYCHOLOGICAL THERAPIES 325

Lambert’s and Wampold’s analyses share one important conclusion.

Common factors have a far greater impact than specific factors in deter-
mining whether or not clients benefit from psychotherapy. The major
impact of common factors on the outcome of psychotherapy provides a
possible explanation for the similarity in outcome of different psycho-
therapy approaches. However, therapists must engage in specific forms
of therapy for common factors to have a medium through which to oper-
ate. For example, in family therapy the process of convening family
meetings, helping family members view individual problems as part of a
pattern of family interaction, and exploring alternative interaction pat-
terns creates a context within which therapists develop good working
alliances with clients (which is one of the most important common fac-
tors affecting treatment outcome).

Categories of common factor

In considering common factors, it is useful to distinguish between client
factors, therapist factors and factors associated with the therapeutic
context, including the dose of therapy received, the quality of the
therapeutic alliance, and therapeutic procedures. Common factors that
contribute to the effectiveness of psychotherapy are listed in Table 10.2.

TABLE 10.2
Therapy, client and therapist ‘common factors’ that affect positive psychotherapy outcome
Therapeutic context factors Client factors Therapist factors
Dose of 20–45 sessions High personal distress Personal adjustment
Positive therapeutic alliance Low symptom severity Therapeutic competence
Empathy Low functional impairment Matching therapy style to patients’ needs
Collaboration and goal Low problem complexity, Over-controlled patients – facilitate insight
consensus chronicity and comorbidity Under-controlled patients – build symptom
Positive regard and Readiness to change and management skills
genuineness lack of resistance Positive past relationships – facilitate insight
Relevant feedback and Early response to therapy Negative past relationships – provide
relevant self-disclosure
Psychological mindedness support
Repair alliance ruptures Ego strength Compliant clients – use directive
Manage transference and interventions
Capacity to make and
countertransference maintain relationships Resistant clients – use self-directed
Common procedures interventions
Social support
Problem exploration Credibility of rationales
High socio-economic status
Credible rationale Problem-solving creativity
Mobilizing client Specific training
Support and catharsis Flexible manual use
Reconceptualizing problem Supervision and personal therapy
Behavioural change Feedback on client recovery
Combining psychotherapy
and medication

Book 1.indb 325 06/03/2012 13:48

 326 C L I N I C A L P S Y C H O L O G Y : A N I N T R O D U C T I O N

Client characteristics
A range of client characteristics are associated with a positive response
to any type of psychological intervention (Clarkin & Levy, 2004; Lambert,
2005). Distressed clients with circumscribed problems of low severity
with little functional impairment who are ready to change, and who show
an improvement early in treatment, respond well to psychotherapy.
High socio-economic status, social support, the capacity to make and
maintain relationships, psychological-mindedness and ego strength are
other client attributes associated with a positive response to psycho-
therapy. Psychologically minded people understand their problems in
intrapsychic terms, rather than blaming them on external factors. Ego
strength is the capacity to tolerate conflict and distress, while showing
flexibility and persistence in pursuing valued goals.

Therapist characteristics
Effective therapists have distinctive profiles (Addis, 2002; Beutler et al.,
2004; Lambert et al., 2003; Lambert & Ogles, 1997; Miller et al., 2005;
Norcross, 2005; Stein & Lambert, 1995). They are technically competent,
credible and creative in their approach to helping clients solve problems.
They have engaged in personal therapy, are well adjusted, well trained,
use therapy manuals flexibly, and use feedback on client progress to
match their therapeutic style to clients’ needs.
There is evidence for the effectiveness of three types of matching.
For reflective, over-controlled clients, an insight-oriented approach is
particularly effective, whereas a symptom-focused, skills-building
approach is more effective with impulsive, under-controlled clients. For
clients who are resistant to directives, a self-directed approach is most
effective, whereas a directive approach is effective with non-resistant
clients. For clients with a history of gratifying early relationships, con-
frontative insight-oriented approaches are effective, whereas supportive
approaches are more effective for clients with histories of problem-
atic early relationships.

Therapeutic common factors

For 50–75% of psychotherapy clients to recover, 20–45 sessions of
therapy are necessary (Hansen et al., 2002). The therapeutic alliance is
the single most important therapeutic common factor and accounts for
about 38% of the effectiveness of psychotherapy (Martin et al., 2000;
Shirk & Karver, 2003). Strong therapeutic alliances have distinctive
features (Norcross, 2002; Orlinsky et al., 2004). For a strong therapeutic
alliance, the therapist must be empathic and collaborative, and the
client must be co-operative and committed to recovery.
Within the therapy relationship, effective therapists show positive
regard, genuineness, and provide clients with both relevant feedback
and relevant self-disclosure information. Ruptures in the therapeutic alli-
ance are common. These may be associated with client transference,
therapist countertransference or a mismatch between clients’ needs and
the therapist’s way of conducting therapy. Strong therapeutic alliances

Book 1.indb 326 06/03/2012 13:48

 10 • EFFECTIVENESS OF PSYCHOLOGICAL THERAPIES 327

are maintained by managing such ruptures in therapeutic alliances and

customizing therapeutic relationships to take account of clients’ needs.
Certain common procedures characterize effective therapy (Frank &
Frank, 1991; Hubble et al., 1999; Karasu, 1986; Lambert & Ogles, 2004;
Norcross & Goldfried, 2003; Sprenkle & Blow, 2004; Wampold, 2001).
Effective therapy involves exploration and reconceptualization of both
conscious and unconscious aspects of clients’ problems; provision of a
credible rationale for conducting therapy; generating hope and the
expectation of improvement; and mobilizing clients to engage in problem
resolution. This mobilization process may involve helping clients develop
more adaptive behaviour patterns and belief systems; more effective
ways of regulating their emotions; and more supportive emotional con-
nections with themselves, their family members and their therapists.
There is also a developmental sequence common to most forms of
psychotherapy in which interventions that support clients (such as reas-
surance and facilitating catharsis and emotional expression) precede
interventions that promote learning to see problems in new ways (such
as reframing and interpretation), and these in turn precede inter-
ventions that promote new forms of behaviour such as facing fears,
regulating behaviour, interpersonal risk-taking, and practising new
skills.
For specific disorders, multimodal programmes in which psychother-
apy and psychotropic medication are combined are more effective than
either alone (Kazdin, 2004; Thase & Jindal, 2004). For example, in chil-
dren with attention deficit hyperactivity disorder, the effectiveness of
psychotherapy, which includes parent-management training, school
intervention, and self-instructional training for the child, can be enhanced
by combining this with stimulant therapy as discussed in Chapter 2. In
adults being treated with antipsychotic medication for schizophrenia,
relapse rates may be reduced by offering psychoeducational family
therapy to reduce family stress and cognitive-behaviour therapy to
improve symptom management, as discussed in Chapter 7.

Specific factors
Common factors have a profound impact on the effectiveness of psycho-
therapy. However, therapists must engage in specific forms of therapy
for common factors to have a medium through which to operate. In
Chapters 2–8, examples of specific evidence-based psychological treat-
ments for particular problems have been given. Comprehensive reviews
of the literature on the effectiveness of psychological interventions con-
cur that effective interventions have been developed for a range of prob-
lems (Carr, 2009a; Nathan & Gorman, 2007; Roth & Fonagy, 2005).
These include mood, anxiety, eating, substance use and sleep disorders
in both children and adults; family relationship problems, pain manage-
ment, adjustment to illnesses such as asthma and diabetes, and adjust-
ment to physical and intellectual disabilities in children and adults;
disruptive behaviour disorders and toileting problems in childhood; and
personality disorders and psychosis in adults.

Book 1.indb 327 06/03/2012 13:48

 328 C L I N I C A L P S Y C H O L O G Y : A N I N T R O D U C T I O N

Summary
Clinical psychologists provide psychotherapy to children and
adults on an individual, couple, family, or group basis, often as
one element of a multimodal programme offered by a multidis-
ciplinary team. In doing so, they engage in evidence-based
practice by taking account of available scientific evidence
about ‘what works’ on one hand, and clients’ unique problems,
needs, rights and preferences on the other, and making bal-
anced, compassionate judgements.
Scientific evidence for the effectiveness of psychotherapy
ranges in persuasiveness from case studies to meta-analyses
of controlled trials. Results of meta-analyses show that approx-
imately two-thirds to three-quarters of people who engage in
psychotherapy improve. Similar improvement rates occur for
children and adults, individuals and families, and for psycho-
therapy from a range of different traditions. The moderate
effect sizes associated with psychotherapy for mental health
problems are similar to those associated with the medical and
surgical treatments for physical health problems.
About one in 10 clients deteriorate following psychotherapy.
Marginalized clients with particularly troublesome disorders
and negative attitudes to psychotherapy are vulnerable to
dropping out of psychotherapy and deterioration. Psychotherapy
has a significant medical cost offset, and those who participate
in psychotherapy use fewer other medical services than those
who do not.
Most forms of psychotherapy are equally effective. This is
due to the fact that they share common factors that contribute
to effectiveness. These common factors include those associ-
ated with the client, the therapist and the therapeutic context.
Distressed clients with circumscribed problems of low severity
and little functional impairment who are ready to change,
who show an improvement early in treatment, are of high
socio-economic status, have a high level of social support,
the capacity to make and maintain relationships, psychological-
mindedness and ego strength respond well to psychotherapy.
Particularly effective therapists are technically competent,
credible and creative in their approach to helping clients solve
problems, have engaged in personal therapy, are well adjusted,
well trained, use therapy manuals flexibly, and use feedback on
client progress to match their therapeutic style to clients’ needs.
At least 20 sessions are required for most clients to recover,
and the therapeutic alliance is the single most important com-
mon therapeutic common factor. For a strong therapeutic alli-
ance, the therapist must be empathic and collaborative, and the
client must be co-operative and committed to recovery.

Book 1.indb 328 06/03/2012 13:48

 10 • EFFECTIVENESS OF PSYCHOLOGICAL THERAPIES 329

The common procedures that characterize effective therapy

include exploration and reconceptualization of conscious
and unconscious aspects of problems; provision of a credible
rationale for conducting therapy; generating hope and the
expectation of improvement; and mobilizing clients to engage
in problem resolution. These broad procedures may involve
using therapeutic techniques such as providing support and
encouraging emotional expression; facilitating new ways of
viewing problems; and helping clients to develop new ways of
behaving adaptively.
For certain disorders, multimodal programmes in which
psychotherapy and pharmacotherapy are combined are more
effective than either alone. Therapists must engage in specific
forms of therapy for common factors to have a medium through
which to operate.

Questions
● What is evidence-based practice in clinical psychology?
● What is the hierarchy of evidence that informs evidence-based
practice in clinical psychology?
● What do the results of broad meta-analyses indicate about the
overall effectiveness of psychotherapy?
● Is there a medical cost offset associated with psychotherapy?
● What is the ‘Dodo bird’ verdict?
● How important are common factors in contributing to the effective-
ness of psychotherapy?
● What common factors contribute to the effectiveness of psycho-
therapy?
● How do specific models of practice contribute to the effectiveness of
psychotherapy?

FURTHER READING
● Carr, A. (2009a). What works with children, adolescents and adults?
A review of research on the effectiveness of psychotherapy. London:
Routledge.
● Nathan, P. & Gorman, J. (2007). A guide to treatments that work (third
edition). New York: Oxford University Press.
● Roth, T. & Fonagy, P. (2005). What works for whom? A critical review of
psychotherapy research (second edition). London: Guilford.

WEBSITE
● Society for Psychotherapy Research:
www.psychotherapyresearch.org

Book 1.indb 329 06/03/2012 13:48

 Glossary
A-CRA. Adolescent Contingency Reinforcement Approach, an evidence-based
therapy for adolescent drug problems in which operant conditioning is the
central intervention.
AACAP practice parameters. Clinical guidelines produced by the American
Academy of Child and Adolescent Psychiatry, which is the US professional
association for child and adolescent psychiatrists. (www.aacap.org/cs/root/
member_information/practice_information/practice_parameters/practice_
parameters)
AACBT. Australian Association for Cognitive and Behaviour Therapy. (www.
aacbtqld.org.au)
AAMFT. American Association for Marital and Family Therapy. (www.aamft.org)
ABCT. Association for Behavioral and Cognitive Therapies (US). (www.abct.
org)
ACPA. Australian Clinical Psychology Association. (www.acpa.org.au)
Addictive personality. A profile of personality traits that predisposes a person
to addiction.
ADHD. Attention deficit hyperactivity disorder. A syndrome characterized by
persistent overactivity, impulsivity and difficulties in sustaining attention. Also
known as attention deficit disorder, hyperkinetic disorder, hyperkinesis and
minimal brain dysfunction.
ADIS. Anxiety Disorders Interview Schedule, for assessing DSM–IV anxiety
disorders. There are adult and child versions.
AFT. Association for Family Therapy (UK) (www.aft.org.uk)
Agoraphobia. A fear of public places, often due to a fear of having panic attacks
in public places.
Alogia. Impoverished thought inferred from speech, common in schizophrenia.
Brief concrete replies are given to questions (poverty of speech) or a normal
amount of speech is produced but conveys little information (poverty of
content) due to repetition, being overly concrete or being overly abstract.
Amygdala. An almond-shaped brain structure within the limbic system, located
in the medial temporal lobes, that subserves the processing of emotional
information and memories. Abnormalities of the amygdala occur in many
psychological disorders.
Anaclitic depression. In Blatt’s psychoanalytic theory, anaclitic (or depen-
dent) depression is characterized by feelings of abandonment in response
to interpersonal loss. It is contrasted with introjective (or self-critical) depres-
sion which is characterized by self-criticism in response to perceived
failure.
Anakastic personality disorder. See Obsessive compulsive personality
disorder.
Anomie. A state characterized by normlessness where the social structures
provided by family, religion and other institutions become destabilized and
leave members of a community feeling alienated. Some disadvantaged

Book 1.indb 330 06/03/2012 13:48

 GLOSSARY 331

communities in which delinquency, drug abuse and suicide occur are

characterized by anomie.
Anorexia nervosa. An eating disorder characterized by over-evaluation of
weight and shape and their control, and a severe weight loss.
Antisocial personality disorder. A personality disorder characterized by a
pervasive disregard for the rights of others and consistent violation of these
rights. Has also been referred to as psychopathy, sociopathy and dissocial
personality disorder.
APA practice guidelines. Evidence-based clinical practice guidelines produced
by the American Psychiatric Association, which is the US professional
association for psychiatrists. (www.psychiatryonline.org)
APA. American Psychological Association (www.apa.org); American Psychiatric
Association (www.psych.org). American Psychoanalytical Association (www.
apsa.org).
APS. Australian Psychological Society (www.psychology.org.au); Australian
Psychoanalytical Society (www.psychoanalysis.asn.au).
ASEBA. Achenbach System of Empirically Based Assessment. Parent, teacher
and self-report rating scales widely used for assessing internalizing and
externalizing behaviour problems in children and adolescents.
Assertive community treatment. An integrated community mental health
service delivery model in which hard-to-reach people with psychosis receive
intensive, continuous individualized treatment, rehabilitation and support
services from community-based multidisciplinary teams.
Assessment. Procedures such as interviewing, psychological testing and
behavioural observation used to evaluate individuals with psychological
problems.
Assistant Psychologists Ireland Google groups. A forum for discussing
issues relevant to getting onto clinical psychology training programmes in
Ireland (ap_ireland@googlegroups.com).
AVE (abstinence violation effect). The cognitive process that leads to the
experience of loss of control and relapse during recovery from drug problems
when a minor slip occurs.
Avoidant personality disorder. A personality disorder characterized by a
pervasive pattern of social inhibition and shyness beginning in adolescence
or early adulthood.
Avolition. A lack of goal-directed activity common in schizophrenia.
BABCP. British Association for Behavioural & Cognitive Psychotherapies.
(www.babcp.com)
Basal ganglia. A subcortical region of the brain which subserves the initiation,
control and modulation of voluntary movement. Damage to the basal
ganglia may lead to excessive involuntary movement or to a slowing
of voluntary movement. Parkinson’s disease, Sydenham’s chorea and
Huntington’s chorea all involve damage to the basal ganglia. Dysfunction of
the basal ganglia underpins obsessive compulsive disorder and Tourette’s
syndrome.
BDI-II. Beck Depression Inventory, second edition, a self-report instrument for
assessing depression.
Behaviourally inhibited temperament. A temperamental trait involving the
tendency to become nervous and withdraw from unfamiliar stimuli and
situations.
Biological model. A conceptual framework which assumes that psychological
problems are symptoms of ‘mental illnesses’ each of which has a discrete
neurobiological cause, a unique course and prognosis, and for which a

Book 1.indb 331 06/03/2012 13:48

 332 C L I N I C A L P S Y C H O L O G Y : A N I N T R O D U C T I O N

specific physical treatment or psychotropic medication will be found. Also

referred to as the biomedical, neurobiological, organic, medical or disease
model.
Biomedical model. See Biological model.
Bipolar disorder. A recurrent mood disorder characterized by episodes of
mania and depression, previously known as manic-depression.
BMI. Body mass index. BMI = W/H2, where W = weight in kilograms and H =
height in metres. The normal range for BMI is 18.5–24.9.
Borderline personality disorder. A personality disorder characterized by
fear of abandonment, impulsivity and a pattern of pervasive instability in
interpersonal relationships, self-image and mood, often leading to self-
harm.
BPRS. Brief Psychiatric Rating Scale, a scale for monitoring psychotic symptom
severity.
BPS. British Psychoanalytical Society (www.psychoanalysis.org.uk); British
Psychological Society (www.bps.org.uk).
BSFT. Brief strategic family therapy, an evidence-based family therapy
intervention for adolescent conduct and drug problems.
Bulimia nervosa. An eating disorder characterized by over-evaluation of weight
and shape and their control, and a cycle of bingeing in response to stressful
events and compensatory purging.
BYI-II. Beck Youth Inventories, second edition, self-report instruments for
assessing depression, anxiety, anger, disruptive behaviour and self-esteem
in children and adolescents.
CAN. Camberwell Assessment of Need, a scale for assessing mental health
service users’ needs in areas such as mental and physical health, drug use,
social relationships, accommodation, transport, budgeting, and activities of
daily living.
Case–control study. A study design in which a group of diagnostically
homogeneous cases about which the researcher is trying to find out more
information is compared to another group of patients with a known condition
or with a normal control group.
Catatonic behaviour. Behaviour that occurs in some cases of schizophrenia,
characterized by a marked reduction or increase in motor activity.
Catatonic schizophrenia. A form of schizophrenia in which catatonic behaviour
is the predominant symptom.
CBCL. Child Behaviour Checklist, for screening children for psychological
problems. There are parent, teacher and child self-report versions. Also
called ASEBA – Achenbach’s System for Empirically Based Assessment.
CBT. Cognitive-behaviour therapy, a form of psychotherapy that involves
helping people improve their mood and adjustment by directly changing
their behaviour and thinking patterns using principles of learning theory and
cognitive psychology.
CDRS. Children’s Depression Rating Scale, for rating severity of depressive
symptoms in children and adolescents.
CFI. Camberwell Family Interview, a structured interview for assessing
expressed emotion which includes criticism, hostility and emotional over-
involvement.
Classical conditioning. An associative learning process that occurs when
two stimuli are regularly paired so that the response originally given to the
second stimulus comes to be given to the first.
Clearing House for Postgraduate Courses in Clinical Psychology. A web-
based system for applying for UK courses. (www.leeds.ac.uk/chpccp)

Book 1.indb 332 06/03/2012 13:48

 GLOSSARY 333

Cognitive rehabilitation. A set of cognitive drills that helps patients ameliorate

or compensate for cognitive deficits due to neurological conditions.
Common factors. Factors common to many forms of psychotherapy that
account for their similar levels of effectiveness.
Comorbid. Having more than one diagnosed psychological disorder or problem
at a time.
Compulsions. Repetitive, ritualistic, stereotyped behaviours that people with
OCD feel compelled to perform to regulate anxiety caused by obsessions.
Conduct disorder. A pervasive and persistent pattern of antisocial behaviour
that extends beyond the family to the school and community and involves
serious violations of rules, characterized by defiance of authority, aggression,
destructiveness, deceitfulness and cruelty.
Conversion hysteria. A condition characterized by deficits in sensory or
motor functioning in the absence of an organic illness, also referred to as
conversion disorder.
Counselling psychology. An applied psychology specialism that places a strong
emphasis on psychotherapeutic processes in effecting change in people facing
a range of normal life challenges as well as psychological disorders.
Countertransference. Therapists’ emotional responses to clients.
CPA. Canadian Psychological Association. (www.cpa.ca)
CRS. Conners Rating Scales: parent, teacher and self-report rating scales
widely used for assessing the severity of ADHD symptoms and other
childhood problems.
Cue exposure treatment. A treatment, based on the classical conditioning
model of addiction, in which recovering drug addicts are exposed to cues that
elicit craving and concurrently use a variety of coping strategies to tolerate
their discomfort and avoid drug-taking.
Cyclothymia. A persistent bipolar disorder characterized by continuous mood
swings from elation to sadness.
DAWBA. Development and Well-Being Assessment, a structured interview
and set of self-report instruments (the Strengths and Difficulties Scales) for
diagnosing childhood psychological disorders.
Defence mechanism. An unconscious psychological strategy for regulating
anxiety about unacceptable emotions or impulses such as sex or aggression.
Delusions. Unfounded and culturally alien beliefs.
Dependent personality disorder. A personality disorder characterized by a
pervasive pattern of submissiveness and dependence on other people.
Depersonalization. A perceptual distortion in which there is a sense of being
detached from the self or observing the self.
Derailment. A speech pattern common in schizophrenia marked by cons-
tant jumping from one topic to another, with only very loose associations
between topics and little logic to what is said, reflecting an underlying thought
disorder.
Derealization. A perceptual distortion in which there is sense of unreality, or
being in a dream.
Dialectical behaviour therapy. An evidence-based cognitive-behavioural
treatment for borderline personality disorder.
Diathesis–stress theory. A model in which a psychological disorder is proposed
to occur when a genetically vulnerable person is exposed to stress.
DID. Dissociative identity disorder, a condition in which two or more distinct
personalities exist within the individual, also known as multiple personality
disorder.
Disease model. See Biological model.

Book 1.indb 333 06/03/2012 13:48

 334 C L I N I C A L P S Y C H O L O G Y : A N I N T R O D U C T I O N

Dissociation. An abnormality of perception, memory or identity that occurs

in response to trauma and may include derealization (seeing the world as
dream-like), depersonalization (viewing the self from an external perspective)
and inability to recall important personal information.
Dizygotic twins. Fraternal twins that come from two separate ova.
Dodo bird verdict. The hypothesis that different forms of psychotherapy have
similar effects: refers to a quotation from Lewis Carroll’s Alice in Wonderland –
At last the Dodo said ‘Everybody has won, and all must have prizes’.
Dopamine. A neurotransmitter involved in the reward system or mesolimbic
dopamine pathway.
DSM-IV-TR. American Psychiatric Association’s (2000) Diagnostic and
Statistical Manual of Mental Disorders, fourth edition, text revision.
Dual diagnosis. A term used to describe cases in which there is a diagnosis
of a substance use disorder and another disorder, e.g. an anxiety, mood or
psychotic disorder.
Dysthymia. A non-episodic chronic mood disorder characterized by depressive
symptomatology.
ECT. Electroconvulsive therapy, an intervention for severe treatment-resistant
depression in which seizures are induced by briefly passing an electric cur-
rent through the brain via electrodes applied to the scalp. ECT is conducted
under general anaesthetic and muscle relaxants are used to prevent body
spasms.
EDE. Eating Disorder Examination, a detailed interview for assessing anorexia,
bulimia and other eating disorders.
EDI. Eating Disorder Inventory, a comprehensive self-report psychological
assessment instrument for evaluating eating pathology and related
psychological traits such as perfectionism and ineffectiveness.
Educational psychology. An applied psychology specialism concerned with
learning problems, and social and emotional problems encountered by
young people in educational settings.
EEG. Electroencephalogram, a procedure for assessing electrical activity
within the brain. Electrodes placed on the scalp are attached by wires to a
machine that records electrical impulses from the brain and displays these as
‘brain waves’ on a paper printout or a computer screen. Used for assessing
seizures, sleep stages and as biofeedback for ADHD.
EFPA. European Foundation for Psychologists and Analysts. (www.efpa.be)
EFTA. European Family Therapy Association. (www.europeanfamilytherapy.eu)
Ego strength. The capacity to tolerate conflict and distress, while showing
flexibility and persistence in pursuing valued goals.
Epidemiology. The study of the distribution of disorders and their correlates
within populations.
Evidence-based practice. The judicious and compassionate use of the best
available scientific evidence to make decisions about patient or client
care.
Executive function. Cognitive processes involved in decision making, following
through on plans and troubleshooting difficulties without being distracted by
irrelevant stimuli or habitual reactions.
Expressed emotion. An attitude of criticism, hostility or emotional over-
involvement expressed by family members of mental health service users,
assessed with the Camberwell Family Interview, and associated with relapse
in mood, and psychotic and other disorders.
Family systems model. A model which assumes that psychological problems
are maintained by patterns of interaction and belief systems within the family

Book 1.indb 334 06/03/2012 13:48

 GLOSSARY 335

and the wider social system of the client, and may be resolved by disrupting
these processes in family therapy.
Family therapy. A psychosocial intervention where the family is the unit of
treatment.
FFT. Functional family therapy, an evidence-based family therapy intervention
for adolescent conduct and drug problems.
Five-factor model of personality traits. A theory which proposes that the ‘Big
5’ personality traits offer the most parsimonious description of personality.
The Big 5 are neuroticism, extraversion, openness to experience, conscien-
tiousness and agreeableness.
Flooding. A behavioural treatment for phobias in which clients are exposed
for a prolonged period to their most anxiety-provoking stimuli until anxiety
responses are extinguished; also called implosion.
Forensic psychology. An applied psychology specialism concerned with the
application of psychology to criminal investigation and the assessment and
treatment of offending behaviour.
FTAI. Family Therapy Association of Ireland. (www.familytherapyireland.com)
GAF. Global Assessment of Functioning scale, a single 100-point scale for
rating the functioning of adult mental health service users.
GAIN. Global Appraisal of Individual Needs, a comprehensive structured
interview for assessing drug use severity and personal, family and school-
related adjustment problems in adolescents.
Gateway drugs. Nicotine, alcohol and cannabis, which may lead to the use of
other drugs such as cocaine and heroin.
Generalized anxiety disorder. Ongoing apprehension that misfortunes of
various sorts will occur and anxiety that this worrying process is uncontrollable.
GRE. Graduate Record Examination. (www.ets.org/gre).
Hallucination. Experiencing a sensation in the absence of an external stimulus.
Harm-avoidance. Interventions such as needle exchanges and safe injection
sites that reduce the harm caused by drug misuse.
HCR-20. Historical, Clinical, Risk Management–20, a rating scale for assessing
risk of violence.
Health psychology. An applied psychology specialism concerned with the
application of psychology to address physical health problems.
Hebephrenic schizophrenia. A form of schizophrenia characterized by
inappropriate or flat affect and disorganization of behaviour and speech.
Histrionic personality disorder. A condition characterized by pervasive
attention-seeking behaviour including inappropriately seductive behaviour
and shallow or exaggerated emotions.
HPA axis. Hypothalamic–pituitary–adrenal axis, a major part of the neuro-
endocrine system involving the hypothalamus, the pituitary gland located
below the hypothalamus, and the adrenal glands (located on top of the
kidneys), which controls stress reactions and other processes including the
immune system, sexuality and digestion, and is dysregulated in anxiety
and mood disorders.
HRS. Hamilton Rating Scale, for rating severity of depressive symptoms in adults.
HSE. Health Service Executive (www.hse.ie), the Irish public health service.
Hull University. The only university in the UK or Ireland that offers an integrated
6-year BSc/DClinPsych (www2.hull.ac.uk).
Humanistic psychotherapy. An overarching term for approaches to explaining
psychological problems using the concepts of self-actualization, the self, the
ideal self and the organism, and treating such problems with non-directive
client-centred therapy.

Book 1.indb 335 06/03/2012 13:48

 336 C L I N I C A L P S Y C H O L O G Y : A N I N T R O D U C T I O N

IAPT. Improving Access to Psychological Therapies (www.iapt.nhs.uk) is

an NHS programme to improve access to evidence-based talking
therapies through an expansion of the psychological therapy workforce and
services.
ICD-10. The World Health Organization’s (1992) International Classification of
Diseases – Tenth Edition. Psychological problems are classified in Chapter 5.
ICP. Irish Council of Psychotherapy. (www.psychotherapy-ireland.com)
Ideas of reference. Incorrect interpretation of events as referring directly to
oneself.
Implosion. A behavioural treatment for phobias in which clients are exposed
for a prolonged period to their most anxiety-provoking stimuli until anxiety
responses are extinguished; also called flooding.
Introjective depression. In Blatt’s psychoanalytic theory introjective (or self-
critical) depression is characterized by self-criticism in response to perceived
failure. It is contrasted with anaclitic (or dependent) depression, which is
characterized by feelings of abandonment in response to interpersonal loss.
IPA. International Psychoanalytical Association. (www.ipa.org.uk)
IPDE. International Personality Disorder Examination, a structured interview for
the diagnosis of personality disorders.
IPT. Interpersonal therapy, an evidence-based treatment for depression and
bulimia in which the focus is on resolving interpersonal difficulties, notably
grief, role disputes, role transitions, and interpersonal deficits, which maintain
the presenting problem.
IUPsyS. International Union of Psychological Science. (www.iupsys.org)
Learning theory. A theoretical framework which posits that behaviour is learned
through the processes of operant and classical conditioning.
Limbic system. A complex of brain structures that subserves the experience
and expression of emotions, which includes the amygdala, hippocampus,
insula and parts of the anterior cingulated cortex
Longitudinal study. A study design in which a group of cases is assessed on
a number of occasions to discover the course of their development over
time.
Major depression. A unipolar recurrent episodic mood disorder involving
low mood, selective attention to negative features of the environment, a
pessimistic belief system, self-defeating behaviour patterns, particularly
within intimate relationships, and a disturbance of sleep and appetite.
MAOI. Monoamine oxidase inhibitors, a type of antidepressant, such as
phenelzine/Nardil which prevents the enzyme monoamine oxidase from
breaking down neurotransmitters in the synaptic cleft and leads to an
increase in neurotransmitter levels.
MCMI-III. Millon Clinical Multiaxial Inventory–III, a self-report inventory for
assessing personality disorders.
MDFT. Multidimensional family therapy, an evidence-based family therapy
intervention for adolescent drug problems.
Medical cost offset. The extent to which clients who avail of psychotherapy
services use fewer medical services and so incur reduced medical costs.
Medical model. See Biological model.
Mentalization-based treatment. An evidence-based psychodynamic treatment
that aims to improve adjustment in borderline personality disorder by
enhancing mentalization skills.
Mentalization. The capacity to understand mental states, motives and intentions
of the self and others, and to conceptualize these states as being separate
from behaviour.

Book 1.indb 336 06/03/2012 13:48

 GLOSSARY 337

Mesolimbic dopamine pathway. The neurobiological system that underpins

reward or reinforcement, involving the ventral tegmental area, the nucleus
accumbens and the prefrontal cortex.
Meta-analysis. A systematic, quantitative approach to reviewing evidence from
multiple studies in which effect sizes are calculated for each study and then
averaged across all studies.
Methadone maintenance. An intervention for opioid dependency involving the
prescription of a daily dose of methadone as a substitute for street opioids
such as heroin.
Minnesota Model. An approach to treating drug problems that integrates the
Narcotics Anonymous/Alcoholics Anonymous 12-step approach with group
and family therapy.
MMPI-2. Minnesota Multiphasic Personality Inventory–2, a self-report inventory
for assessing personality functioning and psychopathology.
Monozygotic twins. Identical twins that come from a single ovum.
Motivational interviewing. A non-directive intervention that motivates people
with drug problems to take steps towards reducing drug use, also called
motivational enhancement therapy.
MST. Multisystemic therapy, a comprehensive evidence-based treatment
approach to treating conduct disorder in which family therapy is the core
intervention but which also involves individual intervention and interventions
with the young person’s wider social network.
Multidisciplinary team. A team of health professionals from a variety of
disciplines such as psychology, medicine and social work.
Multimodal programme. In the mental health field, a programme usually
offered by multidisciplinary teams that includes a number of different types of
intervention; for example, psychotherapy and psychotropic medication.
Multiple personality disorder. A condition in which two or more distinct
personalities exist within the individual, with only one being evident at a time;
also known as dissociative identity disorder.
NA. Narcotics Anonymous, a self-help organization for drug addicts involving a
12-step recovery programme like that used in Alcoholics Anonymous.
Narcissistic personality disorder. A personality disorder characterized by a
pervasive pattern of grandiosity, a need for admiration, and a lack of empathy
for others.
Negative symptoms. Collective term for flattening of affect, poverty of speech
and lack of goal-directed behaviour common in schizophrenia.
NEO-PI-R. Revised NEO Personality Inventory, a self-report inventory for
assessing the Big 5 personality traits and 30 related facets.
Neologisms. Made-up words that only have meaning for the individual, common
in schizophrenia.
Neuroadaptation. A neurobiological process that accompanies drug addiction
and accounts for the phenomena of tolerance, dependence, withdrawal, and
the high rate of relapse among recovered addicts.
Neurobiological model. See Biological model.
Neurodevelopmental hypothesis. The view that prenatal and perinatal adver-
sities interact with a genetic vulnerability to psychosis to give rise to atypical
neuroanatomical development initially in infancy, and later in adolescence,
to cause schizophrenia.
Neuropsychology. A branch of applied psychology concerned with the
assessment and rehabilitation of people with neurological disorders.
Neuroticism. A personality trait characterized by the tendency to experience
negative affect including anxiety, depression and hostility.

Book 1.indb 337 06/03/2012 13:48

 338 C L I N I C A L P S Y C H O L O G Y : A N I N T R O D U C T I O N

Neurotransmitters. Chemicals released into synapses between neurons which

permit messages to be transmitted from one neuron to the next. Dysregulations
of neurotransmitters may occur in certain conditions. For example, there is
dysregulation of the dopamine system in schizophrenia, and the serotonin
system in depression.
NHS. National Health Service (www.nhs.uk): the UK public health service.
NICE Guidelines. Evidence-based guidelines for the treatment of mental and
physical health problems produced by the National Institute for Clinical
Excellence. (http://guidance.nice.org.uk/topic/mentalhealthbehavioural)
NUIG. National University of Ireland Galway (www.nuigalway.ie), which runs
one of the five clinical psychology training programmes in Ireland.
NZPS. New Zealand Psychological Society. (www.psychology.org.nz)
Obsessions. Involuntary, recurrent, persistent and stereotyped thoughts, images
or impulses that concern issues such as danger, violence and obscenity.
Obsessive compulsive personality disorder. A personality disorder charac-
terized by a pervasive pattern of preoccupation with orderliness, perfec-
tionism, ethics, interpersonal control, and fiscal economy, also referred to as
anakastic personality disorder.
OCD. Obsessive compulsive disorder, a condition characterized by distressing
obsessions on one hand and compulsive rituals which reduce the anxiety
associated with the obsessions on the other.
Operant conditioning. A learning process in which responses are strengthened
by reinforcement.
Oppositional defiant disorder. A disorder of conduct confined to the home and
characterized by difficulties with rule-following.
Organic model. See Biological model.
Panic disorder. A condition in which there are recurrent unexpected panic
attacks and an ongoing fear of further attacks, often accompanied by
agoraphobia.
PANSS. Positive and Negative Symptom Scale, a scale for monitoring psychotic
symptom severity.
Paranoid personality disorder. A personality disorder characterized by a
pervasive distrust of others.
Paranoid schizophrenia. A form of schizophrenia in which paranoid delusions
are the predominant feature.
PCL-R. The Psychopathy Checklist, a rating scale for assessing antisocial
personality disorder and risk of violence.
PEI. Personal Experience Inventory, a comprehensive questionnaire for
assessing drug use severity and personal, family and school-related
adjustment problems.
Personality disorder. Conditions characterized by pervasive, enduring,
inflexible patterns of behaviour and experience that deviate markedly
from cultural expectations and that lead to significant personal distress or
significant impairment in social functioning.
PESQ. Personal Experience Screening Questionnaire, a brief screening
instrument for adolescent drug problems.
Phobia. An anxiety disorder characterized by intense fear which occurs when
faced with an object, event or situation from a clearly defined class of stimuli
that is out of proportion to the danger posed by the stimulus.
Positive symptoms. Collective term for delusions and hallucinations common
in schizophrenia.
PRIME theory. PRIME represents plans, responses, impulses and inhibi-
tory forces (felt as urges), motives (felt as wants or needs), and evaluative

Book 1.indb 338 06/03/2012 13:48

 GLOSSARY 339

beliefs – the five components of the motivational system in the PRIME or

synthetic theory of motivation and addiction.
Prodromal phase. The period before the onset of a disorder during which
individuals may show subclinical symptoms.
PsSI. Psychological Society of Ireland (www.psihq.ie)
Psychiatry. A medical specialty concerned with the assessment and treatment
of psychological disorders using both physical and psychological treatments.
Psychoanalytic model. A conceptual framework which assumes that psycho-
logical problems are symptoms of underlying unconscious conflict, which
may be treated with psychoanalytically informed interventions derived from
Sigmund Freud’s psychoanalysis, also referred to as the psychodynamic
model.
Psychological-mindedness. The capacity to understand problems in intrapsy-
chic terms, rather than inaccurately explaining them in terms of external or
physical factors.
Psychotherapy. A contractual process in which trained professionals with
expert knowledge of their discipline interact with clients to help them resolve
psychological problems.
Psyclick. A website giving information about getting onto UK clinical psychology
training programmes (www.psyclick.org.uk)
PTSD. Posttraumatic stress disorder, an anxiety disorder which occurs in
response to a catastrophic trauma perceived to be potentially life-threatening,
characterized by recurrent intrusive memories of the trauma that lead
to intense anxiety coupled with attempts to avoid this by suppressing the
memories and avoiding situations that remind the individual of the trauma.
QUB. Queen’s University Belfast (www.qub.ac.uk), which runs one of the five
clinical psychology training programmes in Ireland.
RANZCP. The Royal Australian & New Zealand College of Psychiatry (www.
ranzcp.org)
RAS. Recovery Assessment Scale: assesses hope, meaning of life, quality of
life, symptoms and empowerment.
RCPsych. Royal College of Psychiatrists (www.rcpsych.ac.uk)
RCT. Randomized controlled trial: an experimental design for evaluating the
effectiveness of a treatment programme, in which cases are randomly
assigned to treatment and control groups and evaluated with pre-tests and
post-tests.
Recovery model. A rehabilitation model that privileges the concepts of optimism,
well-being, personal strengths, supportive relationships, collaboration,
personal choice, adaptive coping, developing a meaningful life, civil rights,
empowerment and inclusion.
Reward system. The mesolimbic dopamine pathway, which involves the ventral
tegmental area, the nucleus accumbens and the prefrontal cortex, and is
activated by drug use and reinforcement.
Schizoid personality disorder. A personality disorder characterized by a
pervasive pattern of detachment from social relationships.
Schizophrenia. A set of conditions characterized by positive symptoms
(delusions and hallucinations), negative symptoms (lack of goal-directed
activity, flattening of affect, poverty of speech) and disorganized speech
(frequent incoherence and derailment or loosening of associations).
Schizotypal personality disorder. A personality disorder characterized by
unusual perceptual experiences, eccentric thoughts and speech, inappropri-
ate or constricted affect, peculiar or eccentric behaviour, and a lack of close
relationships.

Book 1.indb 339 06/03/2012 13:48

 340 C L I N I C A L P S Y C H O L O G Y : A N I N T R O D U C T I O N

Schizotypy. A personality structure or set of traits conferring vulnerability to

schizophrenia, characterized primarily by disorganized thinking similar to
(though less extreme than) that shown in schizophrenia.
SCID-I. Structured Clinical Interview for DSM-IV Axis I Disorders.
SCID-II. Structured Clinical Interview for DSM-IV Personality Disorders.
SDQ. Strengths and Difficulties Questionnaire: brief parent, teacher and self-
report rating scales widely used in the UK for assessing emotional and
behaviour problems in children and adolescents.
Seasonal affective disorder. A unipolar mood disorder in which episodes of
depression occur during the winter months.
Self-medication. The use of street drugs to alleviate negative affective
states.
Separation anxiety disorder. An anxiety disorder that occurs most commonly
in children, characterized by a recurrent and persistent fear when separa-
tion from parents, or other important attachment figures, is anticipated.
Headaches, stomach aches and school refusal may occur.
Serotonin. 5-Hydroxytryptamine or 5-HT, a neurotransmitter involved in the
regulation of mood and appetite. Dysregulation of the serotonin system in
the brain subserves depression and eating disorders.
SNAP-2. Schedule for Nonadaptive and Adaptive Personality–II, a self-report
inventory for assessing personality disorders.
Sociotropy. In Beck’s cognitive theory of depression, sociotropy is a depressive
schema characterized by interpersonal dependency and is contrasted with
the autonomy schema, which is characterized by perfectionism and self-
criticism.
SSRIs. Selective serotonin reuptake inhibitors (e.g., fluoxetine/Prozac), a type
of antidepressant that prevents serotonin from being reabsorbed into the
presynaptic membrane and so increases the efficiency of this neurotransmitter
system. Used for the treatment of depression, anxiety and eating disorders.
Stepped care. A service delivery model in which more intensive interventions
are preceded by less intensive interventions.
Systematic desensitization. A behavioural treatment for phobias in which a
client in a deeply relaxed state is exposed to increasingly anxiety-provoking
stimuli, with progression to the next stimulus occurring once habituation to
the previous one has occurred.
Systemic model. An overarching term for approaches to explaining
psychological problems using ideas from general systems theory and treating
such problems with couples and family therapy.
TCAs. Tricyclic antidepressants (e.g., imipramine/Tofranil), a type of
antidepressant that increases efficiency neurotransmitter systems, which are
dysregulated in depression. They were developed and widely used before
the advent of SSRIs.
TCD. Trinity College Dublin (www.tcd.ie), which runs one of the five clinical
psychology training programmes in Ireland.
Therapeutic community. Residential treatment programme in which a
democratic, participative approach to decision-making is used to facilitate
recovery of people with addictions and chronic, complex mental health
problems.
Thought broadcasting. The feeling that one’s thoughts are known by others.
Thought disorder. Confused thinking common in schizophrenia, characterized
by disorganized and illogical speech.
Thought echo. A form of auditory hallucination in which thoughts are heard
spoken aloud, as they are being thought or a moment or two afterwards.

Book 1.indb 340 06/03/2012 13:48

 GLOSSARY 341

Thought insertion. The feeling that thoughts in one’s mind are not one’s
own, ‘explained’ by the delusion that they have been inserted by an outside
agency.
Thought withdrawal. The feeling that thoughts are missing from one’s mind,
‘explained’ by the delusion that they have been withdrawn by an outside
agency.
Token economy. A therapeutic system used in residential or inpatient settings,
based on learning theory, in which tokens are used as secondary reinforcers
to encourage patients to engage in positive behaviours and to use adaptive
skills. Tokens earned for completing positive behaviours or using adaptive
skills may be exchanged for privileges or valued items.
Transference-focused psychotherapy. An evidence-based psychodynamic
treatment for borderline personality disorder.
Transference. The unconscious repetition in significant adult relationships
of relationship patterns that occurred in childhood with parents. People
unconsciously transfer feelings that they had towards their parents onto
their partners, friends, colleagues and psychotherapists. In psychoanalytic
practice, interpreting transference is a central aspect of therapy.
Transtheoretical stages of change model. An integrative model, widely
influential in the field of drug use and health behaviour, which proposes
that therapeutic change involves movement through the stages of pre-
contemplation, contemplation, preparation, action and maintenance, and
that interventions must be designed to suit the client’s stage of change.
UCD. University College Dublin (www.ucd.ie), which runs one of the five clinical
psychology training programmes in Ireland.
UKCP. UK Council for Psychotherapy (www.psychotherapy.org.uk)
UL. University of Limerick (www.ul.ie), which runs one of the five clinical
psychology training programmes in Ireland.
Unconscious. In psychoanalytic theory, a set of processes, of which the
individual is unaware, that motivate behaviour.
WIAT. Wechsler Individual Achievement Test, a widely used set of attainment
tests for school-aged children. It is now in its third revision. It is designed to
be interpreted in conjunction with the WISC.
Wilderness/adventure therapy. A psychotherapeutic treatment for drug
problems and antisocial behaviour where adolescents are challenged to take
risks and master skills by doing outdoor activities in a ‘wilderness’ location
away form their home community.
WISC. Wechsler Intelligence Scale for Children, the most widely used intelligence
test for school-aged children in the world. It is now in its fourth revision. It is
a downward extension of the WAIS.
WPPSI. Wechsler Preschool and Primary Scale of Intelligence, a widely used
intelligence test for preschoolers. It is now in its third revision. It is a downward
extension of the WISC.

Book 1.indb 341 06/03/2012 13:48

 References
Abraham, K. (1924). The influence of oral eroticism on character formation. In
C. Bryan & A. Strachey (Ed. & trans.), Selected papers on psychoanalysis
(pp. 393–406). London: Hogarth Press.
Abramson, L., Seligman, M., & Teasdale, J. (1978). Learned helplessness in
humans: Critique and reformulation. Journal of Abnormal Psychology, 87,
49–74.
Achenbach, T. M. (2009). ASEBA: Development, findings, theory, and
applications. Burlington, VT: University of Vermont Research Centre for
Children, Youth and Families.
Achenbach, T. M., & Rescorla, L. A. (2000). Manual for ASEBA preschool
forms & profiles. Burlington, VT: University of Vermont, Research Centre for
Children, Youth, & Families.
Achenbach, T. M., & Rescorla, L. A. (2001). Manual for ASEBA school-age
forms & profiles. Burlington, VT: University of Vermont, Research Centre for
Children, Youth, & Families.
Addis, M. (2002). Methods for disseminating research products and increasing
evidence-based practice: Promises, obstacles, and future directions. Clinical
Psychology: Science and Practice, 9, 367–378.
Afifi, T. O., Asmundson, G. H., Taylor, S., & Jang, K. L. (2010). The role of
genes and environment on trauma exposure and posttraumatic stress dis-
order symptoms: A review of twin studies. Clinical Psychology Review, 30,
101–112.
Agras, W. (2010). The Oxford handbook of eating disorders. New York: Oxford
University Press.
Aichorn, A. (1935). Wayward youth. New York: Viking Press.
Aldao, A., Nolen-Hoeksema, S., & Schweizer, S. (2010). Emotion-regulation
strategies across psychopathology: A meta-analytic review. Clinical
Psychology Review, 30, 217–237.
Allen, J., Fonagy, P., & Bateman, A. (2008). Mentalizing in clinical practice.
Washington, DC: American Psychiatric Press.
Alwin, N., Blackburn, R., Davidson, K., Hilton, M., Logan, C., & Shine, J. (2006).
Understanding personality disorder: A report by the British Psychological
Society. Leicester, UK: British Psychological Society.
American Academy of Child and Adolescent Psychiatry (2001). Practice
parameter for the assessment and treatment of children and adolescents
with suicidal behaviour. Journal of the American Academy of Child and
Adolescent Psychiatry, 40 (7 Supplement), 24S–51S.
American Academy of Child and Adolescent Psychiatry (2004). Practice
parameters for use of electroconvulsive therapy with adolescents. Journal of
the American Academy of Child and Adolescent Psychiatry, 43(12), 1521–
1539.
American Academy of Child and Adolescent Psychiatry (2005). Practice
parameters for the assessment and treatment of children and adolescents

Book 1.indb 342 06/03/2012 13:48

 REFERENCES 343

with substance use disorders. American Academy of Child and Adolescent

Psychiatry, 44(6), 609–621.
American Academy of Child and Adolescent Psychiatry (2007a). Practice
parameters for the assessment and treatment of children, adolescents, and
adults with attention-deficit/hyperactivity disorder. Journal of the American
Academy of Child and Adolescent Psychiatry, 46, 894–921.
American Academy of Child and Adolescent Psychiatry (2007b). Practice
parameters for the assessment and treatment of children and adolescents
with oppositional defiant disorder. Journal of the American Academy of Child
and Adolescent Psychiatry, 46, 126–141.
American Academy of Child and Adolescent Psychiatry (2007c). Practice
parameters for the assessment and treatment of children and adolescents
with anxiety disorders. Journal of the American Academy of Child and
Adolescent Psychiatry, 36, 267–283.
American Academy of Child and Adolescent Psychiatry (2007d). Practice
parameters for the assessment and treatment of children and adolescents
with depressive disorders. Journal of the American Academy of Child and
Adolescent Psychiatry, 46, 1503–1526.
American Academy of Child and Adolescent Psychiatry (2009). Practice param-
eters on the use of psychotropic medication in children and adolescents.
Journal of the American Academy of Child & Adolescent Psychiatry, 48,
961–973.
American Academy of Child and Adolescent Psychiatry (2010). Practice
parameters for the assessment and treatment of children and adolescents
with posttraumatic stress disorder. Journal of the American Academy of
Child and Adolescent Psychiatry, 49, 414–430.
American Academy of Paediatrics (2001). Clinical practice guideline: Treatment
of the school-aged child with attention-deficit/hyperactivity disorder.
Paediatrics, 108(4), 1033–1104.
American Psychiatric Association (2000). Diagnostic and Statistical Manual of
the Mental Disorders (fourth edition, text revision, DSM-IV-TR). Washington,
DC: APA.
American Psychiatric Association (2001a). Task force report of the American
Psychiatric Association on the practice of electroconvulsive therapy:
Recommendations for treatment, training, and privileging (second edition).
Washington, DC: American Psychiatric Press.
American Psychiatric Association (2001b). American Psychiatric Association
practice guideline for the treatment of patients with borderline person-
ality disorder (second edition). Washington, DC: American Psychiatric
Association.
American Psychiatric Association (2003). American Psychiatric Association
practice guideline for the assessment and treatment of suicidal behaviour.
Washington, DC: American Psychiatric Association.
American Psychiatric Association (2004a). American Psychiatric Association
practice guideline for the treatment of patients with acute stress disorder
and posttraumatic stress disorder. Washington, DC: American Psychiatric
Association.
American Psychiatric Association (2004b). American Psychiatric Association
practice guideline for the treatment of patients with schizophrenia (second
edition). Washington, DC: American Psychiatric Association.
American Psychiatric Association (2006). American Psychiatric Association
practice guidelines for the treatment of eating disorders (third revision).
Washington, DC: APA.

Book 1.indb 343 06/03/2012 13:48

 344 C L I N I C A L P S Y C H O L O G Y : A N I N T R O D U C T I O N

American Psychiatric Association (2007). American Psychiatric Association

practice guideline for the treatment of patients with obsessive-compulsive
disorder. Washington, DC: American Psychiatric Association.
American Psychiatric Association (2009). American Psychiatric Association
practice guideline for the treatment of patients with panic disorder (second
edition). Washington, DC: APA.
American Psychiatric Association (2010). American Psychiatric Association
practice guideline for the treatment of patients with major depressive disorder
(third edition). Washington, DC: American Psychiatric Association.
American Psychological Association (2007). Getting in: A step-by-step plan
for gaining admission to graduate school in psychology (second edition).
Washington, DC: American Psychological Association.
American Psychological Association Presidential Task Force on Evidence
Based Practice (2006). Evidence-based practice in psychology. American
Psychologist, 61, 271–285.
Anastopoulos, A., Barkley, R., & Shelton, T. (2005). Family based treatment:
Psychosocial intervention for children and adolescents with attention
deficit hyperactivity disorder. In E. Hibbs & P. Jensen (eds.), Psychosocial
treatments for child and adolescent disorders. Empirically based strategies
for clinical practice (second edition, pp. 327–350). Washington, DC: APA.
Anderson, D. A., & Murray, A. D. (2010). Psychological assessment of the eating
disorders. In W. S. Agras (Ed.), The Oxford handbook of eating disorders
(pp. 249–258). New York: Oxford University Press.
Anderson, H. (2003). Postmodern social construction therapies. In T. Sexton,
G. Weeks, & M. Robbins (Eds.), Handbook of family therapy: The science
and practice of working with families and couples (pp. 125–146). New York:
Brunner-Routledge.
Andrews, G., Cuijpers, P., Craske, M. G., McEvoy, P., & Titov, N. (2010). Com-
puter therapy for the anxiety and depressive disorders is effective, acceptable
and practical health care: A meta-analysis. PLoS ONE, 5(10), e13196.
Andrews, J. A., & Hops, H. (2010). The influence of peers on substance use.
In L. Scheier (Ed.), Handbook of drug use aetiology: Theory, methods, and
empirical findings (pp. 403–420). Washington, DC: American Psychological
Association.
Angst, J. (2009). Course and prognosis of mood disorders. In M. Gelder et al.
(Eds.), New Oxford textbook of psychiatry (second edition, Vol. 1, pp. 665–
669). Oxford: Oxford University Press.
Antony, M., & Stein, M. (2009a). Oxford handbook of anxiety and related
disorders. New York: Oxford University Press.
Antony, M., & Stein, M. (2009b). Future directions in anxiety disorders research.
In M. M. Antony & M. B. Stein (Eds.), Oxford handbook of anxiety and related
disorders (pp. 667–677). New York: Oxford University Press.
Aouizerate, B., Rotge, J.-Y., & Martin-Guehl, C. (2006). A systematic review
of psychosurgical treatments for obsessive-compulsive disorder: Does
deep brain stimulation represent the future trend in psychosurgery? Clinical
Neuropsychiatry, 3, 391–403.
Arnett, J. J. (2005). The developmental context of substance use in emerging
adulthood. Journal of Drug Issues, 35, 235–254.
Baer, R. (2003). Mindfulness training as a clinical intervention: A conceptual
and empirical review. Clinical Psychology Science and Practice, 10, 125–
143.
Bakermans-Kranenburg, M. J., & van IJzendoorn, M. H. (2009). The first
10,000 Adult Attachment Interviews: Distributions of adult attachment

Book 1.indb 344 06/03/2012 13:48

 REFERENCES 345

representations in non-clinical and clinical groups. Attachment and Human

Development, 11, 223–263.
Ballenger, J. (2009). Panic disorder and agoraphobia. In M. Gelder et al. (Eds.),
New Oxford textbook of psychiatry (second edition, Vol. 1, pp. 750–765).
Oxford: Oxford University Press.
Bandura, A., & Walters, R. (1959). Adolescent aggression. New York: Ronald
Press.
Barkley, R. (2003). Attention deficit hyperactivity disorder. In E. Mash & R.
Barkley (Eds.), Child psychopathology (second edition, pp. 75–143). New
York: Guilford.
Barkley, R. (2005). Attention deficit hyperactivity disorder: A handbook for
diagnosis and treatment (third edition). New York: Guilford.
Barkley, R., Guevremont, A., Anastopoulas, A., & Fletcher, K. (1992). A com-
parison of three family therapy programs for treating family conflicts in
adolescents with attention deficit hyperactivity disorder. Journal of Consulting
and Clinical Psychology, 60, 450–462.
Barkus, E., & Murray, R. M. (2010). Substance use in adolescence and
psychosis: Clarifying the relationship. Annual Review of Clinical Psychology,
6, 365–389.
Barlow, D. H., Allen, L. B., & Basden, S. L. (2007). Psychological treatments for
panic disorders, phobias, and generalized anxiety disorder. In P. E. Nathan
& J. M. Gorman (Eds.), A guide to treatments that work (third edition, pp.
351–394). New York: Oxford University Press.
Barron (2009a). Barron’s GRE (18th edition). New York: Barron’s Educational
Series.
Barron (2009b). Barron’s GRE psychology: Barron’s how to prepare for the GRE
psychology graduate record examination in psychology (sixth edition). New
York: Barron’s Educational Series.
Barrowclough, C., & Lobban, F. (2008). Family intervention. In K. Mueser & D.
Jeste (Eds.). Clinical handbook of schizophrenia (pp. 214–225). New York:
Guilford Press.
Bartlett, P. & Sandland, R. (2007). Mental health law: Policy and practice (third
edition). Oxford: Oxford University Press.
Bateman, A., & Fonagy, P. (2000). Effectiveness of psychotherapeutic treatment
of personality disorder. British Journal of Psychiatry, 177, 138–143.
Bateman, A. & Fonagy, P. (2010a). Mentalization-based treatment and
borderline personality disorder. In J. Clarkin, O. Fonagy & G. Gabbard (Eds.).
Psychodynamic psychotherapy for personality disorders: A clinical handbook
(pp. 187–208). Arlington, VA: American Psychiatric Publishing.
Bateman, A., & Fonagy, P. (2010b). Mentalization based treatment for borderline
personality disorder. World Psychiatry, 9, 11–15.
Beach, S. R. H., Jones, D. J., & Franklin, K. J. (2009). Marital, family, and
interpersonal therapies for depression in adults. In H. Gotlib & C. Hammen
(Eds.), Handbook of depression (second edition, pp. 624–641). New York:
Guilford Press.
Bebbington, P., & Kuipers, E. (2008). Psychosocial factors. In K. Mueser & D.
Jeste (Eds.). Clinical handbook of schizophrenia (pp. 74–81). New York:
Guilford Press.
Bech, P. (2009). Clinical features of mood disorders and mania. In M. Gelder
et al. (Eds.), New Oxford textbook of psychiatry (second edition, Vol. 1,
pp. 632–637). Oxford: Oxford University Press.
Beck, A. (1976). Cognitive therapy and the emotional disorders. New York:
Meridian.

Book 1.indb 345 06/03/2012 13:48

 346 C L I N I C A L P S Y C H O L O G Y : A N I N T R O D U C T I O N

Beck, A. (2005). The current state of cognitive therapy: A 40-year retrospective.

Archives of General Psychiatry, 62, 953–959.
Beck, A. (2008). The evolution of the cognitive model of depression and its
neurobiological correlates. American Journal of Psychiatry, 165, 969–977.
Beck, A., Epstein, N., Harrison, R. P., & Emery, G. (1983). Development of
the Sociotropy-Autonomy Scale: A measure of personality factors in psycho-
pathology. Unpublished manuscript, University of Pennsylvania, Philadel-
phia.
Beck, A., Freeman, A., & Davis, D. (2003). Cognitive therapy of personality
disorders (second edition). New York: Guilford Press.
Beck, A. Rector, N., Stolar, N., & Grant, P. (2011). Schizophrenia: Cognitive
theory, research and therapy. New York: Guilford.
Beck, A., Rush, A., Shaw, B., & Emery, G. (1979). Cognitive therapy of
depression. New York: Guilford Press.
Beck, A., & Steer, R. (1991). Beck Scale for Suicide Ideation. San Antonio, TX:
Psychological Corporation.
Beck, A., Steer, R., & Brown, G. (1996). Beck Depression Inventory – Second
edition (BDI-II). San Antonio, TX: Psychological Corporation.
Becker, D. R. (2008). Vocational rehabilitation. In K. Mueser & D. Jeste (Eds.),
Clinical handbook of schizophrenia (pp. 261–267). New York: Guilford Press.
Becker, S. P. (2010). Wilderness therapy: Ethical considerations for mental
health professionals. Child & Youth Care Forum, 39, 47–61.
Beinart, H., Kennedy, P., & Llewelyn, S. (2009). Clinical psychology in practice.
London: British Psychological Society–Blackwell.
Bellack, A., Mueser, K., Gingerich, S., & Agresta, J. (2004). Social skill training
for schizophrenia: A step-by-step guide (second edition). New York: Guilford.
Benjamin, L. T., Jr. (2005). A history of clinical psychology as a profession in
America (and a glimpse at its future). Annual Review of Clinical Psychology,
1(1), 1–30.
Bentall, R. (2003). Madness explained: Psychosis and human nature. London:
Penguin.
Berle, D., & Starcevic, V. (2005). Thought–action fusion: Review of the literature
and future directions. Clinical Psychology Review, 25, 263–284.
Berman, A. (2009). Depression and suicide. In H. Gotlib & C. Hammen (Eds.),
Handbook of depression (second edition, pp. 510–533). New York: Guilford
Press.
Bertram, L. (2008). Genetic research in schizophrenia: New tools and future
perspectives. Schizophrenia Bulletin, 34, 806–812.
Beutler, L., Malik, M., Alimohamed, S., Harwood, T., Talebi, H., Noble, S., et
al. (2004). Therapist variables. In M. Lambert (Ed.), Bergin and Garfield’s
handbook of psychotherapy and behaviour change (fifth Edition, pp. 227–
306). New York: Wiley.
Bibring, E. (1965). The mechanism of depression. In P. Greenacre (Ed.),
Affective Disorders (pp. 13–48). New York: International Universities Press.
Bitran, S., Barlow, D., & Spiegel, D. (2009). Generalized anxiety disorders. In
M. Gelder et al. (Eds.), New Oxford textbook of psychiatry (second edition,
Vol. 1, pp. 729–739). Oxford: Oxford University Press.
Blackmore, M., Erwin, B., Heimberg, R., Magee, L., & Fresco, D. (2009). Social
anxiety disorder and specific phobias. In M. Gelder et al. (Eds.), New Oxford
textbook of psychiatry (second edition, Vol. 1, pp. 739–750). Oxford: Oxford
University Press.
Blatt, S. (2004). Experiences of depression: Theoretical, clinical and research
perspectives. Washington, DC: American Psychological Association.

Book 1.indb 346 06/03/2012 13:48

 REFERENCES 347

Bleuler, E. (1911). Dementia praecox or the group of schizophrenias. New York:

International University Press.
Bleuler, E. (1924). Textbook of psychiatry. New York: Macmillan.
Bloch, S., Hanfer, J., Harari, E., & Szmukler, G. (1994). The family in clinical
psychiatry. Oxford: Oxford University Press.
Bögels, S. M., & Brechman-Toussaint, M. L. (2006). Family issues in child
anxiety: Attachment, family functioning, parental rearing and beliefs. Clinical
Psychology Review, 26, 834–856.
Boland, R. J., & Keller, M. B. (2009). Course and outcome of depression. In H.
Gotlib & C. Hammen (Eds.), Handbook of depression (second edition, pp.
23–43). New York: Guilford Press.
Bond, G., Drake, R., Mueser, K., & Latimer, E. (2001). Assertive community
treatment for people with severe mental illness. Critical ingredients and impact
on patients. Disease Management & Health Outcomes, 9(3), 141–159.
Bora, E., Fornito, A., Radua, J., Walterfang, M., Seal, M., Wood, S. J., et al.
(2011). Neuroanatomical abnormalities in schizophrenia: A multimodal
voxelwise meta-analysis and meta-regression analysis. Schizophrenia
Research, 127, 46–57.
Bota, R., Munro, S., Nguyen, C., & Preda, A. (2011). The course of schizophrenia:
What has been learned from longitudinal studies? In M. Ritsner (Ed.),
Handbook of schizophrenia spectrum disorders, Volume II. Phenotypic and
endophenotypic presentations (pp. 281–300). New York: Springer.
Bowlby, J. (1944). Forty-four juvenile lives: Their characters and homelife.
International Journal of Psychoanalysis, 25, 1–57.
Bowlby, J. (1980). Attachment and loss, Volume 3. Loss, sadness and
depression. New York: Basic Books.
Boyle, M. (2002). Schizophrenia: A scientific delusion (second Edition). London:
Routledge.
Bradley, A. J., & Dinan, T. G. (2010). A systematic review of hypothalamic–
pituitary–adrenal axis function in schizophrenia: Implications for mortality.
Journal of Psychopharmacology, 24, 91–118.
Bradley, C. (1937). The behaviour of children receiving Benzedrine. American
Journal of Psychiatry, 94, 577–585.
Brandes, M., & Bienvenu, O. J. (2009). Anxiety disorders and personality
disorders comorbidity. In M. M. Antony & M. B. Stein (Eds.), Oxford handbook
of anxiety and related disorders (pp. 587–595). New York: Oxford University
Press.
Breggin, P. (1991). Toxic psychiatry. London: Harper Collins.
Breggin, P. (2001). Talking back to Ritalin: What doctors aren’t telling you about
stimulants and ADHD. New York: Da Capo Press
Bremner, D. (2005). Brain imaging handbook. New York: Norton.
Brent, D., & Weersing, R. (2008). Depressive disorders in childhood and
adolescence. In M. Rutter et al. (Eds.), Rutter’s child and adolescent
psychiatry (fifth edition, pp. 587–612). London: Blackwell.
Bridge, J. A., Iyengar, S., & Salary, C. B. (2007). Clinical response and risk for
reported suicidal ideation and suicide attempts in paediatric antidepressant
treatment: A meta-analysis of randomized controlled trials. Journal of the
American Medical Association, 297, 1683–1696.
Britton, J. C., & Rauch, S. L. (2009). Neuroanatomy and neuroimaging of anxiety
disorders. In M. M. Antony & M. B. Stein (Eds.), Oxford handbook of anxiety
and related disorders (pp. 97–110). New York: Oxford University Press.
Bronfenbrenner, U., & Morris, P. A. (2006). The bioecological model of human
development. In R. M. Lerner (Ed.), Handbook of child psychology, Volume

Book 1.indb 347 06/03/2012 13:48

 348 C L I N I C A L P S Y C H O L O G Y : A N I N T R O D U C T I O N

1: Theoretical models of human development (sixth Edition, pp. 793–828).

Hoboken, NJ: Wiley.
Brown, T. (2009). ADHD comorbidities: Handbook for ADHD complications in
children and adults. Arlington, VA: American Psychiatric Publishing.
Brown, T., DiNardo, P., & Barlow, D. (1994). Anxiety Disorders Interview
Schedule for DSM-IV. (ADIS-IV). New York: Oxford University Press.
Bruch, H. (1973). Eating disorders. New York: Basic Books.
Bruch, H. (1978).The golden cage: The enigma of anorexia nervosa. Cambridge,
MA: Harvard University Press.
Brunwasser, S. M., Gillham, J. E., & Kim, E. S. (2009). A meta-analytic review
of the Penn Resiliency Program’s effect on depressive symptoms. Journal of
Consulting and Clinical Psychology, 77(6), 1042–1054.
Buchanan, R. W., Kreyenbuhl, J., Kelly, D. L., Noel, J. M., Boggs, D. L., &
Fischer, B. A. (2010). The 2009 schizophrenia PORT psychopharmacological
treatment recommendations and summary statements. Schizophrenia
Bulletin, 36, 71–93.
Busch, F. N., Milrod, B. L., & Shear, K. (2010). Psychodynamic concepts of
anxiety. In D. J. Stein, E. Hollander, & B. O. Rothbaum (Eds.), Textbook of
anxiety disorders (second edition, pp. 117–128). Arlington, VA: American
Psychiatric Publishing.
Butler, A., Chapman, J., Forman, E., & Beck, A. (2006). The empirical status
of cognitive-behavioural therapy: A review of meta-analyses. Clinical
Psychology Review, 36, 17–31.
Byrne, M., Carr, A., & Clarke, M. (2004). The efficacy of couples based
interventions for panic disorder with agoraphobia. Journal of Family Therapy,
26(2), 105–125.
Cain, D., & Seeman, J. (2001). Humanistic psychotherapies: Handbook
of research and practice. Washington, DC: American Psychological
Association.
Caligor, E. (2010). An object relations model of personality and personality
pathology. In J. Clarkin, O. Fonagy, & G. Gabbard (Eds.), Psychodynamic
psychotherapy for personality disorders: A clinical handbook (pp. 3–36).
Arlington, VA: American Psychiatric Publishing.
Campbell, D., Draper, R., & Crutchley, E. (1991). The Milan systemic approach
to family therapy. In A. Gurman & D. Kniskern (Eds.), Handbook of family
therapy (Vol. II, pp. 325–362). New York: Brunner Mazel.
Carlson, G. A., & Cantwell, D. P. (1980). Unmasking masked depression in
children and adolescents. American Journal of Psychiatry, 137(4), 445–
449.
Carney, S., Cowen, P., Geddes, J., Goodwin, G., Rogers, R., Dearness, K., et al.
(2003). Efficacy and safety of electroconvulsive therapy in depressive disorders:
A systematic review and meta-analysis. Lancet, 361(9360), 799–808.
Carpenter, L., Philip, N., & O’Riordan, J. (2009). Advances in neurostimulation
for depression: Electroconvulsive therapy, transcranial magnetic stimulation,
vagus nerve stimulation and deep brain stimulation. In T. L. Schwartz &
T. J. Petersen (Eds.), Depression: Treatment strategies and management
(second edition, pp. 166–185). London: Inform Healthcare
Carr, A. (2000). Clinical psychology in Ireland, Volume 1: Empirical studies of
professional practice. Lampeter, UK: Edwin Mellen Press.
Carr, A. (2006a). Handbook of child and adolescent clinical psychology: A
contextual approach (second edition). London: Routledge.
Carr, A. (2006b). Family therapy: Concepts, process and practice (second
edition). Chichester, UK: Wiley.

Book 1.indb 348 06/03/2012 13:48

 REFERENCES 349

Carr, A. (2009a). What works with children, adolescents and adults? A review of
research on the effectiveness of psychotherapy. London: Routledge.
Carr, A. (2009b). The effectiveness of family therapy and systemic interventions
for child-focused problems. Journal of Family Therapy, 31, 3–45.
Carr, A. (2009c). The effectiveness of family therapy and systemic interventions
for adult-focused problems. Journal of Family Therapy, 31, 46–74.
Carr, A. (2011). Positive psychology: The science of happiness and human
strengths (second edition). London: Routledge.
Carr, A., & McNulty, M. (2006). Handbook of adult clinical psychology: An
evidence based practice approach. London: Brunner-Routledge.
Carr, A., O’Reilly, G., Walsh, P., & McEvoy, J. (2007). Handbook of intellectual
disability and clinical psychology practice. London; Brunner-Routledge.
Casey, R. J., & Berman, J. S. (1985). The outcome of psychotherapy with
children. Psychological Bulletin, 98, 388–400.
Caspi, A., Hariri, A., Holmes, A., Uher, R., & Moffitt, T. (2010). Genetic sensitivity
to the environment: The case of the serotonin transporter gene and its
implications for studying complex diseases and traits. American Journal of
Psychiatry, 167, 509–527.
Caspi, A., McClay, J., Moffitt, T., Mill, J., Martin, J., Craig, I., et al. (2002). Role of
genotype in the cycle of violence in maltreated children. Science, 297, 851–854.
Caspi, O. (2004). How good are we? A meta-analytic study of effect sizes in
medicine. Dissertation Abstracts International, Section B: The Sciences and
Engineering, 65(5-B), 2607.
Cassidy, J., & Shaver, P. (2008). Handbook of attachment (second edition).
New York: Guilford.
Cassin, S., & von Ranson, K. M. (2005). Personality and eating disorders: A
decade in review. Clinical Psychology Review, 25, 895–916.
Castonguay, L., Grosse Holtforth, M., Coombs, M., Beberman, R., Kakouros, A.,
Boswell, J., et al. (2006). Relationship factors in treating dysphoric disorders.
In L. Castonguay & L. Beutler (Eds.), Principles of therapeutic change that
work (pp. 65–82). Oxford: Oxford University Press.
Catalano, R. F., Haggerty, K. P., Hawkins, J. D., & Elgin, J. (2011). Prevention
of substance use and substance use disorders: Role of risk and protective
factors. In Y. Kaminer & K. C. Winters (Eds.), Clinical manual of adolescent
substance abuse treatment (pp. 25–63). Arlington, VA: American Psychiatric
Publishing.
Chambers, R. A., Taylor, J. R., & Potenza, M. N. (2003). Developmental
neurocircuitry of motivation in adolescence: A critical period of addiction
vulnerability. American Journal of Psychiatry, 160, 1041–1052.
Chan, R., Di, X., McAlonan, G. M., & Gong, Q. (2011). Brain anatomical
abnormalities in high-risk individuals, first-episode, and chronic schizophrenia:
An activation likelihood estimation meta-analysis of illness progression.
Schizophrenia Bulletin, 37, 177–188.
Cherkasova, M. V., & Hechtman, L. (2009). Neuroimaging in attention-deficit
hyperactivity disorder: Beyond the frontostriatal circuitry. Canadian Journal
of Psychiatry, 54(10), 651–664.
Cheshire, K., & Pilgrim, D. (2004). A short introduction to clinical psychology.
London: Sage.
Chess, S., & Thomas, A. (1995). Temperament in clinical practice. New York:
Guilford.
Cheung, S. (2009). Solution-focused brief therapy. In J. Bray & M. Stanton
(Eds.), The Wiley–Blackwell handbook of family psychology (pp. 212–225).
Chichester, UK: Wiley–Blackwell.

Book 1.indb 349 06/03/2012 13:48

 350 C L I N I C A L P S Y C H O L O G Y : A N I N T R O D U C T I O N

Chiles, J., Lambert, M., & Hatch, A. (1999). The impact of psychological
interventions on medical cost offset: A meta-analytic review. Clinical
Psychology: Science and Practice, 6, 204–220.
Chung, T., & Martin, C. S. (2011). Prevalence and clinical course of adolescent
substance use and substance use disorders. In Y. Kaminer & K. C. Winters
(Eds.), Clinical manual of adolescent substance abuse treatment (pp. 1–23).
Arlington, VA: American Psychiatric Publishing.
Clare, L. (1995). Successful applicants for clinical training: A descriptive profile
of one trainee cohort. Clinical Psychology Forum, 77, 31–34.
Clark, D., & Beck, A. (2010). Cognitive theory and therapy of anxiety and
depression: Convergence with neurobiological findings. Trends in Cognitive
Sciences, 14(9), 418–424.
Clark, D. A., & Beck, A. T. (2010a). Cognitive therapy of anxiety disorders. New
York: Guilford Press.
Clark, D. A., & Beck, A. T. (2010b). Cognitive theory and therapy of anxiety and
depression: Convergence with neurobiological findings. Trends in Cognitive
Sciences, 14(9), 418–424.
Clark, L. A., Simms, L. J., Wu, K. D., & Casillas, A. (2008). Schedule for
Nonadaptive and Adaptive Personality – Second edition. Minneapolis:
University of Minnesota Press.
Clark, L. A., & Watson, D. (2008). Temperament: An organizing paradigm for
trait psychology. In O. John, R. Robins & L. Pervin (Eds.), Handbook of
personality psychology: Theory and research (third edition, pp. 265–286).
New York: Guilford Press.
Clarkin, J., & Levy, K. (2004). The influence of client variables on psychotherapy.
In M. Lambert (Ed.), Bergin and Garfield’s handbook of psychotherapy and
behaviour change (fifth edition, pp. 194–226). New York: Wiley.
Cleckley, H. (1941). The mask of sanity. St Louis, MO: Mosby Medical Library.
Cloninger, C., Svrakic, D. & Przybeck, T. (1993). A psychobiological model of
temperament and character. Archives of General Psychiatry, 50, 975–990.
Cloward, R., & Ohlin, L. (1960). Delinquency and opportunity. Glencoe, IL: Free
Press.
Coccaro, E. F., & Siever, L. J. (2009). Neurobiology. In J. Oldham, A. Skodol,
& D. Bender (Eds.), Essentials of personality disorders (pp. 103–122).
Arlington, VA: American Psychiatric Publishing.
Cochrane, A. (1972). Effectiveness and efficiency: Random reflections on health
services. London: Nuffield Provincial Hospitals Trust.
Cohen, J. (1988). Statistical power analysis for the behavioural sciences (second
edition). Hillsdale, NJ: Lawrence Erlbaum Associates.
Colapinto, J. (1991). Structural family therapy. In A. Gurman & D. Kniskern (Eds.),
Handbook of family therapy (Vol. II, pp. 417–443). New York: Brunner/Mazel.
Coldwell, C., & Bender, W. (2007). The effectiveness of assertive community
treatment for homeless populations with severe mental illness: A meta-
analysis. American Journal of Psychiatry, 164, 393–399.
Collier, D., & Treasure, J. (2004). The aetiology of eating disorders. British
Journal of Psychiatry, 185, 363–365.
Colligan, R., Morey, L., & Offord, K. (1994). MMPI/MMPI-2 personality disorder
scales: Contemporary norms for adults and adolescents. Journal of Clinical
Psychology, 50, 168–200.
Combrinck-Graham, L. (1986). Family treatment for childhood anxiety disorders.
Family Therapy Collections, 18, 22–30.
Conklin, C. A., & Tiffany, S. T. (2002). Applying extinction research and theory to
cue-exposure addiction treatments. Addiction, 97, 155–167.

Book 1.indb 350 06/03/2012 13:48

 REFERENCES 351

Conners, C. (1997). Conners’ Rating Scales: Revised Technical Manual. North

Tonawanda, NY: Multihealth Systems.
Consensus Development Panel (2000). National Institutes of Health Consensus
Development Conference statement: Diagnosis and treatment of attention-
deficit/hyperactivity disorder (ADHD). Journal of the American Academy of
Child and Adolescent Psychiatry, 39(2), 182–193.
Cook, J., & Razzano, L. (2005). Evidence-based practices in supported
employment. In C. Stout & R. Hayes (Eds.), The evidence-based practice:
Methods, models, and tools for mental health professionals (pp. 10–30).
Hoboken, NJ: Wiley.
Cooper, J., Kendall, R., Gurland, B., Sharp, L., Copeland, J., & Simon, R. (1972).
Psychiatric diagnosis in New York and London. Maudsley Monograph Series
No. 20. London: Oxford University Press.
Corrigan, P. W., Salzer, M., Ralph, R. O., Sangster, Y., & Keck, L. (2004).
Examining the factor structure of the Recovery Assessment Scale.
Schizophrenia Bulletin, 30, 1035–1041.
Costa, P. & Widiger, T. (1994). Personality disorders and the five factor model
of personality. Washington, DC: APA.
Costa, P. T., Jr., & McCrae, R. R. (1992). Revised NEO Personality Inventory
(NEOPI-R) and NEO Five-Factor Inventory (NEO-FFI) professional manual.
Odessa, FL: Psychological Assessment Resources.
Costello, E. J., Mustillo, S., Keeler, G., & Angold, A. (2004). Prevalence of
psychiatric disorders in childhood and adolescence. In B. L. Levin, J. Petrila,
& K. D. Hennessy (Eds.), Mental health services: A public health perspective
(second edition, pp. 111–128). New York: Oxford University Press.
Crane, D. R. (2011). Does family therapy reduce health care costs for more than
the identified patient? Clinical Child Psychology and Psychiatry, 16, 3–4.
Crick, N., & Dodge, K. (1994). A review and reformulation of social information
processing mechanisms in children’s social adjustment. Psychological
Bulletin, 115, 74–101.
Crisp, A. (1983). Anorexia nervosa. British Medical Journal, 287, 855–858.
Crome, I., Ghodse, H., Gilvarry, E., & McArdle, P. (2004). Young people and
substance misuse. London: Gaskell.
Crosnoe, R., & Cavanagh, S. E. (2010). Families with children and adolescents:
A review, critique, and future agenda. Journal of Marriage and Family, 72(3),
594–611.
Crow, T. (1985). The two syndrome concept: Origins and current status.
Schizophrenia Bulletin, 9, 471–486.
Cuijpers, P., Donker, T., van Straten, A., Li, J., & Andersson, G. (2010). Is guided
self-help as effective as face-to-face psychotherapy for depression and
anxiety disorders? A systematic review and meta-analysis of comparative
outcome studies. Psychological Medicine, 40(12), 1943–1957.
Cuijpers, P., Muñoz, R. F., Clarke, G. N., & Lewinsohn, P. M. (2009a). Psycho-
educational treatment and prevention of depression: The “coping with
depression” course thirty years later. Clinical Psychology Review, 29, 449–
458.
Cuijpers, P., van Straten, A., Andersson, G., & van Oppen, P. (2008). Psycho-
therapy for depression in adults: A meta-analysis of comparative outcome
studies. Journal of Consulting and Clinical Psychology, 76, 909–922.
Cuijpers, P., van Straten, A., Warmerdam, L., & Andersson, G. (2009b). Psycho-
therapy versus the combination of psychotherapy and pharmacotherapy in
the treatment of depression: A meta-analysis. Depression and Anxiety, 26,
279–288.

Book 1.indb 351 06/03/2012 13:48

 352 C L I N I C A L P S Y C H O L O G Y : A N I N T R O D U C T I O N

Cunningham-Owens, D., & Johnstone, E. (2009). Treatment and management

of schizophrenia. In M. Gelder et al. (Eds.), New Oxford textbook of psychiatry
(second edition, Vol. 1, pp. 578–595). Oxford: Oxford University Press.
Currin, L., Schmidt, U., Treasure, J., & Jick, H. (2005). Time trends in eating
disorder incidence. British Journal of Psychiatry, 186, 132–135.
Dadds, M., Heard, P., & Rapee, R. (1992). The role of family intervention in the
treatment of child anxiety disorders: Some preliminary findings. Behaviour
Change, 9, 171–177.
Dakof, G. A., Godley, S. H., & Smith, J. E. (2011). The adolescent community
reinforcement approach and multidimensional family therapy: Addressing
relapse during treatment. In Y. Kaminer & K. C. Winters (Eds.), Clinical
manual of adolescent substance abuse treatment (pp. 239–268). Arlington,
VA: American Psychiatric Publishing.
Daley, A., Jolly, K., & MacArthur, C. (2009). The effectiveness of exercise in
the management of post-natal depression: Systematic review and meta-
analysis. Family Practice, 26, 154–162.
Dare, C. (1985). The family therapy of anorexia nervosa. Journal of Psychiatric
Research, 19, 435–453.
Dattilio, F. (2009). Cognitive-behavioural therapy with couples and families: A
comprehensive guide for clinicians. New York: Guilford.
Davidson, R. J., Pizzagalli, D. A., & Nitschke, J. B. (2009). Representation
and regulation of emotion in depression: Perspectives from affective
neuroscience. In H. Gotlib & C. Hammen (Eds.), Handbook of depression
(second edition, pp. 218–248). New York: Guilford Press.
Dawson, G., Ashman, S. B., & Carver, L. J. (2000). The role of early experience
in shaping behavioural and brain development and its implications for social
policy. Development and Psychopathology, 12, 695–712.
Deault, L. C. (2010). A systematic review of parenting in relation to the
development of comorbidities and functional impairments in children with
attention-deficit/hyperactivity disorder (ADHD). Child Psychiatry and Human
Development, 41(2), 168–192.
Degnan, K. A., Almas, A. N., & Fox, N. A. (2010). Temperament and the
environment in the etiology of childhood anxiety. Journal of Child Psychology
and Psychiatry, 51, 497–517.
DeLuca, N. L., Moser, L. L., & Bond, G. R. (2008). Assertive community
treatment. In K. Mueser & D. Jeste (Eds.). Clinical handbook of schizophrenia
(pp. 329–338). New York: Guilford Press.
Dennis, M. (1998), Global Appraisal of Individual Needs (GAIN) manual: Adminis-
tration, scoring and interpretation. Bloomington, IL: Lighthouse Publications.
Dent, M. F., & Bremner, J. D. (2009). Pharmacotherapy for posttraumatic stress
disorder and other trauma-related disorders. In M. M. Antony & M. B. Stein
(Eds.), Oxford handbook of anxiety and related disorders (pp. 405–416).
New York: Oxford University Press.
Department of Health (2007). Drug misuse and dependence: UK guidelines on
clinical management. London: Department of Health.
DePauw, S., & Mervielde, I. (2010). Temperament, personality and developmental
psychopathology: A review based on the conceptual dimensions underlying
childhood traits. Child Psychiatry and Human Development, 41, 313–329.
De Raad, B., & Perugini, M. (2002). Big five assessment. Bern, Switzerland:
Hogrefe & Huber.
DeSilva, P., Rachman, S., & Seligman, M. (1977). Prepared phobias and
obsessions: Therapeutic outcome. Behaviour Research and Therapy, 15,
65–77.

Book 1.indb 352 06/03/2012 13:48

 REFERENCES 353

Diamond, G. (2005). Attachment-based family therapy for depressed and

anxious adolescents. In J. Lebow (Ed.), Handbook of clinical family therapy
(pp. 17–41). Hoboken, NJ: Wiley.
DiClemente, C. (2003). Addiction and change. New York: Guilford.
DiMaggio, C., & Galea, S. (2006). The behavioural consequences of terrorism:
A meta-analysis. Academy of Emergency Medicine, 13, 559–566.
Dishion, T., & Dodge, K. (2005). Peer contagion in interventions for children and
adolescents: Moving towards an understanding of the ecology and dynamics
of change. Journal of Abnormal Child Psychology, 33, 395–400.
Dixon, L. B., Dickerson, F., Bellack, A. S., Bennett, M., Dickinson, D., &
Goldberg, R. (2010). The 2009 schizophrenia PORT psychosocial treatment
recommendations and summary statements. Schizophrenia Bulletin, 36,
48–70.
Dodge, K. (2011). Social information processing patterns as mediators of the
interaction between genetic factors and life experiences in the development
of aggressive behaviour. In P. Shaver & M. Mikulincer (Eds.), Human
aggression and violence: Causes, manifestations, and consequences (pp.
165–185). Washington, DC: American Psychological Association.
Dodge, K., Coie, J., & Lynam, D. (2006). Aggression and antisocial behaviour
in youth. In N. Eisenberg (Ed.), Handbook of child psychology, Volume 3:
Social, emotional and personality development (sixth edition, pp. 719–788).
Hoboken, NJ: Wiley.
Dodge, K. A., & Pettit, G. S. (2003). A biopsychosocial model of the development
of chronic conduct problems in adolescence. Developmental Psychology,
39, 349–371.
Dolder, C. R. (2008). Side effects of antipsychotics. In K. Mueser & D. Jeste
(Eds.), Clinical handbook of schizophrenia (pp. 168–177). New York: Guilford
Press.
Dougherty, L. R., Klein, D. N., Olino, T. M., & Laptook, R. S. (2008). Depression
in children and adolescents. In J. Hunsley & E. J. Mash (Eds.), A guide to
assessments that work (pp. 69–95). New York: Oxford University Press.
Douglas, K. S., Webster, C. D., Hart, S. D., Eaves, D., & Ogloff, J. R. P. (Eds.)
(2001). HCR-20: Violence risk management companion guide. Vancouver,
Canada/Tampa, FL: Mental Health, Law, and Policy Institute, Simon Fraser
University/Department of Mental Health Law & Policy, University of South
Florida.
Douglas, V. (1983). Attention and cognitive problems. In M. Rutter (Ed.),
Developmental neuropsychiatry (pp. 280–329). New York: Guilford.
Downar, J., & Kapur, S. (2008). Biological theories. In K. Mueser & D. Jeste
(Eds.), Clinical handbook of schizophrenia (pp. 25–34). New York: Guilford
Press.
Dozier, M., Stovall-McClough, K., & Albus, K. (2008). Attachment and
psychopathology in adulthood. In J. Cassidy & P. Shaver (Eds.), Handbook
of attachment (second edition, pp. 718–744). New York: Guilford.
Driessen, E., Cuijpers, P., de Maat, S., Abbass, A. A., de Jonghe, F. & Dekker,
J. (2010). The efficacy of short-term psychodynamic psychotherapy for
depression: A meta-analysis. Clinical Psychology Review, 30, 25–36.
Drummond, D., Tiffany, S., Glautier, S. & Remingron, B. (1995). Addictive
behaviour: Cue exposure theory and practice. Chichester, UK: Wiley.
Dugas, M. J., Buhr, K., & Ladoucer, R. (2004). The role of intolerance of
uncertainty in etiology and maintenance. In R. Heimberg, C. Turk, & D.
Mennin (Eds), Generalized anxiety disorder: Advances in research and
practice (pp. 143–163). New York: Guilford Press.

Book 1.indb 353 06/03/2012 13:48

 354 C L I N I C A L P S Y C H O L O G Y : A N I N T R O D U C T I O N

Duggan, C., Huband, N., & Smailagic, N. (2008). The use of pharmacological
treatments for people with personality disorder: A systematic review of
randomized controlled trials. Personality and Mental Health, 2, 119–170.
Duggan, C., Huband, N., Smailagic, N., Ferriter, M., & Adams, C. (2007). The
use of psychological treatments for people with personality disorder: A
systematic review of randomized controlled trials. Personality and Mental
Health, 1, 95–125.
Duvall, J., & Béres, L. (2011). Innovations in narrative therapy: Connecting
practice, training, and research. New York: Norton.
Edens, J. F., Campbell, J. S., & Weir, J. M. (2007). Youth psychopathy and
criminal recidivism: A meta-analysis of the psychopathy checklist measures.
Law and Human Behaviour, 31(1), 53–75.
Edvardsen, J., Torgersen, S., Røysamb, E., Lygren, S., Skre, I., Onstad, S., et
al. (2008). Heritability of bipolar spectrum disorders. Unity or heterogeneity?
Journal of Affective Disorders, 106, 229–240.
Egan, S. J., Wade, T. D., & Shafran, R. (2011). Perfectionism as a transdiagnostic
process: A clinical review. Clinical Psychology Review, 31, 203–212.
Egger, J., Carter, C., Graham, P., Gumley, D., & Soothill, J. (1985). Controlled trial
of oligoantigenic treatment in the hyperkinetic syndrome. Lancet, i, 540–545.
Ehlers, A. (2009). Post-traumatic stress disorder. In M. Gelder et al. (Eds.), New
Oxford textbook of psychiatry (second edition, Vol. 1, pp. 700–713). Oxford:
Oxford University Press.
Eisler, I. (2005). The empirical and theoretical base of family therapy and
multiple family day therapy for adolescent anorexia nervosa. Journal of
Family Therapy, 27, 104–113.
Ellenberger, H. (1970). The discovery of the unconscious. New York: Basic
Books.
Elliott, R., Greenberg, L., & Lietaer, G. (2004). Research on experiential psy-
chotherapies. In M. Lambert (Ed.), Bergin and Garfield’s handbook of psy-
chotherapy and behaviour change (fifth edition, pp. 493–539). New York: Wiley.
Ellman, L. M., & Cannon, T. D. (2008). Environmental pre- and perinatal
influences in aetiology. In K. Mueser & D. Jeste (Eds.), Clinical handbook of
schizophrenia (pp. 65–73). New York: Guilford Press.
Emmelkamp, P. (1982). Phobic and obsessive compulsive disorder. New York:
Plenum.
Erikson, E. (1950). Childhood and society. New York: Norton.
Erikson, E. (1968). Identity, youth and crisis. New York: Norton.
Eyler, L. T. (2008). Brain imaging. In K. Mueser & D. Jeste (Eds.), Clinical
handbook of schizophrenia (pp. 35–43). New York: Guilford Press.
Eysenck, H. (1979). The conditioning model of neurosis. Behavioural and Brain
Sciences, 2, 155–199.
Ezriel, H. (1952). Notes on psychoanalytic group therapy: II. Interpretation.
Research Psychiatry, 15, 119.
Fairburn, C. (2008). Cogntive behaviour therapy and eating disorders. London:
Guilford.
Fairburn, C., Cooper, Z., & O’Connor, E. (2008). The Eating Disorder Examination
(Edition 16.0D). In C. Fairburn (Ed.), Cognitive behaviour therapy and eating
disorders (pp. 265–308). London: Guilford.
Falloon, I., Laporta, M., Fadden, G., & Graham-Hole, V. (1993). Managing stress
in families. London: Routledge.
Faraone, S., Biederman, J., & Mick, E. (2006). The age dependent decline of
attention deficit hyperactivity disorder: A meta-analysis of follow-up studies.
Psychological Medicine, 36, 159–165.

Book 1.indb 354 06/03/2012 13:48

 REFERENCES 355

Farmer, A., & McGuffin, P. (1989). The classification of depressions: Contem-

porary confusions revisited. British Journal of Psychiatry, 155, 437–443.
Farrington, D. (1995). The twelfth Jack Tizard Memorial Lecture. The
development of offending and antisocial behaviour from childhood: Key
findings of the Cambridge Study of Delinquent Development. Journal of Child
Psychology and Psychiatry, 36, 929–964.
Fatemi, S. H., & Folsom, T. D. (2009). The neurodevelopmental hypothesis of
schizophrenia, revisited. Schizophrenia Bulletin, 35, 528–548.
Feingold, B. (1975). Hyperkinesis and learning difficulties linked to artificial food
flavours and colours. American Journal of Nursing, 75, 797–803.
Ferguson, C. (2010). Genetic contributions to antisocial personality and
behaviour: A meta-analytic review from an evolutionary perspective. Journal
of Social Psychology, 150, 160–180.
Fernandez-Alderez, H., Clarkin, J., delCarmen Salgueiro, M., & Critchfield, K.
(2006). Participant factors in treating personality disorders. In L. Castonguay
& L. Beutler (Eds.), Principles of therapeutic change that work (pp. 203–218).
Oxford: Oxford University Press.
Fett, A. J., Viechtbauer, W., Dominguez, M., Penn, D. L., van Os, J., &
Krabbendam, L. (2011). The relationship between neurocognition and
social cognition with functional outcomes in schizophrenia: A meta-analysis.
Neuroscience and Biobehavioural Reviews, 35, 573–588.
First, M., Spitzer, R., Gibbon, M., & Williams, J. (1996). Structured Clinical
Interview for DSM-IV Axis I Disorders, Clinician Version (SCID-CV).
Washington, DC: American Psychiatric Press.
First, M., Spitzer, R., Gibbon M., & Williams, J. (1997). Structured Clinical
Interview for DSM-IV Personality Disorders (SCID-II). Washington, DC:
American Psychiatric Press.
Fleming, I. & Steen, L. (2004). Supervision in clinical psychology: Theory,
practice and perspectives. London: Brunner Routledge.
Follette, W., & Greenberg, L. (2006). Technique factors in treating dysphoric
disorders. In L. Castonguay & L. Beutler (Eds.), Principles of therapeutic
change that work (pp. 83–110). Oxford: Oxford University Press.
Fonagy, P., & Target, M. (1994). The efficacy of psychoanalysis for children
with disruptive disorders. Journal of the American Academy for Child and
Adolescent Psychiatry, 33, 45–55.
Forgatch, M. S., & Patterson, G. R. (2010). Parent management training—Oregon
model: An intervention for antisocial behaviour in children and adolescents.
In J. R. Weisz & A. E. Kazdin (Eds.), Evidence-based psychotherapies for
children and adolescents (second edition, pp. 159–177). New York: Guilford
Press.
Fournier, J., DeRubeis, R., Hollon, S., Dimidjian, S., Amsterdam, J., & Shelton,
R. (2010). Antidepressant drug effects and depression severity. Journal
of the American Medical Association, 303, 47–53.
Frank, J., & Frank, J. (1991). Persuasion and healing: A comparative study of
psychotherapy (third edition). Baltimore: Johns Hopkins University Press.
Franklin, M. E., & Foa, E. B. (2007). Cognitive behavioural treatment of
obsessive-compulsive disorder. In P. E. Nathan & J. M. Gorman (Eds.), A
guide to treatments that work (third edition, pp. 431–446). New York: Oxford
University Press.
Franko, D. L., & Keel, P. K. (2006). Suicidality in eating disorders: Occurrence, cor-
relates, and clinical implications. Clinical Psychology Review, 26(6), 769–782.
Freeman, A., Felgoise, S., Nezu, A., Nezu, C., & Reinecke, M. (2005).
Encyclopaedia of cognitive behaviour therapy. New York: Plenum.

Book 1.indb 355 06/03/2012 13:48

 356 C L I N I C A L P S Y C H O L O G Y : A N I N T R O D U C T I O N

Freud, S. (1900). The interpretation of dreams (trans. J. Strachey). London:

Hogarth Press.
Freud, S. (1901). Psychopathology of everyday life (trans. A. Brill). London:
Fisher Unwin.
Freud, S. (1908). Character and anal eroticism. In J. Strachey (Ed. & trans.),
The standard edition of the complete psychological works of Sigmund Freud
(Vol. 9, pp. 167–175). London: Hogarth Press.
Freud, S. (1909a). The analysis of a phobia in a five year old boy. In J. Strachey
(Ed. & trans.). The standard edition of the complete works of Sigmund Freud
(Vol. 10, pp. 1–147). London: Hogarth Press.
Freud, S. (1909b). Notes upon a case of obsessional neurosis. In J. Strachey
(Ed. & trans). The standard edition of the complete works of Sigmund Freud
(Vol. 10, pp. 151–220). London: Hogarth Press.
Freud, S. (1911). Psycho-analytic notes on an autobiographical account of a
case of paranoia (dementia paranoides). In J. Strachey (Ed. & trans.), The
standard edition of the complete psychological works of Sigmund Freud (Vol.
12, pp. 1–82). London: Hogarth Press.
Freud, S. (1917). Mourning and melancholia. In J. Strachey (Ed & trans.).
The standard edition of the complete works of Sigmund Freud (Vol. 14,
pp. 237–258). London: Hogarth Press.
Frewen, P. A., Dozois, D. J. A., & Lanius, R. A. (2008a). Neuroimaging studies
of psychological interventions for mood and anxiety disorders: Empirical and
methodological review. Clinical Psychology Review, 28, 228–246.
Frewen, P. A., Dozois, D. A., Neufeld, R. W. J., & Lanius, R. A. (2008b). Meta-
analysis of alexithymia in posttraumatic stress disorder. Journal of Trauma
and Stress, 21, 243–246.
Frichter, M., & Pirke, K. (1995). Starvation models and eating disorders. In G.
Szmukler, C. Dare, & J. Treasure (Eds.), Handbook of eating disorders (pp.
83–108). Chichester, UK: Wiley.
Friedman, M. J. (2009). Phenomenology of posttraumatic stress disorder and
acute stress disorder. In M. M. Antony & M. B. Stein (Eds.), Oxford handbook
of anxiety and related disorders (pp. 65–72). New York: Oxford University
Press.
Frischer, M., McArdle, P., & Crome, I. (2004). The epidemiology of substance
misuse in young people. In I. Crome et al. (Eds.), Young people and
substance misuse (pp. 31–50). London: Gaskell.
Furr, J. M., Tiwari, S., Suveg, C., & Kendall, P. C. (2009). Anxiety disorders
in children and adolescents. In M. M. Antony & M. B. Stein (Eds.), Oxford
handbook of anxiety and related disorders (pp. 636–656). New York: Oxford
University Press.
Gabbard, G. O., Lazar, S. G., Hornberger, J., & Spiegel, D. (1997). The economic
impact of psychotherapy: A review. American Journal of Psychiatry, 154,
147–155.
Garber, J. (2010). Vulnerability to depression in childhood and adolescence.
In R. Ingram and J. Price (Eds.), Vulnerability to psychopathology:
Risk across the lifespan (second edition, pp. 189–247). New York: Guilford
Press.
Gardner, M., Barajas, R. G., & Brooks-Gunn, J. (2010). Neighborhood influences
on substance use etiology: Is where you live important? In L. Scheier (Ed.),
Handbook of drug use etiology: Theory, methods, and empirical findings (pp.
423–441). Washington, DC: American Psychological Association.
Garner, D. (2005). Eating Disorder Inventory, third edition (EDI-3). Odessa, FL:
Psychological Assessment Resources.

Book 1.indb 356 06/03/2012 13:48

 REFERENCES 357

Gelernter, J., & Stein, M. B. (2009). Heritability and genetics of anxiety disorders.
In M. M. Antony & M. B. Stein (Eds.), Oxford handbook of anxiety and related
disorders (pp. 87–96). New York: Oxford University Press.
Gillham, J. E., Brunwasser, S. M., Freres, D. R., Abela, J. R. Z., & Hankin, B.
L. (2008). Preventing depression in early adolescence: The Penn Resiliency
Program. In J. Abela & B. Hankin (eds.), Handbook of depression in children
and adolescents (pp. 309–322). New York: Guilford.
Gitlin, M. (2009). Pharmcotherapy and other somatic treatments for depression.
In H. Gotlib & C. Hammen (Eds.), Handbook of depression (second edition,
pp. 554–585). New York: Guilford Press.
Glass, V. (1976). Primary, secondary and meta-analysis of research. Educational
Researcher, 5, 3–8.
Glassman, A. H., & Miller, G. E. (2007). Where there is depression, there is
inflammation. . . sometimes! Biological Psychiatry, 62, 280–281.
Glatt, S. J. (2008). Genetics. In K. Mueser & D. Jeste (Eds.), Clinical handbook
of schizophrenia (pp. 55–64). New York: Guilford Press.
Godley, S. H., Meyers, R. J., Smith, J. E., Karvinen, T., Titus, J. C., Godley,
M. D., et al. (2006). The adolescent community reinforcement approach
for adolescent cannabis users. Cannabis Youth Treatment Series, Vol. 4.
Rockville, MD: Center for Substance Abuse Treatment, Substance Abuse
and Mental Health Services Administration.
Golden, T., Gaynes, B., Ekstrom, D., Hamer, R., Jacobsen, F., Suppes, T., et
al. (2005). The efficacy of light therapy in the treatment of mood disorders: A
review and meta-analysis of the evidence. American Journal of Psychiatry,
162, 656–662.
Goodman, R. (2001). Psychometric properties of the Strengths and Difficulties
Questionnaire (SDQ). Journal of the American Academy of Child and
Adolescent Psychiatry, 40, 1337–1345.
Goodman, R., Ford, T., Richards, H., Gatward, R., & Meltzer, H. (2000). The
Development and Well-Being Assessment: Description and initial validation
of an integrated assessment of child and adolescent psychopathology.
Journal of Child Psychology and Psychiatry, 41, 645–655.
Goodman, S. H., & Brand, S. R. (2009). Depression and early adverse
experiences. In H. Gotlib & C. Hammen (Eds.), Handbook of depression
(second edition, pp. 249–274). New York: Guilford Press.
Gotlib, H., & Hammen, C. (2009). Handbook of depression (second edition).
New York: Guilford Press.
Gottdiener, W. (2006). Individual psychodynamic psychotherapy of schizo-
phrenia: Empirical evidence for the practicing clinician. Psychoanalytic
Psychology, 23, 583–589.
Gregory, R. J., Schwer Canning, S., Lee, T. W., & Wise, J. C. (2004). Cognitive
bibliotherapy for depression: A meta-analysis. Professional Psychology:
Research and Practice, 35, 275–280.
Griffin, K. W. (2010). The epidemiology of substance use among adolescents and
young adults: A developmental perspective. In L. Scheier (Ed.), Handbook
of drug use etiology: Theory, methods, and empirical findings (pp. 73–92).
Washington, DC: American Psychological Association.
Griffin, K. W., & Botvin, G. J. (2010). Evidence-based interventions for preventing
substance use disorders in adolescents. Child and Adolescent Psychiatric
Clinics of North America, 19(3), 505–526.
Grilo, C. M., & McGlashan, T. H. (2009). Course and outcome. In J. Oldham, A.
Skodol, & D. Bender (Eds.), Essentials of personality disorders (pp. 63–82).
Arlington, VA: American Psychiatric Publishing.

Book 1.indb 357 06/03/2012 13:48

 358 C L I N I C A L P S Y C H O L O G Y : A N I N T R O D U C T I O N

Grissom, R. (1996). The magical number. 7 ± .2: Meta-meta-analysis of the

probability of superior outcome in comparisons involving therapy, placebo,
and control. Journal of Consulting and Clinical Psychology, 64, 973–982.
Groth-Marnat, G., & Edkins, G. (1996). Professional psychologists in general
health care settings: A review of financial efficacy of direct treatment inter-
ventions. Professional Psychology: Research and Practice, 27, 161–174.
Grunberg, N. E., Berger, S. S., & Hamilton, K. R. (2011). Stress and drug use. In
R. J. Contrada & A. Baum (Eds.), The handbook of stress science: Biology,
psychology, and health (pp. 287–300). New York: Springer.
Gull, W. (1874). Anorexia nervosa (apesia hysterica, anorexia hysterica).
Transactions of the Clinical Society of London, 7, 22–28.
Gunn, M., & Wheat, K. (2009). General principles of law relating to people with
mental disorder. In M. Gelder et al. (Eds.), New Oxford textbook of psychiatry
(second edition, Vol. 2, pp. 1895–1908). Oxford: Oxford University Press.
Gunter, T. D., Vaughn, M. G., & Philibert, R. A. (2010). Behavioural genetics
in antisocial spectrum disorders and psychopathy: A review of the recent
literature. Behavioural Sciences & the Law, 28, 148–173.
Guzzetta, F., & di Girolamo, G. (2009). Epidemiology of personality disorders. In
M. Gelder et al. (Eds.), New Oxford textbook of psychiatry (second edition,
Vol. 1, pp. 881–886). Oxford: Oxford University Press.
Haaga, D., Hall, S., & Haas, A. (2006). Participant factors in treating substance
use disorders. In L. Castonguay & L. Beutler (Eds.), Principles of therapeutic
change that work (pp. 275–292). Oxford: Oxford University Press.
Haeffel, G., Gibb, B., Metalsky, G., Alloy, L., Abramson, L., & Hankin, B. (2008).
Measuring cognitive vulnerability to depression: Development and validation
of the cognitive style questionnaire. Clinical Psychology Review, 28(5), 824–
836.
Häfner, H., & an der Heiden, W. (2008). Course and outcome. In K. Mueser & D.
Jeste (Eds.), Clinical handbook of schizophrenia (pp. 100–116). New York:
Guilford Press.
Hall, J., & Llewelyn, S. (2006). What is clinical psychology? (fourth edition).
Oxford: Oxford University Press.
Hall, J., Olabi, B., Lawrie, S. M., & McIntosh, A. M. (2010). Hippocampal and
amygdala volumes in borderline personality disorder: A meta-analysis of mag-
netic resonance imaging studies. Personality and Mental Health, 4, 172–179.
Halmi, K. A. (2010). Psychological comorbidity of eating disorders. In W. S.
Agras (Ed.), The Oxford handbook of eating disorders (pp. 292–303). New
York: Oxford University Press.
Hamilton, J. P., Furman, D. J., & Gotlib, I. H. (2011). The neural foundations of
major depression: Classical approaches and new frontiers. In F. F. Lopez-
Munoz & C. Alamo (Eds.), Neurobiology of depression. Boca Raton, FL:
CRC Press.
Hamilton, M. (1967). Development of a rating scale for primary depressive
illness. British Journal of Social and Clinical Psychology, 6, 278–296.
Hammen, C. (2009). Children of depressed parents. In H. Gotlib & C. Hammen
(Eds.), Handbook of depression (second edition, pp. 275–297). New York:
Guilford Press.
Hammen, C., Bistricky, S., & Ingram, R. (2010). Vulnerability to depression in
adulthood. In R. Ingram and J. Price (Eds.), Vulnerability to psychopathology:
Risk across the lifespan (second edition, pp. 248–281). New York: Guilford
Press.
Hankin, B., & Abele, J. (2005). Developmental psychopathology: A vulnerability–
stress perspective. Thousand Oaks, CA: Sage.

Book 1.indb 358 06/03/2012 13:48

 REFERENCES 359

Hansen, N., Lambert, M., & Forman, E. (2002). The psychotherapy dose–
response effect and its implications for treatment delivery services. Clinical
Psychology Science and Practice, 9, 329–343.
Hare, R. D. (2003). Manual for the Revised Psychopathy Checklist (second
edition). Toronto, Canada: Multi-Health Systems.
Hargrove, D. S. (2009). Psychotherapy based on Bowen family systems theory.
In J. Bray & M. Stanton (Eds.), The Wiley–Blackwell handbook of family
psychology (pp. 286–299). Chichester, UK: Wiley–Blackwell.
Harkness, K. L., & Lumley, M. N. (2008). Child abuse and neglect and the
development of depression in children and adolescents. In J. Abela & B.
Hankin (Eds.), Handbook of depression in children and adolescents (pp.
466–488). New York: Guilford Press.
Harrington, R., Campbell, F., Shoebridge, P., & Whittaker, J. (1998). Meta-
analysis of CBT for depression in adolescents. Journal of the American
Academy of Child & Adolescent Psychiatry, 37, 1005–1006.
Harrison, P. (2009). The neurobiology of schizophrenia. In M. Gelder et al.
(Eds.), New Oxford textbook of psychiatry (Vol. 1, second edition, pp. 561–
568). Oxford: Oxford University Press.
Hasin, D. S., & Katz, H. (2010). Genetic and environmental factors in substance
use, abuse, and dependence. In L. Scheier (Ed.), Handbook of drug use
etiology: Theory, methods, and empirical findings (pp. 247–267). Washington,
DC: American Psychological Association.
Hauser, P., Zametkin, A., Martinez, P., Vitietllo, B., Matochik, J., Mixon, A. et
al. (1993). Attention deficit hyperactivity disorder in people with generalized
resistance to thyroid hormone. New England Journal of Medicine, 328, 997–
1001.
Hawton, K., & Fortune, S. (2008). Suicidal behaviour and deliberate self-harm. In
M. Rutter et al. (Eds.), Rutter’s child and adolescent psychiatry (fifth edition,
pp. 648–669). London: Blackwell.
Hawton, K. & Taylor, T. (2009). Treatment of suicide attempters and prevention
of suicide and attempted suicide. In M. Gelder et al. (Eds.), New Oxford
textbook of psychiatry (second edition, Vol. 1, pp. 669–679). Oxford: Oxford
University Press.
Hay, P. J., & Claudino, A. de M. (2010). Evidence-based treatment for the eating
disorders. In W. S. Agras (Ed.), The Oxford Handbook of eating disorders
(pp. 452–479). New York: Oxford University Press.
Hazlett-Stevens, H., Pruitt, L. D., & Collins, A. (2009). Phenomenology of
generalized anxiety disorder. In M. M. Antony & M. B. Stein (Eds.), Oxford
handbook of anxiety and related disorders (pp. 47–55). New York: Oxford
University Press.
Head, L., & Gross, A. (2008). Systematic desensitization. In W. O’Donohue &
J. Fisher (Eds.), Cognitive behaviour therapy: Applying empirically supported
techniques in your practice (second edition, pp. 542–549). Hoboken, NJ: Wiley.
Heath, A., Lynskey, M., & Waldron, M. (2008). Substance use and substance
use disorders. In M. Rutter et al. (Eds.), Rutter’s child and adolescent
psychiatry (fifth edition, pp. 565–586). London: Blackwell.
Heisel, M. J. (2008). Suicide. In K. Mueser & D. Jeste (Eds.), Clinical handbook
of schizophrenia (pp. 491–506). New York: Guilford Press.
Helzer, J., Kraemer, H., Krueger, R., Wittchen, H., Sirovatka, P., & Regier,
D. (2008). Dimensional approaches to diagnostic classification: A critical
appraisal. Arlington, VA: American Psychiatric Association.
Hemmeter, U., Hemmeter-Spernal, J., & Krieg, J. (2010). Sleep deprivation in
depression. Expert Review of Neurotherapeutics, 10, 1101–1115.

Book 1.indb 359 06/03/2012 13:48

 360 C L I N I C A L P S Y C H O L O G Y : A N I N T R O D U C T I O N

Hemmings, R., & Simpson, J. (2008). Investigating the predictive validity of

the Lancaster DClinPsy written shortlisting test on subsequent trainee
performance. Final Report to the Clearing House. Retrieved 24 January
2011 from www.lancs.ac.uk/shm/dhr/courses/dclinpsy/admissions/selection
ProcessReport.pdf
Henggeler, S. W., & Schaeffer, C. (2010). Treating serious antisocial behaviour
using multisystemic therapy. In J. R. Weisz & A. E. Kazdin (Eds.), Evidence-
based psychotherapies for children and adolescents (second edition, pp.
259–276). New York: Guilford Press.
Henggeler, S. W., Sheidow, A. J., & Lee, T. (2009). Multisystemic therapy
(MST). In J. Bray & M. Stanton (Eds.), The Wiley–Blackwell handbook of
family psychology (pp. 370–387). Chichester, UK: Wiley–Blackwell.
Hettema, J. M., Neale, M. C., & Kendler, K. S. (2001). A review and meta-
analysis of the genetic epidemiology of anxiety disorders. American Journal
of Psychiatry, 158, 1568–1578.
Hinshaw, S. (1994). Attention deficits and hyperactivity in children. Thousand
Oaks, CA: Sage.
Hinshaw, S., Klein, R. & Abikoff, H. (2007). Childhood attention-deficit
hyperactivity disorder: Nonpharmacological treatments and their combination
with medication. In P. Nathan & J. Gorman (Eds.), A guide to treatments that
work (third edition, pp. 3–28). New York: Oxford University Press.
Hoek, H. W. (2006). Incidence, prevalence and mortality of anorexia nervosa
and other eating disorders. Current Opinion in Psychiatry, 19, 389–394.
Hofmann, S. G., Alpers, G. W., & Pauli, P. (2009). Phenomenology of panic and
phobic disorders. In M. M. Antony & M. B. Stein (Eds.), Oxford handbook of
anxiety and related disorders (pp. 34–46). New York: Oxford University Press.
Hollis, C. (2008). Schizophrenia and allied disorders. In M. Rutter et al. (Eds.),
Rutter’s child and adolescent psychiatry (fifth edition, pp. 737–758). London:
Blackwell.
Hollon, S., Stewart, M., & Strunk, D. (2006). Enduring effects for cognitive
behaviour therapy in the treatment of depression and anxiety. Annual Review
of Psychology, 57, 285–315.
Hoogenhout, E., van der Elst, W., de Groot, R., van Boxtel, M., & Jolles, J.
(2010). The neurovegetative complaints questionnaire in the Maastricht
aging study: Psychometric properties and normative data. Aging & Mental
Health, 14, 613–623.
Hooley, J. (2007). Expressed emotion and relapse of psychopathology. Annual
Review of Clinical Psychology, 3, 329–352.
Hooley, J. M., & Parker, H. A. (2006). Measuring expressed emotion: An
evaluation of the shortcuts. Journal of Family Psychology, 20(3), 386–396.
Hörz, S., Zanarini, M. C., Frankenburg, F. R., Reich, D. B., & Fitzmaurice, G.
(2010). Ten-year use of mental health services by patients with borderline
personality disorder and with other axis II disorders. Psychiatric Services,
61, 612–616.
Houts, A. (2010). Behavioural treatment for enuresis. In J. Weisz & A. Kazdin
(Eds.), Evidence-based psychotherapies for children and adolescents
(second edition, pp. 359–374). New York: Guilford Press.
Hubble, M., Duncan, B., & Miller, S. (1999). The heart and soul of change: What
works in therapy. Washington, DC: The American Psychological Association.
Hudson, J. L., & Rapee, R. M. (2009). Familial and social environments in the
etiology and maintenance of anxiety disorders. In A. Martin & M. Stein (Eds.),
Handbook of anxiety and anxiety disorders (pp. 173–189). New York: Oxford
University Press.

Book 1.indb 360 06/03/2012 13:48

 REFERENCES 361

Hughes, A., & Byrne, A. (2011). Clinical psychology trainee perceptions of what
facilitates a good placement start. Clinical Psychology Forum, 226 (October),
42–47.
Hughes, J., & Youngson, S. (2009). Personal development and clinical
psychology. Oxford: BPS-Blackwell.
Huizink, A. C., Mulder, E. J. H., & Buitelaar, J. K. (2004). Prenatal stress and risk
for psychopathology: Specific effects or induction of general susceptibility.
Psychological Bulletin, 130, 115–142.
Hunsley, J., & Lee, C. (2009). Introduction to clinical psychology (second
edition). Mississauga, CA: Wiley.
Hunsley, J., & Mash, E. (2008). A guide to assessments that work. New York:
Oxford University Press.
Huppert, J. D. (2009). Anxiety disorders and depression comorbidity. In
M. M. Antony & M. B. Stein (Eds.), Oxford handbook of anxiety and related
disorders (pp. 576–586). New York: Oxford University Press.
Hutchison, K. E. (2010). Substance use disorders: Realizing the promise of
pharmacogenomics and personalized medicine. Annual Review of Clinical
Psychology, 6, 577–589.
In-Albon, T., & Schneider, S. (2007). Psychotherapy of childhood anxiety disorders:
A meta-analysis. Psychotherapy and Psychosomatics, 76(1), 15–24.
International Society for the Study of Trauma and Dissociation. (2011).
Guidelines for treating dissociative identity disorder in adults, third revision.
Journal of Trauma & Dissociation, 12, 115–187.
Jablensky, A. (2009). Course and outcome of schizophrenia and their prediction.
In M. Gelder et al. (Eds.), New Oxford textbook of psychiatry (second edition,
Vol. 1, pp. 568–578). Oxford: Oxford University Press.
Jacobi, C., & Fittig, E. (2010). Psychosocial risk factors for eating disorders. In
W. S. Agras (Ed.), The Oxford handbook of eating disorders (pp. 123–136).
New York: Oxford University Press.
Jacobi, C., Hayward, C., de Zwaan, M., Kraemer, H. C., & Agras, W. S. (2004).
Coming to terms with risk factors for eating disorders: Application of risk
terminology and suggestions for a general taxonomy. Psychological Bulletin,
130, 19–65.
Jacobson, M., & Schardt, D. (1999). Diet, ADHD and behaviour: A quarter
century review. Washington, DC: Centre for Science in the Public Interest.
Jaffe, S. L., & Kelly, J. F. (2011). Twelve-step mutual-help programs for adoles-
cents. In Y. Kaminer & K. C. Winters (Eds.), Clinical manual of adolescent
substance abuse treatment (pp. 269–282). Arlington, VA: American
Psychiatric Publishing.
Javitt, D., Spencer, S., Thaker, G., Winterer, G., & Hajos, M. (2008). Neuro-
physiological biomarkers for drug development in schizophrenia. Nature
Reviews Drug Discovery, 7, 1–17.
Jessor, R., & Jessor, S. (1977). Problem behaviour and psychosocial
development. New York: Academic Press.
Jobe, T. H., & Harrow, M. (2010). Schizophrenia course, long-term outcome,
recovery, and prognosis. Current Directions in Psychological Science, 19,
220–225.
Jochman, K. A., & Fromme, K. (2010). Maturing out of substance use: The other
side of etiology. In L. Scheier (Ed.), Handbook of drug use etiology: Theory,
methods, and empirical findings (pp. 565–578). Washington, DC: American
Psychological Association.
John, O., Naumann, L. P., & Soto, C. J. (2008). Paradigm shift to the integrative
big-five trait taxonomy: History, measurement, and conceptual issues. In

Book 1.indb 361 06/03/2012 13:48

 362 C L I N I C A L P S Y C H O L O G Y : A N I N T R O D U C T I O N

O. P. John, R. W. Robins, & L. A. Pervin (Eds.), Handbook of personality:

Theory and research (third edition, pp. 114–158). New York: Guilford Press.
Johnson, J. G., Bromley, E., & McGeoch, P. G. (2009). Childhood experiences
and development of maladaptive and adaptive personality traits. In J.
Oldham, A. Skodol, & D. Bender (Eds.), Essentials of personality disorders
(pp. 143–160). Arlington, VA: American Psychiatric Publishing.
Johnson, S., & Bradley, B. (2009). Emotionally focused couple therapy: Creating
loving relationships. In J. Bray & M. Stanton (Eds.), The Wiley–Blackwell
handbook of family psychology (pp. 402–415). Chichester, UK: Wiley–
Blackwell.
Johnston, C., & Mash, E. (2001). Families of children with attention-deficit/
hyperactivity disorder: review and recommendations for future research.
Clinical Child and Family Psychology Review, 4(3), 183–207.
Johnstone, L. (1999). Adverse psychological effects of ECT. Journal of Mental
Health, 8, 69–85.
Joiner, T., & Coyne, J. (1999). The interactional nature of depression.
Washington, DC: APA.
Joiner, T., & Timmons, K. A. (2009). Depression in its interpersonal context. In
H. Gotlib & C. Hammen (Eds.), Handbook of depression (second edition, pp.
322–339). New York: Guilford Press.
Jones, K., & Vischi, T. (1979). The impact of alcohol, drug abuse, and mental
health treatment on medical care utilization: A review of the research
literature. Medical Care, 17 (Suppl. 12), 43–131.
Jones, M. (1952). A study of therapeutic communities. London: Tavistock.
Joormann, J. (2009). Cognitive aspects of depression. In H. Gotlib & C. Hammen
(Eds.), Handbook of depression (second edition, pp. 298–321). New York:
Guilford Press.
Kagan, J. (2010). The temperament thread. New York: Dana Press.
Kaminer, Y., Ford, J. D., & Clark, D. (2011a). Assessment and treatment of
internalizing disorders: Depression, anxiety disorders, and posttraumatic
stress disorder. In Y. Kaminer & K. C. Winters (Eds.), Clinical manual of
adolescent substance abuse treatment (pp. 307–347). Arlington, VA:
American Psychiatric Publishing.
Kaminer, Y., & Marsch, L. A. (2011). Pharmacotherapy of adolescent substance
use disorders. In Y. Kaminer & K. C. Winters (Eds.), Clinical manual of
adolescent substance abuse treatment (pp. 163–186). Arlington, VA:
American Psychiatric Publishing.
Kaminer, Y., Spirito, A., & Lewander, W. (2011b). Brief motivational interventions,
cognitive-behavioural therapy, and contingency management for youth
substance use disorders. In Y. Kaminer & K. C. Winters (Eds.), Clinical
manual of adolescent substance abuse treatment (pp. 213–237). Arlington,
VA: American Psychiatric Publishing.
Kaminer, Y., & Winters, K. (2011). Clinical manual of adolescent substance
abuse treatment. Arlington, VA: American Psychiatric Publishing.
Kampman, O., & Poutanen, O. (2011). Can onset and recovery in depression be
predicted by temperament? A systematic review and meta-analysis. Journal
of Affective Disorders, 135, 20–27.
Kaplan (2010a). Kaplan GRE subject test: Psychology (fifth edition). New York:
Kaplan.
Kaplan (2010b). Kaplan GRE 2011 premier with CD-ROM. New York: Kaplan.
Karasu, T. B. (1986). The specificity versus nonspecificity dilemma: Toward
identifying therapeutic change agents. American Journal of Psychiatry, 143,
687–695.

Book 1.indb 362 06/03/2012 13:48

 REFERENCES 363

Karg, K., Burmeister, K., Shedden, K., & Sen, S. (2011). The serotonin
transporter promoter variant (5-HTTLPR), stress, and depression meta-
analysis revisited: Evidence of genetic moderation. Archives of General
Psychiatry, 68, 444–454.
Kaslow, N. J., Broth, M. R., Arnette, N. C., & Collins, M. H. (2009). Family-based
treatment for adolescent depression. In S. Nolen-Hoeksema & L. Hilt (Eds.),
Handbook of depression in adolescents (pp. 531–570). New York: Routledge.
Katzman, D. K., Kanbur, N. O., & Steinegger, C. M. (2010). Medical screening
and management of eating disorders in adolescents. In W. S. Agras (Ed.),
The Oxford handbook of eating disorders (pp. 267–291). New York: Oxford
University Press.
Kavanagh, D. J. (2008). Management of co-occurring substance use disorders.
In K. Mueser & D. Jeste (Eds.), Clinical handbook of schizophrenia (pp. 459–
470). New York: Guilford Press.
Kay, S. R., Opler, L. A., & Fiszbein, A. (1987). The Positive and Negative
Syndrome Scale (PANSS) for schizophrenia. Schizophrenia Bulletin, 13,
261–276.
Kaye, W. (2008). Neurobiology of anorexia and bulimia nervosa. Physiology &
Behaviour, 94(1), 121–135.
Kazdin, A. (1995). Conduct disorders in childhood and adolescence (second
edition). Thousand Oaks, CA: Sage.
Kazdin, A. (2004). Psychotherapy for children and adolescents. In M. Lambert
(Ed.), Bergin and Garfield’s handbook of psychotherapy and behaviour
change (fifth edition, pp. 543–589). New York: Wiley.
Kazdin, A. (2010). Problem-solving skills training and parent management
training for oppositional defiant disorder and conduct disorder. In J. R. Weisz
& A. E. Kazdin (Eds.), Evidence-based psychotherapies for children and
adolescents (second edition, pp. 211–226). New York: Guilford Press.
Kazdin, A., Bass, D., Ayers, W., & Rodgers, A. (1990). Empirical and clinical
focus of child and adolescent psychotherapy research. Journal of Consulting
and Clinical Psychology, 58, 729–740.
Keel, P. K. (2010). Epidemiology and course of eating disorders. In W. S. Agras
(Ed.), The Oxford handbook of eating disorders (pp. 25–32). New York:
Oxford University Press.
Kendell, R. (1976). The classification of depressions: A review of contemporary
confusion. British Journal of Psychiatry, 129, 15–88.
Kendler, K., Aggen, S., Czajkowski, N., Røysamb, E., Tambs, K., & Torgersen, S.
(2008). The structure of genetic and environmental risk factors for personality
disorders: A multivariate twin study. Archives of General Psychiatry, 65,
1438–1446.
Kern, R. S., Glynn, S. M., Horan, W. P., & Marder, S. R. (2009). Psychosocial
treatments to promote functional recovery in schizophrenia. Schizophrenia
Bulletin, 35, 347–361.
Kernberg, O. (1975). Borderline conditions and pathological narcissism. New
York: Jason Aronson.
Kernberg, O. F., & Caligor, E. (2005). A psychoanalytic theory of personality
disorders. In J. Clarkin & M. Lenzenweger (Eds.), Major theories of personality
disorder (second edition, pp. 114–156). New York: Guilford.
Kernberg, P., & Chazan, S. (1991). Children with conduct disorders: A
psychotherapy manual. New York: Basic Books.
Keshavan, M. S., Tandon, R., Boutros, N. N., & Nasrallah, H. A. (2008).
Schizophrenia, “just the facts”: What we know in 2008: Part 3: Neurobiology.
Schizophrenia Research, 106, 89–107.

Book 1.indb 363 06/03/2012 13:48

 364 C L I N I C A L P S Y C H O L O G Y : A N I N T R O D U C T I O N

Kessler, R., Berglund, P., Demler, O., Jin, R., Merikangas, K., & Walters,
E. (2005). Lifetime prevalence and age-of-onset distributions of DSM-
IV disorders in the National Comorbidity Survey Replication. Archives of
General Psychiatry, 62, 593–602.
Kessler, R., Ruscio, A. M., Shear, K., & Wittchen, H. (2009). Epidemiology of
anxiety disorders. In M. M. Antony & M. B. Stein (Eds.), Oxford handbook
of anxiety and related disorders (pp. 19–33). New York: Oxford University
Press.
Kessler, R., & Wang, P. S. (2009). Epidemiology of depression. In H. Gotlib & C.
Hammen (Eds.), Handbook of depression (second edition, pp. 5–22). New
York: Guilford Press.
Khan, S., King, A. P., Abelson, J. L., & Liberzon, I. (2009). Neuroendocrinology
of anxiety disorders. In M. M. Antony & M. B. Stein (Eds.), Oxford handbook
of anxiety and related disorders (pp. 111–122). New York: Oxford University
Press.
Khantzian, E. J. (2003). The self-medication hypothesis revisited: The dually
diagnosed patient. Primary Psychiatry, 10, 47–48, 53–54.
Kim-Cohen, J., Caspi, A., Taylor, A., Williams, B., Newcombe, R. & Craig, I. W.
(2006). MAOA, maltreatment, and gene–environment interaction predicting
children’s mental health: New evidence and a meta-analysis. Molecular
Psychiatry, 11, 903–913.
Kim, S., Thibodeau, R., & Jorgensen, R. S. (2011). Shame, guilt, and depressive
symptoms: A meta-analytic review. Psychological Bulletin, 137, 68–96.
Klein, D. N., Durbin, C. E., & Shankman, S. A. (2009). Personality and mood
disorders. In H. Gotlib & C. Hammen (Eds.), Handbook of depression
(second edition, pp. 93–112). New York: Guilford Press.
Kliem, S., Kroger, C., & Kosfelder, J. (2010). Dialectical behaviour therapy
for borderline personality disorder: A meta-analysis using mixed-effects
modelling. Journal of Consulting and Clinical Psychology, 78, 936–951.
Kliewer, W. (2010). Family processes in drug use etiology. In L. Scheier (Ed.),
Handbook of drug use etiology: Theory, methods, and empirical findings (pp.
365–381). Washington, DC: American Psychological Association.
Klump, K. L., Bulik, C. M., Kaye, W. H., Treasure, J., & Tyson, E. (2009).
Academy for eating disorders position paper: Eating disorders are serious
mental illnesses. International Journal of Eating Disorders, 42, 97–103.
Knight, A. (2002). How to become a clinical psychologist: Getting a foot in the
door. London: Routledge.
Kohut, H. (1968). The psychoanalytic treatment of narcissistic personality
disorders: Outline of a systematic approach. Psychoanalytic Study of the
Child, 23, 86–113.
Kolvin, I., Oustend, C., Humphrey, M., & McNay, A. (1971). Studies of childhood
psychoses. II. Phenomenology of childhood psychoses. British Journal of
Psychiatry, 118, 385–394.
Kotov, R., Gamez, W., Schmidt, F. & Watson, D. (2010). Linking “big” personality
traits to anxiety, depressive, and substance use disorders: A meta-analysis.
Psychological Bulletin, 136(5), 768–821.
Kraepelin, E. (1899). Psychiatrie (sixth edition). Leipzig, Germany: Barth.
Kraepelin, E. (1913). Hysterical insanity. In E. Kraepelin (Ed.), Lectures on clinical
psychiatry (trans. T. Johnstone, pp. 249–258). New York: William Wood.
Kraepelin, E. (1921). Manic-depressive insanity and paranoia. Edinburgh:
Livingstone.
Kretchmer, E. (1936). Physique and character. London: Kegan Paul, Trench &
Trubner.

Book 1.indb 364 06/03/2012 13:48

 REFERENCES 365

Krueger, R. F., & Johnson, W. (2008). Behavioural genetics and personality. In

L. A. Pervin, O. P. John, & R. W. Robins (Eds.), Handbook of personality:
Theory and research (third edition, pp. 287–310). New York: Guilford.
Kuipers, E., Leff, J., & Lam, D. (2002). Family work for schizophrenia (second
edition). London: Gaskell.
Kurtz, M. M. (2011). Neurocognition as a predictor of response to evidence-
based psychosocial interventions in schizophrenia: What is the state of the
evidence? Clinical Psychology Review, 31, 663–672.
Kurtz, M. M., & Mueser, K. T. (2008). A meta-analysis of controlled research
on social skills training for schizophrenia. Journal of Consulting and Clinical
Psychology, 76(3), 491–504.
Kutcher, S., Aman, M., & Brooks, S. (2004). International consensus statement
on attention-deficit/hyperactivity disorder (ADHD) and disruptive behaviour
disorders (DBDs): Clinical implications and treatment practice suggestions.
European Neuropsychopharmacology, 14(1), 11–28.
Kutchins, H. & Kirk, S. (1999). Making us crazy: DSM – The psychiatric bible and
the creation of mental disorders. New York: Constable.
Kutscher, E. C. (2008). Antipsychotics. In K. Mueser & D. Jeste (Eds.), Clinical
handbook of schizophrenia (pp. 159–167). New York: Guilford Press.
Laing, R. D. (2009). Selected works of R. D. Laing, Volumes 1–7. (Vol. 1. The
divided self. Vol. 2. Self and others. Vol. 3. Reason and violence. Vol 4.
Sanity and madness in the family. Vol. 5. The politics of the family. Vol. 6.
Interpersonal perception. Vol. 7. Knots.) London: Routledge.
Lambert, M. (1992). Psychotherapy outcome research: Implications for
integrative and eclectic therapists. In J. Norcross & M. Goldfried (Eds.),
Handbook of psychotherapy integration (pp. 94–129). New York: Basic.
Lambert, M. (2005). Early response in psychotherapy: Further evidence for
the importance of common factors rather than “placebo effects”. Journal of
Clinical Psychology, 61, 855–869.
Lambert, M., & Barley, D. (2002). Research summary on the therapeutic
relationship and psychotherapy outcome. In J. Norcross (Ed.), Relationships
that work (pp. 17–36). Oxford: Oxford University Press.
Lambert, M., & Ogles, B. (1997). The effectiveness of psychotherapy supervision.
In C. E. Watkins Jr. (Ed.), Handbook of psychotherapy supervision (pp. 421–
446). New York: Wiley.
Lambert, M., & Ogles, B. (2004). The efficacy and effectiveness of psychotherapy.
In M. J. Lambert (Ed.), Bergin and Garfield’s handbook of psychotherapy and
behaviour change (fifth edition, pp. 139–193). New York: Wiley.
Lambert, M., Whipple, J., & Hawkins, E. (2003). Is it time for clinicians to routinely
track patient outcome? A meta-analysis. Clinical Psychology: Science and
Practice, 10, 288–301.
Lasègue, E. (1873). De l’anorexie hysterique. Archives Generales de Medicine,
21, 385–403.
Lebow, J. L., & Uliaszek, A. A. (2010). Couples and family therapy for personality
disorders. In J. J. Magnavita (Ed.), Evidence-based treatment of personality
dysfunction: Principles, methods, and processes (pp. 193–221). Washington,
DC: American Psychological Association.
Lees, J., Manning, N., & Rawlings, B. (1999). Therapeutic community
effectiveness: A systematic international review of therapeutic community
treatment for people with personality disorders and mentally disordered
offenders. York, UK: University of York, NHS Centre for Reviews and
Dissemination.
Leff, J., & Vaughn, C. (1985). Expressed emotion in families. New York: Guilford.

Book 1.indb 365 06/03/2012 13:48

 366 C L I N I C A L P S Y C H O L O G Y : A N I N T R O D U C T I O N

Leff, J., Vearnals, S., Brewin, C., Wolff, G., Alexander, B., Asen, E., et al. (2000).
The London Depression Intervention Trial: Randomised controlled trial of
antidepressants versus couple therapy in the treatment and maintenance
of people with depression living with a partner: Clinical outcomes and costs.
British Journal of Psychiatry, 177, 95–100.
le Grange, D. & Rienecke Hoste, R. (2010). Family therapy. In W. S. Agras
(Ed.), The Oxford handbook of eating disorders (pp. 373–385). New York:
Oxford University Press.
Lehman, A., & Steinwachs, D. (1998). At issue: Translating research into
practice: The Schizophrenia Patient Outcomes Research Team (PORT)
treatment recommendations. Schizophrenia Bulletin, 24, 1–10.
Leichsenring, F. (2009). Applications of psychodynamic psychotherapy to
specific disorders: Efficacy and indications. In G. O. Gabbard (Ed.), Textbook
of psychotherapeutic treatments (pp. 97–132). Arlington, VA: American
Psychiatric Publishing.
Leichsenring, F. (2010). Evidence for psychodynamic psychotherapy in
personality disorders: A review. In J. Clarkin, O. Fonagy, & G. Gabbard
(Eds.), Psychodynamic psychotherapy for personality disorders: A clinical
handbook (pp. 421–438). Arlington, VA: American Psychiatric Publishing.
Leichsenring, F., & Leibing, E. (2003). The effectiveness of psychodynamic
therapy and cognitive behaviour therapy in the treatment of personality
disorders: A meta-analysis. American Journal of Psychiatry, 160, 1223–1232.
Leichsenring, F., & Rabung, S. (2008). Effectiveness of long-term psycho-
dynamic psychotherapy: A meta-analysis. Journal of the American Medical
Association, 300, 1551–1565.
Leichsenring, F., & Rabung, S. (2011). Long-term psychodynamic psychotherapy
in complex mental disorders: A meta-analysis. British Journal of Psychiatry,
199, 15–22.
Leichsenring, F., Rabung, S., & Leibing, E. (2004). The efficacy of short-term
psychodynamic psychotherapy in specific psychiatric disorders: A meta-
analysis. Archives of General Psychiatry, 61, 1208–1216.
Leichsenring, F., Salzer, S., Jaeger, U., Kächele, H., Kreische, R., & Leweke, F.
(2009). Short-term psychodynamic psychotherapy and cognitive-behavioural
therapy in generalized anxiety disorder: A randomized, controlled trial.
American Journal of Psychiatry, 166, 875–881.
Lemma, A., Roth, A., & Pilling, S. (2008). The competences required to deliver
effective psychoanalytic/psychodynamic therapy. London: Centre for
Outcomes Research & Effectiveness.
Lemma, A., Target, M., & Fonagy, P. (2010). The development of a brief
psychodynamic protocol for depression: Dynamic interpersonal therapy
(DIT). Psychoanalytic Psychotherapy, 24, 329–346.
Lemma, A., Target, M., & Fonagy, P. (2011). Brief dynamic interpersonal
therapy: A clinician’s guide. Oxford: Oxford University Press.
Lenzenweger, M. (2010). Schizotypy and schizophrenia. New York: Guilford.
Lenzenweger, M. F., & Clarkin, J. F. (2005). The personality disorders: History,
classification, and research issues. In J. Clarkin & M. Lenzenweger (Eds.),
Major theories of personality disorder (second edition, pp. 1–42). New York:
Guilford.
Lenzenweger, M., Lane, M., Loranger, A., & Kessler, R. (2007). DSM IV
personality disorders in the national comorbidity survey replication. Biological
Psychiatry, 62, 533–564.
Leshner, A. (2008). By now, “harm reduction” harms both science and the public
health. Clinical Pharmacology & Therapeutics, 83(4), 513–514.

Book 1.indb 366 06/03/2012 13:48

 REFERENCES 367

Leucht, C., Heres, S., Kane, J. M., Kissling, W., Davis, J. M., & Leucht, S.
(2011). Oral versus depot antipsychotic drugs for schizophrenia—A critical
systematic review and meta-analysis of randomised long-term trials.
Schizophrenia Research, 127, 83–92.
Levine, M. P., & Murnen, S. K. (2009). “Everybody knows that mass media are/
are not a cause of eating disorders”: A critical review of evidence for a causal
link between media, negative body image, and disordered eating in females.
Journal of Social and Clinical Psychology, 28, 9–42.
Levine, M. P., & Smolak, L. (2010). Cultural influences on body image and
the eating disorders. In W. S. Agras (Ed.), The Oxford handbook of eating
disorders (pp. 223–246). New York: Oxford University Press.
Levinson, D. F. (2009). Genetics of major depression. In H. Gotlib & C. Hammen
(Eds.), Handbook of depression (second edition, pp. 165–186). New York:
Guilford Press.
Lewinsohn, P., & Gotlib, I. (1995). Behavioural theory and treatment of
depression. In E. Becker & W. Leber (Eds.), Handbook of depression
(pp. 352–375). New York: Guilford.
Lezak, M., Howieson, D., & Loring, D. (2004). Neuropsychological assessment
(fourth edition). Oxford: Oxford University Press.
Liddle, H. A. (2010). Treating adolescent substance abuse using multidimensional
family therapy. In J. R. Weisz & A. E. Kazdin (Eds.), Evidence-based
psychotherapies for children and adolescents (second edition, pp. 416–432).
New York: Guilford Press.
Lilienfeld, S. (2007). Psychological treatments that cause harm. Perspectives on
Psychological Science, 2, 53–70.
Lin, C., Lane, H., & Tsai, G. E. (2011). Glutamate signaling in the pathophysiology
and therapy of schizophrenia. Pharmacology, Biochemistry and Behaviour.
Advance oinline publication. doi:10.1016/j.pbb.2011.03.023
Linde, K., Berner, M., & Egger, M. (2005). St John’s wort for depression –
Meta-analysis of randomised controlled trials. British Journal of Psychiatry,
86, 99–107.
Linehan, M., Davison, G., Lynch, T., & Sanderson, G. (2006). Technique factors in
treating personality disorders. In L. Castonguay & L. Beutler (Eds.), Principles of
therapeutic change that work (pp. 239–252). Oxford: Oxford University Press.
Links, P. S., & Kolla, N. (2009). Assessing and managing suicide risk. In J.
Oldham, A. Skodol, & D. Bender (Eds.), Essentials of personality disorders
(pp. 343–360). Arlington, VA: American Psychiatric Publishing.
Linscott, R. J., & van Os, J. (2010). Systematic reviews of categorical versus
continuum models in psychosis: Evidence for discontinuous subpopulations
underlying a psychometric continuum: Implications for DSM-V, DSM-VI, and
DSM-VII. Annual Review of Clinical Psychology, 6, 391–419.
Lipsey, M. W. (2009). The primary factors that characterize effective interventions
with juvenile offenders: A meta-analytic overview. Victims & Offenders, 4(2),
124–147.
Liu, R. T., & Alloy, L. B. (2010). Stress generation in depression: A systematic
review of the empirical literature and recommendations for future study.
Clinical Psychology Review, 30, 582–593.
Lochman, J. E., Boxmeyer, C. L., Powell, N. P., Barry, T. D., & Pardini, D. A.
(2010). Anger control training for aggressive youths. In J. R. Weisz & A. E.
Kazdin (Eds.), Evidence-based psychotherapies for children and adolescents
(second edition, pp. 227–242). New York: Guilford Press.
Lock, J., Le Grange, D., Agras, W., & Dare, C. (2001). Treatment manual for
anorexia nervosa: A family based approach. New York: Guilford.

Book 1.indb 367 06/03/2012 13:48

 368 C L I N I C A L P S Y C H O L O G Y : A N I N T R O D U C T I O N

Lopez, S., & Snyder, C. (2009). Oxford handbook of positive psychology (second
edition). New York: Oxford University Press.
Loranger, A. W. (1999). International Personality Disorder Examination. Odessa,
FL: Psychological Assessment Resources.
Lorber, M. F. (2004). The psychophysiology of aggression, psychopathy, and
conduct problems: A meta-analysis. Psychological Bulletin, 130, 531–552.
Losel, F., & Beelmann, A. (2005). Social problem-solving programs for
preventing antisocial behaviour in children and youth. In M. McMurran & J.
McGuire (Eds.), Social problem solving and offending: Evidence, evaluation
and evolution (pp. 127–143). Chichester, UK: Wiley.
Lubman, D., & Yücel, M. (2008). Drugs, mental health and the adolescent
brain: Implications for early intervention. Early Intervention in Psychiatry, 2,
63–66.
Luborsky, L. (1962). Clinicians’ judgements of mental health. Archives of
General Psychiatry, 7, 407–417.
Lucas, R. (2009). Psychotic wavelength: A psychoanalytic perspective for
psychiatry. London: Routledge.
Lukoff, D., Nuechterlein, K., & Ventura, J. (1986). Manual for expanded Brief
Psychiatric Rating Scale (BRS). Schizophrenia Bulletin, 12, 594–602.
Lunt, I. (2008). Psychologist qualifications in Europe: Common standard for
quality and mobility. Australian Psychologist, 43(4), 222–230.
Luty, J., Fekadu, D., & Dhandayudham, A. (2006). Understanding of the term
‘schizophrenia’ by the British public. Psychiatric Bulletin, 30, 435–435.
Luyten, P., Corveleyn, J., & Blatt, S. J. (2005). The convergence among
psychodynamic and cognitive-behavioural theories of depression: A critical
overview of empirical research. In J. Corveleyn, P. Luyten, & S. J. Blatt (Eds.),
The theory and treatment of depression: Towards a dynamic interactionism
model (pp. 107–147). Leuven, Belgium/Mahwah, NJ: Leuven University
Press/Lawrence Erlbaum Associates.
Maag, J. W., Swearer, S. M., & Toland, M. D. (2009). Cognitive-behavioural
interventions for depression in children and adolescents: Meta-analysis,
promising programs, and implications for school personnel. In M. J. Mayer,
J. E. Lochman, & R. Van Acker (Eds.), Cognitive-behavioural interventions
for emotional and behavioural disorders: School-based practice (pp. 235–
265). New York: Guilford Press.
Macgowan, M. J., & Engle, B. (2010). Evidence for optimism: Behavior therapies
and motivational interviewing in adolescent substance abuse treatment.
Child and Adolescent Psychiatric Clinics of North America, 19, 527–545.
Magnavita, J. J. (2009). Psychodynamic family psychotherapy: Toward unified
relational systematics. In J. Bray & M. Stanton (Eds.). The Wiley–Blackwell
handbook of family psychology (pp. 240–257). Chichester, UK: Wiley-
Blackwell.
Maine, M. & Bunnell, D. (2010). A perfect biopsychosocial storm: Gender,
culture, and eating disorders. In M. Maine, B. McGilley, & D. Bunnell (Eds.),
Treatment of eating disorders: Bridging the research–practice gap (pp.
3–16). San Diego, CA: Elsevier.
Makris, N., Biederman, J., Monuteaux, M. C., & Seidman, L. J. (2009). Towards
conceptualizing a neural systems-based anatomy of attention-deficit/
hyperactivity disorder. Developmental Neuroscience, 31, 36–49.
Malan, D. (1995). Individual psychotherapy and the science of psychodynamics
(second edition). London: Butterworth-Heinemann.
Mamah, D., & Barch, D. (2011). Diagnosis and classification of the schizophrenia
spectrum disorders. In M. Ritsner (Ed.), Handbook of schizophrenia spectrum

Book 1.indb 368 06/03/2012 13:48

 REFERENCES 369

disorders, Volume I: Conceptual issues and neurobiological advances (pp.

45–83). New York: Springer.
Marlatt, G. A., & Witkiewitz, K. (2010). Update on harm-reduction policy and
intervention research. Annual Review of Clinical Psychology, 6, 591–606.
Maron, E., Hettema, J. M., & Shlik, J. (2010). Advances in molecular genetics of
panic disorder. Molecular Psychiatry, 15(7), 681–701.
Martin, D., Graske, J., & Davis, M. (2000). Relation of the therapeutic alliance
with outcome and other variables: A meta-analytic review. Journal of
Consulting & Clinical Psychology, 68, 438–450.
Martin, E. I., Ressler, K. J., Binder, E., & Nemeroff, C. B. (2009). The neurobiology
of anxiety disorders: Brain imaging, genetics, and psychoneuroendocrinology.
Psychiatric Clinics of North America, 32(3), 549–575.
Mason, M. J. (2010). Mental health, school problems, and social networks:
Modeling urban adolescent substance use. Journal of Primary Prevention,
31, 321–331.
Masson, J. (1984). Freud’s suppression of seduction theory. New York: Farrar,
Straus, & Giroux.
Mathew, S. J., & Hoffman, E. J. (2009). Pharmacotherapy for generalized
anxiety disorder. In M. M. Antony & M. B. Stein (Eds.), Oxford handbook of
anxiety and related disorders (pp. 350–363). New York: Oxford University
Press.
Mathews, C. A. (2009). Phenomenology of obsessive-compulsive disorder. In
M. M. Antony & M. B. Stein (Eds.), Oxford handbook of anxiety and related
disorders (pp. 56–64). New York: Oxford University Press.
Matthews, K., & Christmas, D. (2009). Neurosurgery for psychiatric disorders. In
M. Gelder, et al. (Eds.), New Oxford textbook of psychiatry (second edition,
Vol. 2, pp. 1266–1272). Oxford: Oxford University Press.
Mazzeo, S. E., & Bulik, C. M. (2009). Environmental and genetic risk factors for
eating disorders: What the clinician needs to know. Child and Adolescent
Psychiatric Clinics of North America, 18(1), 67–82.
Mazzucchelli, T., Kane, R., & Rees, C. (2009). Behavioural activation treatments
for depression in adults: A meta-analysis and review. Clinical Psychology:
Science and Practice, 16, 383–411.
McCart, M., Priester, P., Davies, W., & Azen, R. (2006). Differential effectiveness
of cognitive-behavioural therapy and behavioural parent-training for
antisocial youth: A meta-analysis. Journal of Abnormal Child Psychology,
34(4), 527–543.
McCrae, R. R., & Costa, P. T., Jr. (2008). The five-factor theory of personality.
In O. P. John, R. W. Robins, & L. A. Pervin (Eds.), Handbook of personality:
Theory and research (third edition, pp. 159–181). New York: Guilford Press.
McCullough-Vaillant, L. (1997). Changing character: Short-term anxiety
regulating psychotherapy for restructuring defences, affects and attachments.
New York: Basic Books.
McDermott, L. M., & Ebmeier, K. P. (2009). A meta-analysis of depression
severity and cognitive function. Journal of Affective Disorders, 119, 1–8.
McDermott, R., Tingley, D., Cowden, J., Frazzetto, G., & Johnson, D. D. P.
(2009). Monoamine oxidase A gene (MAOA) predicts behavioural aggression
following provocation. Proceedings of the National Academy of Sciences of
the United States of America, 106, 2118–2123.
McElroy, S. L., Guerdjikova, A. I., O’Melia, A. M., Mori, N., Keck, P. E., Jr. (2010).
Pharmacotherapy of the eating disorders. In W. S. Agras (Ed.), The Oxford
Handbook of eating disorders (pp. 417–451). New York: Oxford University
Press.

Book 1.indb 369 06/03/2012 13:48

 370 C L I N I C A L P S Y C H O L O G Y : A N I N T R O D U C T I O N

McFall, R. M. (2006). Doctoral training in clinical psychology. Annual Review of

Clinical Psychology, 2, 21–49.
McFarlane, W. (2004). Multifamily groups in the treatment of severe psychiatric
disorders. New York: Guilford.
McFarlane, W. R. (2005). Psychoeducational multifamily groups for families with
persons with severe mental illness. In J. Lebow (Ed.), Handbook of clinical
family therapy (pp. 195–227). Hoboken, NJ: Wiley.
McGlashen, T., & Hoffman, R. (2000). Schizophrenia as a disorder of develop-
mentally reduced synaptic connectivity. Archives of General Psychiatry, 57,
637–648.
McGrath, J., Saha, S., Welham, J., Saadi, O., MacCauley, C., & Chant, D. (2004).
A systematic review of the incidence of schizophrenia: The distribution of
rates and the influence of sex, urbanicity, migrant status and methodology.
BMC Medicine, 2, 13.
McLaughlin, K. A., & Nolen-Hoeksema, S. (2011). Rumination as a transdiag-
nostic factor in depression and anxiety. Behaviour Research and Therapy,
49, 186–193.
McLeod, B. D., Weisz, J. R., & Wood, J. J. (2007). Examining the association
between parenting and childhood depression: A meta-analysis. Clinical
Psychology Review, 27, 986–1003.
McMahon, R. J., Witkiewitz, K., Kotler, J. S., & The Conduct Problems Prevention
Research Group. (2010). Predictive validity of callous–unemotional traits
measured in early adolescence with respect to multiple antisocial outcomes.
Journal of Abnormal Psychology, 119(4), 752–763.
McNally, R. F. & Reese, H. E. (2009). Information-processing approaches
to understanding anxiety disorders. In M. M. Antony & M. B. Stein (Eds.),
Oxford handbook of anxiety and related disorders (pp. 136–152). New York:
Oxford University Press.
Medalia, A., & Choi, J. (2009). Cognitive remediation in schizophrenia.
Neuropsychology Review, 19, 353–364.
Meltzer, H., Gatward, R., Goodman, R., & Ford, T. (2000). The Mental Health
of Children and Adolescents in Great Britain: The report of a survey carried
out in 1999 by Social Survey Division of the Office for National Statistics on
behalf of the Department of Health, the Scottish Health Executive and the
National Assembly for Wales. London: The Stationery Office.
Menninger, K. (1958). Theory of psychoanalytic technique. London: Imago.
Meyer, B., Ajchenbrenner, M., & Bowles, D. P. (2005). Sensory sensitivity, at-
tachment experiences, and rejection responses among adults with border-
line and avoidant features. Journal of Personality Disorders, 19, 641–658.
Miller, S., Duncan, B., Sorrell, R., & Brown, G. (2005). The partners for change
outcome management system. Journal of Clinical Psychology, 61, 199–
208.
Miller, W., & Rollnick, S. (2002). Motivational interviewing. Preparing people for
change (second edition). New York: Guilford.
Millon, T. (2009). Millon Clinical Multiaxial Inventory–III manual (fourth edition).
Minneapolis, MN: National Computer Systems.
Milne, D. (2009). Evidence-based clinical supervision: Principles and practice.
Oxford: BPS-Blackwell.
Milrod, B., Leon, A., Busch, F., Rudden, M., Schwalberg, M., Clarkin J., et al.
(2007). A randomized controlled clinical trial of psychoanalytic psychotherapy
for panic disorder. American Journal of Psychiatry, 164, 265–272.
Mindus, P., Rasmussen, S. A., Lindquist, C., & Noren, G. (2001). Neurosurgical
treatment for refractory obsessive-compulsive disorder: Implications for

Book 1.indb 370 06/03/2012 13:48

 REFERENCES 371

understanding frontal lobe function. Arlington, VA: American Psychiatric

Publishing.
Minuchin, S., Rosman, B., & Baker, L. (1978). Psychosomatic families: Anorexia
nervosa in context. Cambridge, MA: Harvard University Press.
Mitchell, J. E., & Crow, S. J. (2010). Medical comorbidities of eating disorders. In
W. S. Agras (Ed.), The Oxford handbook of eating disorders (pp. 259–266).
New York: Oxford University Press.
Moffitt, T. (2005). The new look of behavioural genetics in developmental
psychopathology: Gene–environment interplay in antisocial behaviours.
Psychological Bulletin, 131, 533–554.
Moffitt, T., & Scott, S. (2008). Disorders of attention and activity. In M. Rutter
et al. (Eds.), Rutter’s child and adolescent psychiatry (fifth edition, pp. 543–
564). London: Blackwell.
Mohr, D. (1995). Negative outcome in psychotherapy: A critical review. Clinical
Psychology: Science and Practice, 2, 1–27.
Mojtabai, R., Nicholson, R., & Carpenter, B. (1998). Role of psychosocial
treatments in management of schizophrenia: A meta-analysis review of
controlled outcome studies. Schizophrenia Bulletin, 24, 569–587.
Monroe, S., & Harkness, K. (2005). Life stress, the “kindling” hypothesis, and
the recurrence of depression: Considerations from a life stress perspective.
Psychological Review, 112, 417–445.
Monroe, S., Slavich, G. M., & Georgiades, K. (2009). The social environment
and life stress in depression. In H. Gotlib & C. Hammen (Eds.), Handbook of
depression (second edition, pp. 340–360). New York: Guilford Press.
Montañés, F., & de Lucas Taracena, M. T. (2006). Evolutionary aspects
of affective disorders, critical review and proposal of a new model. Actas
Españolas De Psiquiatría, 34, 264–276.
Monteleone, P., Martiadis, V., & Maj, M. (2010). Circadian rhythms and treatment
implications in depression. Progress in Neuropsychopharmacology &
Biological Psychiatry, 35, 1569–1574.
Morgan, T. B., & Crane, D. R. (2010). Cost-effectiveness of family-based sub-
stance abuse treatment. Journal of Marital and Family Therapy, 36, 486–498.
Moscovitch, D. A., Antony, M. M., & Swinson, R. P. (2009). Exposure-based
treatments for anxiety disorders: Theory and process. In M. M. Antony &
M. B. Stein (Eds.), Oxford handbook of anxiety and related disorders
(pp. 461–475). New York: Oxford University Press.
Moss, E. S., Nicole, C. C., Dubois-Comtois, K., Mazzarello, T., & Berthiaume, C.
(2006). Attachment and behaviour problems in middle childhood as reported
by adult and child informants. Development and Psychopathology, 18(2),
425–444.
Mowrer, O. (1939). A stimulus response analysis of anxiety and its role as a
reinforcing agent. Psychological Review, 46, 553–565.
Mueser, K. & Duva, S. (2011). Schizophrenia. In D. Barlow (Ed.), The Oxford
handbook of clinical psychology (pp. 469–503). New York: Oxford University
Press.
Mueser, K., & Jeste, D. (2008). Clinical handbook of schizophrenia. New York:
Guilford Press.
Mumford, E., Schlesinger, H., Glass, G., Patrick, C., & Cuerdon, T. (1984). A
new look at evidence about reduced cost of medical utilization following
mental health treatment. American Journal of Psychiatry, 141, 1145–1158.
Murray, C., & Lopez, A. (1996). The global burden of disease: A comprehensive
assessment of mortality and disability from diseases, injuries and risk factors
in 1990 and projected to 2020. Cambridge, MA: Harvard University Press.

Book 1.indb 371 06/03/2012 13:48

 372 C L I N I C A L P S Y C H O L O G Y : A N I N T R O D U C T I O N

Murray, R., & Castle, D. (2009). Genetic and environmental risk factors for
schizophrenia. In M. Gelder et al. (Eds.), New Oxford textbook of psychiatry
(second edition, Vol. 1, pp. 553–561). Oxford: Oxford University Press.
Murray, R., & Lewis, S. (1987). Is schizophrenia a neurodevelopmental disorder?
British Medical Journal, 295, 681–682.
Murray, R., & Van Os, J. (1998). Predictors of outcome in schizophrenia. Journal
of Clinical Psychopharmacology, 18, 25–45.
Najavits, L. M. (2007). Psychosocial treatments for posttraumatic stress disorder.
In P. E. Nathan & J. M. Gorman (Eds.), A guide to treatments that work (third
edition, pp. 513–530). New York: Oxford University Press.
Naragon-Gainey, K. (2010). Meta-analysis of the relations of anxiety sensitivity
to the depressive and anxiety disorders. Psychological Bulletin, 136(1),
128–150.
Narcotics Anonymous (2008). Narcotics Anonymous (sixth edition). Chatsworth,
CA: Narcotics Anonymous World Services.
Nasser, M., & Katzman, N. (2003). Sociocultural theories of eating disorders. In
J. Treasure, U. Schmidt, & E. van Furth (Eds.), Handbook of eating disorders
(second edition, pp. 139–150). Chichester, UK: Wiley.
Nathan, P., & Gorman, J. (2007), A guide to treatments that work (third edition).
New York: Oxford University Press.
National Advisory Committee on Drugs and the Drug and Alcohol Information
and Research Unit (2004). Drug use in Ireland and Northern Ireland
2003/2003 Drug Prevalence Survey. Dublin, Ireland and Belfast, UK: Health
Board (Ireland) and Social Service Board (Northern Ireland).
National Centre for Social Research and the National Foundation for Educational
Research (2002). Drug use, smoking and drinking among young people in
England in 2001. London: NCSR and NFER.
National Institute of Mental Health in England (2003). Personality disorder:
No longer a diagnosis of exclusion. Leeds, UK: National Institute of Mental
Health in England.
Nestler, E., & Charney, D. (2008). Neurobiology of mental illness (third edition).
Oxford: Oxford University Press.
Newman, M., Crits-Christoph, P., Connoly Gibbons, M., & Erickson, T. (2006a).
Participant factors in treating anxiety disorders. In L. Castonguay & L. Beutler
(Eds.), Principles of therapeutic change that work (pp. 121–154). Oxford:
Oxford University Press.
Newman, M., Stiles, W., Woody, S. & Janeck, A. (2006b). Integration of
therapeutic factors in anxiety disorders. In L. Castonguay & L. Beutler (Eds.),
Principles of therapeutic change that work (pp. 187–202). Oxford: Oxford
University Press.
Newton-Howes, G., Tyrer, P., & Johnson, T. (2006). Personality disorder and the
outcome of depression: Meta-analysis of published studies. British Journal of
Psychiatry, 188, 13–20.
NICE (2004a). Eating disorders: Core interventions in the treatment and
management of anorexia nervosa, bulimia nervosa and related disorders.
London: National Institute for Clinical Excellence.
NICE (2004b). Self-harm: The short-term physical and psychological
management and secondary prevention of self-harm in primary and
secondary care (Clinical guideline 16). London: National Institute of Clinical
Excellence.
NICE (2005a). Post-traumatic stress disorder: The management of PTSD in
adults and children in primary and secondary care (Clinical guideline 26).
London: National Institute of Clinical Excellence.

Book 1.indb 372 06/03/2012 13:48

 REFERENCES 373

NICE (2005b). Obsessive compulsive disorder: Core interventions in

the treatment of obsessive compulsive disorder and body dysmorphic
disorder (Clinical guideline 31). London: National Institute for Clinical
Excellence.
NICE (2005c). Depression in children and young people: Identification and
management in primary, community and secondary care (Clinical guideline
28). London: National Institute of Clinical Excellence.
NICE (2006a). Parent-training/education programmes in the management of
children with conduct disorders. NICE technology appraisal guidance 102.
London: National Institute of Clinical Excellence.
NICE (2006b). Computerized cognitive behaviour therapy for depression and
anxiety (Technology appraisal 97). London: NICE.
NICE (2008a). Attention deficit hyperactivity disorder. Diagnosis and
management of ADHD in children, young people and adults. NICE guideline
72. London: National Institute of Clinical Excellence.
NICE (2008b). Drug misuse: Psychosocial interventions. National clinical
practice guideline 51. London: British Psychological Society and the Royal
College of Psychiatrists.
NICE (2009a). Depression: The treatment and management of depression in
adults (update) (Clinical guideline 90). London: National Institute of Clinical
Excellence.
NICE (2009b). Core interventions in the treatment and management of
schizophrenia in primary and secondary care (update). (Clinical guideline
82). London: National Institute of Clinical Excellence.
NICE (2009c). Antisocial personality disorder: Treatment, management and
prevention (Clinical guideline 77). London: National Institute of Clinical
Excellence.
NICE (2009d). Borderline personality disorder: Treatment and management
(Clinical guideline 78). London: National Institute of Clinical Excellence.
NICE (2011). Generalized anxiety disorder and panic disorder, with and without
agoraphobia. Management in primary, secondary and community care
(Clinical guideline 113). London: National Institute of Clinical Excellence.
Nigg, J. (2001). Is ADHD an inhibitory disorder. Psychological Bulletin, 125,
571–596.
Nigg, J. (2005). Neuropsychologic theory and findings in attention-deficit/
hyperactivity disorder: The state of the field and salient challenges for the
coming decade. Biological Psychiatry, 57, 1424–1435.
Nigg, J., & Huang-Pollock, C. L. (2003). An early onset model of the role of
executive functions and intelligence in conduct disorder/delinquency. In
B. B. Lahey, T. Moffitt, & A. Caspi (Eds.), The causes of conduct disorder and
serious juvenile delinquency (pp. 227–253). New York: Guilford.
Nolen-Hoeksema, S., & Hilt, L. M. (2009a). Handbook of depression in
adolescents. New York: Routledge.
Nolen-Hoeksema, S., & Hilt, L. M. (2009b). Gender differences in depression.
In H. Gotlib & C. Hammen (Eds.), Handbook of depression (second edition,
pp. 386–404). New York: Guilford Press.
Norcross, J. (2002). Psychotherapy relationships that work. Oxford: Oxford
University Press.
Norcross, J. (2005). The psychotherapist’s own psychotherapy: Educating and
developing psychologists. American Psychologist, 60(8), 840–850.
Norcross, J., Beutler, L., & Levant, R. (2006). Evidence-based practices in mental
health: Debate and dialogue on the fundamental questions. Washington, DC:
American Psychological Association.

Book 1.indb 373 06/03/2012 13:48

 374 C L I N I C A L P S Y C H O L O G Y : A N I N T R O D U C T I O N

Norcross, J. C., Ellis, J. L., & Sayette, M. A. (2010). Getting in and getting
money: A comparative analysis of admission standards, acceptance rates,
and financial assistance across the research–practice continuum in clinical
psychology programs. Training and Education in Professional Psychology,
4(2), 99–104.
Norcross, J., & Goldfried, M. (Eds.) (2003). Handbook of psychotherapy
integration (second edition). New York: Basic Books.
Norton, P., & Price, E. (2007). A meta-analytic review of adult cognitive-
behavioural treatment outcome across the anxiety disorders. Journal of
Nervous and Mental Disease, 195(6), 521–531.
Nunez-Smith, M., Wolf, E., Huang, H. M., Chen, P. G., Lee, L., Emanuel, E. J.,
et al. (2010). Media exposure and tobacco, illicit drugs, and alcohol use
among children and adolescents: A systematic review. Substance Abuse,
31, 174–192.
O’Brien, C., Childress, A., McLellan, A., & Ehrman, R. (1992). A learning model
of addiction. Research Publication of the Association of Research on Nervous
and Mental Diseases, 70, 157–177.
Olatunji, B. O., Cisler, J. M., & Deacon, B. J. (2010). Efficacy of cognitive
behavioural therapy for anxiety disorders: A review of meta-analytic findings.
Psychiatric Clinics of North America, 33(3), 557–577.
Orlinsky, D., Tonnestad, M., & Willutzki, U. (2004). Fifty years of psychotherapy
process–outcome research: Continuity and change. In M. Lambert (Ed.),
Bergin and Garfield’s handbook of psychotherapy and behaviour change
(fifth edition, pp. 307–389). New York: Wiley.
Orth, U., Robins, R. W., & Roberts, B. W. (2008). Low self-esteem prospectively
predicts depression in adolescence and young adulthood. Journal of
Personality and Social Psychology, 95, 695–708.
O’Shea, G., & Byrne, M. (2010). In pursuit of clinical training. Irish Psychologist,
36(4), 79–81.
O’Shea, G., & Byrne, M. (2011a). A profile of entrants to Irish clinical training
programmes. Irish Psychologist, 37(5), 118–123.
O’Shea, G., & Byrne, M. (2011b). Entrants’ experiences of the clinical psychology
programme selection process. Irish Psychologist, 37(6), 150–157.
Ozer, E., Best, S., Lipsey, T., & Weiss, D. (2003). Predictors of posttraumatic
stress disorder and symptoms in adults: A meta-analysis. Psychological
Bulletin, 129, 52–73.
Pachana, N., O’Donovan, A., & Helmes, E. (2006). Australian clinical psychology
training program directors survey. Australian Psychologist, 41(3), 168–178.
Pachana, N., Sofronoff, K., & O’Brien, M. (2008). Focus on clinical psychology
postgraduate training: Taking the curriculum into the next decade. Australian
Psychologist, 43(4), 219–221.
Page, A. & Stritzke, W. (2006). Clinical psychology for trainees. Cambridge, UK:
Cambridge University Press.
Palmer, B. W., Dawes, S. E., & Heaton, R. K. (2009). What do we know about
neuropsychological aspects of schizophrenia? Neuropsychology Review,
19, 365–384.
Papworth, M. (2004). Getting on clinical psychology training courses: Responses
to frequently asked questions. Clinical Psychology, 42, 32–36.
Papworth, M. (2007). Getting on clinical psychology training courses: Responses
to frequently asked questions (part 2). Clinical Psychology Forum, 177,
37–41.
Pardini, D. A., Frick, P. J., & Moffitt, T. E. (2010). Building an evidence base
for DSM-V conceptualizations of oppositional defiant disorder and conduct

Book 1.indb 374 06/03/2012 13:48

 REFERENCES 375

disorder: Introduction to the special section. Journal of Abnormal Psychology,

119(4), 683–688.
Paris, J. (1996). Social factors in the personality disorders: A biopsychosocial
approach to etiology and treatment. New York: Cambridge University Press.
Parker, G. (2009). Diagnosis, classification and differential diagnosis of the
mood disorders. In M. Gelder et al. (Eds.) New Oxford textbook of psychiatry
(second edition, Vol. 1, pp. 637–645). Oxford: Oxford University Press.
Patterson, G. (1982). Coercive family process. Eugene, OR: Castalia.
Paykel, E., & Scott, J. (2009). Treatment of mood disorders. In M. Gelder
et al. (Eds.), New Oxford textbook of psychiatry (second edition, Vol. 1,
pp. 6669–6680). Oxford: Oxford University Press.
Paykina, N., Greenhill, L., & Gorman, J. (2007). Pharmacological treatments
for attention-deficit hyperactivity disorder. In P. Nathan & J. Gorman (Eds.),
A guide to treatments that work (third edition, pp. 29–70). New York: Oxford
University Press.
Peckham, A. D., McHugh, R. K., & Otto, M. W. (2010). A meta-analysis of the
magnitude of biased attention in depression. Depression and Anxiety, 27,
1135–1142.
Perlmutter, R. (1996). A family approach to psychiatric disorders. Washington,
DC: American Psychiatric Press.
Persons, J. B., & Fresco, D. M. (2008). Adult depression. In J. Hunsley & E. J.
Mash (Eds.), A guide to assessments that work (pp. 96–120). New York:
Oxford University Press.
Peterson, C., & Villanova, P. (1988). An expanded Attributional Style
Questionnaire. Journal of Abnormal Psychology, 97, 87–89.
Pfammatter, M., Junghan, U., & Brenner, H. (2006). Efficacy of psychological
therapy in schizophrenia: Conclusions from meta-analyses. Schizophrenia
Bulletin, 32(Suppl. 1), S64–S80.
Phillips, A., Hatton, C., & Gray, I. (2001). Which selection methods do clinical
psychology courses use? Clinical Psychology, 8, 19–23.
Phillips, A., Hatton, C., & Gray, I. (2004). Factors predicting the short-listing
and selection of trainee clinical psychologists: A prospective national cohort
study. Clinical Psychology and Psychotherapy, 11, 111–125.
Phillips, L. J., Francey, S. M., Edwards, J., & McMurray, N. (2007). Stress and
psychosis: Towards the development of new models of investigation. Clinical
Psychology Review, 27, 307–317.
Phillips, P., McKeown, O., & Sandford, T. (2010). Dual diagnosis: Practice in
context. Oxford: Wiley–Blackwell.
Phillips, W. J., Hine, D. W., & Thorsteinsson, E. B. (2010). Implicit cognition and
depression: A meta-analysis. Clinical Psychology Review, 30, 691–709.
Pine, D. & Klein, R. (2008). Anxiety disorders. In M. Rutter et al. (Eds.),
Rutter’s child and adolescent psychiatry (fifth edition, pp. 628–647). London:
Blackwell.
Plante, T. (2009). Contemporary clinical psychology (third edition). Hoboken,
NJ: Wiley.
Pliszka, S. R. (2007). Pharmacologic treatment of attention-deficit/hyperactivity
disorder: Efficacy, safety and mechanisms of action. Neuropsychology
Review, 17(1), 61–72.
Polanski, E., & Mokros, H. (1999). Children’s Depression Rating Scale –
Revised. Los Angeles: Western Psychological Services.
Pollack, M. H., & Simon, N. M. (2009). Pharmacotherapy for panic disorder and
agoraphobia. In M. M. Antony & M. B. Stein (Eds.), Oxford handbook of anxiety
and related disorders (pp. 295–307). New York: Oxford University Press.

Book 1.indb 375 06/03/2012 13:48

 376 C L I N I C A L P S Y C H O L O G Y : A N I N T R O D U C T I O N

Princeton Review (2010a). Cracking the GRE 2011 edition. Framingham, MA:
Princeton Review.
Princeton Review (2010b). Cracking the GRE psychology subject test (eighth
edition). Framingham, MA: Princeton Review.
Prochaska, J., DiClemente, C., & Norcross, J. (1992). In search of how people
change: Applications to addictive behaviours. American Psychologist, 47,
1102–1114.
Raine, A. (1996). Autonomic nervous system activity and violence. In D. M. Stoff
& R. B. Cairns (Eds.), Aggression and violence: Genetic, neurobiological
and biological perspectives (pp. 145–168). Mahwah, NJ: Lawrence Erlbaum
Associates.
Raine, A., & Yang, Y. (2006). Neural foundations to moral reasoning and antisocial
behaviour. Social, Cognitive, and Affective Neuroscience, 1, 203–213.
Rapee, R. M., Schniering, C. A., & Hudson, J. L. (2009). Anxiety disorders
during childhood and adolescence: Origins and treatment. Annual Review of
Clinical Psychology, 5, 311–341.
Rapoport, J., & Shaw, P. (2008). Obsessive compulsive disorders. In M. Rutter
et al. (Eds.), Rutter’s child and adolescent psychiatry (fifth edition, pp. 698–
718). London: Blackwell.
Rapp, C., & Goscha, R. (2006). The strengths model: Case management
with people with psychiatric disabilities (second edition). New York: Oxford
University Press.
Rapp, C., & Goscha, R. (2008). Strengths-based case management. In K.
Mueser & D. Jeste (Eds.), Clinical handbook of schizophrenia (pp. 319–328).
New York: Guilford Press.
Rapport, M. & Moffitt, C. (2002). Attention deficit/hyperactivity disorder and
methylphenidate: A review of height/weight, cardiovascular, and somatic
complaint side effects. Clinical Psychology Review, 22, 1107–1131.
Read, J., & Bentall, R. (2010). The effectiveness of electroconvulsive therapy: A
literature review. Epidemiologia e Psichiatria Sociale, 19, 333–347.
Reichborn-Kjennerud, T. (2010). The genetic epidemiology of personality
disorders. Dialogues in Clinical Neuroscience, 12, 103–114.
Retz, W., Retz-Junginger, P., Supprian, T., Thome, J., & Rosler, M. (2004).
Association of serotonin transporter promoter gene polymorphism with
violence: Relation with personality disorders, impulsivity and childhood
ADHD psychopathology. Behavioural Sciences and the Law, 22, 415–425.
Rholes, S., & Simpson, J. (2004). Adult attachment: Theory, research, and
clinical implications. New York: Guilford.
Rietkerk, T., Boks, M. P. M., Sommer, I. E., Liddle, P. F., Ophoff, R. A., & Kahn,
R. S. (2008). The genetics of symptom dimensions of schizophrenia: Review
and meta-analysis. Schizophrenia Research, 102, 197–205.
Ritsner, M., & Gottesman, I. (2011). The schizophrenia construct after 100 years
of challenges. In M. Ritsner (Ed.), Handbook of schizophrenia spectrum
disorders, Volume I: Conceptual issues and neurobiological advances
(pp. 1–44). New York: Springer.
Robbins, M. S., Horigian, V., Szapocznik, J., & Ucha, J. (2010). Treating
Hispanic youths using brief strategic family therapy. In J. R. Weisz & A. E.
Kazdin (Eds.), Evidence-based psychotherapies for children and adolescents
(second edition, pp. 375–390). New York: Guilford Press.
Robbins, M. S., Szapocznik, J., & Horigian, V. E. (2009). Brief strategic family
therapy for adolescents with behaviour problems. In J. Bray & M. Stanton
(Eds.), The Wiley–Blackwell handbook of family psychology (pp. 416–430).
Chichester, UK: Wiley-Blackwell.

Book 1.indb 376 06/03/2012 13:48

 REFERENCES 377

Robins, L. (1966). Deviant children growing up. Baltimore: Williams and Wilkins.
Roe, D., & Davidson, L. (2008). Recovery. In K. Mueser & D. Jeste (Eds.),
Clinical handbook of schizophrenia (pp. 566–574). New York: Guilford Press.
Rosenhan, D. (1973). On being sane in insane places. Science, 179, 250–258.
Rosenthal, N. E. (2009). Issues for DSM-V: Seasonal affective disorder and
seasonality. American Journal of Psychiatry, 166, 852–853.
Rosenthal, R. (1994). Parametric measures of effect size. In H. Cooper and
L. Hedges (Eds.), The handbook of research synthesis (pp. 231–260).
New York: Sage.
Rosenthal., R., & Rubin, D. (1982). A simple, general purpose display of
magnitude of experimental effect. Journal of Educational Psychology, 74,
166–196.
Rosenzweig, S. (1936). Some implicit common factors in diverse methods of
psychotherapy: “At last the Dodo bird said, ‘Everybody has won and all must
have prizes.’” American Journal of Orthopsychiatry, 6, 412–415.
Roth, G., & Buchheim, A. (2010). Neurobiology of personality disorders. In J.
Clarkin, O. Fonagy, & G. Gabbard (Eds.). Psychodynamic psychotherapy
for personality disorders: A clinical handbook (pp. 89–124). Arlington, VA:
American Psychiatric Publishing.
Roth, T. (1998). Getting on clinical training courses. The Psychologist, 11(12),
589–592.
Roth, T. & Fonagy, P. (2005). What works for whom? A critical review of
psychotherapy research (second edition). London: Guilford.
Roth, T., & Leiper, R. (1995). Selecting for clinical training. The Psychologist,
8(1), 25–28.
Rothbart, M. K., & Bates, J. E. (2006). Temperament. In W. Damon & R. M.
Lerner (Series Eds.) & N. Eisenberg (Volume Ed.), Handbook of child
psychology, Volume 3: Social, emotional, and personality development (sixth
edition, pp. 99–166). New York: Wiley.
Rowe, D. L., Robinson, P. A., Lazzaro, I. L., Powles, R. C., Gordon, E., &
Williams, L. M. (2005). Biophysical modeling of tonic cortical electrical
activity in attention deficit hyperactivity disorder. International Journal of
Neuroscience, 115(9), 1273–1305.
Royal College of Psychiatrists (2005). The ECT handbook (second edition): The
third report of the Royal College of Psychiatrists’ Special Committee on ECT
(Council Report CR128). London: Royal College of Psychiatrists.
Rudd, D. N., Cordero, L., & Bryan, C. J. (2009). What every psychologist should
know about the Food and Drug Administration’s black box warning label
for antidepressants. Professional Psychology: Research and Practice, 40,
321–326.
Russell, G. (1979). Bulimia nervosa: An ominous variant of anorexia nervosa?
Psychological Medicine, 9, 429–448.
Sackett, D., Rosenberg, W., Gray, J., Haynes, R., & Richardson, W. (1996).
Evidence-based medicine: What it is and what it isn’t. British Medical Journal,
312, 71–72.
Sackett, D., Straus, S., Richardson, W., Rosenberg, W., & Haynes, R. (2000).
Evidence based medicine: How to practice and teach EBM (second edition).
London: Churchill Livingstone.
Saha, S., Chant, D., Welham, J., & McGrath, J. (2005). A systematic review of
the prevalence of schizophrenia. PLoS Medicine, 2, 413–433.
Sajatovic, M., Madhusoodanan, S., & Fuller, M. A. (2008). Clozapine. In K.
Mueser & D. Jeste (Eds.), Clinical handbook of schizophrenia (pp. 178–185).
New York: Guilford Press.

Book 1.indb 377 06/03/2012 13:48

 378 C L I N I C A L P S Y C H O L O G Y : A N I N T R O D U C T I O N

Salloum, A. (2010). Minimal therapist-assisted cognitive-behavioural therapy

interventions in stepped care for childhood anxiety. Professional Psychology:
Research and Practice, 41(1), 41–47.
Sammons, M., Paige, R., & Levant, R. (2003). Prescriptive authority for
psychologists: A history and guide. Washington, DC: American Psychological
Association.
Samuel, D. B., & Widiger, T. A. (2008). A meta-analytic review of the relationships
between the five-factor model and personality disorders: A facet level
analysis. Clinical Psychology Review, 28, 1326–1342.
Savla, G. N., Moore, D. J., & Palmer, B. W. (2008). Cognitive functioning. In K.
Mueser & D. Jeste (Eds.), Clinical handbook of schizophrenia (pp. 91–99).
New York: Guilford Press.
Sayette, M., Mayne, T., & Norcross, J. (2010). Insider’s guide to graduate
programs in clinical and counseling psychology: 2010/2011 (seventh edition).
New York: Guilford.
Scaife, J. (2010). Supervising the reflective practitioner: An essential guide to
theory and practice. London: Brunner-Routledge.
Schachar, R. (1991). Childhood hyperactivity. Journal of Child Psychology and
Psychiatry, 32, 155–191.
Scheier, L. (2010). Handbook of drug use etiology: Theory, methods, and
empirical findings. Washington, DC: American Psychological Association.
Schennach-Wolff, R., Seemuller, F., Musil, R., Spellmann, I. Holler, H., & Riedel,
M. (2011). Suicidality and the outcome of schizophrenia. In M. Ritsner (Ed.),
Handbook of schizophrenia spectrum disorders, Volume III: Therapeutic
approaches, comorbidity and outcome (pp. 365–382). New York: Springer.
Scherag, S., Hebebrand, J., & Hinney, A. (2010). Eating disorders: The
current status of molecular genetic research. European Child & Adolescent
Psychiatry, 19, 211–226.
Schmahl, C., & Bremner, J. D. (2006). Neuroimaging in borderline personality
disorder. Journal of Psychiatric Research, 40, 419–427.
Schneider, K. (1923). Die Psychopathischen Persönlichkeiten. Berlin: Springer.
Schuckit, M. (1994). Low level of response to alcohol as a predictor of future
alcoholism. American Journal of Psychiatry, 151, 184–189.
Schulteis, G., & Koob, G. (1996). Reinforcement processes in opiate addiction:
A homeostatic model. Neurochemical Research, 21, 1437–1454.
Schultz, D., & Schultz, S. (2008). Theories of personality (ninth edition). Belmont,
CA: Wadsworth.
Schwartz, S. J., Forthun, L. F., Ravert, R. D., Zamboanga, B. L., Umaña-Taylor,
A. J., & Filton, B. J. (2010). Identity consolidation and health risk behaviours
in college students. American Journal of Health Behaviour, 34, 214–224.
Scior, K., Gray, J., Halsey, R., & Roth, A. (2007). Selection for clinical
psychology training: Is there evidence of any bias against applicants from
ethnic minorities? Clinical Psychology Forum, 175, 7–11.
Scott, C. L., & Resnick, P. J. (2006). Violence risk assessment in persons with
mental illness. Aggression and Violent Behaviour, 11, 598–611.
Scott, S. (2009). Conduct disorders in childhood and adolescence. In M. Gelder
et al. (Eds.), New Oxford textbook of psychiatry (second edition, Vol. 2,
pp. 1654–1664). Oxford: Oxford University Press.
Seeman, P. (2011). All roads to schizophrenia lead to dopamine supersensitivity
and elevated dopamine D2 receptors. CNS Neuroscience & Therapeutics,
17, 118–132.
Segal, L. (1991). Brief therapy: The MRI approach. In A. Gurman & D. Kniskern
(Eds.), Handbook of family therapy (Vol. 2, pp. 17–199). New York: Brunner/
Mazel.

Book 1.indb 378 06/03/2012 13:48

 REFERENCES 379

Selvini Palazzoli, S. (1988). The work of Mara Selvini Palazzoli. New York:
Jason Aronson
Semkovska, M., & McLoughlin, D. M. (2010). Objective cognitive performance
associated with electroconvulsive therapy for depression: A systematic
review and meta-analysis. Biological Psychiatry, 68, 568–577.
Serpell, L., & Troup, N. (2003). Sociocultural theories of eating disorders. In J.
Treasure, U. Schmidt, & E. van Furth (Eds.), Handbook of eating disorders
(second edition, pp. 151–167). Chichester, UK: Wiley.
Sexton, T. L. (2009). Functional family therapy: Traditional theory to evidence-
based practice. In J. Bray & M. Stanton (Eds.), The Wiley–Blackwell handbook
of family psychology (pp. 327–340). Chichester, UK: Wiley-Blackwell.
Sexton, T., & Alexander, J. (2003). Functional family therapy: A mature clinical
model for working with at-risk adolescents and their families. In T. Sexton, G.
Weeks, & M. Robbins (Eds.), Handbook of family therapy (third edition, pp.
323–350). New York: Brunner-Routledge.
Shadish, W., & Baldwin, S. (2003). Meta-analysis of MFT interventions. Journal
of Marital and Family Therapy, 29, 547–570.
Shadish, W., Matt, G., Navarro, A., Siegle, G., Crits-Cristoph, P., Hazelrigg,
H., et al. (1997). Evidence that therapy works in clinically representative
conditions. Journal of Consulting Psychology, 65, 355–365.
Shaham, Y., & Hope, B. (2005). The role of neuroadaptations in relapse to drug
seeking. Nature Neuroscience, 8, 1437–1439.
Shapiro, D. A., & Shapiro, D. (1982). Meta-analysis of comparative therapy
outcome studies: A replication and refinement. Psychological Bulletin, 92,
581–604.
Shaw, P. (2010). The shape of things to come in attention deficit hyperactivity
disorder. American Journal of Psychiatry, 167(4), 363–365.
Shedler, J. (2010). The efficacy of psychodynamic psychotherapy. American
Psychologist, 65, 98–109.
Sherlin, L., Arns, M., Lubar, J., & Sokhadze, E. (2010). A position paper on
neurofeedback for the treatment of ADHD. Journal of Neurotherapy, 14(2),
66–78.
Shevlin, M., Houston, J. E., Dorahy, M. J., & Adamson, G. (2008). Cumulative
traumas and psychosis: An analysis of the national comorbidity survey and
the British psychiatric morbidity survey. Schizophrenia Bulletin, 34, 193–199.
Shibley-Hyde, J., Mezulis, A., & Abramson, L. (2008). The ABCs of depression:
Integrating affective, biological, and cognitive models to explain the
emergence of the gender difference in depression. Psychological Review,
115, 291–313
Shirk, S., & Karver, M. (2003). Prediction of treatment outcome from relationship
variables in child and adolescent therapy: A meta-analytic review. Journal of
Consulting and Clinical Psychology, 71, 452–464.
Shyn, S. I., & Hamilton, S. P. (2010). The genetics of major depression: Moving
beyond the monoamine hypothesis. Psychiatric Clinics of North America, 33,
125–140.
Siegel, A. B. (2010). Dream interpretation in clinical practice: A century after
Freud. Sleep Medicine Clinics, 5(2), 299–313.
Siever, L., & Davis, L. (1991). A psychobiological perspective on the personality
disorders. American Journal of Psychiatry, 148, 1647–1658.
Silverman, W. K., & Albano, A. M. (1996). The Anxiety Disorder Interview
Schedule for Children–IV–Child and Parent Version. Boulder, CO: Graywind.
Silvia, P. J., & Kaufman, J. C. (2010). Creativity and mental illness. In J. Kaufman
& R. Sternberg (Eds.), The Cambridge handbook of creativity (pp. 381–394).
New York: Cambridge University Press.

Book 1.indb 379 06/03/2012 13:48

 380 C L I N I C A L P S Y C H O L O G Y : A N I N T R O D U C T I O N

Singh, A. (2002). Recent and conceptualized basic research activities for eating
disorder: A review and future directions. International Medical Journal, 9,
83–85.
Skelton, R. (2006). The Edinburgh international encyclopaedia of psychoanalysis.
Edinburgh: Edinburgh University Press.
Skodol, A. E., Gunderson, J. G., Shea, M. T., McGlashan, T. H., Morey, L. C.,
Sanislow, C. A., et al. (2005). The Collaborative Longitudinal Personality
Disorders Study (CLPS). Journal of Personality Disorders, 19, 487–504.
Slade, M. (2009). Personal recovery and mental illness: A guide for mental
health professional. Cambridge, UK: Cambridge University Press.
Slade, M., Loftus, L., Phelan, M., Thornicroft, G., & Wykes, T. (1999). The
Camberwell Assessment of Need. London: Gaskell.
Smith, D. K., & Chamberlain, P. (2010). Multidimensional treatment foster care
for adolescents: Processes and outcomes. In J. R. Weisz & A. E. Kazdin
(Eds.), Evidence-based psychotherapies for children and adolescents
(second edition, pp. 243–258). New York: Guilford Press.
Smith, L., Gates, S., & Foxcroft, D. (2006). Therapeutic communities for substance
related disorder. Cochrane Database of Systematic Reviews, Issue 1, Art. No.
CD005338. Published inline. doi:10.1002/14651858.CD005338.pub2
Smith, M., & Glass, G. (1977). Meta-analysis of psychotherapy outcome studies.
American Psychologist, 32, 752–760.
Snyder, L. B., & Nadorff, P. G. (2010). Youth substance use and the media.
In L. Scheier (Ed.), Handbook of drug use etiology: Theory, methods, and
empirical findings (pp. 475–491). Washington, DC: American Psychological
Association.
Soeteman, D., Hakkaart-van Roijen, L., Verheul, R., & Busschbach, J. (2008).
The economic burden of personality disorders in mental health care. Journal
of Clinical Psychiatry, 69, 259–265.
Solanto, M. (1998). Neuropsychopharmacological mechanisms of stimulant drug
action in attention-deficit hyperactivity disorder: A review and integration.
Behavioural Brain Research, 94, 127–152.
Spoont, M. R. (1992). Modulatory role of serotonin in neural information
processing: Implications for human psychopathology. Psychological Bulletin,
112, 330–350.
Sprenkle, D., & Blow, A. (2004). Common factors and our sacred models.
Journal of Marital and Family Therapy, 30, 113–130.
Stampfl, T. G., & Levis, D. J. (1968). Implosive therapy—A behavioural therapy.
Behaviour Research and Therapy, 6, 31–36.
Stanley, B., & Brodsky, B. S. (2009). Dialectical behaviour therapy. In J. Oldham,
A. Skodol, & D. Bender (Eds.), Essentials of personality disorders (pp. 235–
252). Arlington, VA: American Psychiatric Publishing.
Starcevic, V., & Berle, D. (2006). Cognitive specificity of anxiety disorders: A
review of selected key constructs. Depression and Anxiety, 23, 51–61.
Steer, R., Beck, J., Beck, A., & Jolly, J. (2005). Beck Youth Inventories for
Children and Adolescents (second edition) (BYI-II). San Antonio, TX:
Psychological Corporation.
Stein, D., & Lambert, M. (1995). Graduate training in psychotherapy: Are
therapy outcomes enhanced? Journal of Consulting & Clinical Psychology,
63, 182–196.
Steinhausen, J. (2002). The outcome of anorexia nervosa in the 20th century.
American Journal of Psychiatry, 159, 1284–1293.
Stern, A. (1938). Psychoanalytic investigation of and therapy in the borderline
group of neuroses. Psychoanalytic Quarterly, 7, 467–489.

Book 1.indb 380 06/03/2012 13:48

 REFERENCES 381

Stevenson, J. (2010). Recent research on food additives: Implications for

CAMH. Child and Adolescent Mental Health, 15(3), 130–133.
Stewart, D. G., & Davis, K. L. (2008). Neuropathology. In K. Mueser & D. Jeste
(Eds.), Clinical handbook of schizophrenia (pp. 44–54). New York: Guilford
Press.
Stewart, S. E., Jenike, E., & Jenike, M. A. (2009). Biological treatment for
obsessive-compulsive disorder. In M. M. Antony & M. B. Stein (Eds.), Oxford
handbook of anxiety and related disorders (pp. 375–390). New York: Oxford
University Press.
Stice, E. (2002). Risk and maintenance factors for eating pathology: A meta-
analytic review. Psychological Bulletin, 825–848.
Stice, E., Agras, S., & Hammer, L. (1999). Risk factors for the development of
childhood eating disturbances: A five year prospective study. International
Journal of Eating Disorders, 25, 375–387.
Stiles, W., & Wolfe, B. (2006). Relationship factors in treating anxiety disorders.
In L. Castonguay & L. Beutler (Eds.), Principles of therapeutic change that
work (pp. 155–166). Oxford: Oxford University Press.
Still, G. (1902). The Coulstonian lectures on some abnormal physical conditions
in children, Lancet i, 1008–1012, 1077–1082, 1163–1169.
Strack, S. (2010). Evidence-based assessment and instrumentation for
personality disorders. In J. J. Magnavita (Ed.), Evidence-based treatment
of personality dysfunction: Principles, methods, and processes (pp. 19–48).
Washington, DC: American Psychological Association.
Strauss, A. & Lehtinen, L. (1947). Psychopathology and education of the brain-
injured child. New York: Grune & Stratton.
Striegel-Moore, R. H., & Bulik, C. M. (2007). Risk factors for eating disorders.
American Psychologist (Special Issue: Eating Disorders), 62(3), 181–198.
Sullivan, H. S. (1953). The interpersonal theory of psychiatry. New York: Norton.
Sullivan, P., Kendler, K., & Neale, M. (2003). Schizophrenia as a complex
trait—Evidence from a meta-analysis of twin studies. Archives of General
Psychiatry, 60, 1187–1192.
Sullivan, P., Neale, M., & Kendler, K. (2000). Genetic epidemiology of major
depression: Review and meta-analysis. American Journal of Psychiatry, 157,
1552–1562.
Sumner, J. A., Griffith, J., & Mineka, S. (2010). Overgeneral autobiographical
memory as a predictor of the course of depression: A meta-analysis.
Behaviour Research and Therapy, 48, 614–625.
Susman, E. J. (2006). Psychobiology of persistent antisocial behaviour: Stress,
early vulnerabilities and the attenuation hypothesis. Neuroscience and
Biobehavioural Reviews, 30, 376–389.
Svartberg, M., & McCullough, L. (2010). Cluster C personality disorders:
Prevalence, phenomenology, treatment effects, and principles of treatment.
In J. Clarkin, O. Fonagy, & G. Gabbard (Eds.), Psychodynamic psychotherapy
for personality disorders: A clinical handbook (pp. 337–368). Arlington, VA:
American Psychiatric Publishing.
Swanson, J. M., & Volkow, N. D. (2009). Psychopharmacology: Concepts and
opinions about the use of stimulant medications. Journal of Child Psychology
and Psychiatry, 50(1–2), 180–193.
Szasz, T. (2010). Psychiatry, anti-psychiatry, critical psychiatry: What do these
terms mean? Philosophy, Psychiatry, & Psychology, 17, 229–232.
Taft, C. T., Watkins, L. E., Stafford, J., Street, A. E., & Monson, C. M. (2011).
Posttraumatic stress disorder and intimate relationship problems: A meta-
analysis. Journal of Consulting and Clinical Psychology, 79, 22–33.

Book 1.indb 381 06/03/2012 13:48

 382 C L I N I C A L P S Y C H O L O G Y : A N I N T R O D U C T I O N

Tai, S., & Turkington, D. (2009). The evolution of cognitive behaviour therapy
for schizophrenia: Current practice and recent developments. Schizophrenia
Bulletin, 35, 865–873.
Tammenmaa, I. A., Sailas, E., McGrath, J. J., Soares-Weiser, K., & Wahlbeck,
K. (2004). Systematic review of cholinergic drugs for neuroleptic-induced
tardive dyskinesia: A meta-analysis of randomized controlled trials. Progress
in Neuro-Psychopharmacology & Biological Psychiatry, 28(7), 1099–1107.
Tandon, R., Keshavan, M. S., & Nasrallah, H. A. (2008a). Schizophrenia,
“just the facts”: What we know in 2008. Part 1: Overview. Schizophrenia
Research, 100, 4–19.
Tandon, R., Keshavan, M. S., & Nasrallah, H. A. (2008b). Schizophrenia, “just
the facts”: What we know in 2008. Part 2: Epidemiology and aetiology.
Schizophrenia Research, 102, 1–18.
Tandon, R., Nasrallah, H. A., & Keshavan, M. S. (2009). Schizophrenia, “just the
facts” 4. Clinical features and conceptualization. Schizophrenia Research,
110, 1–23.
Tandon, R., Nasrallah, H. A., & Keshavan, M. S. (2010). Schizophrenia, “just the
facts” 5. Treatment and prevention past, present and future. Schizophrenia
Research, 122, 1–23.
Tanofsky-Kraff, M., & Wilfley, D. E. (2010). Interpersonal psychotherapy for the
treatment of eating disorders. In W. S. Agras (Ed.), The Oxford handbook of
eating disorders (pp. 348–372). New York: Oxford University Press.
Taylor, E. (2008). Disorders of attention and activity. In M. Rutter et al. (Eds.),
Rutter’s child and adolescent psychiatry (fifth edition, pp. 521–542). London:
Blackwell.
Taylor, E., & Rogers, J. W. (2005). Practitioner review: Early adversity and
developmental disorders. Journal of Child Psychology and Psychiatry, 46(5),
451–467.
Teichner, G., & Golden, C. J. (2000). The relationship of neuropsychological
impairment to conduct disorder in adolescence: A conceptual review.
Aggression and Violent Behaviour, 5, 509–528.
Tenhula, W. N., & Bellack, A. S. (2008). Social skills training. In K. Mueser &
D. Jeste (Eds.), Clinical handbook of schizophrenia (pp. 240–248). New
York: Guilford Press.
Tevyaw, T., & Monti, P. (2004). Motivational enhancement and other brief
interventions for adolescent substance abuse: Foundations, applications and
evaluations. Addiction, 99, 63–75.
Thapar, A., & Scourfield, J. (2002). Childhood disorders. In P. McGuffin, M.
Owen, & I. Gottesman (Eds.), Psychiatric genetics and genomics (pp. 147–
180). Oxford: Oxford University Press.
Thapar, A., & Stergiakouli, E. (2008). An overview on the genetics of ADHD.
Acta Psychologica Sinica (Special Issue: Behavioural Genetics), 40(10),
1088–1098.
Thase, M. (2009). Neurobiological aspects of depression. In H. Gotlib &
C. Hammen (Eds.), Handbook of depression (second edition, pp. 187–217).
New York: Guilford Press.
Thase, M., & Jindal, R. (2004). Combining psychotherapy and pharmacotherapy
for treatment of mental disorders. In M. Lambert (Ed.), Bergin and Garfield’s
handbook of psychotherapy and behaviour change (fifth edition, pp. 743–
766). New York: Wiley.
Thompson, P., Vidal, C., Giedd, J., Gochman, P. Blumenthal, J., Nicolson, R.,
et al. (2001). Mapping adolescent brain change reveals dynamic wave of
accelerated gray matter loss in very early-onset schizophrenia. Proceedings

Book 1.indb 382 06/03/2012 13:48

 REFERENCES 383

of the National Academy of Sciences of the United States of America, 98,

11650–11655.
Thompson-Brenner, H., Glass, S., & Westen, D. (2003). A multidimensional
meta-analysis of psychotherapy for bulimia nervosa. Clinical Psychology:
Science and Practice, 10, 268–287.
Thompson-Brenner, H., Weingeroff, J., & Westen, D. (2009). Empirical support
for psychodynamic psychotherapy for eating disorders. In R. A. Levy & J. S.
Ablon (Eds.), Handbook of evidence-based psychodynamic psychotherapy:
Bridging the gap between science and practice (pp. 67–92). Totowa, NJ:
Humana Press.
Tomás, P., Fuentes, I., Roder, V., & Ruiz, J. (2010). Cognitive rehabilitation
programs in schizophrenia: Current status and perspectives international.
Journal of Psychology and Psychological Therapy, 10, 191–204.
Toplak, M. E., Connors, L., Shuster, J., Knezevic, B., & Parks, S. (2008). Review
of cognitive, cognitive-behavioural, and neural-based interventions for
attention-deficit/hyperactivity disorder (ADHD). Clinical Psychology Review,
28(5), 801–823.
Torgersen, S. (2009). Prevalence, sociodemographics, and functional impair-
ment. In J. Oldham, A. Skodol, & D. Bender (Eds.), Essentials of personality
disorders (pp. 83–102). Arlington, VA: American Psychiatric Publishing.
Toumbourou, J. W., Stockwell, T., Neighbors, C., Marlatt, G. A., Sturge, J., &
Rehm, J. (2007). Interventions to reduce harm associated with adolescent
substance use. The Lancet, 369(9570), 1391–1401.
Trauer, T., Tobias, G., & Slade, M. (2008). Development and evaluation of a
patient-rated version of the Camberwell Assessment of Need Short Appraisal
Schedule (CANSAS-P). Community Mental Health Journal, 44, 113–124.
Turner, E. H., Matthews, A. M., Linardatos, E., Tell, R. A., & Rosenthal, R.
(2008). Selective publication of antidepressant trials and its influence on
apparent efficacy. New England Journal of Medicine, 358, 252–260.
Udechuku, A., Nguyen, T., Hill, R., & Szego, K. (2010). Antidepressants in
pregnancy: A systematic review. Australian and New Zealand Journal of
Psychiatry, 44, 978–996.
US–UK Team (1974). The diagnosis and psychopathology of schizophrenia in
New York and London. Schizophrenia Bulletin, 1, 80–102.
Vahia, I. V., & Cohen, C. I. (2008). Psychopathology. In K. Mueser & D. Jeste (Eds.),
Clinical handbook of schizophrenia (pp. 82–90). New York: Guilford Press.
Van Ameringen, M., Mancini, C., & Patterson, B. (2009). Pharmacotherapy for
social anxiety disorder and specific phobia. In M. M. Antony & M. B. Stein
(Eds.), Oxford handbook of anxiety and related disorders (pp. 321–333).
New York: Oxford University Press.
van Goozen, S. H. M., Fairchild, G., & Harold, G. T. (2008). The role of
neurobiological deficits in childhood antisocial behaviour. Current Directions
in Psychological Science, 17(3), 224–228.
van Goozen, S. H. M., Fairchild, G., Snoek, H., & Harold, G. T. (2007). The
evidence for a neurobiological model of childhood antisocial behaviour.
Psychological Bulletin, 133(1), 149–182.
Vittengl, J., Clark, L., Dunn, T., & Jarrett, R. (2007). Reducing relapse and
recurrence in unipolar depression: A comparative meta-analysis of cognitive-
behavioural therapy. Journal of Consulting and Clinical Psychology, 75, 475–
488.
Vögele, C., & Gibson, E. L. (2010). Mood, emotions, and eating disorders. In
W. S. Agras (Ed.), The Oxford handbook of eating disorders (pp. 180–205).
New York: Oxford University Press.

Book 1.indb 383 06/03/2012 13:48

 384 C L I N I C A L P S Y C H O L O G Y : A N I N T R O D U C T I O N

Wade, T. D. (2010). Genetic influences on eating and the eating disorders. In

W. S. Agras (Ed.), The Oxford handbook of eating disorders (pp. 103–122).
New York: Oxford University Press.
Waldron, H. B., & Brody, J. L. (2010). Functional family therapy for adolescent
substance use disorders. In J. R. Weisz & A. E. Kazdin (Eds.), Evidence-
based psychotherapies for children and adolescents (second edition,
pp. 401–415). New York: Guilford Press.
Waldron, H. B., & Turner, C. W. (2008). Evidence-based psychosocial treatments
for adolescent substance abuse. Journal of Clinical Child and Adolescent
Psychology (Special Issue: Evidence-Based Psychosocial Treatments for
Children and Adolescents: A Ten Year Update), 37, 238–261.
Walker, E., Kestler, L. & Bollini, A. (2004). Schizophrenia: Aetiology and course.
Annual Review of Psychology, 55, 401–430.
Walker, E., Mittal, V., & Tessner, K. (2008). Stress and the hypothalamic pituitary
adrenal axis in the developmental course of schizophrenia. Annual Review of
Clinical Psychology, 4, 189–216.
Walton, K. E., Ormel, J., & Krueger, R. F. (2011). The dimensional nature of
externalizing behaviours in adolescence: Evidence from a direct comparison
of categorical, dimensional, and hybrid models. Journal of Abnormal Child
Psychology, 39, 553–561.
Wampold, B. (2001). The great psychotherapy debate: Models, methods, and
findings. Mahwah, NJ: Lawrence Erlbaum Associates.
Watson, D. (2009). Differentiating the mood and anxiety disorders: A quadripartite
model. Annual Review of Clinical Psychology, 5, 221–247.
Watson, H. J., & Rees, C. S. (2008). Meta-analysis of randomized, controlled
treatment trials for pediatric obsessive-compulsive disorder. Journal of Child
Psychology and Psychiatry, 49(5), 489–498.
Webster-Stratton, C., & Reid, M. J. (2010). The Incredible Years parents,
teachers, and children training series: A multifaceted treatment approach for
young children with conduct disorders. In J. R. Weisz & A. E. Kazdin (Eds.),
Evidence-based psychotherapies for children and adolescents (second
edition, pp. 194–210). New York: Guilford Press.
Wechsler, D. (2004a). Wechsler Intelligence Scale for Children. Fourth Edition
UK (WISC-IVuk). San Antonio, TX: Psychological Corporation.
Wechsler, D. (2004b). Wechsler Preschool and Primary Scale of Intelligence–III
UK (WPPSI-IIIuk). San Antonio, TX: Psychological Corporation.
Wechsler, D. (2005). Wechsler Individual Achievement Test–II UK (WIAT-IIuk).
San Antonio, TX: Psychological Corporation.
Wechsler, D. (2009). Wechsler Adult Intelligence Scale–Fourth Edition UK
(WAIS-IVuk). San Antonio, TX: Psychological Corporation.
Weeks, J. W., Heimberg, R. G., Fresco, D. M., Hart, T. A., Turk, C. L., Schnieier,
F. R., et al. (2005). Empirical validation and psychometric evaluation of
the Brief Fear of Negative Evaluation Scale in patients with social anxiety
disorder. Psychological Assessment, 17, 179–190.
Weinberg, W., Harper, C., & Brumback, R. (2002). Substance use and
abuse: Epidemiology, pharmacological considerations, identification and
suggestions towards management. In M. Rutter & E. Taylor (Eds.), Child
and adolescent psychiatry (fourth edition, pp. 437–454). Oxford: Blackwell.
Weissman, A., & Beck, A. (1978). Development and validation of the Dysfunc-
tional Attitudes Scale. Paper presented at AABT, Chicago. Scale is on pp.
100–104 of Williams, M. (1992). The Psychological treatment of depression
(second edition). London: Routledge.

Book 1.indb 384 06/03/2012 13:48

 REFERENCES 385

Weisz, J., Weiss, B., Alicke, M., & Klotz, M. (1987). Effectiveness of
psychotherapy with children and adolescents: A meta-analysis for clinicians.
Journal of Consulting and Clinical Psychology, 55, 542–549.
Weisz, J., Weiss, B., Han, S. & Granger, D. (1995). Effects of psychotherapy with
children and adolescents revisited: A meta-analysis of treatment outcome
studies. Psychological Bulletin, 117, 450–468.
West, R. (2006). Theory of addiction. Oxford: Blackwell.
Wetchler, J., & Piercy, F. (1996). Experiential family therapies. In F. Piercy et al.
(Eds.), Family therapy sourcebook (second edition, pp. 79–105). New York:
Guilford.
Widiger, T. A. (2008). Personality disorders. In J. Hunsley & E. J. Mash (Eds.), A
guide to assessments that work (pp. 413–435). New York: Oxford University
Press.
Widiger, T. A., & Mullins-Sweatt, S. N. (2010). Clinical utility of a dimensional
model of personality disorder. Professional Psychology: Research and
Practice, 41, 488–494.
Wieder, H. & Kaplan, E. (1969). Drug use in adolescents: Psychodynamic mean-
ing and pharmacological effect. Psychoanalytic Study of the Child, 24, 399.
Wierzbicki, M., & Pekarik, G. (1993). A meta-analysis of psychotherapy dropout.
Professional Psychology: Research & Practice, 24, 190–195.
Wikler, A. (1973). Dynamics of drug dependence. Archives of General
Psychiatry, 28, 611–616.
Williams, R. & Chang, S. (2000). A comprehensive and comparative review
of adolescent substance abuse treatment outcome. Clinical Psychology:
Science and Practice, 7, 138–166.
Williams, W. (2001). Relevant experience. The Psychologist, 14(4), 188–189.
Wills, T. A., & Ainette, M. G. (2010). Temperament, self-control, and adolescent
substance use: A two-factor model of etiological processes. In L. Scheier
(Ed.), Handbook of drug use etiology: Theory, methods, and empirical findings
(pp. 127–146). Washington, DC: American Psychological Association.
Wilson, G. (2010). Cognitive behavioural therapy for eating disorders. In
W. S. Agras (Ed.), The Oxford handbook of eating disorders (pp. 331–347).
New York: Oxford University Press.
Wilson, G., & Fairburn, C. (2007). Treatments for eating disorders. In P. Nathan
& J. Gorman (Eds.), A guide to treatments that work (third edition, pp. 579–
609). New York: Oxford University Press.
Winkelmann, K., Stefini, A., Hartmann, M., Geiser-Elze, A., Kromüller, A.,
Schenkenbach, C., et al. (2005). Efficacy of psychodynamic short-term
psychotherapy for children and adolescents with behavioural disorders.
Praxis der Kinderpsychologie und Kinderpsychiatrie, 54, 598–614.
Winter, D., & Viney, L. (2005). Personal construct psychotherapy: Advances in
theory, practice and research. London: Whurr.
Winters, K. (1991). Personal Experience Screening Questionnaire. Los Angeles:
Western Psychological Services.
Winters, K., & Henly, G. (1989). Personal Experience Inventory. Los Angeles:
Western Psychological Services.
Winters, K. C., Stinchfield, R. D., Opland, E., Weller, C., & Latimer, W. W.
(2000). The effectiveness of the Minnesota Model approach in the treatment
of adolescent drug abusers. Addiction, 95, 601–612.
Witkiewitz, K., & Marlatt, G. A. (2004). Relapse prevention for alcohol and drug
problems: That was zen, this is tao. American Psychologist, 59, 224–235.
Wolpe, J. (1969). The practice of behaviour therapy. New York: Pergamon
Press.

Book 1.indb 385 06/03/2012 13:48

 386 C L I N I C A L P S Y C H O L O G Y : A N I N T R O D U C T I O N

Woods, R., & Clare, L. (2008). Handbook of the clinical psychology of ageing
(second edition). Chichester, UK: Wiley.
Woody, S., & Ollendick, T. (2006). Technique factors in treating anxiety
disorders. In L. Castonguay & L. Beutler (Eds.), Principles of therapeutic
change that work (pp. 167–186). Oxford: Oxford University Press.
World Health Organization (1992). The ICD-10 Classification of Mental and
Behavioural Disorders. Geneva, Switzerland: WHO.
Xie, P., Kranzler, H., Poling, J., Stein, M., Anton, R., Brady, K., et al. (2009).
Interactive effect of stressful life events and the serotonin transporter
5-HTTLPR genotype on posttraumatic stress disorder diagnosis in
2 independent populations. Archives of General Psychiatry, 66, 1201–1209.
Yeomans, F. E., & Diamond, D. (2010). Transference-focused psychotherapy
and borderline personality disorder. In J. Clarkin, O. Fonagy, & G. Gabbard
(Eds.), Psychodynamic psychotherapy for personality disorders: A clinical
handbook (pp. 209–238). Arlington, VA: American Psychiatric Publishing.
Young, S., & Amarasinghe, J. M. (2010). Practitioner review: Non-
pharmacological treatments for ADHD: A lifespan approach. Journal of Child
Psychology and Psychiatry, 51(2), 116–133.
Zahradnik, M., & Stewart, S. H. (2009). Anxiety disorders and substance use
disorder comorbidity. In M. M. Antony & M. B. Stein (Eds.), Oxford handbook
of anxiety and related disorders (pp. 565–575). New York: Oxford University
Press.
Zajecka, J., & Goldstein, C. (2009). Combining medications to achieve remission.
In T. L. Schwartz & T. J. Petersen (Eds.), Depression: Treatment strategies
and management (second edition, pp. 54–100). London: Inform Healthcare.
Zgierska, A., Rabago, D., Chawla, N., Kushner, K., Koehler, R., & Marlatt, A.
(2009). Mindfulness meditation for substance use disorders: A systematic
review. Substance Abuse, 30, 266–294.
Ziguras, S., & Stuart, G. (2000). A meta-analysis of the effectiveness of mental
health case management over 20 years. Psychiatric Services, 51, 1410–
1421.
Zimmerman, M., Chelminski, I., & Young, D. (2008). The frequency of personality
disorders in psychiatric patients. Psychiatric Clinics of North America, 31,
405–420.
Zohar, J., Fostick, L. & Juven-Wetzler, E. (2009). Obsessive-compulsive
disorder. In M. Gelder et al. (Eds.), New Oxford textbook of psychiatry
(second edition, Vol. 1, pp. 765–774). Oxford: Oxford University Press.
Zubin, J., & Spring, B. (1977). Vulnerability: A new view of schizophrenia.
Journal of Abnormal Psychology, 86, 103–126.
Zuckerman, M. (2007). Sensation seeking and risky behaviour. Washington,
DC: American Psychological Association.

Book 1.indb 386 06/03/2012 13:48

 Index
A-CRA 113 anorexia nervosa 73–94; cognitive behavioural
abstinence violation effect assessment 90; case theories 153–6; coping
114 study 75–9; clinical strategies 151; course
addictive personality features 80–2; 145–6; DSM IV 127;
110 cognitive behavioural epidemiology 145–6;
ADHD 36–49, 105, 297; theories 85–7; family systems theory
assessment 47–8; controversies 92; 157–8; family therapy
case example 36–8; course 79; diagnostic 158; formulation
clinical features 39; criteria 74; DSM IV 129, 132, 135, 139,
cognitive behavioural 74; EDE 90; EDI 90; 160; GABA 148–9;
approaches 44–5; epidemiology 79; generalized anxiety
Connors Rating Scale family therapy 88–89; disorder 131–3;
47; controversies formulation 78, 91; genetics 147; HPA
68–9; DAWBA 47; genetics 83; ICD 10 74; axis 147; ICD 10 127;
diagnostic criteria 40; interpersonal therapy neurobiology 148–9;
diet 43; drug misuse 90; intervention 91–2; obsessive compulsive
105; epidemiology mood dysregulation 84; disorder (OCD)
39–41; executive psychoanalytic theories 137–40; panic disorder
function 45; formulation 84–5; risk factors 133–6; personality
38, 48; genetics 79–80; SSRI 84; traits 150; phobias
41–2; hypo-arousal starvation 84; stress 130–1; posttraumatic
44; methylphenidate 88; systemic theories stress disorder (PTSD)
43, 49; MTA 43; 87–90; TCA 84 136–7; psychoanalytic
neurofeedback 49; antidepressants 84, 149, theories 151–3; PTSD
neurotransmitter 161, 181, 201 136–7; risk factors
dysregulation 43; antipsychotic medication 145–6; separation
organic deficits 42–3; 227 anxiety disorder
parent training 49; antisocial personality 127–30; SSRI 149,
systemic theory disorder 254–6; case 161; stepped care
46–7; theories 41–47; example 255–6; 160–1; systematic
treatment 48–9 clinical features desensitization 130;
ADIS 159 254–5; neurobiology temperament 149–50;
adult mental health 7 267–8 treatment 160–2;
alcohol misuse, adolescent anxiety disorders 126–166; triangles of conflict
95–125 ADIS 159; assessment and person 153
alogia 208 159–60; attentional anxious avoidant
anakastic personality bias 150; clinical personality disorder
disorder 250 features 140–5; 250

Book 1.indb 387 06/03/2012 13:48

 388 I N D E X

ASEBA 65 260; clinical features factors 79–80; SSRI

assertive community 260 84; starvation 84;
treatment 236 avolition 208 stress 88; systemic
assessment, ADHD 47–8; theories 87–90;
anxiety disorders BDI 196 TCA 84
159–60; conduct behavioural theory of BYI 196
disorder 65–6; depression 190
depression 196; biological model 292–8; CAN 237
drug misuse 119–20; achievements 292–5; cannabis 110
eating disorders 90; assumptions 292; case example, ADHD
personality disorders limitations 295–8 36–8; conduct disorder
280; schizophrenia bipolar disorder 168, 176–7 49–54; depression
237–8 Bleuler’s theory of 169–72; drug misuse
attachment theory, schizophrenia 221, 233 96–9; eating disorders
conduct disorder 60–1; borderline personality 75–79; generalized
depression 185 disorder 256–7; case anxiety disorder 131–3;
attention deficit example 257; clinical OCD 137–40; panic
hyperactivity disorder features 256–7; disorder 133–6; PTSD
36–49; assessment dialectical behaviour 136–7; schizophrenia
47–8; case therapy 276–7; 208–13; separation
example 36–8; mentalization based anxiety disorder
clinical features 39; psychotherapy 274–5; 127–30; personality
cognitive behavioural neurobiology 266–7; disorders 248–263
approaches 44–5; transference focused case series 313
Connors Rating Scale psychotherapy 269–74 case studies 311–2
47; controversies BPRS 237 catatonic behaviour 208,
68–9; DAWBA 47; brief strategic family 213, 216
diagnostic criteria 40; therapy 115 catatonic schizophrenia 217
diet 43; drug misuse bulimia nervosa 73–94; CFI 238
105; epidemiology assessment 90; child abuse 300; conduct
39–41; executive case study 75–9; disorder 64; drug
function 45; formulation clinical features misuse 111; multiple
38, 48; genetics 80–2; cognitive personality disorder
41–2; hypo-arousal behavioural theories 241; personality
44; methylphenidate 85–7; controversies 92; disorders 268
43, 49; MTA 43; course 79; diagnostic child and adolescent mental
neurofeedback 49; criteria 74; drug health 6
neurotransmitter misuse 105; DSM childhood disorders 35–71
dysregulation 43; IV 74; EDE 90; EDI circadian rhythms 182
organic deficits 42–3; 90; epidemiology 79; classical conditioning, drug
parent training 49; family therapy 88–89; misuse 113
systemic theory 46–7; formulation 78, 91; classification 294;
treatment 48–9 genetics 83; ICD 10 74; depression 176–7;
attentional bias 150 interpersonal therapy drug misuse 99–101;
attributional style 90; intervention 91–2; schizophrenia 217
questionnaire 193 mood dysregulation 84; client-centred humanistic
avoidant personality psychoanalytic psychotherapy 305,
disorder, case example theories 84–5; risk 318

Book 1.indb 388 06/03/2012 13:48

 INDEX 389

clinical features, ADHD 39; cognitive remediation contamination, behaviour

anxiety disorders in schizophrenia problems 68
140–5; conduct 233 continuing professional
disorder 54–6; cognitive theory of development 5
depression 172–6; depression 190–3 controversies, ADHD 68–9;
drug misuse 101–5; common factors 322–7 clinical psychololgy
eating disorders 80–2; conduct disorder 49–68; 29–31; conduct
personality disorders antisocial personality disorder 68–9;
248–63; schizophrenia disorder 255; ASEBA depression 200–3;
213 65; assessment 65–6; drug misuse 121–2;
clinical psychology 1–33; attachment theory eating disorders 92;
adult mental health 7; 60–1; case example personality disorders
child and adolescent 49–54; child abuse 281–8; schizophrenia
mental health 6; 64; clinical features 239–44
clinical psychology 54–6; coercive family coping, anxiety disorders
training 9–27; process 62–3; cognitive 151; depression 185
continuing professional behavioural theory COPT 216
development 5; 61–63; controversies cue exposure treatment
controversies 29–31; 68–9; diagnostic criteria 113
intellectual disability 50–1; drug misuse cyclothymia 176
7–8; neuropsychology 105; executive function
8; older adults 7; related 59–60; formulation DAWBA 47, 196
professions 27–9; roles 54, 66; genetics defence mechanisms
3–9; the discipline 56; hypoarousal 271–2
2; the profession 2; 58–9; intervention delusions 207–8, 213–15,
training 9–27 66–8; modelling 231–2
coercive family process 62; multisystemic dementia praecox 221
62–3 ecological theory 64–5; dependent personality
cognitive behavioural multisystemic therapy disorder 260–1; case
model 300–303; 65; neuroanatomical example 261; clinical
achievements 301–2; abnormalities 57; features 260–1
assumptions 300–1; neuropsychological depression 167–206;
limitations 302–3 deficits 59–60; antidepressants 181,
cognitive behaviour therapy neurotransmitter 201; assessment
(CBT) 61–63; 300–3; dysregulation 57–8; 196; attachment 185;
318–9; ADHD 44–5; psychoanalysis 60; BDI 196; behavioural
anxiety disorders psychodynamic theory 190; case
153–6; conduct theories 60–1; SDQ example 169–72;
disorder 61–63; 65; social information circadian rhythms 182;
depression 189–94; processing 61–2; classification 176–7;
drug misuse 112–14; social skills 62; clinical features 172–6;
eating disorders 85–7; sociological theory 64; cognitive behavioural
personality disorders systems theory 63–4; theories 189–94;
276–8; schizophrenia temperament 59 cognitive bias 185;
230–2 Connors Rating Scale cognitive theory 190–3;
cognitive bias, anxiety 47 controversies 200–3;
disorders 150; constructivist coping 185; course
depression 185 psychotherapy 305–6 177–8; cyclothymia

Book 1.indb 389 06/03/2012 13:48

 390 I N D E X

176; diagnostic criteria of conflict and person classical conditioning

168; DSM IV 168; 189 113; classification
dysthymia 176; ECT derailment 215 99–101; clinical
201–2; endogenous deterioration 321 features 101–5;
depression 177; diagnostic criteria, ADHD, cognitive behavioural
epidemiology 177–8; 40; conduct disorder, theories 112–14;
executive function 185; 50–1; depression controversies 121–2;
expressed emotion 168; drug misuse cue exposure treatment
186; family therapy 100; eating disorders 113; dependence
195; formulation 172, 74; oppositional syndrome 100;
197; gender 202–3; defiant disorder 50–1; diagnostic criteria
genetics 179–80; schizophrenia 209 100; disease model
HPA axis 181–2; dialectical behaviour 106; DSM IV 100;
HRS 196; ICD 10 therapy for borderline dual diagnosis 105;
168; interpersonal personality disorder epidemiology 99–101;
style 185–6; learned 276–7 family therapy 115;
helplessness 193–4; diathesis stress theory formulation 97, 120;
MAOI 181; masked 292, 296; personality functional family
depression 177; disorders 263; therapy 115; GAIN
meloncholia172–3; schizophrenia 219, 119; genetics 107; ICD
mentalizing 189; 227–8 10 100; identity 112;
mindfulness 200; diet, ADHD 43–4 learning difficulties
neurobiology 180; dimensional approaches 111–12; methadone
neurotic depression 296; childhood 110; motivational
177; neurotransmitters disorders 68–9; interviewing 114;
180–1; Penn Resiliency personality disorders multidimensional
Programme 193; 281–3; schizophrenia family therapy 115;
personality traits 221, 240–1 multisystemic therapy
184–5; psychoanalytic disease model 292; drug 115; Narcotics
theory 186–9; psychotic misuse 106 Anonymous 106,
depression 173, 177; disorganized schizophrenia 121; neurobiology
reactive depression 217 108–10; norms 117;
177; risk assessment dissocial personality operant conditioning
196–9; risk factors disorder 250 112–13; peer group
177–8; SCID 196; dissociative identity 116; PRIME 118–19;
seasonal affective disorder 241–2 risk factors 99–102;
disorder 168, 182; dopamine hypothesis of schizophrenia 219–20;
self-harm 176; sleep schizophrenia 224–5 self-medication 111;
182; social skills dopamine-2 antagonists sexual abuse 111;
186; sociotropy 184, drop-out from social disadvantage
186; SSRI 181, 201; psychotherapy 321 116; stages of change
stepped care 200; drug misuse 95–125; 117; stress 111;
stress 182–3; suicide A-CRA 113; abstinence substance dependence
176, 196–9; system violation effect 114; 100; systemic theories
theory 194–5; TCA addictive personality 114–117; temperament
181, 201; temperament 110; ADHD 105; 107–8; treatment
183–4; treatment assessment 119–20; 119; twelve steps of
199–200; triangles case study 96–9; Narcotics Anonymous

Book 1.indb 390 06/03/2012 13:48

 INDEX 391

106; wilderness therapy depression 177–8; foster care 67

108 drug misuse 99–101; functional family therapy
DSM IV 294; ADHD 40; eating disorders 79; 67, 115
anxiety disorders 127; oppositional defiant
conduct disorder, disorder 56; personality GABA 148–9
50–1; depression disorders 263–4; GAF 237
168; drug misuse schizophrenia 218 GAIN 119
100; eating disorder evidence-based practice generalized anxiety
74; multiaxial system 311 disorder (GAD) 131–3
248; oppositional executive function 59–60; genetics, ADHD 41–2;
defiant disorder 50–1; ADHD 45; conduct anxiety disorders 147;
schizophrenia 209 disorder 59–60; conduct disorder 56;
dual diagnosis 105 depression 185; depression 179–80;
dysthymia 176 schizophrenia 215, drug misuse 107;
224 eating disorders 83;
eating disorders 73–94; expressed emotion, personality disorders
assessment 90; case depression 186; 265–6; schizophrenia
study 75–9; clinical schizophrenia 212, 222–3
features 80–2; cognitive 220, 228, 238 glutamate hypothesis
behavioural theories eye movements 224 of schizophrenia
85–7; controversies 92; 224–6
course 79; diagnostic family systems model
criteria 74; DSM IV 303–5; achievements hallucinations 207–8,
74; EDE 90; EDI 90; 304–5; assumptions 213–14, 231
epidemiology 79; 303–4; limitations HCR-20 279
family therapy 88–9; 305 hebephrenic schizophrenia
formulation 78, 91; family therapy 303–5, 319; 216–17
genetics 83; ICD 10 74; anxiety disorders 158; histrionic personality
interpersonal therapy conduct disorders 67; disorder, case example
90; intervention 91–2; depression 195; drug 258; clinical features
mood dysregulation 84; misuse 115; eating 257–8
psychoanalytic theories disorders 88–89; HIV/AIDS 216
84–5; risk factors 79– schizophrenia 229–30 HPA axis 181–2; anxiety
80; SSRI 84; starvation formulation, ADHD 38, 48; disorders 147;
84; stress 88; systemic anxiety disorders 129, schizophrenia 220,
theories 87–90; TCA 84 132, 135, 139, 160; 228, 230
ECT 201–2, 297 conduct disorder 54, HRS 196
EDE 90 66; depression 172, hypoarousal 44, 58–9
EDI 90 197; drug misuse 97,
EEG 224 120; eating disorders ICD 10 204; ADHD 40;
effectiveness studies 316–7 78, 91; generalized anxiety disorders 127;
efficacy studies 316–7 anxiety disorder conduct disorder,
endogenous depression 132; OCD 139; 50–1; depression
177 panic disorder 135; 168; drug misuse
epidemiology, ADHD psychoanalytic 153; 100; eating disorders
39–41; anxiety schizophrenia 212, 74; oppositional
disorders 145–6; 238; separation anxiety defiant disorder 50–1;
conduct disorder 56; disorder 129 schizophrenia 209

Book 1.indb 391 06/03/2012 13:48

 392 I N D E X

identity 112 psychoanalytic model 148–9; conduct

intellectual disability 7–8 298–300 disorder 57–8;
interpersonal style 185–6 motivational interviewing depression 180–1;
interpersonal therapy 90 114 eating disorders 84;
IPDE 280 MTA trail 43 personality disorders
multiaxial system 248 266–8; schizophrenia
Kraepelin’s theory of multidimensional family 224
schizophrenia 221, 233 therapy 115
multimodal treatment 310; obsessive compulsive
learned helplessness ADHD 48; depression disorder (OCD)
193–4 200; schizophrenia 137–40, 287
learning difficulties 111–12 228–9 obsessive compulsive
LSD 110 multiple personality personality disorder,
disorder 241–2, 250 case example 26–32;
MAOI 181 multisystemic therapy clinical features 261–2;
marital therapy 278, 319 (MST) 65, 115 genetics 268
masked depression 177 obstetric complications 223
MCMI 279 narcissistic personality older adults 7
MDMA 110 disorder, case example operant conditioning, drug
medical cost offset 259; clinical features misuse 112–13
321–2 258–9 oppositional defiant
medical model 292 Narcotics Anonymous 106, disorder 49–68
melancholia 172–3 121
mentalizing, depression negative symptoms of panic disorder 133–6
189; borderline schizophrenia 207–8, PANSS 237
personality disorder 217, 232 paranoid personality
274–5 NEO-PI 280 disorder 217, 250–2;
meta-analysis 314–16 neologisms 215 case example 250–2;
methadone 110 neurobiological model 292 clinical features 250
methylphenidate 43 neurobiology, ADHD 42–3; paranoid schizophrenia 217
mindfulness 200 anxiety disorders parent training, ADHD 49;
MMPI 279 148–9; conduct oppositional defiant
modelling 62 disorder 57; drug use disorder 67
models of clinical 108–10; depression PCL 279
psychology 291–309; 180; eating disorders peer group, drug misuse
biological model 84; personality 116
292–8; client-centred disorders 266–8; PEI 119
humanistic model schizophrenia 224 Penn Resiliency
305; cognitive neurodevelopmental Programme 193
behavioural model hypothesis of personality disorders
300–3; constructivist schizophrenia 219, 223 247–90; anakastic
psychotherapy 305–6; neurofeedback 49 personality disorder
disease model 292; neuropsychology 8, 250; antisocial
family systems model conduct disorder 59–60 personality disorder
303–5; medical model neurotic depression 177 254–6; anxious
292; neurobiological neurotransmitter avoidant personality
model 292; positive dysregulation, ADHD disorder 250;
psychology 306; 43; anxiety disorders assessment 280;

Book 1.indb 392 06/03/2012 13:48

 INDEX 393

avoidant personality 266–8; obsessive assumptions 298–9;

disorder 260; borderline compulsive personality conduct disorder
personality disorder disorder 261–3; 60–1; depression
256–7; case examples paranoid personality 186–9; eating disorders
248–263; child abuse disorder 250–2; PCL 84–5; limitations
268; clinical features 279; personality traits 300; personality
248–63; cluster A, odd 281–3; psychotherapy disorders 269–76;
eccentric 250–4; cluster 269–78, 80–1; psychotherapy, 14,
B, dramatic, emotional, risk assessment, 28, 152–3, 161,188–9,
erratic 254–9; cluster violence 278; schizoid 199–200, 243–4,
C, anxious, fearful personality disorder 269–76, 298–300, 305,
259–63; cognitive 252–3; schizotypal 310–29; schizophrenia
behaviour therapy personality disorder 243–4
277–8; conduct 253–4; SCID II 280; psychosis 207–46
disorder and antisocial SNAP 279; stress psychotherapy, 14, 28,
personality disorder 268; temperament 152–3, 161,188–9,
255; controversies 265; therapeutic 199–200, 243–4,
281–8; defence communities 287; 269–76, 299–300, 305,
mechanisms 271–2; transference focused 310–29
dependent personality psychotherapy for psychotic depression 173,
disorder 260–1; borderline personality 177
dialectical behaviour disorder 269–74; PTSD 111, 136–7
therapy for borderline triangles of conflict and
personality disorder person 275–6 randomized controlled trials
276–7; diathesis stress personality traits, anxiety 313–4
theory 263; dimensional disorders 150; reactive depression 177
approaches 281–3; depression 184–5; recovery model 234–5, 238
dissocial personality personality disorders reward system 108–9
disorder 250; DSM 281–3; schizophrenia risk assessment,
IV multiaxial system 240 suicide196–9; violence
248; epidemiology PESQ 119 278
263–4; genetics 265–6; phobias 130–1 risk factors, anxiety
HCR-20 279; histrionic placebo 323 disorders 145–6;
personality disorder positive psychology 306 depression 177–8;
257–8; IPDE 280; positive symptoms of drug misuse 99–102;
marital therapy 278; schizophrenia 207–8, eating disorders 79–80;
MCMI 279; medication 217 schizophrenia 218–20
269; mentalization posttraumatic stress
based psychotherapy disorder (PTSD) 136–7 schizoaffective disorder 217
for borderline PRIME 118–19 schizoid personality
personality disorder prodromal phase, disorder 217, 252–3;
274–5; MMPI 279; schizophrenia 215 case example 253;
multiaxial system 248; psychoanalytic/ clinical features 252–3
multiple personality psychodynamic schizophrenia 217, 207–46,
disorder 241, 250; model 60–1, 243–4, 283, 296; alogia
narcissistic personality 298–300; achievements 208; antipsychotic
disorder 258–9; NEO- 299–300; anxiety medication 227;
PI 280; neurobiology disorders 151–3; assertive community

Book 1.indb 393 06/03/2012 13:48

 394 I N D E X

treatment 236; ICD 10 209; Kraepelin’s self-harm 176

assessment 237–8; theory 221, 233; self-medication 111
avolition 208; Bleuler’s multimodal intervention separation anxiety disorder
theory 221, 233; case 228–9; negative 127–30, 286
example 208–13; symptoms 207–8, sexual abuse 111, 300
catatonic behaviour 217, 232; neologisms sleep, depression 182;
208, 213, 216; 215; neuroanatomical schizophrenia 224
catatonic schizophrenia abnormalities 224; SNAP 279
217; classification neurodevelopmental social disadvantage 116
217; clinical features hypothesis 219, 223; social information
213; cognitive neurotransmitters 224; processing 61–2
behaviour therapy obstetric complications social skills, conduct
230–2; cognitive 223; paranoid disorder 62; depression
remediation 233; schizophrenia 217; 186; schizophrenia 233
controversies 239–44; positive symptoms sociotropy 184, 186
course 218; delusions 207–8, 217; split-personality 241–2
207–8, 213–15, 231–2; prodromal phase 215; SSRI 84, 149, 161, 181,
dementia praecox psychoanalysis 243–4; 201
221; derailment 215; recovery model 234–5, stages of change 117
diagnostic criteria 238; risk factors 218– starvation 84
209; diathesis- 20; sleep 224; social stepped care, anxiety
stress theory 219, skills training 233; disorders 160–1;
227–8; dimensional strengths based case depression 200
approach 221, 240–1; management 235–6; strengths based case
disorganization 207–8, stress 227–8; stress management 235–6
217; disorganized vulnerability theory stress 297; depression
schizophrenia 217; 227–8; substance use 182–3; drug misuse
dissociative identity 219–20; treatment 111; eating disorders
disorder 241–2; 239; two syndrome 88; personality
dopamine hypothesis hypothesis 226, 233; disorders 268;
224–5; dopamine-2 vocational rehabilitation schizophrenia 227–8
antagonists; DSM IV 234 stress vulnerability theory
209; epidemiology schizophrenia spectrum 227–8, 292
218; executive disorders 217 substance use 95–125;
function 215, 224; schizophreniform disorder A-CRA 113; abstinence
expressed emotion 217 violation effect 114;
212, 220, 228, 238; schizotypal personality addictive personality
eye movements 224; disorder 217, 253–4; 110; ADHD 105;
family therapy 229–30; case example 253–4; assessment 119–20;
formulation 212, clinical features 253; case study 96–9;
238; genetics 222–3; neurobiology 266 classical conditioning
glutamate hypothesis schizotypy 240 113; classification
224–6; hallucinations SCID 196 99–101; clinical
207–8, 213–14, SCID 237 features 101–5;
231; hebephrenic SCID II 280 cognitive behavioural
schizophrenia 216–17; SDQ 65 theories 112–14;
HIV/AIDS 216; HPA seasonal affective disorder controversies 121–2;
axis 220, 228, 230; 168, 182 cue exposure treatment

Book 1.indb 394 06/03/2012 13:48

 INDEX 395

113; dependence 117; stress 111; borderline personality

syndrome 100; substance dependence disorder 269–74
diagnostic criteria 100; systemic theories treatment, ADHD 48–9;
100; disease model 114–117; temperament anxiety disorders
106; DSM IV 100; 107–8; treatment 160–2; conduct
dual diagnosis 105; 119; twelve steps of disorder 66–8;
epidemiology 99–101; Narcotics Anonymous depression 199–200;
family therapy 115; 106; wilderness drug misuse 119;
formulation 97, 120; therapy 108 eating disorders 91–2;
functional family suicide 176, 196–9, 294 personality disorders
therapy 115; GAIN system theory 303–5, 280–1; schizophrenia
119; genetics 107; 319; ADHD 46–7; 239
ICD 10 100; identity conduct disorder 63–4, triangles of conflict and
112; learning difficulties depression 194–5; person, anxiety
111–12; methadone drug misuse 114–117; disorders 153;
110; motivational eating disorders 87–90 depression 189;
interviewing 114; systematic desensitization personality disorders
multidimensional 130 275–6
family therapy 115; twelve steps of Narcotics
multisystemic therapy talking cure 300 Anonymous 106
115; Narcotics TCA 84, 181, 201 two syndrome hypothesis
Anonymous 106, temperament 59; anxiety of schizophrenia
121; neurobiology disorders 149–50; 226, 233
108–10; norms 117; conduct disorder 59;
operant conditioning depression 183–4; unconscious 298–9
112–13; peer group drug misuse 107–8;
116; PRIME 118–19; personality disorders violence 278
risk factors 99–102; 265 vocational rehabilitation 234
schizophrenia 219–20; therapeutic communities
self-medication 111; 287 WIAT-II47
sexual abuse 111; transference 298–9 wilderness therapy 108
social disadvantage transference focused WISC-IV 47
116; stages of change psychotherapy for WPPSI-III 47

Book 1.indb 395 06/03/2012 13:48

Book 1.indb 396 06/03/2012 13:48
Book 1.indb 397 06/03/2012 13:48
Book 1.indb 398 06/03/2012 13:48